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Monitoring Changes in Attitudes and Practices among Family Planning Providers and Clinics

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Morbidity and Mortality Weekly Report
www.cdc.gov/mmwr

Recommendations and Reports

June 18, 2010 / Vol. 59 / No. RR-4

U.S. Medical Eligibility Criteria for
Contraceptive Use, 2010
Adapted from the World Health Organization
Medical Eligibility Criteria for Contraceptive Use, 4th edition

Continuing Education Examination available at http://w ww.cdc.gov/mmwr/cme/conted.html

department of health and human services
Centers for Disease Control and Prevention

MMWR

The MMWR series of publications is published by the Oﬃce of
Surveillance, Epidemiology, and Laboratory Services, Centers for
Disease Control and Prevention (CDC), U.S. Department of Health
and Human Services, Atlanta, GA 30333.
Suggested Citation: Centers for Disease Control and Prevention.

[Title]. MMWR 2010;59(No. RR-#):[inclusive page numbers].

CONTENTS

Introduction .............................................................................. 1
Methods ................................................................................... 2
How to Use This Document ......................................................... 2
Using the Categories in Practice............................................... 3
Recommendations for Use of Contraceptive Methods ................. 3

Centers for Disease Control and Prevention
Thomas R. Frieden, MD, MPH
Director
Peter A. Briss, MD, MPH
Acting Associate Director for Science
James W. Stephens, PhD
Oﬃce of the Associate Director for Science
Stephen B. Thacker, MD, MSc
Deputy Director for
Surveillance, Epidemiology, and Laboratory Services
Editorial and Production Staff
Frederic E. Shaw, MD, JD
Editor, MMWR Series
Christine G. Casey, MD
Deputy Editor, MMWR Series
Teresa F. Rutledge
Managing Editor, MMWR Series
David C. Johnson
Lead Technical Writer-Editor
Karen L. Foster, MA
Project Editor
Martha F. Boyd
Lead Visual Information Specialist
Malbea A. LaPete
Stephen R. Spriggs
Terraye M. Starr
Visual Information Specialists
Quang M. Doan, MBA
Phyllis H. King
Information Technology Specialists
Editorial Board
William L. Roper, MD, MPH, Chapel Hill, NC, Chairman
Virginia A. Caine, MD, Indianapolis, IN
Jonathan E. Fielding, MD, MPH, MBA, Los Angeles, CA
David W. Fleming, MD, Seattle, WA
William E. Halperin, MD, DrPH, MPH, Newark, NJ
King K. Holmes, MD, PhD, Seattle, WA
Deborah Holtzman, PhD, Atlanta, GA
John K. Iglehart, Bethesda, MD
Dennis G. Maki, MD, Madison, WI
Patricia Quinlisk, MD, MPH, Des Moines, IA
Patrick L. Remington, MD, MPH, Madison, WI
Barbara K. Rimer, DrPH, Chapel Hill, NC
John V. Rullan, MD, MPH, San Juan, PR
William Schaﬀner, MD, Nashville, TN
Anne Schuchat, MD, Atlanta, GA
Dixie E. Snider, MD, MPH, Atlanta, GA
John W. Ward, MD, Atlanta, GA

Contraceptive Method Choice.................................................. 4
Contraceptive Method Effectiveness.......................................... 4
Unintended Pregnancy and Increased Health Risk ..................... 4
Keeping Guidance Up to Date .................................................... 4
Appendices
A. Summary of Changes from WHO MEC to U.S. MEC ............ 7
B. Combined Hormonal Contraceptives .................................. 11
C. Progestin-Only Contraceptives........................................... 34
D. Emergency Contraceptive Pills ........................................... 50
E. Intrauterine Devices........................................................... 52
F. Copper IUDs for Emergency Contraception.......................... 64
G. Barrier Methods ............................................................... 65
H. Fertility Awareness–Based Methods ................................... 71
I. Lactational Amenorrhea Method ......................................... 73
J. Coitus Interruptus (Withdrawal) .......................................... 74
K. Sterilization...................................................................... 75
L. Summary of Hormonal Contraceptives and IUDs.................. 76
M. Potential Drug Interactions: Hormonal Contraceptives
and Antiretroviral Drugs ..................................................... 82
Abbreviations and Acronyms ................................................... 84
Participants ............................................................................. 85

Disclosure of Relationship

CDC, our planners, and our presenters wish to disclose they have
no ﬁnancial interests or other relationships with the manufacturers
of commercial products, suppliers of commercial services, or commercial supporters.
This document will not include any discussion of the unlabeled use
of a product or a product under investigational use, with the exception that some of the recommendations included in this document
may be inconsistent with package labeling.
There was no commercial support for this activity.

Vol. 59 / RR-4

Recommendations and Reports

U S. Medical Eligibility Criteria for Contraceptive Use, 2010
Adapted from the World Health Organization Medical Eligibility Criteria
for Contraceptive Use, 4th edition
Prepared by
Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion

Summary
CDC created U.S. Medical Eligibility Criteria for Contraceptive Use, 2010, from guidance developed by the World Health
Organization (WHO) and ﬁnalized the recommendations after consultation with a group of health professionals who met in
Atlanta, Georgia, during February 2009. This guidance comprises recommendations for the use of speciﬁc contraceptive methods by
women and men who have certain characteristics or medical conditions. The majority of the U.S. guidance does not diﬀer from the
WHO guidance and covers >60 characteristics or medical conditions. However, some WHO recommendations were modiﬁed for
use in the United States, including recommendations about contraceptive use for women with venous thromboembolism, valvular
heart disease, ovarian cancer, and uterine ﬁbroids and for postpartum and breastfeeding women. Recommendations were added
to the U.S. guidance for women with rheumatoid arthritis, history of bariatric surgery, peripartum cardiomyopathy, endometrial
hyperplasia, inﬂammatory bowel disease, and solid organ transplantation. The recommendations in this document are intended
to assist health-care providers when they counsel women, men, and couples about contraceptive method choice. Although these
recommendations are meant to serve as a source of clinical guidance, health-care providers should always consider the individual
clinical circumstances of each person seeking family planning services.

Introduction
In 1996, the World Health Organization (WHO) published the ﬁrst edition of the Medical Eligibility Criteria for
Contraceptive Use (MEC), which gave evidence-based guidance
on the safety of contraceptive method use for women and
men worldwide who had speciﬁc characteristics and medical
conditions. Since that time, WHO has regularly updated its
guidance on the basis of new evidence, and the WHO MEC
is now in its fourth edition (1).
CDC, through close collaboration with WHO, has contributed substantially during the last 15 years to creation of
WHO’s global family planning guidance, which includes four
documents: the medical eligibility criteria for contraceptive
use, the selected practice recommendations for contraceptive
use, a decision-making tool for clients and providers, and a
global family planning handbook. This WHO guidance has
been based on the best available scientiﬁc evidence, and CDC
has served as the lead for establishing that evidence base and
presenting the evidence to WHO for use during its expert
working group meetings to create and update the guidance.
WHO has always intended for its global guidance to be used
by local or regional policy makers, managers of family planning
Corresponding preparer: Kathryn M. Curtis, PhD, Division of
Reproductive Health, CDC, MS K-34, 4770 Buford Highway NE,
Atlanta, GA 30341; Telephone 770-488-6397; Fax: 770-488-6391;
E-mail [email protected]

programs, and the scientiﬁc community as a reference when
they develop family planning guidance at the country or program level. The United Kingdom is one example of a country
that has adapted the WHO MEC for its own use (2).
CDC undertook a formal process to adapt the WHO MEC
at this time because the fourth edition of the WHO guidance is
unlikely to undergo major revisions in the near future. Although
the WHO guidance is already available in the United States
through inclusion in textbooks, use by professional organizations,
and incorporation into training programs, the adaptation of the
guidance ensures its appropriateness for use in the United States
and allows for further dissemination and implementation among
U.S. health-care providers. Most of the U.S. guidance does not
diﬀer from the WHO guidance and covers approximately 60 characteristics or medical conditions. However, several changes have
been made, including adaptations of selected WHO recommendations, addition of recommendations for new medical conditions,
and removal of recommendations for contraceptive methods not
currently available in the United States (Appendix A).
This document contains recommendations for health-care
providers for the safe use of contraceptive methods by women
and men with various characteristics and medical conditions. It is
intended to assist health-care providers when they counsel women,
men, and couples about contraceptive method choice. These
recommendations are meant to be a source of clinical guidance;
health-care providers should always consider the individual
clinical circumstances of each person seeking family planning
services.

MMWR

Methods
The process for adapting the WHO MEC for the United
States comprised four major steps: 1) determination of the
scope of and process for the adaptation, including a small
meeting; 2) preparation and peer review of systematic reviews
of the evidence to be used for the adaptation; 3) organization
of a larger meeting to examine the evidence and provide input
on the recommendations; and 4) ﬁnalization of the recommendations by CDC.
In June 2008, CDC held a 2-day meeting of eight key
partners and U.S. family planning experts to determine the
scope of and process for a U.S. adaptation of the WHO MEC.
Participants were family planning providers, who also had
expertise in conducting research on contraceptive safety and
translating research evidence into guidance. WHO guidance is
used widely around the world, including in the United States,
and contains approximately 1,800 separate recommendations.
In most cases, the evidence base would be the same for the
U.S. and the WHO recommendation, and—because of the
extensive collaboration between WHO and CDC in creating
the international guidance—the process for determining the
recommendations also would be the same. Therefore, CDC
determined that the global guidance also should be the U.S.
guidance, except when a compelling reason existed for adaptation, and that CDC would accept the majority of WHO
guidance for use in the United States.
During the June 2008 meeting, CDC identiﬁed speciﬁc
WHO recommendations for which a compelling reason
existed to consider modiﬁcation for the United States because
of the availability of new scientiﬁc evidence or the context in
which family planning services are provided in the United
States. CDC also identiﬁed areas in which WHO guidance
was inconsistent with current U.S. practice by contacting
numerous professional and service organizations and individual
providers. In addition, CDC assessed the need for adding recommendations for medical conditions not currently included
in the WHO MEC. Through this process, a list was developed
of existing WHO recommendations to consider adapting and
new medical conditions to consider adding to the guidance.
A systematic review of the scientiﬁc evidence was conducted
for each of the WHO recommendations considered for adaptation and for each of the medical conditions considered for
addition to the guidance. The purpose of these systematic
reviews was to identify direct evidence about the safety of
contraceptive method use by women (or men) with selected
conditions (e.g., risk for disease progression or other adverse
health eﬀects in women with rheumatoid arthritis who use
combined oral contraceptives). Information about indirect
evidence (e.g., evidence from healthy women or animal studies)

June 18, 2010

or theoretical considerations was obtained when direct evidence
was not available. CDC conducted systematic reviews following standard guidelines (3,4), included thorough searches of
PubMed and other databases of the scientiﬁc literature, and
used the U.S. Preventive Services Task Force system to grade
the strength and quality of the evidence (5). Each systematic
review was peer-reviewed by two or three experts before being
used in the adaptation process. These systematic reviews have
been submitted for publication in peer-reviewed journals.
For most recommendations in this document, a limited
number of studies address the use of a speciﬁc contraceptive
method by women with a speciﬁc condition. Therefore, within
the WHO guidance, as well as with this U.S. adaptation of
the guidance, most of the decisions about medical eligibility
criteria were often necessarily based on 1) extrapolations from
studies that primarily included healthy women, 2) theoretical
considerations about risks and beneﬁts, and 3) expert opinion.
Evidence was particularly limited for newer contraceptive
methods. The total body of evidence for each recommendation
included evidence based on direct studies or observations of
the contraceptive method used by women (or men) with the
condition and may have included 1) evidence derived from
eﬀects of the contraceptive method used by women (or men)
without the condition and 2) indirect evidence or theoretical
concerns based on studies of suitable animal models, human
laboratory studies, or analogous clinical situations.
In February 2009, CDC held a meeting of 31 experts who
were invited to provide their individual perspective on the
scientiﬁc evidence presented and the discussions on potential recommendations that followed. This group included
obstetricians/gynecologists, pediatricians, family physicians,
nurse-midwives, nurse practitioners, epidemiologists, and
others with expertise in contraceptive safety and provision.
For each topic discussed, the evidence from the systematic
review was presented; for most of the topics, an expert in the
speciﬁc medical condition (e.g., rheumatoid arthritis) also gave
a brief presentation on the condition and speciﬁc issues about
contraceptive safety. CDC gathered input from the experts
during the meeting and ﬁnalized the recommendations in
this document. CDC plans to develop a research agenda to
address topics identiﬁed during the meeting that need further
investigation.

How to Use This Document
These recommendations are intended to help health-care providers determine the safe use of contraceptive methods among
women and men with various characteristics and medical conditions. Providers also can use the synthesis of information in
these recommendations when consulting with women, men,

Vol. 59 / RR-4

Recommendations and Reports

and couples about their selection of contraceptive methods.
The tables in this document include recommendations for the
use of contraceptive methods by women and men with particular characteristics or medical conditions. Each condition
was deﬁned as representing either an individual’s characteristics (e.g., age, history of pregnancy) or a known preexisting
medical/pathologic condition (e.g., diabetes and hypertension).
The recommendations refer to contraceptive methods being
used for contraceptive purposes; the recommendations do
not consider the use of contraceptive methods for treatment
of medical conditions because the eligibility criteria in these
cases may diﬀer. The conditions aﬀecting eligibility for the
use of each contraceptive method were classiﬁed under one of
four categories (Box 1).

BOX 1. Categories of medical eligibility criteria for
contraceptive use

Using the Categories in Practice

When the categories diﬀer for initiation and continuation,
these diﬀerences are noted in the columns Initiation and
Continuation. Where Initiation and Continuation are not
denoted, the category is the same for initiation and continuation of use.
On the basis of this classiﬁcation system, the eligibility criteria for initiating and continuing use of a speciﬁc contraceptive
method are presented in tables (Appendices A–M). In these
tables, the ﬁrst column indicates the condition. Several conditions were divided into subconditions to diﬀerentiate between
varying types or severity of the condition. The second column
classiﬁes the condition for initiation and/or continuation into
Category 1, 2, 3, or 4. For some conditions, the numeric classiﬁcation does not adequately capture the recommendation;
in this case, the third column clariﬁes the numeric category.
These clariﬁcations were determined during the discussions of
the scientiﬁc evidence and the numeric classiﬁcation and are
considered a necessary element of the recommendation. The
third column also summarizes the evidence for the recommendation, where evidence exists. The recommendations for
which no evidence is cited are based on expert opinion from
either the WHO or U.S. expert working group meetings and
may be based on evidence from sources other than systematic
reviews and presented at those meetings. For selected recommendations, additional comments appear in the third column
and generally come from the WHO or the U.S. expert working
group participants.

Health-care providers can use these categories when assessing
the safety of contraceptive method use for women and men
with speciﬁc medical conditions or characteristics. Category
1 comprises conditions for which no restrictions exist for
use of the contraceptive method. Classiﬁcation of a method/
condition as Category 2 indicates the method generally can
be used, but careful follow-up may be required. For a method/
condition classiﬁed as Category 3, use of that method usually
is not recommended unless other more appropriate methods
are not available or acceptable. The severity of the condition
and the availability, practicality, and acceptability of alternative
methods should be taken into account, and careful follow-up
will be required. Hence, provision of a method to a woman
with a condition classiﬁed as Category 3 requires careful
clinical judgement and access to clinical services. Category 4
comprises conditions that represent an unacceptable health
risk if the method is used. For example, a smoker aged <35
years generally can use combined oral contraceptives (COCs)
(Category 2). However, for a woman aged ≥35 years who
smokes <15 cigarettes per day, the use of COCs usually is
not recommended unless other methods are not available or
acceptable to her (Category 3). A woman aged ≥35 years who
smokes ≥15 cigarettes per day should not use COCs because
of unacceptable health risks, primarily the risk for myocardial
infarction and stroke (Category 4). The programmatic implications of these categories may depend on the circumstances of
particular professional or service organizations (e.g., in some
settings, a Category 3 may mean that special consultation is
warranted).
The recommendations address medical eligibility criteria for
the initiation and continued use of all methods evaluated. The
issue of continuation criteria is clinically relevant whenever a
woman develops the condition while she is using the method.

Recommendations for Use of
Contraceptive Methods
The classiﬁcations for whether women with certain medical
conditions or characteristics can use speciﬁc contraceptive
methods are provided for combined hormonal contraceptive methods, including low-dose (containing ≤35 µg ethi-

MMWR

nyl estradiol) combined oral contraceptive pills, combined
hormonal patch, and combined vaginal ring (Appendix B);
progestin-only contraceptive methods, including progestinonly pills, depot medroxyprogesterone acetate injections, and
etonogestrel implants (Appendix C); emergency contraceptive
pills (Appendix D); intrauterine contraception, including the
copper intrauterine device (IUD) and the levonorgestrel IUD
(Appendix E); use of copper IUDs for emergency contraception (Appendix F); barrier contraceptive methods, including
male and female condoms, spermicides, diaphragm with
spermicide, and cervical cap (Appendix G); fertility awarenessbased methods (Appendix H); lactational amenorrhea method
(Appendix I); coitus interruptus (Appendix J); and female
and male sterilization (Appendix K). Tables at the end of the
document summarize the classiﬁcations for the hormonal and
intrauterine methods (Appendix L) and the evidence about
potential drug interactions between hormonal contraceptives
and antiretroviral therapies (Appendix M).

Contraceptive Method Choice
Many elements need to be considered by women, men, or
couples at any given point in their lifetimes when choosing
the most appropriate contraceptive method. These elements
include safety, eﬀectiveness, availability (including accessibility and aﬀordability), and acceptability. The guidance in this
document focuses primarily on the safety of a given contraceptive method for a person with a particular characteristic or
medical condition. Therefore, the classiﬁcation of Category 1
means that the method can be used in that circumstance with
no restrictions with regard to safety but does not necessarily
imply that the method is the best choice for that person; other
factors, such as eﬀectiveness, availability, and acceptability, may
play a key role in determining the most appropriate choice.
Voluntary informed choice of contraceptive methods is an
essential guiding principle, and contraceptive counseling,
where applicable, may be an important contributor to the
successful use of contraceptive methods.
In choosing a method of contraception, the risk for sexually
transmitted infections (STIs), including human immunodeﬁciency virus (HIV), also must be considered. Although hormonal
contraceptives and IUDs are highly eﬀective at preventing
pregnancy, they do not protect against STIs. Consistent and
correct use of the male latex condom reduces the risk for STIs
(6). When a male condom cannot be used properly for infection
prevention, a female condom should be considered (7). Women
who use contraceptive methods other than condoms should be
counseled about the use of condoms and the risk for STIs (7).
Additional information about prevention and treatment of STIs

June 18, 2010

is available from CDC’s Sexually Transmitted Diseases Treatment
Guidelines (http://www.cdc.gov/std/treatment) (7).

Contraceptive Method Effectiveness
Contraceptive method eﬀectiveness is critically important
in minimizing the risk for unintended pregnancy, particularly
among women for whom an unintended pregnancy would
pose additional health risks. The eﬀectiveness of contraceptive
methods depends both on the inherent eﬀectiveness of the
method itself and on how consistently and correctly it is used
(Table 1). Methods that depend on consistent and correct use
have a wide range of eﬀectiveness.

Unintended Pregnancy and Increased
Health Risk
For women with conditions that may make unintended pregnancy an unacceptable health risk, long-acting, highly eﬀective contraceptive methods may be the best choice (Table 1).
Women with these conditions should be advised that sole
use of barrier methods for contraception and behavior-based
methods of contraception may not be the most appropriate
choice because of their relatively higher typical-use rates of
failure (Table 1). Conditions included in the U.S. MEC for
which unintended pregnancy presents an unacceptable health
risk are identiﬁed throughout the document (Box 2).

Keeping Guidance Up to Date
As with any evidence-based guidance document, a key challenge is keeping the recommendations up to date as new scientiﬁc evidence becomes available. CDC will continue to work
with WHO to identify and assess all new relevant evidence
and to determine whether changes to the recommendations
are warranted (4). In most cases, the U.S. MEC will follow any
updates in the WHO guidance, which typically occur every
3–4 years (or sooner if warranted by new data). However,
CDC will review any WHO updates for their application in
the United States. CDC also will identify and assess any new
literature for the recommendations and medical conditions that
are not included in the WHO guidance. CDC will completely
review the U.S. MEC every 3–4 years as well. Updates to the
guidance will appear on the CDC U.S. MEC website: http://
www.cdc.gov/reproductivehealth/UnintendedPregnancy/
USMEC.htm.

Vol. 59 / RR-4

Recommendations and Reports

No
Spermicides**
Withdrawal
Fertility awareness–based methods
Standard Days method††
TwoDay method™††
Ovulation method††
Sponge
Parous women
Nulliparous women
Diaphragm§§
Condom¶¶
Female (Reality®)
Male
Combined pill and progestin-only pill
Evra patch®
NuvaRing®
Depo-Provera®
Intrauterine device
ParaGard® (copper T)
Mirena® (LNG-IUS)
Implanon®
Female sterilization
Male sterilization
Emergency contraceptive pills***
Lactational amenorrhea methods†††

Typical use*
85%
29%
27%
25%

Perfect use†
85%
18%
4%

Women continuing use at 1 year§
42%
43%
51%

5%
4%
3%
32%
16%
16%

20%
9%
6%

46%
57%
57%

21%
15%
8%
8%
8%
3%

5%
2%
0.3%
0.3%
0.3%
0.3%

49%
53%
68%
68%
68%
56%

0.8%
0.2%
0.05%
0.5%
0.15%
Not applicable
Not applicable

0.6%
0.2%
0.05%
0.5%
0.10%
Not applicable
Not applicable

78%
80%
84%
100%
100%
Not applicable
Not applicable

Adapted from Trussell J. Contraceptive efficacy. In Hatcher RA, Trussell J, Nelson AL, Cates W, Stewart FH, Kowal D. Contraceptive technology. 19th revised
ed. New York, NY: Ardent Media; 2007.
* Among typical couples who initiate use of a method (not necessarily for the first time), the percentage who experience an unintended pregnancy during
the first year if they do not stop use for any other reason. Estimates of the probability of pregnancy during the first year of typical use for spermicides, withdrawal, fertility awareness-based methods, the diaphragm, the male condom, the pill, and Depo-Provera are taken from the 1995 National Survey of Family
Growth corrected for underreporting of abortion; see the text for the derivation of estimates for the other methods.
† Among couples who initiate use of a method (not necessarily for the first time) and who use it perfectly (both consistently and correctly), the percentage
who experience an unintended pregnancy during the first year if they do not stop use for any other reason. See the text for the derivation of the estimate
for each method.
§ Among couples attempting to avoid pregnancy, the percentage who continue to use a method for 1 year.
¶ The percentages becoming pregnant in the typical use and perfect use columns are based on data from populations where contraception is not used
and from women who cease using contraception to become pregnant. Of these, approximately 89% become pregnant within 1 year. This estimate was
lowered slightly (to 85%) to represent the percentage who would become pregnant within 1 year among women now relying on reversible methods of
contraception if they abandoned contraception altogether.
** Foams, creams, gels, vaginal suppositories, and vaginal film.
†† The TwoDay and Ovulation methods are based on evaluation of cervical mucus. The Standard Days method avoids intercourse on cycle days 8–19.
§§ With spermicidal cream or jelly.
¶¶ Without spermicides.
*** Treatment initiated within 72 hours after unprotected intercourse reduces the risk for pregnancy by at least 75%. The treatment schedule is 1 dose within
120 hours after unprotected intercourse and a second dose 12 hours after the first dose. Both doses of Plan B can be taken at the same time. Plan B (1
dose is 1 white pill) is the only dedicated product specifically marketed for emergency contraception. The Food and Drug Administration has in addition
declared the following 22 brands of oral contraceptives to be safe and effective for emergency contraception: Ogestrel or Ovral (1 dose is 2 white pills);
Levlen or Nordette (1 dose is 4 light-orange pills); Cryselle, Levora, Low-Ogestrel, Lo/Ovral, or Quasence (1 dose is 4 white pills); Tri-Levlen or Triphasil
(1 dose is 4 yellow pills); Jolessa, Portia, Seasonale, or Trivora (1 dose is 4 pink pills); Seasonique (1 dose is 4 light blue-green pills); Empresse (1 dose
is 4 orange pills); Alesse, Lessina, or Levlite (1 dose is 5 pink pills); Aviane (1 dose is 5 orange pills); and Lutera (1 dose is 5 white pills).
††† Lactational amenorrhea method is a highly effective temporary method of contraception. However, to maintain effective protection against pregnancy,
another method of contraception must be used as soon as menstruation resumes, the frequency or duration of breastfeeding is reduced, bottle feeds
are introduced, or the baby reaches 6 months of age.

MMWR

BOX 2. Conditions associated with increased risk for adverse
health events as a result of unintended pregnancy

Breast cancer
Complicated valvular heart disease
Diabetes: insulin-dependent; with nephropathy/
retinopathy/neuropathy or other vascular disease; or
of >20 years’ duration
Endometrial or ovarian cancer
Epilepsy
Hypertension (systolic >160 mm Hg or diastolic
>100 mm Hg)
History of bariatric surgery within the past 2 years
HIV/AIDS
Ischemic heart disease
Malignant gestational trophoblastic disease
Malignant liver tumors (hepatoma) and
hepatocellular carcinoma of the liver
Peripartum cardiomyopathy
Schistosomiasis with ﬁbrosis of the liver
Severe (decompensated) cirrhosis
Sickle cell disease
Solid organ transplantation within the past 2 years
Stroke
Systemic lupus erythematosus
Thrombogenic mutations
Tuberculosis

June 18, 2010
Acknowledgements

This report is based in part on the work of the Promoting Family
Planning Team, Department of Reproductive Health and Research,
World Health Organization, and its development of the WHO
Medical Eligibility Criteria for Contraceptive Use, 4th edition.
References
1. WHO. Medical eligibility criteria for contraceptive use. 4th ed. Geneva:
WHO; 2009. Available at http://www.who.int/reproductivehealth/publications/family_planning/9789241563888/en/index.html.
2. Faculty of Family Planning and Reproductive Health Care, Royal College
of Obstetricians and Gynecologists. UK medical eligibility criteria for
contraceptive use, 2005–2006. London: Faculty of Family Planning and
Reproductive Health Care, 2006.
3. Stroup DF, Berlin JA, Morton SC, et al. Meta-analysis of observational
studies in epidemiology: a proposal for reporting. Meta-analysis Of
Observational Studies in Epidemiology (MOOSE) group. JAMA
2000;283:2008–12.
4. Mohllajee AP, Curtis KM, Flanagan RG, et al. Keeping up with evidence
a new system for WHO’s evidence-based family planning guidance. Am
J Prev Med 2005;28:483–90.
5. Harris RP, Helfand M, Woolf SH, et al. Current methods of the US
Preventive Services Task Force: a review of the process. Am J Prev Med
2001;20:21–35.
6. CDC. Condom fact sheet in brief. Available at http://www.cdc.gov/
condomeﬀectiveness/docs/Condom_fact_Sheet_in_Brief.pdf.
7. CDC. Sexually transmitted diseases treatment guidelines, 2006. MMWR
2006;55(RR No. 11).

Vol. 59 / RR-4

Recommendations and Reports

Appendix A
Summary of Changes to the World Health Organization Medical Eligibility
Criteria for Contraceptive Use, 4th Edition, to Create the U.S. Medical
Eligibility Criteria for Contraceptive Use, 2010
The classiﬁcation additions, deletions, and modiﬁcations
from the World Health Organization (WHO) Medical
Eligibility Criteria for Contraceptive Use, 4th Edition, are
summarized below (Tables 1–3). For conditions for which

classiﬁcation changed for ≥1 methods or the condition description underwent a major modiﬁcation, WHO conditions and
recommendations appear in curly brackets.

BOX. Categories for Classifying Hormonal Contraceptives and Intrauterine Devices

1 = A condition for which there is no restriction for the use of the contraceptive method.
2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks.
3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method.
4 = A condition that represents an unacceptable health risk if the contraceptive method is used.
TABLE 1. Summary of changes in classifications from WHO Medical Eligibility Criteria for Contraceptive Use, 4th edition*†
Condition
Breastfeeding
a. <1 mo postpartum {WHO:
<6 wks postpartum}
b. 1 mo to <6 mos {WHO: ≥6
wks to <6 mos postpartum}

COC/P/R
3§ {4}

POP
2§ {3}

DMPA
2§ {3}

Implants

Cu-IUD

2§ {3}

2 {1 if not
breastfeeding and 3 if
breastfeeding}
2 {3}

2{3}

2 {3}

2 {1}

3 {4}
2 {3}

2 {3}

Clarification
The US Department of Health
and Human Services recommends that infants be exclusively
breastfed during the first 4–6
months of life, preferably for a
full 6 months. Ideally, breastfeeding should continue through the
first year of life (1). {Not included
in WHO MEC}

2§ {3}

Postpartum (in breastfeeding
or nonbreastfeeding women),
including post caesarean
section
a. <10 min after delivery of
the placenta {WHO: <48
hrs, including insertion immediately after delivery of
the placenta}
b. 10 min after delivery of the
placenta to <4 wks {WHO:
≥48 hrs to <4 wks}
Deep venous thrombosis
(DVT)/pulmonary embolism
(PE)
a. History of DVT/PE, not on
anticoagulant therapy
ii. Lower risk for recurrent
DVT/PE (no risk factors)
b. Acute DVT/PE
c. DVT/PE and established on
anticoagulant therapy for at
least 3 mos

LNG-IUD

MMWR

June 18, 2010

TABLE 1. (Continued) Summary of changes in classifications from WHO Medical Eligibility Criteria for Contraceptive Use,
4th edition*†
Condition

COC/P/R

POP

DMPA

Implants

LNG-IUD

i. Higher risk for recurrent
DVT/PE (≥1 risk factors)
r,OPXOUISPNCPQIJMJB
including
antiphospholipid
syndrome
r"DUJWFDBODFS
(metastatic, on therapy,
or within 6 mos after
clinical remission),
excluding nonmelanoma skin cancer
r)JTUPSZPGSFDVSSFOU
DVT/PE
ii. Lower risk for recurrent
DVT/PE (no risk factors)

Valvular heart disease
b. Complicated¶ (pulmonary
hypertension, risk for
atrial fibrillation, history
of subacute bacterial
endocarditis)

Cu-IUD

Clarification

2 {1}

3§ {4}

2 {1}

1 {2}

Women on anticoagulant therapy
are at risk for gynecologic complications of therapy such as
hemorrhagic ovarian cysts and
severe menorrhagia. Hormonal
contraceptive methods can be of
benefit in preventing or treating
these complications. When a
contraceptive method is used
as a therapy, rather than solely
to prevent pregnancy, the risk/
benefit ratio may be different and
should be considered on a caseby-case basis. {Not included in
WHO MEC}

1 {2}

Ovarian cancer¶

1 {Initiation = 3,
Continuation = 2}

Uterine fibroids

2 {1 if no uterine
distortion and 4 if
uterine distortion
is present}

2 {1 if no uterine
distortion and 4 if
uterine distortion is
present}

* For conditions for which classification changed for ≥1 methods or the condition description underwent a major modification, WHO conditions and recommendations appear in curly brackets.
† Abbreviations: WHO = World Health Organization; COC = combined oral contraceptive; P = combined hormonal contraceptive patch; R = combined
hormonal vaginal ring; POP = progestin-only pill; DMPA = depot medroxyprogesterone acetate; LNG-IUD = levonorgestrel-releasing intrauterine device;
Cu-IUD = copper intrauterine device; DVT = deep venous thrombosis; PE = pulmonary embolism; VTE = venous thromboembolism.
§ Consult the clarification column for this classification.
¶ Condition that exposes a women to increased risk as a result of unintended pregnancy.

Vol. 59 / RR-4

Recommendations and Reports

TABLE 2. Summary of recommendations for medical conditions added to the U.S. Medical Eligibility Criteria for Contraceptive Use*
Condition

COC/P/R POP

History of bariatric surgery†
a. Restrictive procedures: decrease storage
1
capacity of the stomach (vertical banded
gastroplasty, laparoscopic adjustable
gastric band, laparoscopic sleeve
gastrectomy)
b. Malabsorptive procedures: decrease
COCs: 3
absorption of nutrients and calories
P/R: 1
by shortening the functional length of
the small intestine (Roux-en-Y gastric
bypass, biliopancreatic diversion)
Peripartum cardiomyopathy†
a. Normal or mildly impaired cardiac
function (New York Heart Association
Functional Class I or II: patients with no
limitation of activities or patients with
slight, mild limitation of activity) (2)
i <6 mos
ii ≥6 mos
b. Moderately or severely impaired cardiac
function (New York Heart Association
Functional Class III or IV: patients with
marked limitation of activity or patients
who should be at complete rest) (2)

4
3
4

DMPA Implants

LNG-IUD

Cu-IUD

1
1
2

2
2
2

2/3§

Clarification

b. Not on immunosuppressive therapy

ContinuaContinuation
Initiation
tion
1
2
1
DMPA use among women on long-term corticosteroid therapy with a history of, or risk factors
for, nontraumatic fractures is classified as Category 3. Otherwise, DMPA use for women with
rheumatoid arthritis is classified as Category 2.
1
1

Endometrial hyperplasia

2/3§

Rheumatoid arthritis
a. On immunosuppressive therapy

Inflammatory bowel disease (IBD)
(ulcerative colitis, Crohn disease)

Initiation
2

Solid organ transplantation†
Initiation
a. Complicated: graft failure (acute or
chronic), rejection, cardiac allograft
vasculopathy

b. Uncomplicated

2§

For women with mild IBD, with no other risk
factors for VTE, the benefits of COC/P/R use
generally outweigh the risks (Category 2).
However, for women with IBD with increased
risk for VTE (e.g., those with active or extensive
disease, surgery, immobilization, corticosteroid
use, vitamin deficiencies, fluid depletion), the
risks for COC/P/R use generally outweigh the
benefits (Category 3).

ContinuaContinuation
Initiation
tion

Women with Budd-Chiari syndrome should not
use COC/P/R because of the increased risk for
thrombosis.

* Abbreviations: COC = combined oral contraceptive; P = combined hormonal contraceptive patch; R = combined hormonal vaginal ring: POP = progestin-only pill; DMPA = depot
medroxyprogesterone acetate; LNG-IUD = levonorgestrel-releasing intrauterine device; Cu-IUD = copper intrauterine device; IBD = inflammatory bowel disease; VTE = venous
thromboembolism.
† Condition that exposes a women to increased risk as a result of unintended pregnancy.
§ Consult the clarification column for this classification.

MMWR

June 18, 2010

TABLE 3. Summary of additional changes to the U.S. Medical Eligibility Criteria for Contraceptive Use
Condition/Contraceptive method

Change

Emergency contraceptive pills

History of bariatric surgery, rheumatoid arthritis, inflammatory bowel disease, and solid organ transplantation
were added to Appendix D and given a Category 1.

Barrier methods

For 6 conditions—history of bariatric surgery, peripartum cardiomyopathy, rheumatoid arthritis, endometrial
hyperplasia, inflammatory bowel disease, and solid organ transplantation—the barrier methods are classified
as Category 1.

Sterilization

In general, no medical conditions would absolutely restrict a person’s eligibility for sterilization.
Recommendations from the World Health Organization (WHO) Medical Eligibility Criteria for Contraceptive
Use about specific settings and surgical procedures for sterilization are not included here. The guidance has
been replaced with general text on sterilization.

Other deleted items

Guidance for combined injectables, levonorgestrel implants, and norethisterone enanthate has been removed because these methods are not currently available in the United States.
Guidance for “blood pressure measurement unavailable” and “history of hypertension, where blood pressure
CANNOT be evaluated (including hypertension in pregnancy)” has been removed.

Unintended pregnancy and increased
health risk

The following conditions have been added to the WHO list of conditions that expose a woman to increased
risk as a result of unintended pregnancy: history of bariatric surgery within the past 2 years, peripartum cardiomyopathy, and receiving a solid organ transplant within 2 years.

References
1. Oﬃce on Women’s Health, US Department of Health and Human
Services. HHS blueprint for action on breastfeeding. Washington, DC:
US Department of Health and Human Services, Oﬃce on Women’s
Health; 2000.

2. The Criteria Committee of the New York Heart Association. Nomenclature
and criteria for diagnosis of diseases of the heart and great vessels. 9th ed.
Boston, MA: Little, Brown & Co; 1994.

Vol. 59 / RR-4

Recommendations and Reports

Appendix B
Classifications for Combined Hormonal Contraceptives
Combined hormonal contraceptives (CHCs) include lowdose (containing ≤35 µg ethinyl estradiol [EE]) combined oral
contraceptives (COCs), the combined hormonal patch, and
the combined vaginal ring. The combined hormonal patch and
vaginal ring are relatively new contraceptive methods. Limited
information is available about the safety of these methods
among women with speciﬁc medical conditions. Moreover,
epidemiologic data on the long-term eﬀects of the combined
hormonal patch and the vaginal ring were not available for
review. Evidence indicates that the combined hormonal patch
and the combined vaginal ring provide comparable safety

and pharmacokinetic proﬁles to COCs with similar hormone
formulations (1–33). Pending further studies, the evidence
available for recommendations about COCs applies to the
recommendations for the combined hormonal patch and vaginal ring. Therefore, the patch and ring should have the same
categories (Box) as COCs, except where noted. The assigned
categories should, therefore, be considered a preliminary, best
judgement, which will be reevaluated as new data become
available. CHCs do not protect against sexually transmitted
infections (STIs) or human immunodeﬁciency virus (HIV).

BOX. Categories for Classifying Combined Hormonal Contraceptives

TABLE. Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Condition

Category

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy
Age
a. Menarche to <40 yrs
b. ≥40 yrs

Not applicable

Clarification: Use of COCs, P, or R is not required. There is no known harm to the woman, the course of
her pregnancy, or the fetus if COCs, P, or R are inadvertently used during pregnancy.

1
2

Evidence: Adolescents using 20 μg EE-containing COCs have lower BMD than do nonusers, and higher
dose-containing COCs have little to no effect. (34–41). In premenopausal adult women, COC use has little
to no effect on bone health while appearing to preserve bone mass in perimenopausal women (26,42–90).
Postmenopausal women who have ever used COCs have similar BMD to postmenopausal women who
have never used COCs (54,58,68,81,91–110). BMD in adolescent or premenopausal women may not accurately predict postmenopausal fracture risk (109,111–122).
Comment: The risk for cardiovascular disease increases with age and might increase with CHC use. In the
absence of other adverse clinical conditions, CHCs can be used until menopause.

Parity
a. Nulliparous
b. Parous

1
1

Breastfeeding
a. <1 mo postpartum
b. 1 mo to <6 mos postpartum
c. ≥6 mos postpartum

3
2
2

Clarification: The U.S. Department of Health and Human Services recommends that infants be exclusively
breastfed during the first 4–6 months of life, preferably for a full 6 months. Ideally, breastfeeding should
continue through the first year of life (123).
Evidence: Clinical studies demonstrate conflicting results about effects on milk volume in women exposed
to COCs during lactation; no consistent effect on infant weight has been reported. Adverse health outcomes
or manifestations of exogenous estrogen in infants exposed to CHCs through breast milk have not been
demonstrated (124–133). In general, these studies are of poor quality, lack standard definitions of breastfeeding or outcome measures, and have not included premature or ill infants. Theoretical concerns about
effects of CHCs on breast milk production are greater in the early postpartum period when milk flow is being
established.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Condition

Category

Postpartum (in nonbreastfeeding
women)
a. <21 days
b. ≥21 days

3
1

Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic abortion

1
1
1

Past ectopic pregnancy

History of pelvic surgery

Smoking
a. Age <35 yrs
b. Age ≥35 yrs
i. <15 Cigarettes/day
ii. ≥15 Cigarettes/day
Obesity
a. ≥30 kg/m2 BMI
b. Menarche to <18 yrs and
≥30 kg/m2 BMI

History of bariatric surgery§
a. Restrictive procedures: decrease
storage capacity of the stomach
(vertical banded gastroplasty,
laparoscopic adjustable gastric band,
laparoscopic sleeve gastrectomy)
b. Malabsorptive procedures: decrease
absorption of nutrients and calories
by shortening the functional length of
the small intestine (Roux-en-Y gastric bypass, biliopancreatic diversion)

2
3
4

Clarifications/Evidence/Comments

Comment: Theoretical concern exists about the association between CHC use up to 3 weeks postpartum
and risk for thrombosis in the mother. Blood coagulation and fibrinolysis are essentially normalized by 3
weeks postpartum.
Clarification: COCs, P, or R may be started immediately postabortion.
Evidence: Women who started taking COCs immediately after first trimester medical or surgical abortion
did not experience more side effects or adverse vaginal bleeding outcomes or clinically significant changes
in coagulation parameters than did women who used a placebo, an IUD, a nonhormonal contraceptive
method, or delayed COC initiation (134–140). Limited evidence on women using the ring immediately after
first trimester medical or surgical abortion found no serious adverse events and no infection related to use
of the combined vaginal contraceptive ring during 3 cycles of follow-up postabortion (141).
Comment: The risk for future ectopic pregnancy is increased among women who have had an ectopic
pregnancy in the past. CHCs protect against pregnancy in general, including ectopic gestation.

Evidence: COC users who smoked were at increased risk for cardiovascular diseases, especially myocardial infarction, than those who did not smoke. Studies also showed an increased risk for myocardial infarction with increasing number of cigarettes smoked per day (142–153).

2
2

Evidence: Obese women who use COCs are more likely than obese women who do not use COCs to
experience VTE. The absolute risk for VTE in healthy women of reproductive age is small. Limited evidence
suggests that obese women who use COCs do not have a higher risk for acute myocardial infarction or
stroke than do obese nonusers (147,153–159). Limited evidence is inconsistent about whether COC effectiveness varies by body weight or BMI (160–165). Limited evidence suggests obese women are no more
likely to gain weight after 3 cycles of the vaginal ring or COC than overweight or normal weight women.
A similar weight gain during the 3 months was noted between the COC group and the vaginal ring group
across all BMI categories (166). The effectiveness of the patch decreased among women who weighed >90
kg; however, no association was found between pregnancy risk and BMI (18).

Evidence: Limited evidence demonstrated no substantial decrease in effectiveness of oral contraceptives
among women who underwent laparoscopic placement of an adjustable gastric band (167).

COCs: 3

Evidence: Limited evidence demonstrated no substantial decrease in effectiveness of oral contraceptives
among women who underwent a biliopancreatic diversion (168); however, evidence from pharmacokinetic
studies reported conflicting results of oral contraceptive effectiveness among women who underwent a
jejunoileal bypass (169,170).

P/R: 1

Comment: Bariatric surgical procedures involving a malabsorptive component have the potential to decrease oral contraceptive effectiveness, perhaps further decreased by postoperative complications, such as
long-term diarrhea and/or vomiting.

Cardiovascular Disease
Multiple risk factors for arterial cardiovascular disease (such
as older age, smoking, diabetes, and
hypertension)

3/4

Clarification: When a woman has multiple major risk factors, any of which alone would substantially
increase her risk for cardiovascular disease, use of COCs, P, or R might increase her risk to an unacceptable level. However, a simple addition of categories for multiple risk factors is not intended; for example, a
combination of two risk factors assigned a category 2 might not necessarily warrant a higher category.

Hypertension
For all categories of hypertension, classifications are based on the assumption that no other risk factors exist for cardiovascular disease. When multiple risk factors do exist,
risk for cardiovascular disease might increase substantially. A single reading of blood pressure level is not sufficient to classify a woman as hypertensive.
a. Adequately controlled hypertension
3
Clarification: Women adequately treated for hypertension are at reduced risk for acute myocardial
infarction and stroke compared with untreated women. Although no data exist, COC, P, or R users with
adequately controlled and monitored hypertension should be at reduced risk for acute myocardial infarction
and stroke compared with untreated hypertensive COC, P, or R users.
b. Elevated blood pressure levels
(properly taken measurements)

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Condition
i. Systolic 140–159 mm Hg or
diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic
≥100 mm Hg§
c. Vascular disease
History of high blood pressure during
pregnancy (where current blood pressure is measurable and normal)

Category
3

Clarifications/Evidence/Comments
Evidence: Among women with hypertension, COC users were at higher risk than nonusers for
stroke, acute myocardial infarction, and peripheral arterial disease (142,144,151–153,155,171–186).
Discontinuation of COCs in women with hypertension might improve blood pressure control (187).

4
4
2

Deep venous thrombosis (DVT)/
Pulmonary embolism (PE)
a. History of DVT/PE, not on anticoagulant therapy
i. Higher risk for recurrent DVT/PE
(≥1 risk factors)

Evidence: Women with a history of high blood pressure in pregnancy, who also used COCs, had a
higher risk for myocardial infarction and VTE than did COC users who did not have a history of high blood
pressure during pregnancy. The absolute risks for acute myocardial infarction and VTE in this population
remained small (153,172,184–186,188–193).

r )JTUPSZPGFTUSPHFOBTTPDJBUFE
DVT/PE
r 1SFHOBODZBTTPDJBUFE%751&
r *EJPQBUIJD%751&
r ,OPXOUISPNCPQIJMJB
JODMVEJOH
antiphospholipid syndrome
r "DUJWFDBODFS NFUBTUBUJD
PO
therapy, or within 6 mos after
clinical remission), excluding
non-melanoma skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii. Lower risk for recurrent DVT/PE
(no risk factors)
b. Acute DVT/PE
c. DVT/PE and established on anticoagulant therapy for at least 3 mos
i. Higher risk for recurrent DVT/PE
(≥1 risk factors)

3
4

Clarification: Women on anticoagulant therapy are at risk for gynecologic complications of therapy, such
as hemorrhagic ovarian cysts and severe menorrhagia. Hormonal contraceptive methods can be of benefit
in preventing or treating these complications. When a contraceptive method is used as a therapy, rather
than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-bycase basis.

Clarification: Women on anticoagulant therapy are at risk for gynecologic complications of therapy, such
as hemorrhagic ovarian cysts and severe menorrhagia. Hormonal contraceptive methods can be of benefit
in preventing or treating these complications. When a contraceptive method is used as a therapy, rather
than solely to prevent pregnancy, the risk/benefit ratio may differ and should be considered on a case-bycase basis.
Comment: Some conditions that increase the risk for DVT/PE are heritable.

r ,OPXOUISPNCPQIJMJB
JODMVEJOH
antiphospholipid syndrome
r "DUJWFDBODFS NFUBTUBUJD
PO
therapy, or within 6 mos after
clinical remission), excluding
non-melanoma skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii. Lower risk for recurrent DVT/PE
(no risk factors)

d. Family history (first-degree relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged immobilization
f. Minor surgery without immobilization
Known thrombogenic mutations§
(e.g., factor V Leiden; prothrombin mutation; protein S, protein C, and antithrombin deficiencies)
Superficial venous thrombosis
a. Varicose veins
b. Superficial thrombophlebitis

2
4
2
1
4

Clarification: Routine screening is not appropriate because of the rarity of the conditions and the high cost
of screening.
Evidence: Among women with thrombogenic mutations, COC users had a 2-fold to 20-fold higher risk for
thrombosis than did nonusers (159,194–216).

1
2

Current and history of ischemic heart
disease§

Stroke§ (history of cerebrovascular
accident)

Comment: Varicose veins are not risk factors for DVT/PE

MMWR

June 18, 2010

TABLE. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Condition
Known hyperlipidemias

Valvular heart disease
a. Uncomplicated
b. Complicated§ (pulmonary hypertension, risk for atrial fibrillation, history
of subacute bacterial endocarditis)

Category

Clarifications/Evidence/Comments

2/3

Clarification: Routine screening is not appropriate because of the rarity of the conditions and the high cost
of screening. Although some types of hyperlipidemias are risk factors for vascular disease, the category
should be assessed according to the type, its severity, and the presence of other cardiovascular risk
factors.

2
4

Peripartum cardiomyopathy§
a. Normal or mildly impaired cardiac function (New York Heart
Association Functional Class I or II:
patients with no limitation of activities
or patients with slight, mild limitation
of activity) (217)
i. <6 mos
ii. ≥6 mos
b. Moderately or severely impaired
cardiac function (New York Heart
Association Functional Class III or
IV: patients with marked limitation of
activity or patients who should be at
complete rest) (217)

Comment: Among women with valvular heart disease, CHC use may further increase the risk for arterial
thrombosis; women with complicated valvular heart disease are at greatest risk.

Evidence: No direct evidence exists about the safety of COCs/P/R among women with peripartum
cardiomyopathy. Limited indirect evidence from noncomparative studies of women with cardiac disease
demonstrated few cases of hypertension and transient ischemic attack in women with cardiac disease using
COCs. No cases of heart failure were reported (218).
Comment: COCs might increase fluid retention in healthy women; fluid retention may worsen heart failure
in women with peripartum cardiomyopathy. COCs might induce cardiac arrhythmias in healthy women;
women with peripartum cardiomyopathy have a high incidence of cardiac arrhythmias.
4
3
4

2
2

Evidence: Limited evidence shows no consistent pattern of improvement or worsening of rheumatoid arthritis with use of oral contraceptives (240–245), progesterone (246), or estrogen (247).

Neurologic Conditions
Headaches

a. Non-migrainous (mild or severe)
b. Migraine
i. Without aura
r "HFZST
r "HFŜZST
ii. With aura, at any age

Initiation Continuation Clarification: Classification depends on accurate diagnosis of those severe headaches that are migrainous
and those headaches that are not. Any new headaches or marked changes in headaches should be evaluated. Classification is for women without any other risk factors for stroke. Risk for stroke increases with age,
hypertension and smoking.
1
2
Evidence: Among women with migraine, women who also had aura had a higher risk for stroke than did
those without aura (248–250). Women with a history of migraine who use COCs are about 2–4 times as
likely to have an ischemic stroke as nonusers with a history of migraine (142,157,179,180,249-254).
2
3
3
4
Comment: Aura is a specific focal neurologic symptom. For more information about this and other diag4
4
nostic criteria, see: Headache Classification Subcommittee of the International Headache Society. The
International Classification of Headache Disorders, 2nd ed. Cephalalgia. 2004;24(Suppl 1). Available http://
www.i-h-s.org/upload/ct_clas/ihc_II_main_no_print.pdf.

Epilepsy§

Clarification: If a woman is taking anticonvulsants, refer to the section on drug interactions. Certain anticonvulsants lower COC effectiveness. The extent to which P or R use is similar to COC use in this regard
remains unclear.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Condition

Category

Clarifications/Evidence/Comments

Clarification: The classification is based on data for women with selected depressive disorders. No data on
bipolar disorder or postpartum depression were available. Drug interactions potentially can occur between
certain antidepressant medications and hormonal contraceptives.

Depressive Disorders
Depressive disorders

Evidence: COC use did not increase depressive symptoms in women with depression compared with baseline or with nonusers with depression (255–264).

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without heavy
bleeding
b. Heavy or prolonged bleeding (includes regular and irregular patterns)

Unexplained vaginal bleeding
(suspicious for serious condition)
Before evaluation

Comment: Irregular menstrual bleeding patterns are common among healthy women.

Clarification: Unusually heavy bleeding should raise suspicion of a serious underlying condition.
Evidence: A Cochrane Collaboration Review identified 1 randomized controlled trial evaluating the effectiveness of COC use compared with naproxen and danazol in treating menorrhagic women. Women with
menorrhagia did not report worsening of the condition or any adverse events related to COC use (265).

Clarification: If pregnancy or an underlying pathological condition (such as pelvic malignancy) is suspected, it must be evaluated and the category adjusted after evaluation.
Comment: No conditions that cause vaginal bleeding will be worsened in the short term by use of CHCs.

Endometriosis

Benign ovarian tumors (including cysts)

Severe dysmenorrhea

Evidence: Risk for side effects with COC use was not higher among women with dysmenorrhea than
among women not using COCs. Some COC users had a reduction in pain and bleeding (267,268).

Evidence: After molar pregnancy evacuation, the balance of evidence found COC use did not increase
the risk for postmolar trophoblastic disease, and β-hCG levels regressed more rapidly in some COC users
than in nonusers (269–275). Limited evidence suggests that use of COCs during chemotherapy does not
significantly affect the regression or treatment of postmolar trophoblastic disease compared with women
who used a nonhormonal contraceptive method or DMPA during chemotherapy (276).

Gestational trophoblastic disease
a. Decreasing or undetectable β–hCG
levels
b. Persistently elevated β-hCG levels or
malignant disease§

Evidence: A Cochrane Collaboration Review identified 1 randomized controlled trial evaluating the effectiveness of COC use compared with a gonadotropin-releasing hormone analogue in treating the symptoms
of endometriosis. Women with endometriosis did not report worsening of the condition or any adverse
events related to COC use (266).

Cervical ectropion

Comment: Cervical ectropion is not a risk factor for cervical cancer, and restriction of CHC use is
unnecessary.

Cervical intraepithelial neoplasia

Evidence: Among women with persistent HPV infection, long-term COC use (≥5 years) might increase
the risk for carcinoma in situ and invasive carcinoma (21,277). Limited evidence on women with low-grade
squamous intraepithelial lesions found use of the vaginal ring did not worsen the condition (21).

Cervical cancer (awaiting treatment)

Comment: Theoretical concern exists that CHC use might affect prognosis of the existing disease. While
awaiting treatment, women may use CHCs. In general, treatment of this condition can render a woman
sterile.

Breast Disease
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer

2
1
1

Clarification: The woman should be evaluated as early as possible.

d. Breast cancer§
i. Current
ii. Past and no evidence of current
disease for 5 yrs
Endometrial hyperplasia
Endometrial cancer§

4
3

Evidence: Women with breast cancer susceptibility genes (such as BRCA1 and BRCA2) have a higher
baseline risk for breast cancer than do women without these genes. The baseline risk for breast cancer is
also higher among women with a family history of breast cancer than among those who do not have such
a history. However, current evidence does not suggest that the increased risk for breast cancer among
women with either a family history of breast cancer or breast cancer susceptibility genes is modified by the
use of COCs (278–295).
Comment: Breast cancer is a hormonally sensitive tumor, and the prognosis for women with current or
recent breast cancer might worsen with CHC use.

1
1

Comment: COC use reduces the risk for endometrial cancer; whether P or R use reduces the risk for
endometrial cancer is not known. While awaiting treatment, women may use COCs, P, or R. In general,
treatment of this condition renders a woman sterile.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Category

Clarifications/Evidence/Comments

Ovarian cancer§

Comment: COC use reduces the risk for ovarian cancer; whether P or R use reduces the risk for ovarian
cancer is not known. While awaiting treatment, women may use COCs, P, or R. In general, treatment of this
condition can render a woman sterile.

Uterine fibroids

Comment: COCs do not appear to cause growth of uterine fibroids, and P and R also are not expected to
cause growth.

Condition

Pelvic inflammatory disease (PID)
a. Past PID (assuming no current risk
factors for STIs)
i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID
STIs
a. Current purulent cervicitis or chlamydial infection or gonorrhea
b. Other STIs (excluding HIV and
hepatitis)
c. Vaginitis (including Trichomonas
vaginalis and bacterial vaginosis)
d. Increased risk for STIs

Comment: COCs might reduce the risk for PID among women with STIs but do not protect against HIV
or lower genital tract STIs. Whether use of P or R reduces the risk for PID among women with STIs is
unknown, but they do not protect against HIV or lower genital tract STIs.
1
1
1
1
1
1
1

Evidence: Evidence suggests that chlamydial cervicitis may be increased among COC users at high risk
for STIs. For other STIs, there is either evidence of no association between COC use and STI acquisition or
too limited evidence to draw any conclusions (296–376).

High risk for HIV

Evidence: The balance of the evidence suggests no association between oral contraceptive use and HIV
acquisition, although findings from studies conducted among higher risk populations have been inconsistent
(377–415).

HIV infection§

Evidence: Most studies suggest no increased risk for HIV disease progression with hormonal contraceptive
use, as measured by changes in CD4 cell count, viral load, or survival. Studies observing that women with
HIV who use hormonal contraception have increased risks of acquiring STIs are generally consistent with
reports among uninfected women. One direct study found no association between hormonal contraceptive
use and an increased risk for HIV transmission to uninfected partners; several indirect studies reported
mixed results about whether hormonal contraception is associated with increased risk for HIV-1 DNA or
RNA shedding from the genital tract (377,416–432).

AIDS§

Clarification: Drug interactions may occur between hormonal contraceptives and ARV therapy; refer to the
section on drug interactions.

Evidence: Among women with uncomplicated schistosomiasis, COC use had no adverse effects on liver
function (433–439).

HIV/AIDS

Other Infections
Schistosomiasis
a. Uncomplicated
b. Fibrosis of liver§ (if severe, see
cirrhosis)

Tuberculosis§
a. Nonpelvic
b. Pelvic

1
1

Malaria

Clarification: If a woman is taking rifampicin, refer to the section on drug interactions. Rifampicin is likely to
decrease COC effectiveness. The extent to which P or R use is similar to COC use in this regard remains
unclear.

Endocrine Conditions
Diabetes
a. History of gestational disease

b. Nonvascular disease
i. Noninsulin-dependent
ii. Insulin-dependent§
c. Nephropathy/retinopathy/
neuropathy§
d. Other vascular disease or diabetes of
>20 yrs’ duration§

3/4

Evidence: The development of noninsulin-dependant diabetes in women with a history of gestational
diabetes is not increased by use of COCs (440–447). Likewise, lipid levels appear to be unaffected by COC
use (448–450).
Evidence: Among women with insulin- or noninsulin-dependent diabetes, COC use had limited effect on
daily insulin requirements and no effect on long-term diabetes control (e.g., glycosylated hemoglobin levels)
or progression to retinopathy. Changes in lipid profile and hemostatic markers were limited, and most
changes remained within normal values (451–460).
Clarification: The category should be assessed according to the severity of the condition.

3/4

Clarification: The category should be assessed according to the severity of the condition.

2
2

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Condition
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Category

Clarifications/Evidence/Comments

1
1
1

Gastrointestinal Conditions
Inflammatory bowel disease (IBD)
(ulcerative colitis, Crohn disease)

2/3

Clarification: For women with mild IBD and no other risk factor for VTE, the benefits of COC/P/R use
generally outweigh the risks (Category 2). However, for women with IBD who are at increased risk for VTE
(e.g., those with active or extensive disease, surgery, immobilization, corticosteroid use, vitamin deficiencies, or fluid depletion), the risks of COC/P/R use generally outweigh the benefits (Category 3).
Evidence: Risk for disease relapse was not significantly higher among women with IBD using oral contraceptives (most studies did not specify formulation) than among nonusers (461–465).
Absorption of COCs among women with mild ulcerative colitis and no or small ileal resections was similar to
the absorption among healthy women (466,467). Findings might not apply to women with Crohn disease or
more extensive bowel resections.
No data exist that evaluate the increased risk for VTE among women with IBD using COCs/P/R. However,
women with IBD are at higher risk than unaffected women for VTE (468).

Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic

2
3
3
2

History of cholestasis
a. Pregnancy-related

b. Past COC-related

Viral hepatitis
a. Acute or flare
b. Carrier
c. Chronic

Comment: COCs, P, or R might cause a small increased risk for gallbladder disease. COCs, P, or R might
worsen existing gallbladder disease.

Comment: History of pregnancy-related cholestasis might predict an increased risk for COC-related
cholestasis.
Comment: History of COC-related cholestasis predicts an increased risk with subsequent COC use.

Initiation Continuation
3/4
2
Clarification for initiation: The category should be assessed according to the severity of the condition.
1
1
Evidence: Data suggest that in women with chronic hepatitis, COC use does not increase the rate or sever1
1
ity of cirrhotic fibrosis, nor does it increase the risk for hepatocellular carcinoma (469,470). For women who
are carriers, COC use does not appear to trigger liver failure or severe dysfunction (471-473). Evidence is
limited for COC use during active hepatitis (474).

Cirrhosis
a. Mild (compensated)
b. Severe§ (decompensated)

1
4

Liver tumors
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma§
b. Malignant§ (hepatoma)

2
4
4

Evidence: Limited direct evidence suggests that hormonal contraceptive use does not influence either
progression or regression of liver lesions among women with focal nodular hyperplasia (475,476).

Anemias
Thalassemia

Comment: Anecdotal evidence from countries where thalassemia is prevalent indicates that COC use does
not worsen the condition.

Sickle cell disease§

Iron deficiency anemia

Comment: CHC use may decrease menstrual blood loss.

Evidence: Limited evidence of COC and P users indicated no overall changes in biochemical measures.
However, one study reported discontinuations of COC use in 2 (8%) of 26 women as a result of serious
medical complications, and in one case report, a woman developed cholestasis associated with high-dose
COC use (477–480).
Clarification: Women with Budd-Chiari syndrome should not use COC/P/R because of the increased risk
for thrombosis.

Solid Organ Transplantation
Solid organ transplantation§
a. Complicated: graft failure (acute or
chronic), rejection, cardiac allograft
vasculopathy
b. Uncomplicated

MMWR

June 18, 2010

TABLE. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring*†
Condition

Category

Clarifications/Evidence/Comments

Drug Interactions
Antiretroviral (ARV) therapy
a. Nucleoside reverse transcriptase
inhibitors (NRTIs)
b. Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
c. Ritonavir-boosted protease inhibitors

Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin,
carbamazepine, barbiturates, primidone, topiramate, oxcarbazepine)

1
2
3

Clarification: ARV drugs have the potential to either decrease or increase the bioavailability of steroid
hormones in hormonal contraceptives. Limited data (summarized in Appendix M) suggest potential drug
interactions between many ARV drugs (particularly some non-NNRTIs and ritonavir-boosted protease
inhibitors) and hormonal contraceptives. These interactions might alter the safety and effectiveness of both
the hormonal contraceptive and the ARV drug. Thus, if a woman on ARV treatment decides to initiate or
continue hormonal contraceptive use, the consistent use of condoms is recommended to both prevent HIV
transmission and compensate for any possible reduction in the effectiveness of the hormonal contraceptive.
When a COC is chosen, a preparation containing a minimum of 30 µg EE should be used.
Clarification: Although the interaction of certain anticonvulsants with COCs, P, or R is not harmful to
women, it is likely to reduce the effectiveness of COCs, P, or R. Use of other contraceptives should be encouraged for women who are long-term users of any of these drugs. When a COC is chosen, a preparation
containing a minimum of 30 µg EE should be used.
Evidence: Use of certain anticonvulsants might decrease the effectiveness of COCs (481–484).

b. Lamotrigine

Clarification: The recommendation for lamotrigine applies only for situations where lamotrigine monotherapy is taken concurrently with COCs. Anticonvulsant treatment regimens that combine lamotrigine and
nonenzyme-inducing antiepileptic drugs (such as sodium valproate) do not interact with COCs.
Evidence: Pharmacokinetic studies show levels of lamotrigine decrease significantly during COC use
(485–489). Some women who used both COCs and lamotrigine experienced increased seizure activity in
one trial (485).

Antimicrobial therapy
a. Broad-spectrum antibiotics

Evidence: Most broad-spectrum antibiotics do not affect the contraceptive effectiveness of COCs(490–
526), P (527) or R (528).

b. Antifungals

Evidence: Studies of antifungal agents have shown no clinically significant pharmacokinetic interactions
with COCs (529–538) or R (539).

c. Antiparasitics

Evidence: Studies of antiparasitic agents have shown no clinically significant pharmacokinetic interactions
with COCs (433,540–544).

d. Rifampicin or rifabutin therapy

Clarification: Although the interaction of rifampicin or rifabutin therapy with COCs, P, or R is not harmful
to women, it is likely to reduce the effectiveness of COCs, P, or R. Use of other contraceptives should be
encouraged for women who are long-term users of either of these drugs. When a COC is chosen, a preparation containing a minimum of 30 µg EE should be used.
Evidence: The balance of the evidence suggests that rifampicin reduces the effectiveness of COCs
(545–560). Data on rifabutin are limited, but effects on metabolism of COCs are less than with rifampicin,
and small studies have not shown evidence of ovulation (547,554).

* Abbreviations: STI = sexually transmitted infection; HIV = human immunodeficiency virus; COC = combined oral contraceptive; P = patch; R = ring; EE = ethinyl estradiol;
BMD = bone mineral density; CHC = combined hormonal contraceptive; IUD = intrauterine device; VTE = venous thromboembolism; BMI = body mass index; DVT = deep
venous thrombosis; PE = pulmonary embolism; SLE = systemic lupus erythematosus; MEC = Medical Eligibility Criteria; hCG = human chorionic gonadotropin; DMPA = depot
medroxyprogesterone acetate; HPV = human papillomavirus; PID = pelvic inflammatory disease; AIDS = acquired immunodeficiency syndrome; ARV = antiretroviral; IBD =
inflammatory bowel disease; NRTI = nucleoside reverse transcriptase inhibitor; NNRTI = non-nucleoside reverse transcriptase inhibitor.
† COCs/P/R do not protect against STI/HIV. If risk for STI/HIV (including during pregnancy or postpartum) exists, the correct and consistent use of condoms is recommended,
either alone or with another contraceptive method. Consistent and correct use of the male latex condom reduces the risk for STI/HIV transmission.
§ Condition that exposes a woman to increased risk as a result of unintended pregnancy.

References
1. Abrams LS, Skee D, Natarajan J, Wong FA, Lasseter KC. Multiple-dose
pharmacokinetics of a contraceptive patch in healthy women participants. Contraception 2001;64:287–94.
2. Audet M-C, Moreau M, Koltun WD, et al. Evaluation of contraceptive
eﬃcacy and cycle control of a transdermal contraceptive patch vs. an
oral contraceptive: a randomized trial. JAMA 2001;285:2347–54.
3. Boonyarangkul A, Taneepanichskul S. Comparison of cycle control
and side effects between transdermal contraceptive patch and an
oral contraceptive in women older than 35 years. J Med Assoc Thai
2007;90:1715–9.
4. Burkman RT. The transdermal contraceptive patch: a new approach to
hormonal contraception. Int J Fertil 2002;47:69–76.
5. Cole JA, Norman H, Doherty M, Walker AM. Venous thromboembolism, myocardial infarction, and stroke among transdermal contraceptive
system users. Obstet Gynecol 2007;109:339–46.

6. Devineni D, Skee D, Vaccaro N, et al. Pharmacokinetics and pharmacodynamics of a transdermal contraceptive patch and an oral contraceptive.
J Clin Pharmacol 2007;47:497–509.
7. Dittrich R, Parker L, Rosen JB, et al. Transdermal contraception: evaluation of three transdermal norelgestromin/ethinyl estradiol doses in a
randomized, multicenter, dose-response study. Am J Obstet Gynecol
2002;186:15–20.
8. Helmerhorst FM, Cronje HS, Hedon B, et al. Comparison of eﬃcacy,
cycle control, compliance and safety in users of a contraceptive patch
vs. an oral contraceptive. Int J Gynaecol Obstet 2000;70:78.
9. Jick S, Kaye J, Li L, Jick H. Further results on the risk of nonfatal venous
thromboembolism in users of the contraceptive transdermal patch compared to users of oral contraceptives containing norgestimate and 35 µg
of ethinyl estradiol. Contraception 2007;76:4–7.

Vol. 59 / RR-4

Recommendations and Reports

10. Jick SS, Jick H. Cerebral venous sinus thrombosis in users of four hormonal
contraceptives: levonorgestrel-containing oral contraceptives, norgestimatecontaining oral contraceptives, desogestrel-containing oral contraceptives
and the contraceptive patch. Contraception 2006;74:290–2.
11. Jick SS, Kaye J, Russmaann S, Jick H. Risk of nonfatal venous thromboembolism in women using a contraceptive transdermal patch and
oral contraceptives containing norgestimate and 35 microg of ethinyl
estradiol. Contraception 2006;73:223–8.
12. Jick SS, Jick H. The contraceptive patch in relation to ischemic stroke
and acute myocardial infarction. Pharmacotherapy 2007;27:218–20.
13. Pierson RA, Archer DF, Moreau M, et al. Ortho EvraEvra versus oral
contraceptives: follicular development and ovulation in normal cycles
and after an intentional dosing error. Fertil Steril 2003;80:34–42.
14. Radowicki S, Skorzeqska K, Szlendak K. Safety evaluation of a transdermal contraceptive system with an oral contraceptive. Ginekologia Polska
2005;76:884–9.
15. Smallwood GH, Meador ML, Lenihan JP, et al. Eﬃcacy and safety of a
transdermal contraceptive system. Obstet Gynecol 2001;98:799–805.
16. Urdl W, Apter D, Alperstein A, et al. Contraceptive eﬃcacy, compliance
and beyond: factors related to satisfaction with once-weekly transdermal
compared with oral contraception. Eur J Obstet Gynecol Reprod Biol
2005;121:202–10.
17. White T, Ozel B, Jain JK, Stanczyk FZ. Eﬀects of transdermal and oral
contraceptives on estrogen-sensitive hepatic proteins. Contraception
2006;74:293–6.
18. Zieman M, Guillebaud JG, Weisberg E, et al. Contraceptive eﬃcacy and
cycle control with the Ortho Evra/Evra transdermal system: the analysis
of pooled data. Fertil Steril 2002;77:s13–s18.
19. Ahrendt HJ, Nisand I, Bastianelli C, et al. Eﬃcacy, acceptability and
tolerability of the combined contraceptive ring, NuvaRing, compared
with an oral contraceptive containing 30 microg of ethinyl estradiol and
3 mg of drospirene. Contraception 2006;74:451–7.
20. Bjarnadottir RI, Tuppurainen M, Killick SR. Comparison of cycle control with a combined contraceptive vaginal ring and oral levonorgestrel/
ethinyl estradiol. Am J Obstet Gynecol 2002;186:389–95.
21. Dieben T, Roumen FJ, Apter D. Eﬃcacy, cycle control, and user acceptibility of a novel combined contraceptive vaginal ring. Obstet Gynecol
2002;100:585–93.
22. Duijkers I, Killick SR, Bigrigg A, et al. A comparative study on the
eﬀects of a contraceptive vaginal ring NuvaRing and an oral contraceptive on carbohydrate metabolism and adrenal and thyroid function. Eur
J Contracept Reprod Health Care 2004;9:131–40.
23. Duijkers I, Klipping C, Verhoeven CH, et al. Ovarian function with the
contraceptive vaginal ring or an oral contraceptive: a randomized study.
Hum Reprod 2004;19:2668–73.
24. Elkind-Hirsch KE, Darensbourg C, Ogden B, et al. Contraceptive
vaginal ring use for women has less adverse metabolic eﬀets than an oral
contraceptive. Contraception 2007;76:348–56.
25. Magnusdottir EM, Bjarnadottir RI, Onundarson PT, et al. The contraceptive vaginal ring (NuvaRing) and hemostasis: a comparative study.
Contraception 2004;69:461–7.
26. Massai R, Makarainen L, Kuukankorpi A, Klipping C, Duijkers I, Dieben
T. The combined contraceptive vaginal ring and bone mineral density
in healthy pre-menopausal women. Hum Reprod 2005;20:2764–8.
27. Milsom I, Lete I, Bjertnaes A, et al. Eﬀects on cycle control and
bodyweight of the combined contraceptive ring, NuvaRing, versus an
oral contraceptive containing 30 microg ethinyl estradiol and 3 mg
drospirenone. Hum Reprod 2006;21:2304–11.
28. Oddsson K, Leifels-Fischer B, de Melo NR, et al. Eﬃcacy and safety of
a contraceptive vaginal ring (NuvaRing) compared with a combined oral
contraceptive: a 1-year randomized trial. Contraception 2005;71:176–82.
29. Sabatini R, Cagiano R. Comparison proﬁles of cycle control, side eﬀects
and sexual satisfaction of three hormonal contraceptives. Contraception
2006;74:220–3.

30. Timmer CJ, Mulders TM. Pharmacokinetics of etonogestrel and ethinylestradiol released from a combined contraceptive vaginal ring. Clin
Pharmacokinet 2000;39:233–42.
31. Tuppurainen M, Klimscheﬀskij R, Venhola M, et al. The
The combined contraceptive vaginal ring (NuvaRing) and lipid metabolism: a comparative
study. Contraception 2004;69:389–94.
32. van den Heuvel MW, van Bragt AJM, Alnabawy AKM, Kaptein MCJ.
Comparison of ethylestradiol pharmacokinetics in three hormonal
contraceptive formulations: the vaginal ring, the transdermal patch and
an oral contraceptive. Contraception 2005;72:168–74.
33. Veres S, Miller L, Burington B. A comparison between the vaginal ring
and oral contraceptives. Obstet Gynecol 2004;104:555–63.
34. Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral
density in adolescents using norethisterone enanthate, depot-medroxyprogesterone acetate or combined oral contraceptives for contraception.
Contraception 2007;75:438–43.
35. Cromer BA, Blair JM, Mahan JD, Zibners L, Naumovski Z. A prospective comparison of bone density in adolescent girls receiving depot
medroxyprogesterone acetate (Depo-Provera), levonorgestrel (Norplant),
or oral contraceptives. J Pediatr 1996;129:671–6.
36. Cromer BA, Stager M, Bonny A, et al. Depot medroxyprogesterone
acetate, oral contraceptives and bone mineral density in a cohort of
adolescent girls. J Adolesc Health 2004;35:434–41.
37. Lara-Torre E, Edwards CP, Perlman S, Hertweck SP. Bone mineral density
in adolescent females using depot medroxyprogesterone acetate. J Pediatr
Adolesc Gynecol 2004;17:17–21.
38. Lloyd T, Taylor DS, Lin HM, et al. Oral contraceptive use by teenage
women does not aﬀect peak bone mass: a longitudinal study. Fertil Steril
2000;74:734–8.
39. Lloyd T, Petit MA, Lin HM, Beck TJ. Lifestyle factors and the development of bone mass and bone strength in young women. J Pediatr
2004;144:776–82.
40. Polatti F, Perotti F, Filippa N, Gallina D, Nappi RE. Bone mass and
long-term monophasic oral contraceptive treatment in young women.
Contraception 1995;51:221–4.
41. Wallace LS, Ballard JE. Lifetime physical activity and calcium intake
related to bone density in young women. J Womens Health Gend Based
Med 2002;11:389–98.
42. Afghani A, Abbott AV, Wiswell RA, et al. Bone mineral density in
Hispanic women: role of aerobic capacity, fat-free mass, and adiposity.
Int J Sports Med 2004;25:384–90.
43. Bahamondes L, Juliato CT, Villarreal M, et al. Bone mineral density in
users of two kinds of once-a-month combined injectable contraceptives.
Contraception 2006;74:259–63.
44. Berenson AB, Radecki CM, Grady JJ, Rickert VI, Thomas A. A prospective, controlled study of the eﬀects of hormonal contraception on bone
mineral density. Obstet Gynecol 2001;98:576–82.
45. Berenson AB, Breitkopf CR, Grady JJ, Rickert VI, Thomas A. Eﬀects
of hormonal contraception on bone mineral density after 24 months of
use. Obstet Gynecol 2004;103:899–906.
46. Burr DB, Yoshikawa T, Teegarden D, et al. Exercise and oral contraceptive use suppress the normal age-related increase in bone mass
and strength of the femoral neck in women 18–31 years of age. Bone
2000;27:855–63.
47. Castelo-Branco C, Martinez de Osaba MJ, Pons F, Vanrell JA. Eﬀects
on bone mass of two oral contraceptives containing ethinylestradiol and
cyproterone acetate or desogestrel: results of a 2-year follow-up. Eur J
Contracept Reprod Health Care 1998;3:79–84.
48. Cobb KL, Kelsey JL, Sidney S, Ettinger B, Lewis CE. Oral contraceptives and bone mineral density in white and black women in CARDIA.
Coronary Risk Development in Young Adults. Osteoporos Int
2002;13:893–900.
49. Collins C, Thomas K, Harding A, et al. The eﬀect of oral contraceptives
on lumbar bone density in premenopausal women. J La State Med Soc
1988;140:35–9.

MMWR

50. de Papp AE, Bone HG, Caulﬁeld MP, et al. A cross-sectional study
of bone turnover markers in healthy premenopausal women. Bone
2007;40:1222–30.
51. Elgan C, Samsioe G, Dykes AK. Inﬂuence of smoking and oral contraceptives on bone mineral density and bone remodeling in young women:
a 2-year study. Contraception 2003;67:439–47.
52. Elgan C, Dykes AK, Samsioe G. Bone mineral density changes in young
women: a two year study. Gynecol Endocrinol 2004;19:169–77.
53. Endrikat J, Mih E, Dusterberg B, et al. A 3-year double-blind, randomized, controlled study on the inﬂuence of two oral contraceptives
containing either 20 microg or 30 microg ethinylestradiol in combination with levonorgestrel on bone mineral density. Contraception
2004;69:179–87.
54. Fortney JA, Feldblum PJ, Talmage RV, Zhang J, Godwin SE. Bone
mineral density and history of oral contraceptive use. J Reprod Med
1994;39:105–9.
55. Garnero P, Sornay-Rendu E, Delmas PD. Decreased bone turnover in
oral contraceptive users. Bone 1995;16:499–503.
56. Goldsmith N, Johnston J. Bone mineral: eﬀects of oral contraceptives, pregnancy, and lactation. J Bone Joint Surg (American) 1975;57–A:657–68.
57. Hall ML, Heavens J, Cullum ID, Ell PJ. The range of bone density in
normal British women. Br J Radiol 1990;63:266–9.
58. Hansen M, Overgaard K, Riis B, Christiansen C. Potential risk factors
for development of postmenopausal osteoporosis—examined over a
12-year period. Osteoporos Int 1991;1:95–102.
59. Hartard M, Bottermann P, Bartenstein P, Jeschke D, Schwaiger M. Eﬀects
on bone mineral density of low-dosed oral contraceptives compared to
and combined with physical activity. Contraception 1997;55:87–90.
60. Hartard M, Kleinmond C, Wiseman M, Weissenbacher ER, Felsenberg
D, Erben RG. Detrimental eﬀect of oral contraceptives on parameters
of bone mass and geometry in a cohort of 248 young women. Bone
2007;40:444–50.
61. Hawker GA, Forsmo S, Cadarette SM, et al. Correlates of forearm bone
mineral density in young Norwegian women: The Nord-Trondelag health
study. Am J Epidemiol 2002;156:01.
62. Hreshchyshyn MM, Hopkins A, Zylstra S, Anbar M. Associations of
parity, breast-feeding, and birth control pills with lumbar spine and
femoral neck bone densities. Am J Obstet Gynecol 1988;159:318–22.
63. Kanders B, Lindsay R, Dempster D, Markhard L, Valiquette G.
Determinants of bone mass in young healthy women. In: Christiansen,
C Arnaud CD, Nordin BEC, Parfitt AM, Peck WA, Riggs BL,
eds. Osteoporosis: proceedings of the Copenhagen Symposium on
Osteoporosis. Copenhagen: Department of Clinical Chemistry, Glostrup
Hospital: 1984:337–40.
64. Kleerekoper M, Brienza RS, Schultz LR, Johnson CC. Oral contraceptive
use may protect against low bone mass. Henry Ford Hospital Osteoporosis
Cooperative Research Group. Arch Intern Med 1991;151:1971–6.
65. Kritz-Silverstein D, Barrett-Connor E. Bone mineral density in postmenopausal women as determined by prior oral contraceptive use. Am
J Public Health 1993;83:100–2.
66. Laitinen K, Valimaki M, Keto P. Bone mineral density measured by
dual-energy X-ray absorptiometry in healthy Finnish women. Calcif
Tissue Int 1991;48:224–31.
67. Lau EMC, Lynn H, Woo J, Melton III LJ. Areal and volumetric bone
density in Hong Kong Chinese: A comparison with Caucasians living
in the United States. Osteoporos Int 2003;14:01.
68. Lindsay R, Tohme J, Kanders B. The eﬀect of oral contraceptive use on
vertebral bone mass in pre- and post-menopausal women. Contraception
1986;34:333–40.
69. Lloyd T, Buchanan JR, Ursino GR, et al. Long-term oral contraceptive use does not aﬀect trabecular bone density. Am J Obstet Gynecol
1989;160:402–4.
70. MacDougall J, Davies MC, Overton CE, et al. Bone density in a population of long term oral contraceptive pill users does not diﬀer from that
in menstruating women. Br J Fam Plann 1999;25:96–100.

June 18, 2010

71. Mais V, Fruzzetti F, Ajossa S, et al. Bone metabolism in young women
taking a monophasic pill containing 20 mcg ethinylestradiol: a prospective study. Contraception 1993;48:445–52.
72. Masaryk P, Lunt M, Benevolenskaya L, et al. Eﬀects of menstrual history and use of medications on bone mineral density: the EVOS Study.
Calcif Tissue Int 1998;63:271–6.
73. Mazess RB, Barden HS. Bone density in premenopausal women: eﬀects
of age, dietary intake, physical activity, smoking, and birth-control pills.
Am J Clin Nutr 1991;53:132–42.
74. Melton III LJ, Bryant SC, Wahner HW, et al. Inﬂuence of breastfeeding
and other reproductive factors on bone mass later in life. Osteoporos Int
1993;3:76–83.
75. Murphy S, Khaw KT, Compston JE. Lack of relationship between hip
and spine bone mineral density and oral contraceptive use. Eur J Clin
Invest 1993;23:108–11.
76. Nappi C, Di Spiezio SA, Acunzo G, et al. Eﬀects of a low-dose and
ultra–low-dose combined oral contraceptive use on bone turnover and
bone mineral density in young fertile women: a prospective controlled
randomized study. Contraception 2003;67:355–9.
77. Nappi C, Di Spiezio SA, Greco E, et al. Eﬀects of an oral contraceptive
containing drospirenone on bone turnover and bone mineral density.
Obstet Gynecol 2005;105:53–60.
78. Nelson M, Mayer AB, Rutherford O, Jones D. Calcium intake, physical
activity and bone mass in pre-menopausal women. J Hum Nutr Diet
1991;4:171–8.
79. Ott SM, Scholes D, LaCroix AZ, et al. Eﬀects of contraceptive use on
bone biochemical markers in young women. J Clin Endocrinol Metab
2001;86:179–85.
80. Paoletti AM, Orru M, Lello S, et al. Short-term variations in bone remodeling markers of an oral contraception formulation containing 3 mg of
drospirenone plus 30 microg of ethinyl estradiol: observational study
in young postadolescent women. Contraception 2004;70:293–8.
81. Pasco JA, Kotowicz MA, Henry MJ, et al. Oral contraceptives and
bone mineral density: A population-based study. Am J Obstet Gynecol
2000;182:265–9.
82. Perrotti M, Bahamondes L, Petta C, Castro S. Forearm bone density in
long-term users of oral combined contraceptives and depot medroxyprogesterone acetate. Fertil Steril 2001;76:469–73.
83. Petitti DB, Piaggio G, Mehta S, Cravioto MC, Meirik O. Steroid
hormone contraception and bone mineral density: a cross-sectional
study in an international population. The WHO Study of Hormonal
Contraception and Bone Health. Obstet Gynecol 2000;95:736–44.
84. Picard D, Ste-Marie LG, Coutu D, et al. Premenopausal bone mineral
content relates to height, weight and calcium intake during early adulthood. Bone Miner 1988;4:299–309.
85. Prior JC, Kirkland SA, Joseph L, et al. Oral contraceptive use and bone
mineral density in premenopausal women: cross-sectional, populationbased data from the Canadian Multicentre Osteoporosis Study. Can
Med Assoc J 2001;165:1023–9.
86. Recker RR, Davies KM, Hinders SM, et al. Bone gain in young adult
women. JAMA 1992;268:2403–8.
87. Reed SD, Scholes D, LaCroix AZ, et al. Longitudinal changes in
bone density in relation to oral contraceptive use. Contraception
2003;68:177–82.
88. Rodin A, Chapman M, Fogelman I. Bone density in users of combined
oral contraception. Preliminary reports of a pilot study. Br J Fam Plann
1991;16:125–9.
89. Shoepe HA, Snow CM. Oral contraceptive use in young women is associated with lower bone mineral density than that of controls. Osteoporos
Int 2005;16:1538–44.
90. Stevenson JC, Lees B, Devenport M, Cust MP, Ganger KF. Determinants
of bone density in normal women: risk factors for future osteoporosis?
BMJ 1989;298;924–8.

Vol. 59 / RR-4

Recommendations and Reports

91. Beksinska M, Smit J, Kleinschmidt I, Farley T, Mbatha F. Bone mineral
density in women aged 40–49 years using depot-medroxyprogesterone
acetate, norethisterone enanthate or combined oral contraceptives for
contraception. Contraception 2005;71:170–5.
92. Berning B, van KC, Schutte HE, et al. Determinants of lumbar bone
mineral density in normal weight, non-smoking women soon after
menopause. A study using clinical data and quantitative computed
tomography. Bone Miner 1993;21:129–39.
93. Forsmo S, Schei B, Langhammer A, Forsen L. How do reproductive
and lifestyle factors inﬂuence bone density in distal and ultradistal
radius of early postmenopausal women? The Nord-Trondelag Health
Survey, Norway. Osteoporos Int 2001;12:222–9.
94. Gambacciani M, Spinetti A, Taponeco F, et al. Longitudinal evaluation of perimenopausal vertebral bone loss: eﬀects of a low-dose oral
contraceptive preparation on bone mineral density and metabolism.
Obstet Gynecol 1994;83:392–6.
95. Gambacciani M, Spinetti A, Cappagli B, et al. Hormone replacement
therapy in perimenopausal women with a low dose oral contraceptive
preparation: eﬀects on bone mineral density and metabolism. Maturitas
1994;19(2):25–31).
96. Gambacciani M, Cappagli B, Ciaponi M, Benussi C, Genazzani AR.
Hormone replacement therapy in perimenopause: eﬀect of a low dose
oral contraceptive preparation on bone quantitative ultrasound characteristics. Menopause 1999;6:43–8.
97. Gambacciani M, Ciaponi M, Cappagli B, Benussi C, Genazzani AR.
Longitudinal evaluation of perimenopausal femoral bone loss: eﬀects
of a low-dose oral contraceptive preparation on bone mineral density
and metabolism. Osteoporos Int 2000;11:544–8.
98. Gambacciani M, Cappagli B, Lazzarini V, et al. Longitudinal evaluation of perimenopausal bone loss: eﬀects of diﬀerent low dose oral
contraceptive preparations on bone mineral density. Maturitas
2006;54:176–80.
99. Grainge MJ, Coupland CAC, Cliﬀe SJ, Chilvers CED, Hosking DJ.
Reproductive, menstrual and menopausal factors: which are associated
with bone mineral density in early postmenopausal women? Osteoporos
Int 2001;12:777–87.
100. Johnell O, Nilsson BE. Life-style and bone mineral mass in perimenopausal women. Calcif Tissue Int 1984;36:354–6.
101. Liu SL, Lebrun CM. Eﬀect of oral contraceptives and hormone replacement therapy on bone mineral density in premenopausal and perimenopausal women: a systematic review. Br J Sports Med 2006;40:11–24.
102. Progetto Menopausa Italia Study Group. Risk of low bone density in women attending menopause clinics in Italy. Maturitas
2002;42:105–11.
103. Shargil AA. Hormone replacement therapy in perimenopausal women
with a triphasic contraceptive compound: a three-year prospective study.
Int J Fertil 1985;30.
104. Sowers MF, Wallace RB, Lemke JH. Correlates of forearm bone
mass among women during maximal bone mineralization. Prev Med
1985;14:585–96..
105. Sultana S, Choudhury S, Choudhury SA. Eﬀect of combined oral
contraceptives on bone mineral density in pre and postmenopausal
women. Mymensingh Med J 2002;11:12–4.
106. Taechakraichana N, Limpaphayom K, Ninlagarn T, et al. A randomized
trial of oral contraceptive and hormone replacement therapy on bone
mineral density and coronary heart disease risk factors in postmenopausal women. Obstet Gynecol 2000;95:87–94.

107. Taechakraichana N, Jaisamrarn U, Panyakhamlerd K, Chaikittisilpa S,
Limpaphayom K. Diﬀerence in bone acquisition among hormonally
treated postmenopausal women with normal and low bone mass. J
Med Assoc Thai 2001;84 Suppl 2:S586–S592.
108. Tavani A, La Vecchia C, Franceschi S. Oral contraceptives and bone
mineral density. Am J Obstet Gynecol 2001;184:249–50.
109. Tuppurainen M, Kroger H, Saarikoski S, Honkanen R, Alhava E. The
eﬀect of previous oral contraceptive use on bone mineral density in
perimenopausal women. Osteoporos Int 1994;4:93-8.
110. Volpe A, Amram A, Cagnacci A, Battaglia C. Biochemical aspects of
hormonal contraception: eﬀects on bone metabolism. Eur J Contracept
Reprod Health Care 1997;2:123-6.
111. Barad D, Kooperberg C, Wactawski-Wende J, et al. Prior oral contraception and postmenopausal fracture: a Women’s Health Initiative
observational cohort study. Fertil Steril 2005;84:374–83.
112. Cobb KL, Bachrach LK, Sowers M, et al. The eﬀect of oral contraceptives on bone mass and stress fractures in female runners. Med Sci
Sports Exerc 2007;39:1464–73.
113. Cooper C, Hannaford P, Croft P, Kay CR. Oral contraceptive pill use
and fractures in women: a prospective study. Bone 1993;14:41–5.
114. Johansson C, Mellstrom D. An earlier fracture as a risk factor for
new fracture and its association with smoking and menopausal age in
women. Maturitas 1996;24:97–106.
115. La Vecchia C, Tavani A, Gallus S. Oral contraceptives and risk of hip
fractures. Lancet 1999;354:335–6.
116. Mallmin H, Ljunghall S, Persson I, Bergstrom R. Risk factors for
fractures of the distal forearm: a population-based case-control study.
Osteoporos Int 1994;4:298–304.
117. Michaelsson K, Baron JA, Farahmand BY, Persson I, Ljunghall S. Oralcontraceptive use and risk of hip fracture: a case-control study. Lancet
1999;353:1481–4.
118. Michaelsson K, Baron JA, Farahmand BY, Ljunghall S. Inﬂuence
of parity and lactation on hip fracture risk. Am J Epidemiol
2001;153:1166–72.
119. O’Neill TW, Marsden D, Adams JE, Silman AJ. Risk factors, falls,
and fracture of the distal forearm in Manchester, UK. J Epidemiol
Community Health 1996;50:288–92.
120. O’Neill TW, Silman AJ, Naves DM, et al. Inﬂuence of hormonal and
reproductive factors on the risk of vertebral deformity in European
women. European Vertebral Osteoporosis Study Group. Osteoporos
Int 1997;7:72–8.
121. Vessey M, Mant J, Painter R. Oral contraception and other factors
in relation to hospital referral for fracture. Findings in a large cohort
study. Contraception 1998;57:231–5.
122. Vestergaard P, Rejnmark L, Mosekilde L. Oral contraceptive use and
risk of fractures. Contraception 2006;73:571–6.
123. Oﬃce on Women’s Health, US Department of Health and Human
Services. HHS blueprint for action on breastfeeding. Washington, DC:
US Department of Health and Human Services, Oﬃce on Women’s
Health; 2000.
124. Kaern T. Eﬀect of an oral contraceptive immediately post partum on
initiation of lactation. Br Med J 1967;3:644–5.
125. Miller GH, Hughes LR. Lactation and genital involution eﬀects of a
new low-dose oral contraceptive on breast-feeding mothers and their
infants. Obstet Gynecol 1970;35:44–50.
126. Gambrell RD. Immediate postpartum oral contraception. Obstet
Gynecol 1970;36:101–6.
127. Guiloﬀ E, Ibarrapo A, Zanartu J, et al. Eﬀect of contraception on
lactation. Am J Obstet Gynecol 1974;118:42–5.

MMWR

128. Diaz S, Peralta O, Juez G, et al. Fertility regulation in nursing women.
3. Short-term inﬂuence of a low-dose combined oral-contraceptive
upon lactation and infant growth. Contraception 1983;27:1–11.
129. Croxatto HB, Diaz S, Peralta O, et al. Fertility regulation in nursing
women. 4. Long-term inﬂuence of a low-dose combined oral-contraceptive initiated at day 30 postpartum upon lactation and infant
growth. Contraception 1983;27:13–25.
130. Peralta O, Diaz S, Juez G, et al. Fertility regulation in nursing women. 5.
Long-term nﬂuence of a low-dose combined oral-contraceptive initiated
at day 90 postpartum upon lactation and infant growth. Contraception
1983;27:27–38.
131. World Health Organization Special Programme of Research
Development and Research Training in Human Reproduction. Eﬀects
of hormonal contraceptives on milk volume and infant growth.
Contraception 1984;30:505–22.
132. Nilsson S, Melbin T, Hofvander Y, et al. Long-term follow-up of children breast-fed by women using oral contraceptives. Contraception
1986;34:443–53.
133. World Health Organization Task Force on Oral Contraceptives Special
Programme of Research Development and Research Training in Human
Reproduction. Eﬀects of hormonal contraceptives on breast milk
composition and infant growth. Stud Fam Plann 1988;19:361–9.
134. Lahteenmaki P. Inﬂuence of oral contraceptives on immediate postabortal pituitary-ovarian function. Acta Obstet Gynecol Scand 1978;Suppl
76:1–43.
135. Lahteenmaki P, Rasi V, Luukkainen T, Myllyä G. Coagulation factors in
women using oral contraceptives or intrauterine contraceptive devices
immediately after abortion. Am J Obstet Gynecol 1981;141:175–9.
136. Martin CW, Brown AH, Baird DT. A pilot study of the eﬀect of
methotrexate or combined oral contraceptive on bleeding patterns after
induction of abortion with mifepristone and a prostaglandin pessary.
Contraception 1998;58:99–103.
137. Niswonger JWH, London GD, Anderson GV, Wolfe L. Oral contraceptives during immediate postabortal period. Obstet Gynecol
1968;32:325–7.
138. Peterson WF. Contraceptive therapy following therapeutic abortion.
Obstet Gynecol 1974;44:853–7.
139. Tang OS, et al. A randomized double-blind placebo-controlled study
to assess the eﬀect of oral contraceptive pills on the outcome of
medical abortion with mifepristone and misoprostol. Hum Reprod
1999;14:722–5.
140. Tang OS, Gao PP, Cheng L, Lee SW, Ho PC. The eﬀect of contraceptive
pills on the measured blood loss in medical termination of pregnancy
by mifepristone and misoprostol: a randomized placebo controlled
trial. Hum Reprod 2002;17:99–102.
141. Fine PM, Tryggestad J, Meyers NJ, Sangi-Haghpeykar H. Safety and
acceptability with the use of a contraceptive vaginal ring after surgical
or medical abortion. Contraception 2007;75:367–71.
142. Gillum LA, Mamidipudi SK, Johnston SC. Ischaemic stroke risk with
oral contraceptives: a meta-analysis. JAMA 2000;284:72–8.
143. Jick SS, Walker AM, Stergachis A, Jick H. Oral contraceptives and
breast cancer. Br J Cancer 1989;59:618–21.
144. Khader YS, Rice J, John L, Abueita O. Oral contraceptive use and
the risk of myocardial infarction: a meta-analysis. Contraception
2003;68:11–7.
145. Lawson DH, Davidson JF, Jick H. Oral contraceptive use and
venous thromboembolism: absence of an eﬀect of smoking. BMJ
1977;2:729–30.

June 18, 2010

146. Lidegaard O, Edstrom B, Kreiner S. Oral contraceptives and
venous thromboembolism. A case-control study. Contraception
1998;57:291–301.
147. Nightingale AL, Lawrenson RA, Simpson EL, Williams TJ, MacRae
KD, Farmer RD. The eﬀects of age, body mass index, smoking and
general health on the risk of venous thromboembolism in users of
combined oral contraceptives. Eur J Contracept Reprod Health Care
2000;5:265–74.
148. Petitti D, Wingerd J, Pellegrin F, Ramcharan S. Risk of vascular disease
in women. Smoking, oral contraceptives, noncontraceptive estrogens,
and other factors. JAMA 1979;242:1150–4.
149. Rosenberg L, Palmer JR, Rao RS, Shapiro S. Low-dose oral contraceptive use and the risk of myocardial infarction. Arch Intern Med
2001;161:1065–70.
150. Straneva P, Hinderliter A, Wells E, Lenahan H, Girdler S. Smoking, oral
contraceptives, and cardiovascular reactivity to stress. Obstet Gynecol
2000;95:78–83.
151. Tanis BC, van den Bosch MA, Kemmeren JM, et al. Oral contraceptives and the risk of myocardial infarction. N Engl J Med
2001;345:1787–93.
152. van den Bosch MA, Kemmeren JM, Tanis BC, et al. The RATIO study:
oral contraceptives and the risk of peripheral arterial disease in young
women. J Thromb Haemost 2003;1:439–44.
153. World Health Organization. Venous thromboembolic disease and
combined oral contraceptives: results of international multicentre
case-control study. Lancet 1995;346:1575–82.
154. Abdollahi M, Cushman M, Rosendaal FR. Obesity: risk of venous
thrombosis and the interaction with coagulation factor levels and oral
contraceptive use. Thromb Haemost 2003;89:493–8.
155. Lidegaard O, Edstrom B, Kreiner S. Oral contraceptives and
venous thromboembolism: a ﬁve-year national case-control study.
Contraception 2002;65:187–96.
156. Pomp ER, le CS, Rosendaal FR, Doggen CJ. Risk of venous thrombosis:
obesity and its joint eﬀect with oral contraceptive use and prothrombotic mutations. Br J Haematol 2007;139:289–96.
157. Schwartz SM, Petitti DB, Siscovick DS, et al. Stroke and use of lowdose oral contraceptives in young women: a pooled analysis of two US
studies. Stroke 1998;29:2277–84.
158. Sidney S, Siscovick DS, Petitti DB, et al. Myocardial infarction and
use of low-dose oral contraceptives: a pooled analysis of 2 US studies.
Circulation 1998;98:1058–63.
159. Sidney S, Petitti DB, Soﬀ GA, et al. Venous thromboembolic disease in
users of low-estrogen combined estrogen-progestin oral contraceptives.
Contraception 2004;70:3–10.
160. Brunner Huber LR, Hogue CJ, Stein AD, Drews C, Zieman M. Body
mass index and risk for oral contraceptive failure: a case-cohort study
in South Carolina. Ann Epidemiol 2006;16:637–43.
161. Brunner Huber LR, Toth JL. Obesity and oral contraceptive failure:
ﬁndings from the 2002 National Survey of Family Growth. Am J
Epidemiol 2007;166:1306–11.
162. Brunner LR, Hogue CJ. The role of body weight in oral contraceptive
failure: results from the 1995 National Survey of Family Growth. Ann
Epidemiol 2005;15:492–9.
163. Holt VL, Cushing-Haugen KL, Daling JR. Body weight and risk of
oral contraceptive failure. Obstet Gynecol 2002;99:820–7.
164. Holt VL, Scholes D, Wicklund KG, Cushing-Haugen KL, Daling JR.
Body mass index, weight, and oral contraceptive failure risk. Obstet
Gynecol 2005;105:46–52.

Vol. 59 / RR-4

Recommendations and Reports

165. Vessey M. Oral contraceptive failures and body weight: ﬁndings in a
large cohort study. J Fam Plann Reprod Health Care 2001;27:90–1.
166. O’Connell KJ, Osborne LM, Westoﬀ C. Measured and reported weight
change for women using a vaginal contraceptive ring vs. a low-dose
oral contraceptive. Contraception 2005;72:323–7.
167. Weiss HG, Nehoda H, Labeck B, et al. Pregnancies after adjustable
gastric banding. Obes Surg 2001;11:303–6.
168. Gerrits EG, Ceulemans R, van HR, Hendrickx L, Totte E. Contraceptive
treatment after biliopancreatic diversion needs consensus. Obes Surg
2003;13:378–82.
169. Victor A, Odlind V, Kral JG. Oral contraceptive absorption and sex
hormone binding globulins in obese women: eﬀects of jejunoileal
bypass. Gastroenterol Clin North Am 1987;16:483–91.
170. Andersen AN, Lebech PE, Sorensen TI, Borggaard B. Sex hormone levels and intestinal absorption of estradiol and D-norgestrel in women following bypass surgery for morbid obesity. Int J Obes 1982;6:91–6.
171. Collaborative Group for the Study of Stroke in Young Women. Oral
contraceptives and stroke in young women: associated risk factors.
JAMA 1975;231:718–22.
172. Croft P, Hannaford P. Risk factors for acute myocardial infarction in
women: evidence from the Royal College of General Practitioners’ Oral
Contraception Study. BMJ 1989;298:165–8.
173. D’Avanzo B, La Vecchia C, Negri E, Parazzini F, Franceschi S. Oral
contraceptive use and risk of myocardial infarction: an Italian casecontrol study. J Epidemiol Community Health 1994;48:324–8.
174. Dunn NR, Faragher B, Thorogood M, et al. Risk of myocardial infarction in young female smokers. Heart 1999;82:581–3.
175. Hannaford P, Croft P, Kay CR. Oral contraception and stroke: evidence
from the Royal College of General Practitioners’ Oral Contraception
Study. Stroke 1994;25:935–42.
176. Heinemann LA, Lewis MA, Spitzer WO, Thorogood M, GuggenmoosHolzmann I, Bruppacher R. Thromboembolic stroke in young women.
A European case-control study on oral contraceptives. Contraception
1998;57:29–37.
177. Kemmeren JM, Tanis BC, van den Bosch MA, et al. Risk of
Arterial Thrombosis in Relation to Oral Contraceptives (RATIO)
study: oral contraceptives and the risk of ischemic stroke. Stroke
2002;33:1202–8.
178. Lewis MA, Heinemann LA, Spitzer WO, MacRae KD, Bruppacher R.
The use of oral contraceptives and the occurrence of acute myocardial
infarction in young women. Results from the Transnational Study on
Oral Contraceptives and the Health of Young Women. Contraception
1997;56:129–40.
179. Lidegaard O. Oral contraception and risk of a cerebral thromboembolic
attack: results of a case-control study. BMJ 1993;306:956–63.
180. Lidegaard O. Oral contraceptives, pregnancy and the risk of cerebral thromboembolism: the influence of diabetes, hypertension,
migraine and previous thrombotic disease. Br J Obstet Gynaecol
1995;102:153–9.
181. Lubianca JN, Faccin CS, Fuchs FD. Oral contraceptives: a risk factor for uncontrolled blood pressure among hypertensive women.
Contraception 2003;67:19–24.
182. Narkiewicz K, Graniero GR, D’Este D, Mattarei M, Zonzin P,
Palatini P. Ambulatory blood pressure in mild hypertensive women
taking oral contraceptives. A case-control study. Am J Hypertens
1995;8:249–53.
183. Siritho S, Thrift AG, McNeil JJ, et al. Risk of ischemic stroke among
users of the oral contraceptive pill: The Melbourne Risk Factor Study
(MERFS) Group. Stroke 2003;34:1575–80.

184. World Health Organization. Haemorrhagic stroke, overall stroke
risk, and combined oral contraceptives: results of an international,
multicentre, case-control study. WHO Collaborative Study of
Cardiovascular Disease and Steroid Hormone Contraception. Lancet
1996;348:505–10.
185. World Health Organization. Ischaemic stroke and combined oral contraceptives: results of an international, multicentre, case-control study.
WHO Collaborative Study on Cardiovascular Disease and Steroid
Hromone Contraception. Lancet 1996;348:498–505.
186. World Health Organization. Acute myocardial infarction and combined
oral contraceptives: results of an international multicentre case-control
study. WHO Collaborative Study on Cardiovascular Disease and
Steroid Hormone Contraception. Lancet 1997;349:1202–9.
187. Lubianca JN, Moreira LB, Gus M, Fuchs FD. Stopping oral contraceptives: an eﬀective blood pressure-lowering intervention in women with
hypertension. J Hum Hypertens 2005;19:451–5.
188. Aberg H, Karlsson L, Melander S. Studies on toxaemia of pregnancy
with special reference to blood pressure. ll. Results after 6–11 years’
follow-up. Ups J Me Sci 1978;83:97–102.
189. Carmichael SM, Taylor MM, Ayers CR. Oral contraceptives, hypertension, and toxemia. Obstet Gynecol 1970;35:371–6.
190. Meinel H, Ihle R, Laschinski M. Eﬀect of hormonal contraceptives on
blood pressure following pregnancy-induced hypertension [in German].
Zentralbl Gynäkol 1987;109:527–31.
191. Pritchard JA, Pritchard SA. Blood pressure response to estrogenporgestin oral contraceptive after pregnancy-induced hypertension.
Am J Obstet Gynecol 1977;129:733–9.
192. Sibai BM, Taslimi MM, el-Nazer A, Amon E, Mabie BC, Ryan GM.
Maternal-perinatal outcome associated with the syndrome of hemolysis, elevated liver enzymes, and low platelets in severe preeclampsiaeclampsia. Am J Obstet Gynecol 1986;155:501–9.
193. Sibai BM, Ramadan MK, Chari RS, Friedman SA. Pregnancies complicated by HELLP syndrome (hemolysis, elevated liver enzymes, and
low platelets): subsequent pregnancy outcome and long-term prognosis.
Am J Obstet Gynecol 1995;172:125–9.
194. Anderson BS, Olsen J, Nielsen GL, et al. Third generation oral contraceptives and heritable thrombophilia as risk factors of non-fatal venous
thromboembolism. Thromb Haemost 1998;79:28–31.
195. Aznar J, Mira Y, Vaya A, et al. Factor V Leiden and prothrombin
G20210A mutations in young adults with cryptogenic ischemic stroke.
Thromb Haemost 2004;91:1031–4.
196. Bennet L, Odeberg H. Resistance to activated protein C, highly prevalent amongst users of oral contraceptives with venous thromboembolism. J Intern Med 1998;244:27–32.
197. Bloemenkamp KW, Rosendaal FR, Helmerhorst FM, et al.
Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation
progestagen [comment]. Lancet 1995;346:1593–6.
198. Bloemenkamp KW, Rosendaal FR, Helmerhorst FM, et al. Higher
risk of venous thrombosis during early use of oral contraceptives in
women with inherited clotting defects [comment]. Arch Intern Med
2000;160:49–52.
199. de Bruijn SF, Stam J, Koopman MM, et al. Case-control study of risk of
cerebral sinu thrombosis in oral contraceptive users and in [correction of
who are] carriers of heriditary prothrombotic conditions. The Cerebral
Venous Sinus Thrombosis Study Group. BMJ 1998;316:589–92.

MMWR

200. Emmerich J, Rosendaal FR, Cattaneo M, et al. Combined eﬀect
of factor V Leiden and prothrombin 20210A on the risk of venous
thromboembolism—pooled analysis of 8 case-control studies including 2310 cases and 3204 controls. Study Group for Pooled-Analysis
in Venous Thromboembolism. Thromb Haemost 2001;86:809–16.
201. Gadelha T, Andre C, Juca AA, et al. Prothrombin 20210A and oral
contraceptive use as risk factors for cerebral venous thrombosis.
Cerebrovasc Dis 2005;19:49–52.
202. Legnani C, Palareti G, Guazzaloca G, et al. Venous thromboembolism
in young women: role of throbophilic mutations and oral contraceptive
use. Eur Heart J 2002;23:984–90.
203. Martinelli I, Sacchi E, Landi G, et al. High risk of cerebral-vein thrombosis in carriers of a prothrombin-gene mutation and in users of oral
contraceptives [comment]. N Eng J Med 1998;338:1793–7.
204. Martinelli I, Taioli E, Bucciarelli P, et al. Interaction between the
G20210A mutation of the prothrombin gene and oral contraceptive use in deep vein thrombosis. Arterioscler Thromb Vasc Biol
1999;19:700–3.
205. Martinelli I, Battaglioli T, Bucciarelli P, et al. Risk factors and recurrence rate of primary deep vein thrombosis of the upper extremities.
Circulation 2004;110:566–70.
206. Martinelli I, Battaglia C, Burgo I, et al. Oral contraceptive use, thrombophilia and their interaction in young women with ischemic stroke.
Haematologica 2006;91:844–7.
207. Middeldorp S, Meinardi JR, Koopman MM, et al. A prospective study
of asymptomatic carriers of the factor V Leiden mutation to determine
the incidence of venous thromboembolism [comment]. Ann Intern
Med 2001;135:322–7.
208. Pabinger I, Schneider B. Thrombotic risk of women with hereditary
antithrombin lll-, protein C- and protein S-deﬁciency taking oral contraceptive medication. The GTH Study Group on Natural Inhibitors.
Thromb Haemost 1994;71:548–52.
209. Pezzini A, Grassi M, Iacoviello L, et al. Inherited thrombophilia and
stratiﬁcation of ischaemic stroke risk among users of oral contraceptives.
J Neurol Neurosurg Psychiatry 2007;78:271–6.
210. Santamaria A, Mateo J, Oliver A, et al. Risk of thrombosis associated with
oral contraceptives of women from 97 families with inherited thrombophilia: high risk of thrombosis in carriers of the G20210A mutation
of the prothrombin gene. Haematologica 2001;86:965–71.
211. Slooter AJ, Rosendaal FR, Tanis BC, et al. Prothrombotic conditions,
oral contraceptives, and the risk of ischemic stroke. J Thromb Haemost
2005;3:1213–7.
212. Spannagl M, Heinemann LA, Schramm W. Are factor V Leiden carriers
who use oral contraceptives at extreme risk of venous thromboembolism? Eur J Contracept Reprod Health Care 2000;5:105–12.
213. van Boven HH, Vandenbroucke JP, Briet E, et al. Gene-gene and geneenvironment interactions determine risk of thrombosis in families with
inherited antithrombin deﬁciency. Blood 1999;94:2590–4.
214. van Vlijmen EF, Brouwer JL, Veeger NJ, et al. Oral contraceptives and
the absolute risk of venous thromboembolism in women with single
or multiple thrombophilic defects: results from a retrospective family
cohort study. Arch Intern Med 2007;167:282–9.
215. Vandenbroucke JP, Koster T, Briet E, et al. Increased risk of venous
thrombosis in oral-contraceptive users who are carriers of factor V
Leiden mutation [comment]. Lancet 1994;344:1453–7.
216. Vaya AM. Prothrombin G20210A mutation and oral contraceptive use
increase upper-extremity deep vein thrombotic risk. Thromb Haemost
2003;89:452–7.

June 18, 2010

217. The Criteria Committee of the New York Heart Association.
Nomenclature and criteria for diagnosis of diseases of the heart and
great vessels. 9th ed. Boston, MA: Little, Brown & Co; 1994.
218. Avila WS, Grinberg M, Melo NR, Aristodemo PJ, Pileggi F.
Contraceptive use in women with heart disease [in Portuguese]. Arq
Bras Cardiol 1996;66:205–11.
219. Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated with abnormal Pap results in systemic lupus erythematosus.
Rheumatology (Oxford) 2004;43:1386–9.
220. Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures
and breast cancer in a sample of women with systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1178–81.
221. Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin
gene mutation, and thrombosis risk in patients with antiphospholipid
antibodies. J Rheumatol 2002;29:1683–8.
222. Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional
Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. Arthritis Rheum
2001;44:2331–7.
223. Julkunen HA. Oral contraceptives in systemic lupus erythematosus:
side-eﬀects and inﬂuence on the activity of SLE. Scand J Rheumatol
1991;20:427–33.
224. Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women with
systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30.
225. Jungers P, Dougados M, Pelissier C, et al. Inﬂuence
Inﬂuence of oral contraceptive therapy on the activity of systemic lupus erythematosus. Arthritis
Rheum 1982;25:618–23.
226. Manzi S, Meilahn EN, Rairie JE, et al. Age-speciﬁc incidence rates of
myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study. Am J Epidemiol
1997;145:408–15.
227. McAlindon T, Giannotta L, Taub N, et al. Environmental factors
predicting nephristis in systemic lupus erythematosus. Ann Rheum
Dis 1993;52:720–4.
228. McDonald J, Stewart J, Urowitz MB, et al. Peripheral vascular disease in patients with systemic lupus erythematosus. Ann Rheum Dis
1992;51:56–60.
229. Mintz G, Gutierrez G, Deleze M, et al. Contraception with progestogens
in systemic lupus erythematosus. Contraception 1984;30:29–38.
230. Petri M. Musculoskeletal complications of systemic lupus erythematosus in the Hopkins Lupus Cohort: an update. Arthritis Care Res
1995;8:137–45.
231. Petri M, Kim MY, Kalunian KC, et al. Combined oral contraceptives in women with systemic lupus erythematosus. N Engl J Med
2005;353:2550–8.
232. Petri M. Lupus in Baltimore: evidence-based ‘clinical perarls’ from the
Hopkins Lupus Cohort. Lupus 2005;14:970–3.
233. Sanchez-Guerrero J, Uribe AG, Jimenez-Santana L, et al. A trial of
contraceptive methods in women with systemic lupus erythematosus.
N Engl J Med 2005;353:2539–49.
234. Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and
venous thrombosis after diagnosis of systemic lupus erythematosus.
Arthritis Rheum 2005;53:609–12.
235. Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrel-releasing intrauterine system in the management of menorrhagia in women
with hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–3.
236. Somers E, Magder LS, Petri M. Antiphospholipid antibodies and
incidence of venous thrombosis in a cohort of patients with systemic
lupus erythematosus. J Rheumatol 2002;29:2531–6.

Vol. 59 / RR-4

Recommendations and Reports

237. Urowitz MB, Bookman AA, Koehler BE, et al. The bimodal mortality
pattern of systemic lupus erythematosus. Am J Med 1976;60:221–5.
238. Choojitarom K, Verasertniyom O, Totemchokchyakarn K, et al. Lupus
nephritis and Raynaud’s phenomenon are signiﬁcant risk factors for
vascular thrombosis in SLE patients with positive antiphospholipid
antibodies. Clin Rheumatol 2008;27:345–51.
239. Wahl DG, Guillemin F, de Maistre E, et al. Risk for venous thrombosis
related to antiphospholipid antibodies in systemic lupus erythematosus—a meta-analysis. Lupus 1997;6:467–73.
240. Demers R, Blais JA, Pretty H. Rheumatoid arthritis treated by norethynodrel associated with mestranol: clinical aspects and laboratory
tests [in French]. Can Med Assoc J 1966;95:350–4.
241. Drossaers-Bakker KW, Zwinderman AH, Van ZD, Breedveld FC,
Hazes JM. Pregnancy and oral contraceptive use do not signiﬁcantly
inﬂuence outcome in long term rheumatoid arthritis. Ann Rheum Dis
2002;61:405-8.
242. Gilbert M, Rotstein J, Cunningham C, et al. Norethynodrel with mestranol in treatment of rheumatoid arthritis. JAMA 1964;190:235.
243. Gill D. Rheumatic complaints of women using anti-ovulatory drugs.
An evaluation. J Chronic Dis 1968;21:435–44.
244. Hazes JM, Dijkmans BA, Vandenbroucke JP, Cats A. Oral contraceptive treatment for rheumatoid arthritis: an open study in 10 female
patients. Br J Rheumatol 1989;28 Suppl 1:28–30.
245. Ostensen M, Aune B, Husby G. Eﬀect of pregnancy and hormonal
changes on the activity of rheumatoid arthritis. Scand J Rheumatol
1983;12:69–72.
246. Vignos PJ, Dorfman RI. Eﬀect of large doses of progesterone in rheumatoid arthritis. Am J Med Sci 1951;222:29–34.
247. Bijlsma JW, Huber-Bruning O, Thijssen JH. Eﬀect of oestrogen treatment on clinical and laboratory manifestations of rheumatoid arthritis.
Ann Rheum Dis 1987;46:777–9.
248. Carolei A, Marini C, De Matteis G. History of migraine and risk of cerebral ischaemia in young adults. The Italian National Research Council
Study Group on Stroke in the Young. Lancet 1996;347:1503–6.
249. Chang CL, Donaghy M, Poulter N. Migraine and stroke in young
women: case-control study. The World Health Organisation
Collaborative Study of Cardiovascular Disease and Steroid Hormone
Contraception. BMJ 1999;318:13–8.
250. Tzourio C, Tehindrazanarivelo A, Iglesias S, et al. Case-control study
of migraine and risk of ischaemic stroke in young women. BMJ
1995;310:830–3.
251. Oral contraceptives and stroke in young women. Associated risk factors.
JAMA 1975;231:718–22.
252. Etminan M, Takkouche B, Isorna FC, Samii A. Risk of ischaemic
stroke in people with migraine: systematic review and meta-analysis
of observational studies. BMJ 2005;330:63.
253. Lidegaard O. Oral contraceptives, pregnancy, and the risk of cerebral
thromboembolism: the inﬂuence of diabetes, hypertension, migraine
and previous thrombotic disease [letter]. Br J Obstet Gynaecol
1996;103:94.
254. Nightingale AL, Farmer RD. Ischemic stroke in young women: a nested
case-control study using the UK General Practice Research Database.
Stroke 2004;35:1574–8.
255. Cromer BA, Smith RD, Blair JM, Dwyer J, Brown RT. A prospective study of adolescents who choose among levonorgestrel implant
(Norplant), medroxyprogesterone acetate (Depo-Provera), or
the combined oral contraceptive pill as contraception. Pediatrics
1994;94:687–94.

256. Deijen JB, Duyn KJ, Jansen WA, Klitsie JW. Use of a monophasic, lowdose oral contraceptive in relation to mental functioning. Contraception
1992;46:359–67.
257. Duke JM, Sibbritt DW, Young AF. Is there an association between the
use of oral contraception and depressive symptoms in young Australian
women? Contraception 2007;75:27–31.
258. Gupta N, O’Brien R, Jacobsen LJ, et al. Mood changes in adolescents
using depo-medroxyprogesterone acetate for contraception: a prospective study. Am J Obstet Gynecol 2001;14:71–6.
259. Herzberg BN, Draper KC, Johnson AL, Nicol GC. Oral contraceptives,
depression, and libido. BMJ 1971;3:495–500.
260. Koke SC, Brown EB, Miner CM. Safety and eﬃcacy of ﬂuoxetine in
patients who receive oral contraceptive therapy. Am J Obstet Gynecol
2002;187:551–5.
261. O’Connell K, Davis AR, Kerns J. Oral contraceptives: side eﬀects and
depression in adolescent girls. Contraception 2007;75:299–304.
262. Westoﬀ C, Truman C. Depressive symptoms and Depo-Provera.
Contraception 1998;57:237–40.
263. Westoﬀ C, Truman C, Kalmuss D, et al. Depressive symptoms and
Norplant contraceptive implants. Contraception 1998;57:241–5.
264. Young EA, Kornstein SG, Harvey AT, et al. Inﬂuences of hormonebased contraception on depressive symptoms in premenopausal women
with major depression. Psychoneuroendocrinology 2007;32:843–53.
265. Iyer V, Farquhar C, Jepson R. Oral contraceptive pills for heavy menstrual
bleeding [review]. Cochrane Database Syst Rev 2000;CD000154.
266. Davis L, Kennedy SS, Moore J, Prentice A. Modern combined oral
contraceptives for pain associated with endometriosis. Cochrane
Database Syst Rev 2007;CD001019.
267. Hendrix SL, Alexander NJ. Primary dysmenorrhea treatment with
a desogetrel-containing low-dose oral contraceptive. Contraception
2002;66:393–9.
268. Proctor ML, Roberts H, Farquhar C. Combined oral contraceptive pill
(OCP) as treatment for primary dysmenorrhoea. Cochrane Database
Syste Rev 2001;CD002120.
269. Adewole IF, Oladokun A, Fawole AO, Olawuyi JF, Adeleye JA. Fertility
regulatory methods and development of complications after evacuation
of complete hydatidiform mole. J Obstet Gynecol 2000;20:68–9.
270. Berkowitz RS, Goldstein DP, Marean AR, Bernstein M. Oral contraceptives and post-molar trophoblastic disease. Obstet Gynecol
1981;58:474–7.
271. Curry SL, Schlaerth JB, Kohorn EI, et al. Hormonal contraception
and trophoblastic sequelae after hydatidiform mole (a Gynecologic
Oncology Group Study). Am J Obstet Gynecol 1989;160:805–9.
272. Deicas RE, Miller DS, Rademaker AW, Lurain JR. The role of contraception in the development of postmolar trophoblastic tumour. Obstet
Gynecol 1991;78:221–6.
273. Goldberg GL, Cloete K, Bloch B, Wiswedel K, Altaras MM.
Medroxyprogesterone acetate in non-metastatic gestational trophoblastic disease. Br J Obstet Gynaecol 1987;94:22–5.
274. Ho Yuen B, Burch P. Relationship of oral contraceptives and the intrauterine contraceptive devices to the regression of concentration of the
beta subunit of human chorionic gonadotropin and invasive complications after molar pregnancy. Am J Obstet Gynecol 1983;145:214–7.
275. Morrow P, Nakamura R, Schlaerth J, Gaddis O, Eddy G. The inﬂuence
of oral contraceptives on the postmolar human chorionic gonadotropin
regression curve. Am J Obstet Gynecol 1985;151:906–14.
276. Eddy GL, Schlaerth JB, Natlick RH, et al. Postmolar trophoblastic
disease in women using hormonal contraception with and without
estrogen. Obstet Gynecol 1983;62:736–40.

MMWR

277. Smith JS. Cervical cancer and use of hormonal conraceptives: a systematic review. Lancet 2003;361:1159–67.
278. Black MM, Barclay THC, Polednak A, et al. Family history, oral contraceptive useage, and breast cancer. Cancer 1983;51:2147–51.
279. Brinton LA, Hoover R, Szklo M, Fraumeni JF. Oral contraceptives and
breast cancer. Int J Epidemiol 1982;11:316–22.
280. Brohet RM, Goldgar DE, Easton DF, et al. Oral contraceptives and
breast cancer risk in the International BRCA1/2 Carrier Cohort Study: a
report from EMBRACE, GENEPSO, GEO-HEBON, and the IBCCS
Collaborating Group. J Clin Oncol 2007;25 :3831–6.
281. Claus EB, Stowe M, Carter D. Oral contraceptives and the risk of ductal
breast carcinoma in situ. Breast Cancer Res Treat 2003;81:129–36.
282. Collaborative Group on Hormonal Factors in Breast Cancer. Familial
breast cancer: collaborative reanalysis of individual data from 52 epidemiological studies including 58 209 women with breast cancer and
101 986 women without the disease. Lancet 2001;358:1389–99.
283. Grabrick DM, Hartmann LC, Cerhan JR, et al. Risk of breast cancer
with oral contraceptive use in women with a family history of breast
cancer [comment]. JAMA 2000;284:1791–8.
284. Gronwald J, Byrski T, Huzarski T, et al. Inﬂuence of selected lifestyle
factors on breast and ovarian cancer risk in BRCA1 mutation carriers
from Poland. Breast Cancer Res Treat 2006;95:105–9.
285. Haile RW, Thomas DC, McGuire V, et al. BRCA1 and BRCA2 mutation carriers, oral contraceptive use, and breast cancer before age 50.
Cancer Epidemiol Biomarkers Prev 2006;15:1863–70.
286. Harris NV, Weiss NS, Francis AM, Polissar L. Breast cancer in
relation to patterns of oral contraceptive use. Am J Epidemiol
1982;116:643–51.
287. Hennekens CH, Speizer FE, Lipnick RJ, et al. A case-control study
of oral contraceptive use and breast cancer. J Natl Cancer Inst
1984;72:39–42.
288. Jernstrom H, Loman N, Johannsson OT, Borg A, Olsson H. Impact
of teenage oral contraceptive use in a population-based series of earlyonset breast cancer cases who have undergone BRCA mutation testing.
Eur J Cancer 2005;41:2312–20.
289. Marchbanks PA, McDonald JA, Wilson HG, et al. Oral contraceptives
and the risk of breast cancer. N Engl J Med 2002;346:2025–32.
290. Milne RL, Knight JA, John EM, et al. Oral contraceptive use and
risk of early-onset breast cancer in carriers and noncarriers of BRCA1
and BRCA2 mutations. Cancer Epidemiol Biomarkers Prev 2005;14
:350–6.
291. Narod S, Dube MP, Klijn J, et al. Oral contraceptives and the risk of
breast cancer in BRCA1 and BRCA2 mutation carriers. J Natl Cancer
Inst 2002;94:1773–9.
292. Rosenberg L, Palmer JR, Rao RS, et al. Case-control study of
oral contraceptive use and risk of breast cancer. Am J Epidemiol
1996;143:25–37.
293. Silvera SAN, Miller AB, Rohan TE. Oral contraceptive use and risk of
breast cancer among women with a family history of breast cancer: a
prospective cohort study. Cancer Causes Control 2005;16:1059–63.
294. Ursin G, Henderson BE, Haile RW, et al. Does oral contraceptive use
increase the risk of breast cancer in women with BRCA1/BRCA2 mutations more than in other women? Cancer Res 1997;57:3678–81.
295. Ursin G, Ross RK, Sullivan-Halley J, et al. Use of oral contraceptives
and risk of breast cancer in young women. Breast Cancer Res Treat
1998;50:175–84.
296. Determinants of cervical Chlamydia trachomatis infection in Italy. The
Italian MEGIC Group. Genitourin Med 1993;69:123–5.

June 18, 2010

297. Ackers JP, Lumsden WH, Catterall RD, Coyle R. Antitrichomonal
antibody in the vaginal secretions of women infected with T. vaginalis.
Br J Vener Dis 1975;51:319–23.
298. Acosta-Cazares B, Ruiz-Maya L, Escobedo dlP. Prevalence and risk
factors for Chlamydia trachomatis infection in low-income rural and
suburban populations of Mexico. Sex Transm Dis 1996;23:283–8.
299. Addiss DG, Vaughn ML, Holzhueter MA, Bakken LL, Davis JP.
Selective screening for Chlamydia trachomatis infection in nonurban family planning clinics in Wisconsin. Fam Plann Perspect
1987;19:252–6.
300. Arya OP, Mallinson H, Goddard AD. Epidemiological and clinical correlates of chlamydial infection of the cervix. Br J Vener Dis
1981;57:118–24.
301. Austin H, Louv WC, Alexander WJ. A case-control study of spermicides
and gonorrhea. JAMA 1984;251:2822–4.
302. Avonts D, Sercu M, Heyerick P, et al. Incidence of uncomplicated
genital infections in women using oral contraception or an intrauterine
device: a prospective study. Sex Transm Dis 1990;17:23–9.
303. Baeten JM, Nyange PM, Richardson BA, et al. Hormonal contraception and risk of sexually transmitted disease acquisition: results from
a prospective study. Am J Obstet Gynecol 2001;185:380–5.
304. Barbone F, Austin H, Louv WC, Alexander WJ. A follow-up study
of methods of contraception, sexual activity, and rates of trichomoniasis, candidiasis, and bacterial vaginosis. Am J Obstet Gynecol
1990;163:510–4.
305. Barnes RC, Katz BP, Rolfs RT, et al. Quantitative culture of endocervical
Chlamydia trachomatis. J Clin Microbiol 1990;28:774–80.
306. Berger GS, Keith L, Moss W. Prevalence of gonorrhoea among
women using various methods of contraception. Br J Vener Dis
1975;51:307–9.
307. Bhattacharyya MN, Jephcott AE. Diagnosis of gonorrhea in
women—inﬂuence of the contraceptive pill. J Am Vener Dis Assoc
1976;2:21–4.
308. Blum M, Pery J, Kitai E. The link between contraceptive methods and
Chlamydia trachomatis infection. Adv Contracept 1988;4:233–9.
309. Bontis J, Vavilis D, Panidis D, et al. Detection of Chlamydia trachomatis
in asymptomatic women: relationship to history, contraception, and
cervicitis. Adv Contracept 1994;10:309–15.
310. Bramley M, Kinghorn G. Do oral contraceptives inhibit Trichomonas
vaginalis? Sex Transm Dis 1979;6:261–3.
311. Bro F, Juul S. Predictors of Chlamydia trachomatis infection in women
in general practice. Fam Pract 1990;7:138–43.
312. Burns DC, Darougar S, Thin RN, Lothian L, Nicol CS. Isolation of
Chlamydia from women attending a clinic for sexually transmitted
disease. Br J Vener Dis 1975;51:314–8.
313. Ceruti M, Canestrelli M, Condemi V, et al. Methods of contraception and rates of genital infections. Clin Exp Obstet Gynecol
1994;21:119–23.
314. Chacko M, Lovchik J. Chlamydia trachomatis infection in sexually active
adolescents: prevalence and risk factors. Pediatrics 1984;73:836–40.
315. Cottingham J, Hunter D. Chlamydia trachomatis and oral contraceptive
use: a quantitative review. Genitourin Med 1992;68:209–16.
316. Crowley T, Horner P, Hughes A, et al. Hormonal factors and the laboratory detection of Chlamydia trachomatis in women: implications for
screening? Int J STD AIDS 1997;8:25–31.
317. Edwards D, Phillips D, Stancombe S. Chlamydia trachomatis infection
at a family planning clinic. N Z Med J 1985;98:333–5.
318. Evans BA, Kell PD, Bond RA, et al. Predictors of seropositivity to herpes
simplex virus type 2 in women. Int J STD AIDS 2003;14:30–6.

Vol. 59 / RR-4

Recommendations and Reports

319. Evans DL, Demetriou E, Shalaby H, Waner JL. Detection of Chlamydia
trachomatis in adolescent females using direct immunoﬂuorescence.
Clin Pediatr (Phila) 1988;27:223–8.
320. Fish AN, Fairweather DV, Oriel JD, Ridgway GL. Chlamydia trachomatis infection in a gynaecology clinic population: identiﬁcation of
high-risk groups and the value of contact tracing. Eur J Obstet Gynecol
Reprod Biol 1989;31:67–74.
321. Fouts AC, Kraus SJ. Trichomonas vaginalis: reevaluation of its clinical presentation and laboratory diagnosis. J Infect Dis 1980;141:137–43.
322. Fraser JJ, Jr., Rettig PJ, Kaplan DW. Prevalence of cervical Chlamydia
trachomatis and Neisseria gonorrhoeae in female adolescents. Pediatrics
1983;71:333–6.
323. Gertig DM, Kapiga SH, Shao JF, Hunter DJ. Risk factors for sexually
transmitted diseases among women attending family planning clinics
in Dar-es-Salaam, Tanzania. Genitourin Med 1997;73:39–43.
324. Green J, de Gonzalez AB, Smith JS, et al. Human papillomavirus infection and use of oral contraceptives. Br J Cancer 2003;88:1713–20.
325. Griﬃths M, Hindley D. Gonococcal pelvic inﬂammatory disease, oral
contraceptives, and cervical mucus. Genitourin Med 1985;61:67.
326. Han Y, Morse DL, Lawrence CE, Murphy D, Hipp S. Risk proﬁle for
Chlamydia infection in women from public health clinics in New York
State. J Community Health 1993;18:1–9.
327. Handsﬁeld HH, Jasman LL, Roberts PL, et al. Criteria for selective
screening for Chlamydia trachomatis infection in women attending
family planning clinics. JAMA 1986;255:1730–4.
328. Hanna NF, Taylor-Robinson D, Kalodiki-Karamanoli M, Harris JR,
McFadyen IR. The relation between vaginal pH and the microbiological
status in vaginitis. Br J Obstet Gynaecol 1985;92:1267–71.
329. Harrison HR, Costin M, Meder JB, et al. Cervical Chlamydia trachomatis infection in university women: relationship to history, contraception,
ectopy, and cervicitis. Am J Obstet Gynecol 1985;153:244–51.
330. Hart G. Factors associated with genital chlamydial and gonococcal
infection in females. Genitourin Med 1992;68:217–20.
331. Herrmann B, Espinoza F, Villegas RR, et al. Genital chlamydial infection among women in Nicaragua: validity of direct ﬂuorescent antibody
testing, prevalence, risk factors and clinical manifestations. Genitourin
Med 1996;72:20–6.
332. Hewitt AB. Oral contraception among special clinic patients. With
particular reference to the diagnosis of gonorrhoea. Br J Vener Dis
1970;46:106–7.
333. Hilton AL, Richmond SJ, Milne JD, Hindley F, Clarke SK. Chlamydia
A in the female genital tract. Br J Vener Dis 1974;50:1–10.
334. Hiltunen-Back E, Haikala O, Kautiainen H, Paavonen J, Reunala T.
A nationwide sentinel clinic survey of Chlamydia trachomatis infection
in Finland. Sex Transm Dis 2001;28:252–8.
335. Jacobson DL, Peralta L, Farmer M, et al. Relationship of hormonal
contraception and cervical ectopy as measured by computerized
planimetry to chlamydial infection in adolescents. Sex Transm Dis
2000;27:313–9.
336. Jaﬀe LR, Siqueira LM, Diamond SB, Diaz A, Spielsinger NA. Chlamydia
trachomatis detection in adolescents. A comparison of direct specimen
and tissue culture methods. J Adolesc Health Care 1986;7:401–4.
337. Jick H, Hannan MT, Stergachis A, et al. Vaginal spermicides and
gonorrhea. JAMA 1982;248:1619–21.
338. Johannisson G, Karamustafa A, Brorson J. Inﬂuence of copper salts on
gonococci. Br J Vener Dis 1976;52:176–7.
339. Keith L, Berer GS, Moss W. Cervical gonorrhea in women using diﬀerent methods of contraception. J Am Vener Dis Assoc 1976;3:17–9.

340. Kinghorn GR, Waugh MA. Oral contraceptive use and prevalence
of infection with Chlamydia trachomatis in women. Br J Vener Dis
1981;57:187–90.
341. Lavreys L, Chohan B, Ashley R, et al. Human herpesvirus 8: seroprevalence and correlates in prostitutes in Mombasa, Kenya. J Infect Dis
2003;187:359–63.
342. Lefevre JC, Averous S, Bauriaud R, et al. Lower genital tract infections
in women: comparison of clinical and epidemiologic ﬁndings with
microbiology. Sex Transm Dis 1988;15:110–3.
343. Louv WC, Austin H, Perlman J, Alexander WJ. Oral contraceptive
use and the risk of chlamydial and gonococcal infections. Am J Obstet
Gynecol 1989;160:396–402.
344. Lowe TL, Kraus SJ. Quantitation of Neisseria gonorrhoeae from women
with gonorrhea. J Infect Dis 1976;133:621–6.
345. Lycke E, Lowhagen GB, Hallhagen G, Johannisson G, Ramstedt K.
The risk of transmission of genital Chlamydia trachomatis infection is
less than that of genital Neisseria gonorrhoeae infection. Sex Transm Dis
1980;7:6–10.
346. Macaulay ME, Riordan T, James JM, et al. A prospective study of genital
infections in a family-planning clinic. 2. Chlamydia infection—the identiﬁcation of a high-risk group. Epidemiol Infect 1990;104:55–61.
347. Magder LS, Harrison HR, Ehret JM, Anderson TS, Judson FN.
Factors related to genital Chlamydia trachomatis and its diagnosis
by culture in a sexually transmitted disease clinic. Am J Epidemiol
1988;128:298–308.
348. Magder LS, Klontz KC, Bush LH, Barnes RC. Eﬀect of patient
characteristics on performance of an enzyme immunoassay for
detecting cervical Chlamydia trachomatis infection. J Clin Microbiol
1990;28:781–4.
349. Masse R, Laperriere H, Rousseau H, Lefebvre J, Remis RS. Chlamydia
trachomatis cervical infection: prevalence and determinants among
women presenting for routine gynecologic examination. Can Med
Assoc J 1991;145:953–61.
350. McCormack WM, Reynolds GH. Effect of menstrual cycle and
method of contraception on recovery of Neisseria gonorrhoeae. JAMA
1982;247:1292–4.
351. Morrison CS, Bright P, Wong EL, et al. Hormonal contraceptive use,
cervical ectopy, and the acquisition of cervical infections. Sex Transm
Dis 2004;31:561–7.
352. Nayyar KC, O’Neill JJ, Hambling MH, Waugh MA. Isolation of
Chlamydia trachomatis from women attending a clinic for sexually
transmitted diseases. Br J Vener Dis 1976;52:396–8.
353. Oh MK, Feinstein RA, Soileau EJ, Cloud GA, Pass RF. Chlamydia trachomatis cervical infection and oral contraceptive use among adolescent
girls. J Adolesc Health Care 1989;10:376–81.
354. Oriel JD, Powis PA, Reeve P, Miller A, Nicol CS. Chlamydial infections
of the cervix. Br J Vener Dis 1974;50:11–6.
355. Oriel JD, Johnson AL, Barlow D, et al. Infection of the uterine cervix
with Chlamydia trachomatis. J Infect Dis 1978;137:443–51.
356. Paavonen J, Vesterinen E. Chlamydia trachomatis in cervicitis and
urethritis in women. Scand J Infect Dis Suppl 1982;32:45–54.
357. Park BJ, Stergachis A, Scholes D, et al. Contraceptive methods and
the risk of Chlamydia trachomatis infection in young women. Am J
Epidemiol 1995;142:771–8.
358. Pereira LH, Embil JA, Haase DA, Manley KM. Cytomegalovirus
infection among women attending a sexually transmitted disease clinic:
association with clinical symptoms and other sexually transmitted
diseases. Am J Epidemiol 1990;131:683–92.

MMWR

359. Rahm VA, Odlind V, Pettersson R. Chlamydia trachomatis in sexually
active teenage girls. Factors related to genital chlamydial infection: a
prospective study. Genitourin Med 1991;67:317–21.
360. Reed BD, Huck W, Zazove P. Diﬀerentiation of Gardnerella vaginalis,
Candida albicans, and Trichomonas vaginalis infections of the vagina.
J Fam Pract 1989;28:673–80.
361. Ripa KT, Svensson L, Mardh PA, Westrom L. Chlamydia trachomatis cervicitis in gynecologic outpatients. Obstet Gynecol
1978;52:698–702.
362. Ruijs GJ, Kauer FM, van Gijssel PM, Schirm J, Schroder FP. Direct
immunoﬂuorescence for Chlamydia trachomatis on urogenital smears
for epidemiological purposes. Eur J Obstet Gynecol Reprod Biol
1988;27:289–97.
363. Schachter J, Stoner E, Moncada J. Screening for chlamydial infections in women attending family planning clinics. West J Med
1983;138:375–9.
364. Sellors JW, Karwalajtys TL, Kaczorowski J, et al. Incidence, clearance
and predictors of human papillomavirus infection in women. Can Med
Assoc J 2003;168:421–5.
365. Sessa R, Latino MA, Magliano EM, et al. Epidemiology of urogenital
infections caused by Chlamydia trachomatis and outline of characteristic
features of patients at risk. J Med Microbiol 1994;41:168–72.
366. Shafer MA, Beck A, Blain B, et al. Chlamydia trachomatis: important
relationships to race, contraception, lower genital tract infection, and
Papanicolaou smear. J Pediatr 1984;104:141–6.
367. Smith JS, Herrero R, Munoz N, et al. Prevalence and risk factors for
herpes simplex virus type 2 infection among middle-age women in
Brazil and the Philippines. Sex Transm Dis 2001;28:187–94.
368. Staerfelt F, Gundersen TJ, Halsos AM, et al. A survey of genital infections in patients attending a clinic for sexually transmitted diseases.
Scand J Infect Dis Suppl 1983;40:53–7.
369. Svensson L, Westrom L, Mardh PA. Chlamydia trachomatis in women
attending a gynaecological outpatient clinic with lower genital tract
infection. Br J Vener Dis 1981;57:259–62.
370. Tait IA, Rees E, Hobson D, Byng RE, Tweedie MC. Chlamydial infection of the cervix in contacts of men with nongonococcal urethritis. Br
J Vener Dis 1980;56:37–45.
371. Vaccarella S, Herrero R, Dai M, et al. Reproductive factors, oral contraceptive use, and human papillomavirus infection: pooled analysis
of the IARC HPV prevalence surveys. Cancer Epidemiol Biomarkers
Prev 2006;15:2148–53.
372. Willmott FE, Mair HJ. Genital herpesvirus infection in women attending a venereal diseases clinic. Br J Vener Dis 1978;54:341–3.
373. Winer RL, Lee SK, Hughes JP, et al. Genital human papillomavirus
infection: incidence and risk factors in a cohort of female university students. Am J Epidemiol 2003;157:218–26. Erratum in Am J Epidemiol.
2003;157:858.
374. Winter L, Goldy AS, Baer C. Prevalence and epidemiologic correlates
of Chlamydia trachomatis in rural and urban populations. Sex Transm
Dis 1990;17:30–6.
375. Wolinska WH, Melamed MR. Herpes genitalis in women attending
Planned Parenthood of New York City. Acta Cytol 1970;14:239–42.
376. Woolﬁtt JM, Watt L. Chlamydial infection of the urogenital tract
in promiscuous and non-promiscuous women. Br J Vener Dis
1977;53:93–5.
377. European Study Group on Heterosexual Transmission of HIV.
Comparison of female to male and male to female transmission of
HIV in 563 stable couples. BMJ 1992;304:809–13.

June 18, 2010

378. Aklilu M, Messele T, Tsegaye A, et al. Factors associated with HIV-1
infection among sex workers of Addis Ababa, Ethiopia. AIDS
2001;15:87–96.
379. Allen S, Seruﬁlira A, Gruber V, et al. Pregnancy and contraception use
among urban Rwandan women after HIV testing and counseling. Am
J Public Health 1993;83:705–10.
380. Baeten JM, Benki S, Chohan V, et al. Hormonal contraceptive use,
herpes simplex virus infection, and risk of HIV-1 acquisition among
Kenyan women. AIDS 2007;21:1771–7.
381. Chao A, Bulterys M, Musanganire F, et al. Risk factors associated
with prevalent HIV-1 infection among pregnant women in Rwanda.
National University of Rwanda–Johns Hopkins University AIDS
Research Team. Int J Epidemiol 1994;23:371–80.
382. Cohen CR, Duerr A, Pruithithada N, et al. Bacterial vaginosis and
HIV seroprevalence among female commercial sex workers in Chiang
Mai, Thailand. AIDS 1995;9:1093–7.
383. Criniti A, Mwachari CW, Meier AS, et al. Association of hormonal
contraception and HIV-seroprevalence in Nairobi, Kenya. AIDS
2003;17:2667–9.
384. de Vincenzi I. A longitudinal study of human immunodeﬁciency
virus transmission by heterosexual partners. European Study Group
on Heterosexual Transmission of HIV [comment]. N Engl J Med
1994;331:341–6.
385. Ellerbrock TV, Lieb S, Harrington PE, et al. Heterosexually transmitted human immunodeﬁciency virus infection among pregnant
women in a rural Florida community [comment]. N Engl J Med
1992;327:1704–9.
386. Gray JA, Dore GJ, Li Y, et al. HIV-1 infection among female commercial sex workers in rural Thailand. AIDS 1997;11:89–94.
387. Guimaraes MD, Munoz A, Boschi-Pinto C, Castilho EA. HIV infection
among female partners of seropositive men in Brazil. Rio de Janeiro
Heterosexual Study Group. Am J Epidemiol 1995;142:538–47.
388. Hira SK, Kamanga J, Macuacua R, Feldblum PJ. Oral contraceptive
use and HIV infection. Int J STD AIDS 1990;1:447–8.
389. Kapiga SH, Shao JF, Lwihula GK, Hunter DJ. Risk factors for HIV
infection among women in Dar-es-Salaam, Tanzania. J Acquir Immune
Deﬁc Syndr 1994;7:301–9.
390. Kapiga SH, Lyamuya EF, Lwihula GK, Hunter DJ. The incidence of
HIV infection among women using family planning methods in Dar
es Salaam, Tanzania. AIDS 1998;12:75–84.
391. Kilmarx PH, Limpakarnjanarat K, Mastro TD, et al. HIV-1 seroconversion in a prospective study of female sex workers in northern
Thailand: continued high incidence among brothel-based women.
AIDS 1998;12:1889–98.
392. Kunanusont C, Foy HM, Kreiss JK, et al. HIV-1 subtypes and maleto-female transmission in Thailand. Lancet 1995;345:1078–83.
393. Laga M, Manoka A, Kivuvu M, et al. Non-ulcerative sexually transmitted diseases as risk factors for HIV-1 transmission in women: results
from a cohort study [comment]. AIDS 1993;7:95–102.
394. Lavreys L, Baeten JM, Martin HL, Jr., et al. Hormonal contraception
and risk of HIV-1 acquisition: results of a 10-year prospective study.
AIDS 2004;18:695–7.
395. Limpakarnjanarat K, Mastro TD, Saisorn S, et al. HIV-1 and other
sexually transmitted infections in a cohort of female sex workers in
Chiang Rai, Thailand. Sex Transm Infect 1999;75:30–5.
396. Martin HL, Jr, Nyange PM, Richardson BA, et al. Hormonal contraception, sexually transmitted diseases, and risk of heterosexual
transmission of human immunodeﬁciency virus type 1. J Infect Dis
1998;178:1053–9.

Vol. 59 / RR-4

Recommendations and Reports

397. Mati JK, Hunter DJ, Maggwa BN, Tukei PM. Contraceptive use and
the risk of HIV infection in Nairobi, Kenya. Int J Gynaecol Obstet
1995;48:61–7.
398. Morrison CS, Richardson BA, Mmiro F, et al. Hormonal contraception
and the risk of HIV acquisition. AIDS 2007;21:85–95.
399. Moss GB, Clemetson D, D’Costa L, et al. Association of cervical
ectopy with heterosexual transmission of human immunodeﬁciency
virus: results of a study of couples in Nairobi, Kenya. J Infect Dis
1991;164:588–91.
400. Myer L, Denny L, Wright TC, Kuhn L. Prospective study of hormonal
contraception and women’s risk of HIV infection in South Africa. Int
J Epidemiol 2007;36:166–74.
401. Nagachinta T, Duerr A, Suriyanon V, et al. Risk factors for HIV-1
transmission from HIV-seropositive male blood donors to their regular
female partners in northern Thailand. AIDS 1997;11:1765–72.
402. Nicolosi A, Correa Leite ML, Musicco M, et al. The eﬃciency of
male-to-female and female-to-male sexual transmission of the human
immunodeﬁciency virus: a study of 730 stable couples. Italian Study
Group on HIV Heterosexual Transmission [comment]. Epidemiology
1994;5:570–5.
403. Nzila N, Laga M, Thiam MA, et al. HIV and other sexually
transmitted diseases among female prostitutes in Kinshasa. AIDS
1991;5:715–21.
404. Pineda JA, Aguado I, Rivero A, et al. HIV-1 infection among nonintravenous drug user female prostitutes in Spain. No evidence of
evolution to pattern II. AIDS 1992;6:1365–9.
405. Plourde PJ, Plummer FA, Pepin J, et al. Human immunodeﬁciency virus
type 1 infection in women attending a sexually transmitted diseases
clinic in Kenya [comment]. J Infect Dis 1992;166:86–92.
406. Plummer FA, Simonsen JN, Cameron DW, et al. Cofactors in malefemale sexual transmission of human immunodeﬁciency virus type 1
[comment]. J Infect Dis 1991;163:233–9.
407. Rehle T, Brinkmann UK, Siraprapasiri T, et al. Risk factors of HIV-1
infection among female prostitutes in Khon Kaen, northeast Thailand.
Infection 1992;20:328–31.
408. Saracco A, Musicco M, Nicolosi A, et al. Man-to-woman sexual transmission of HIV: longitudinal study of 343 steady partners of infected
men. J Acquir Immune Deﬁc Syndr 1993;6:497–502.
409. Simonsen JN, Plummer FA, Ngugi EN, et al. HIV infection
among lower socioeconomic strata prostitutes in Nairobi. AIDS
1990;4:139–44.
410. Sinei SK, Fortney JA, Kigondu CS, et al. Contraceptive use and HIV
infection in Kenyan family planning clinic attenders. Int J STD AIDS
1996;7:65–70.
411. Siraprapasiri T, Thanprasertsuk S, Rodklay A, et al. Risk factors for HIV
among prostitutes in Chiangmai, Thailand. AIDS 1991;5:579–82.
412. Spence MR, Robbins SM, Polansky M, Schable CA. Seroprevalence of
human immunodeﬁciency virus type I (HIV-1) antibodies in a familyplanning population. Sex Transm Dis 1991;18:143–5.
413. Taneepanichskul S, Phuapradit W, Chaturachinda K. Association of
contraceptives and HIV-1 infection in Thai female commercial sex
workers. Aust N Z J Obstet Gynaecol 1997;37:86–8.
414. Temmerman M, Chomba EN, Ndinya-Achola J, et al. Maternal human
immunodeﬁciency virus-1 infection and pregnancy outcome. Obstet
Gynecol 1994;83:495–501.

415. Ungchusak K, Rehle T, Thammapornpilap P, et al. Determinants of
HIV infection among female commercial sex workers in northeastern
Thailand: results from a longitudinal study. J Acquir Immune Deﬁc
Syndr Hum Retrovirol 1996;12:500–7. Eerratum in J Acquir Immune
Deﬁc Syndr Hum Retrovirol 1998;18:192.
416. Allen S, Stephenson R, Weiss H, et al. Pregnancy, hormonal contraceptive use, and HIV-related death in Rwanda. J Womens Health (Larchmt
) 2007;16:1017–27.
417. Cejtin HE, Jacobson L, Springer G, et al. Eﬀect of hormonal contraceptive use on plasma HIV-1-RNA levels among HIV-infected women.
AIDS 2003;17:1702–4.
418. Clark RA, Kissinger P, Williams T. Contraceptive and sexually
transmitted diseases protection among adult and adolescent women
infected with human immunodeﬁciency virus. Int J STD AIDS
1996;7:439–42.
419. Clark RA, Theall KP, Amedee AM, et al. Lack of association between
genital tract HIV-1 RNA shedding and hormonal contraceptive use
in a cohort of Louisiana women. Sex Transm Dis 2007;34:870–2.
420. Clemetson DB, Moss GB, Willerford DM, et al. Detection of HIV
DNA in cervical and vaginal secretions. Prevalence and correlates among
women in Nairobi, Kenya. JAMA 1993;269:2860–4.
421. Kaul R, Kimani J, Nagelkerke NJ, et al. Risk factors for genital ulcerations in Kenyan sex workers. The role of human immunodeﬁciency
virus type 1 infection. Sex Transm Dis 1997;24:387–92.
422. Kilmarx PH, Limpakarnjanarat K, Kaewkungwal J, et al. Disease
progression and survival with human immunodeﬁciency virus type 1
subtype E infection among female sex workers in Thailand. J Infect
Dis 2000;181:1598–606.
423. Kovacs A, Wasserman SS, Burns D, et al. Determinants of HIV-1
shedding in the genital tract of women. Lancet 2001;358:1593–601.
424. Kreiss J, Willerford DM, Hensel M, et al. Association between cervical
inﬂammation and cervical shedding of human immunodeﬁciency virus
DNA. J Infect Dis 1994;170:1597–601.
425. Lavreys L, Chohan V, Overbaugh J, et al. Hormonal contraception and
risk of cervical infections among HIV-1-seropositive Kenyan women.
AIDS 2004;18:2179–84.
426. Mostad SB, Overbaugh J, DeVange DM, et al. Hormonal contraception, vitamin A deﬁciency, and other risk factors for shedding of HIV-1
infected cells from the cervix and vagina. Lancet 1997;350:922–7.
427. Richardson BA, Otieno PA, Mbori-Ngacha D, et al. Hormonal contraception and HIV-1 disease progression among postpartum Kenyan
women. AIDS 2007;21:749–53.
428. Seck K, Samb N, Tempesta S, et al. Prevalence and risk factors of cervicovaginal HIV shedding among HIV-1 and HIV-2 infected women
in Dakar, Senegal. Sex Transm Infect 2001;77:190–3.
429. Stringer EM, Kaseba C, Levy J, et al. A randomized trial of the intrauterine contraceptive device vs hormonal contraception in women who
are infected with the human immunodeﬁciency virus. Am J Obstet
Gynecol 2007;197:144–8.
430. Taneepanichskul S, Intaraprasert S, Phuapradit W, Chaturachinda K.
Use of Norplant implants in asymptomatic HIV-1 infected women.
Contraception 1997;55:205–7.
431. Taneepanichskul S, Tanprasertkul C. Use of Norplant implants in the
immediate postpartum period among asymptomatic HIV-1-positive
mothers. Contraception 2001;64:39–41.
432. Wang CC, McClelland RS, Overbaugh J, et al. The eﬀect of hormonal contraception on genital tract shedding of HIV-1. AIDS
2004;18:205–9.

MMWR

433. el-Raghy L, Black DJ, Osman F, Orme ML, Fathalla M. Contraceptive
steroid concentrations in women with early active schistosomiasis: lack
of eﬀect of antischistosomal drugs. Contraception 1986;33:373–7.
434. Gad-el-Mawla N, Abdallah A. Liver function in bilharzial females
receiving contraceptive pills. Acta Hepato 1969;16:308–10.
435. Gad-el-Mawla N, el-Roubi O, Sabet S, Abdallah A. Plasma lipids and
lipoproteins in bilharzial females during oral contraceptive therapy. J
Egypt Med Assoc 1972;55:137–47.
436. Shaaban MM, Hammad WA, Falthalla MF, et al. Eﬀects of oral contraception on liver function tests and serum proteins in women with
active schistosomiasis. Contraception 1982;26:75–82.
437. Shaaban MM, Ghaneimah SA, Mohamed MA, Abdel-Chani S, Mostafa
SA. Eﬀective of oral contraception on serum bile acid. Int J Gynaecol
Obstet 1984;22:111–5.
438. Sy FS, Osteria TS, Opiniano V, Gler S. Eﬀect of oral contraceptive on
liver function tests of women with schistosomiasis in the Philippines.
Contraception 1986;34:283–94.
439. Tagy AH, Saker ME, Moussa AA, Kolgah A. The eﬀect of low-dose
combined oral contraceptive pills versus injectable contracetpive (Depot
Provera) on liver function tests of women with compensated bilharzial
liver ﬁbrosis. Contraception 2001;64:173–6.
440. Beck P, Wells SA. Comparison of the mechanisms underlying carbohydrate intolerance in subclinical diabetic women during pregnancy
and during post-partum oral contraceptive steroid treatment. J Clin
Endocrinol Metab 1969;29:807–18.
441. Kjos SL, Peters RK, Xiang A, et al. Contraception and the risk of type
2 diabetes mellitus in Latina women with prior gestational diabetes
mellitus. JAMA 1998;280:533–8.
442. Kung AW, Ma JT, Wong VC, et al. Glucose and lipid metabolism
with triphasic oral contraceptives in women with history of gestational
diabetes. Contraception 1987;35:257–69.
443. Radberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies in
gestational diabetic women during contraceptive treatment: eﬀects on
glucose tolerance and fatty acid composition of serum lipids. Gynecol
Obstet Invest 1982;13:17–29.
444. Skouby SO, Molsted-Pedersen L, Kuhl C. Low dosage oral contraception in women with previous gestational diabetes. Obstet Gynecol
1982;59:325–8.
445. Skouby SO, Andersen O, Kuhl C. Oral contraceptives and insulin
receptor binding in normal women and those with previous gestational
diabetes. Am J Obstet Gynecol 1986;155:802–7.
446. Skouby SO, Andersen O, Saurbrey N, Kuhl C. Oral contraception
and insulin sensitivity: in vivo assessment in normal women and
women with previous gestational diabetes. J Clin Endocrinol Metab
1987;64:519–23.
447. Xiang AH, Kawakubo M, Kjos SL, Buchanan TA. Long-acting
injectable progestin contraception and risk of type 2 diabetes in
Latino women with prior gestational diabetes mellitus. Diabetes Care
2006;29:613–7.
448. Kjos SL, Shoupe D, Douyan S, et al. Eﬀect of low-dose oral contraceptives on carbohydrate and lipid metabolism in women with recent
gestational diabetes: results of a controlled, randomized, prospective
study. Am J Obstet Gynecol 1990;163:1822–7.
449. Radberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies
in women with previous gestational diabetes during contraceptive
treatment: eﬀects on serum lipids and high density lipoproteins. Acta
Endocrinol (Copenh) 1982;101:134–9.

June 18, 2010

450. Skouby SO, Kuhl C, Molsted-Pedersen L, Petersen K, Christensen
MS. Triphasic oral contraception: metabolic eﬀects in normal women
and those with previous gestational diabetes. Am J Obstet Gynecol
1985;153:495–500.
451. Beck P, Arnett DM, Alsever RN, Eaton RP. Eﬀect of contraceptive steroids on arginine-stimulated glucagon and insulin secretion in women.
ll. Carbohydrate and lipid phsiology in insulin-dependent diabetics.
Metabolism 1976;25:23–31.
452. Diab KM, Zaki MM. Contraception in diabetic women: comparative metabolic study of norplant, depot medroxyprogesterone acetate,
low dose oral contraceptive pill and CuT380A. J Obstet Gynecol Res
2000;26:17–26.
453. Garg SK, Chase P, Marshall G, et al. Oral contraceptives and renal and
retinal complications in young women with insulin-dependent diabetes
mellitus. JAMA 1994;271:1099–102.
454. Grigoryan OR, Grodnitskaya EE, Andreeva EN, et al. Contraception
in perimenopausal women with diabetes mellitus. Gynecol Endocrinol
2006;22:198–206.
455. Margolis KL, Adami H-O, Luo J, Ye W, Weiderpass E. A prospective
study of oral contraceptive use and risk of myocardial infarction among
Swedish women. Fertil Steril 2007;88:310–6.
456. Petersen KR, Skouby SO, Sidelmann J, Jespersen J. Assessment of
endothelial function during oral contraception on women with insulindependent diabetes mellitus. Metabolism 1994;43:1379–83.
457. Petersen KR, Skouby SO, Jespersen J. Balance of coagulation activity with ﬁbrinolysis during use of oral contraceptives in women with
insulin-dependent diabetes millitus. Int J Fertil 1995;40:105–11.
458. Radberg T, Gustafson A, Skryten A, Karlsson k. Oral contraception
in diabetic women. A cross-over study on seum and high density
lipoprotein (HDL) lipids and diabetes control during progestogen
and combined estrogen/progestogen contraception. Horm Metab Res
1982;14:61–5.
459. Skouby SO, Jensen BM, Kuhl C, et al. Hormonal contraception in
diabetic women: acceptability and inﬂuence on diabetes control and
ovarian function of a nonalkylated estrogen/progestogen compound.
Contraception 1985;32:23–31.
460. Skouby SO, Molsted-Petersen L, Kuhl C, Bennet P. Oral contraceptives
in diabetic womne: metabolic eﬀects of four compounds with diﬀerent
estrogen/progestogen proﬁles. Fertil Steril 1986;46:858–64.
461. Bitton A, Peppercorn MA, Antonioli DA, et al. Clinical, biological,
and histologic parameters as predictors of relapse in ulcerative colitis.
Gastroenterology 2001;120:13–20.
462. Cosnes J, Carbonnel F, Carrat F, Beaugerie L, Gendre JP. Oral contraceptive use and the clinical course of Crohn’s disease: a prospective
cohort study. Gut 1999;45:218–22.
463. Sutherland LR, Ramcharan S, Bryant H, Fick G. Eﬀect of oral contraceptive use on reoperation following surgery for Crohn’s disease. Dig
Dis Sci 1992;37:1377–82.
464. Timmer A, Sutherland LR, Martin F. Oral contraceptive use and
smoking are risk factors for relapse in Crohn’s disease. The Canadian
Mesalamine for Remission of Crohn’s Disease Study Group.
Gastroenterology 1998;114:1143–50.
465. Wright JP. Factors inﬂuencing ﬁrst relapse in patients with Crohn’s
disease. J Clin Gastroenterol 1992;15:12–6.
466. Grimmer SF, Back DJ, Orme ML, et al. The bioavailability of
ethinyloestradiol and levonorgestrel in patients with an ileostomy.
Contraception 1986;33:51–9.

Vol. 59 / RR-4

Recommendations and Reports

467. Nilsson LO, Victor A, Kral JG, Johansson ED, Kock NG. Absorption of
an oral contraceptive gestagen in ulcerative colitis before and after proctocolectomy and construction of a continent ileostomy. Contraception
1985;31:195–204.
468. Bernstein CN, Blanchard JF, Houston DS, Wajda A. The incidence
of deep venous thrombosis and pulmonary embolism among patients
with inﬂammatory bowel disease: a population-based cohort study.
Thromb Haemost 2001;85:430–4.
469. Di Martino V, Lebray P, Myers RP, et al. Progression of liver ﬁbrosis
in women infected with hepatitis C: long-term beneﬁt of estrogen
exposure. Hepatology 2004;40:1426–33.
470. Libbrecht L, Craninx M, Nevens F, Desmet V, Roskams T. Predictive
value of liver cell dysplasia for development of hepatocellular carcinoma
in patients with non-cirrhotic and cirrhotic chronic viral hepatitis.
Histopathology 2001;39:66–73.
471. Eisalo A, Konttinen A, Hietala O. Oral contraceptives after liver disease.
Br Med J 1971;3:561–2.
472. Peishan Wang, Zemin Lai, Jinlan Tang, et al. Safety of hormonal
steroid contraceptive use for hepatitis B virus carrier women.
Pharmacoepidemiol Drug Saf 2000;9:245–6.
473. Shaaban MM, Hammad WA, Fathalla MF, et al. Eﬀects of oral contraception on liver function tests and serum proteins in women with
past viral hepatitis. Contraception 1982;26:65–74.
474. Schweitzer IL, Weiner JM, McPeak CM, Thursby MW. Oral contraceptives in acute viral hepatitis. JAMA 1975;233:979–80.
475. D’halluin V, Vilgrain V, Pelletier G, et al. Natural history of focal
nodular hyperplasia. A retrospective study of 44 cases [in French].
Gastroenterol Clin Biol 2001;25:1008–10.
476. Mathieu D, Kobeiter H, Maison P, et al. Oral contraceptive use and focal
nodular hyperplasia of the liver. Gastroenterology 2000;118:560–4.
477. Pietrzak B, Bobrowska K, Jabiry-Zieniewicz Z, et al. Oral and transdermal hormonal contraception in women after kidney transplantation.
Transplant Proc 2007;39:2759–62.
478. Pietrzak B, Kaminski P, Wielgos M, Bobrowska K, Durlik M.
Combined oral contraception in women after renal transplantation.
Neuro Endocrinol Lett 2 006;27:679–82.
479. Jabiry-Zieniewicz Z, Bobrowska K, Kaminski P, et al. Low-dose
hormonal contraception after liver transplantation. Transplant Proc
2007;39:1530–2.
480. Fedorkow DM, Corenblum B, Shaﬀer EA. Cholestasis induced by
oestrogen after liver transplantation. BMJ 1989;299:1080–1.
481. Back DJ, Bates M, Bowden A, et al. The interaction of phenobarbital
and other anticonvulsants with oral contraceptive steroid therapy.
Contraception 1980;22:495–503.
482. Doose DR, Wang S, Padmanabhan M, et al. Eﬀects of topiramate
or carbamazepine on the pharmacokinetics of an oral contraceptive
containing norethindrone and ethinyl estradiol in healthy obese and
nonobese female subjects. Epilepsia 2003;44:540–9.
483. Fattore C, Cipolla G, Gatti G, et al. Induction of ethinylestradiol
and levonorgestrel metabolism by oxcarbazepine in healthy women.
Epilepsia 1999;40:783–7.
484. Rosenfeld WE, Doose DR, Walker SA, Nayak RK. Eﬀect of topiramate on the pharmacokinetics of an oral contraceptive containing
norethindrone and ethinyl estradiol in patients with epilepsy. Epilepsia
1997;38:317–23.
485. Christensen J, Petrenaite V, Atterman J, et al. Oral contraceptives
induce lamotrigine metabolism: evidence from a double-blind, placebocontrolled trial. Epilepsia 2007;48:484–9.

486. Contin M, Albani F, Ambrosetto G, et al. Variation in lamotrigine
plasma concentrations with hormonal contraceptive monthly cycles
in partiens with epilepsy. Epilepsia 2006;47:1573–5.
487. Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens, reduces lamotrigine serum concentrations. Epilepsia
2005;46:1414–7.
488. Sabers A, Buchholt JM, Uldall P, Hansen EL. Lamotrigine plasma levels
reduced by oral contraceptives. Epilepsy Res 2001;47:151–4.
489. Sabers A, Ohman I, Christensen J, Tomson T. Oral contraceptives
reduce lamotrigine plasma levels. Neurology 2003;61:570–1.
490. Back DJ, Breckenridge AM, MacIver M, et al. The eﬀects of ampicillin on oral contraceptive steroids in women. Br J Clin Pharmacol
1982;14:43–8.
491. Back DJ, Grimmer SF, Orme ML, et al. Evaluation of the Committee
on Safety of Medicines yellow card reports on oral contraceptive-drug
interactions with anticonvulsants and antibiotics. Br J Clin Pharmacol
1988;25:527–32.
492. Back DJ, Tjia J, Martin C, et al. The lack of interaction between
temaﬂoxacin and combined oral contraceptive steroids. Contraception
1991;43:317–23.
493. Bacon JF, Shenﬁeld GM. Pregnancy attributable to interaction between
tetracycline and oral contraceptives. BMJ 1980;280:293.
494. Bainton R. Interaction between antibiotic therapy and contraceptive
medication. Oral Surg Oral Med Oral Pathol 1986;61:453–5.
495. Bollen M. Use of antibiotics when taking the oral contraceptive pill
[comment]. Aust Fam Physician 1995;24:928–9.
496. Bromham DR. Knowledge and use of secondary contraception among
patients requesting termination of pregnancy. BMJ 1993;306:556–7.
497. Cote J. Interaction of griseofulvin and oral contraceptives [comment].
J Am Acad Dermatol 1990;22:124–5.
498. Csemiczky G, Alvendal C, Landgren BM. Risk for ovulation in women
taking a low-dose oral contraceptive (Microgynon) when receiving antibacterial treatment with a ﬂuoroquinoline (oﬂoxacin). Adv Contracept
1996;12:101–9.
499. de Groot AC, Eshuis H, Stricker BH. Ineﬃciency of oral contraception during use of minocycline [in Dutch]. Ned Tijdschr Geneeskd
1990;134:1227–9.
500. DeSano EA Jr, Hurley SC. Possible interactions of antihistamines
and antibiotics with oral contraceptive eﬀectiveness. Fertil Steril
1982;37:853–4.
501. Donley TG, Smith RF, Roy B. Reduced oral contraceptive eﬀectiveness
with concurrent antibiotic use: a protocol for prescribing antibiotics
to women of childbearing age. Compendium 1990;11:392–6.
502. Friedman CI, Huneke AL, Kim MH, Powell J. The eﬀect of ampicillin
on oral contraceptive eﬀectiveness. Obstet Gynecol 1980;55:33–7.
503. Grimmer SF, Allen WL, Back DJ, et al. The eﬀect of cotrimoxazole on
oral contraceptive steroids in women. Contraception 1983;28:53–9.
504. Helms SE, Bredle DL, Zajic J, et al. Oral contraceptive failure rates
and oral antibiotics. J Am Acad Dermatol 1997;36:705–10.
505. Hempel E, Bohm W, Carol W, Klinger G. Enzyme induction by
drugs and hormonal contraception [in German]. Zentralbl Gynakol
1973;95:1451–7.
506. Hempel E, Zorn C, Graf K. Eﬀect of chemotherapy agents and antibiotics on hormonal contraception [in German]. Z Arztl Forbild (Jena)
1978;72:924–6.
507. Hetenyi G. Possible interactions between antibiotics and oral contraceptives. Ther Hung 1989;37:86–9.
508. Hughes BR, Cunliﬀe WJ. Interactions between the oral contraceptive
pill and antibiotics [comment]. Br J Dermatol 1990;122:717–8.

MMWR

509. Joshi JV, Joshi UM, Sankholi GM, et al. A study of interaction of lowdose combination oral contraceptive with ampicillin and metronidazole.
Contraception 1980;22:643–52.
510. Kakouris H, Kovacs GT. Pill failure and nonuse of secondary precautions. Br J Fam Plann 1992;18:41–4.
511. Kakouris H, Kovacs GT. How common are predisposing factors to pill
failure among pill users? Br J Fam Plann 1994;20:33–5.
512. Kovacs GT, Riddoch G, Duncombe P, et al. Inadvertent pregnancies
in oral contraceptive users. Med J Aust 1989;150:549–51.
513. Lequeux A. Pregnancy under oral contraceptives after treatment with
tetracycline] [in French]. Louv Med 1980;99:413–4.
514. London BM, Lookingbill DP. Frequency of pregnancy in acne
patients taking oral antibiotics and oral contraceptives. Arch Dermatol
1994;130:392–3.
515. Maggiolo F, Puricelli G, Dottorini M, et al. The eﬀects of ciproﬂoxacin on oral contraceptive steroid treatments. Drugs Exp Clin Res
1991;17:451–4.
516. Murphy AA, Zacur HA, Charache P, Burkman RT. The eﬀect of
tetracycline on levels of oral contraceptives. Am J Obstet Gynecol
1991;164:28–33.
517. Neely JL, Abate M, Swinker M, D’Angio R. The eﬀect of doxycycline
on serum levels of ethinyl estradiol, noretindrone, and endogenous
progesterone. Obstet Gynecol 1991;77:416–20.
518. Pillans PI, Sparrow MJ. Pregnancy associated with a combined oral contraceptive and itraconazole [comment]. N Z Med J 1993;106:436.
519. Scholten PC, Droppert RM, Zwinkels MG, et al. No interaction
between ciproﬂoxacin and an oral contraceptive. Antimicrob Agents
Chemother 1998;42:3266–8.
520. Silber TJ. Apparent oral contraceptive failure associated with antibiotic
administration. J Adolesc Health Care 1983;4:287–9.
521. Sparrow MJ. Pill method failures. N Z Med J 1987;100:102–5.
522. Sparrow MJ. Pregnancies in reliable pill takers. N Z Med J
1989;102:575–7.
523. Sparrow MJ. Pill method failures in women seeking abortion—fourteen
years experience. N Z Med J 1998;111:386–8.
524. van Dijke CP, Weber JC. Interaction between oral contraceptives and
griseofulvin. Br Med J (Clin Res Ed) 1984;288:1125–6.
525. Wermeling DP, Chandler MH, Sides GD, Collins D, Muse KN.
Dirithromycin increases ethinyl estradiol clearance without allowing
ovulation. Obstet Gynecol 1995;86:78–84.
526. Young LK, Farquhar CM, McCowan LM, Roberts HE, Taylor J. The
contraceptive practices of women seeking termination of pregnancy in
an Auckland clinic. N Z Med J 1994;107:189–92.
527. Abrams LS, Skee D, Natarajan J, Wong FA. Pharmocokinetic overview
of Ortho Evra/Evra. Fertil Steril 2002;77:s3–s12.
528. Dogterom P, van den Heuvel MW, Thomsen T. Absence of pharmacokinetic interactions of the combined contraceptive vaginal ring
NuvaRing with oral amoxicillin or doxycycline in two randomized
trials. Clin Pharmacokinet 2005;44:429–38.
529. Devenport MH, Crook D, Wynn V, Lees LJ. Metabolic eﬀects of
low-dose ﬂuconazole in healthy female users and non-users of oral
contraceptives. Br J Clin Pharmacol 1989;27:851–9.
530. Hilbert J, Messig M, Kuye O. Evaluation of interaction between ﬂuconazole and an oral contraceptive in healthy women. Obstet Gynecol
2001;98:218–23.
531. Kovacs I, Somos P, Hamori M. Examination of the potential interaction
between ketoconazole (Nizoral) and oral contraceptives with special
regard to products of low hormone content (Rigevidon, anteovin).
Ther Hung 1986;34:167–70.

June 18, 2010

532. Lunell NO, Pschera H, Zador G, Carlstrom K. Evaluation of the
possible interaction of the antifungal triazole SCH 39304 with oral
contraceptives in normal health women. Gynecol Obstet Invest
1991;32:91–7.
533. McDaniel PA, Cladroney RD. Oral contraceptives and griseofulvin
interactions. Drug Intell Clin Pharm 1986;20:384.
534. Meyboom RH, van Puijenbroek EP, Vinks MH, Lastdrager CJ.
Disturbance of withdrawal bleeding during concomitant use of itraconazole and oral contraceptives. N Z Med J 1997;110:300.
535. Rieth H, Sauerbrey N. Interaction studies with ﬂuconazole, a new
tirazole antifungal drug [in German]. Wien Med Wochenschr
1989;139:370–4.
536. Sinofsky FE, Pasquale SA. The eﬀect of ﬂuconazole on circulating
ethinyl estradiol levels in women taking oral contraceptives. Am J
Obstet Gynecol 1998;178:300–4.
537. van Puijenbroek EP, Feenstra J, Meyboom RH. Pill cycle disturbance
in simultaneous use of itraconazole and oral contraceptives [in Dutch].
Ned Tijedschr Geneeskd 1998;142:146–9.
538. van Puijenbroek EP, Egberts AC, Meyboom RH, Leufkens HG.
Signalling possible drug-drug interactions in a spontaneous reporting system: delay of withdrawal bleeding during concomitant
use of oral contraceptives and itraconazole. Br J Clin Pharmacol
1999;47:689–93.
539. Verhoeven CH, van den Heuvel MW, Mulders TM, Dieben TO. The
contraceptive vaginal ring, NuvaRing, and antimycotic co-medication.
Contraception 2004;69:129–32.
540. Back DJ, Breckenridge AM, Grimmer SF, Orme ML, Purba HS.
Pharmacokinetics of oral contraceptive steroids following the administration of the antimalarial drugs primaquine and chloroquine.
Contraception 1984;30:289–95.
541. Croft AM, Herxheimer A. Adverse eﬀects of the antimalaria drug,
meﬂoquine: due to primary liver damage with secondary thyroid
involvement? BMC Public Health 2002;2:6.
542. Karbwang J, Looareesuwan S, Back DJ, Migasana S, Bunnag D. Eﬀect
of oral contraceptive steroids on the clinical course of malaria infection
and on the pharmacokinetics of meﬂoquine in Thai women. Bull World
Health Organ 1988;66:763–7.
543. McGready R, Stepniewska K, Seaton E, et al. Pregnancy and use of oral
contaceptives reduces the biotransformation of proguanil to cycloguanil.
Eur J Clin Pharmacol 2003;59:553–7.
544. Wanwimolruk S, Kaewvichit S, Tanthayaphinant O, Suwannarach
C, Oranratnachai A. Lack of eﬀect of oral contraceptive use on the
pharmacokinetics of quinine. Br J Clin Pharmacol 1991;31:179–81.
545. Back DJ, Breckenridge AM, Crawford FE, et al. The eﬀect of rifampicin on norethisterone pharmacokinetics. Eur J Clin Pharmacol
1979;15:193–7.
546. Back DJ, Breckenridge AM, Crawford FE, et al. The eﬀect of rifampicin
on the pharmacokinetics of ethynylestradiol in women. Contraception
1980;21:135–43.
547. Barditch-Crovo P, Trapnell CB, Ette E, et al. The eﬀects of rifampicin
and rifabutin on the pharmacokinetics and pharmacodynamics of a combination oral contraceptive. Clin Pharmacol Ther 1999;65:428–38.
548. Bolt HM, Bolt M, Kappus H. Interaction of rifampicin treatment with
pharmacokinetics and metabolism of ethinyloestradiol in man. Acta
Endocrinol (Copenh) 1977;85:189–97.
549. Gupta KC, Ali MY. Failure of oral contraceptive with rifampicin. Med
J Zambia 1981;15:23.
550. Hirsch A. Sleeping pills [letter] [in French]. Nouv Presse Med
1973;2:2957.

Vol. 59 / RR-4

Recommendations and Reports

551. Hirsch A, Tillement JP, Chretien J. Eﬀets contrariants de la rifampicine
sur les contraceptifs oraux: a propos de trois grossesses non desiree chez
trois malades. Rev Fr Mal Respir 1975;2:174–82.
552. Joshi JV, Joshi UM, Sankholi GM, et al. A study of interaction of a
low-dose combination oral contraceptive with anti-tubercular drugs.
Contraception 1980;21:617–29.
553. Kropp R. Rifampicin and oral cotnraceptives (author’s transl) [in
German]. Prax Pneumol 1974;28:270–2.
554. LeBel M, Masson E, Guilbert E, et al. Eﬀects of rifabutin and rifampicin
on the pharmacokinetics of ethinylestradiol and norethindrone. J Clin
Pharmacol 1998;38:1042–50.
555. Meyer B, Muller F, Wessels P, Maree J. A model to detect interactions
between roxithromycin and oral contraceptives. Clin Pharmacol Ther
1990;47:671–4.

556. Nocke-Finke L, Breuer H, Reimers D. Eﬀects of rifampicin on the menstrual cycle and on oestrogen excretion in patients taking oral contraceptives [in German]. Deutsche Med Wochenschr 1973;98:1521–3.
557. Piguet B, Muglioni JF, Chaline G. Oral contraception and rifampicin
[letter] [in French]. Nouv Presse Med 1975;4:115–6.
558. Reimers D, Jezek A. The simultaneous use of rifampicin and other antitubercular agents with oral contraceptives [in German]. Prax Pneumol
1971;25:255–62.
559. Skolnick JL, Stoler BS, Katz DB, Anderson WH. Rifampicin, oral
contraceptives, and pregnancy. JAMA 1976;236:1382.
560. Szoka PR, Edgren RA. Drug interactions with oral contraceptives:
compilation and analysis of an adverse experience report database.
Fertil Steril 1988;49:s31–s38.

MMWR

June 18, 2010

Appendix C
Classifications for Progestin-Only Contraceptives
Classiﬁcations for progestin-only contraceptives (POCs)
include those for progestin-only pills, depot medroxyprogesterone acetate, and progestin-only implants (Box). POCs do

not protect against sexually transmitted infections (STIs) or
human immunodeﬁciency virus (HIV).

BOX. Categories for Classifying Progestin-Only Contraceptives

TABLE. Classifications for progestin-only contraceptives, including progestin-only pills, DMPA, and implants*†
Category
Condition

POP

DMPA

Implants

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy

Not applicable

Clarification: Use of POCs is not required. There is no
known harm to the woman, the course of her pregnancy, or
the fetus if POCs are inadvertently used during pregnancy.
However, the relation between DMPA use during pregnancy
and its effects on the fetus remains unclear.

Age
a. Menarche to <18 yrs
b. 18–45 yrs
c. >45 yrs

1
1
1

2
1
2

1
1
1

Evidence: Most studies have found that women lose
BMD while using DMPA but regain BMD after discontinuing DMPA. It is not known whether DMPA use among
adolescents affects peak bone mass levels or whether adult
women with long duration of DMPA use can regain BMD
to baseline levels before entering menopause. The relation
between DMPA-associated changes in BMD during the reproductive years and future fracture risk is unknown (1–41).
Studies find no effect or have inconsistent results about the
effects of POCs other than DMPA on BMD (42–54).

Parity
a. Nulliparous
b. Parous

1
1

Breastfeeding
a. <1 mo postpartum
b. 1 mo to <6 mos postpartum
c. ≥6 mos postpartum

2
1
1

Clarification: The U.S. Department of Health and Human
Services recommends that infants be exclusively breastfed
during the first 4–6 months of life, preferably for a full 6
months. Ideally, breastfeeding should continue through the
first year of life (55).
Evidence: Despite anecdotal clinical reports that POCs
might diminish milk production, direct evidence from available clinical studies demonstrates no significant negative
effect of POCs on breastfeeding performance (56–90) or on
the health of the infant (66,70,72,76–81,91–93). In general,
these studies are of poor quality, lack standard definitions of
breastfeeding or outcome measures, and have not included
premature or ill infants. Theoretical concerns about effects
of progestin exposure on the developing, neonatal brain
are based on studies of progesterone effects in animals;
whether similar effects occur after progestin exposure in
human neonates is not known.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
Condition

POP

DMPA

Implants

Clarifications/Evidence/Comments

Postpartum (in nonbreastfeeding
women)
a. <21 days
b. ≥21 days

1
1

Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic abortion

1
1
1

Past ectopic pregnancy

History of pelvic surgery

1
1

1
2

1
1

Evidence: Limited evidence demonstrated no substantial
decrease in effectiveness of oral contraceptives among
women who underwent laparoscopic placement of an
adjustable gastric band (106).

Evidence: Limited evidence demonstrated no substantial
decrease in effectiveness of oral contraceptives among
women who underwent a biliopancreatic diversion (107);
however, evidence from pharmacokinetic studies suggested
conflicting results of oral contraceptive effectiveness among
women who underwent a jejunoileal bypass (108,109).

Smoking
a. Age <35 yrs
b. Age ≥35 yrs
i. <15 Cigarettes/day
ii. ≥15 Cigarettes/day
Obesity
a. ≥30 kg/m2 BMI
b. Menarche to <18 yrs and
≥30 kg/m2 BMI

History of bariatric surgery§
a. Restrictive procedures: decrease
storage capacity of the stomach
(vertical banded gastroplasty,
laparoscopic adjustable gastric
band, laparoscopic sleeve
gastrectomy)
b. Malabsorptive procedures:
decrease absorption of nutrients
and calories by shortening the
functional length of the small
intestine (Roux-en-Y gastric
bypass, biliopancreatic diversion)

Clarification: POCs may be started immediately
postabortion.
Evidence: Limited evidence suggests that there are no
adverse side effects when implants (Norplant) or progestinonly injectables (NET-EN) are initiated after first trimester
abortion (94–97).
Comments: POP users have a higher absolute rate of
ectopic pregnancy than do users of other POCs but still less
than using no method.

Evidence: Obese adolescents who used DMPA were
more likely than obese nonusers, obese COC users, and
nonobese DMPA users to gain weight. These associations
were not observed among adult women. One small study
did not observe increases in weight gain among adolescent
Norplant users by any category of baseline weight (98–105).

Comment: Bariatric surgical procedures involving a malabsorptive component have the potential to decrease oral
contraceptive effectiveness, perhaps further decreased by
postoperative complications, such as long-term diarrhea
and/or vomiting.

Cardiovascular Disease
Multiple risk factors for arterial
cardiovascular disease (such as
older age, smoking, diabetes, and
hypertension)

Clarification: When multiple major risk factors exist, risk for
cardiovascular disease might increase substantially. Some
POCs might increase the risk for thrombosis, although this
increase is substantially less than with COCs. The effects of
DMPA might persist for some time after discontinuation.

Clarification: Women adequately treated for hypertension
are at lower risk for acute myocardial infarction and stroke
than are untreated women. Although no data exist, POC users with adequately controlled and monitored hypertension
should be at lower risk for acute myocardial infarction and
stroke than are untreated hypertensive POC users.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
Condition
b. Elevated blood pressure levels
(properly taken measurements)
i. Systolic 140–159 mm Hg or
diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or
diastolic ≥100 mm Hg§
c. Vascular disease

History of high blood pressure during pregnancy (where current blood
pressure is measurable and normal)
Deep venous thrombosis (DVT)/
Pulmonary embolism (PE)
a. History of DVT/PE, not on anticoagulant therapy
i. Higher risk for recurrent DVT/
PE (≥1 risk factors)
r )JTUPSZPGFTUSPHFOBTTPDJated DVT/PE

POP

DMPA

Implants

Clarifications/Evidence/Comments

Evidence: Limited evidence suggests that among women
with hypertension, those who used POPs or progestin-only
injectables had a small increased risk for cardiovascular
events than did women who did not use these methods
(110).
Comment: Concern exists about hypo-estrogenic effects
and reduced HDL levels, particularly among users of DMPA.
However, there is little concern about these effects with regard to POPs. The effects of DMPA might persist for some
time after discontinuation

r 1SFHOBODZBTTPDJBUFE
DVT/PE
r *EJPQBUIJD%751&
r ,OPXOUISPNCPQIJMJB
including antiphospholipid
syndrome
r "DUJWFDBODFS NFUBTUBUJD
on therapy, or within 6 mos
after clinical remission),
excluding non-melanoma
skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii Lower risk for recurrent DVT/
PE (no risk factors)
b. Acute DVT/PE

c. DVT/PE and established on
anticoagulant therapy for at least
3 mos
i. Higher risk for recurrent DVT/
PE (≥1 risk factors)
r ,OPXOUISPNCPQIJMJB
including antiphospholipid
syndrome

Evidence: No direct evidence exists on use of POCs
among women with DVT/PE on anticoagulant therapy.
Although findings on the risk for venous thrombosis with
use of POCs are inconsistent in otherwise healthy women,
any small increased risk is substantially less than that with
COCs (110–112).
Limited evidence indicates that intramuscular injections of
DMPA in women on chronic anticoagulation therapy does
not pose a significant risk for hematoma at the injection site
or increase the risk for heavy or irregular vaginal bleeding
(113).

r "DUJWFDBODFS NFUBTUBUJD
on therapy, or within 6 mos
after clinical remission),
excluding non-melanoma
skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii. Lower risk for recurrent DVT/
PE (no risk factors)
d. Family history
(first-degree relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged
immobilization
f. Minor surgery without
immobilization

2
1

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
POP

DMPA

Implants

Clarifications/Evidence/Comments

Clarification: Routine screening is not appropriate because
of the rarity of the conditions and the high cost of screening.

Superficial venous thrombosis
a. Varicose veins
b. Superficial thrombophlebitis

1
1

Current and history of ischemic
heart disease§

Initiation Continuation
2
3

Stroke§ (history of cerebrovascular
accident)

Initiation Continuation
2
3

1
1

Condition
mutations§

Known thrombogenic
(e.g., factor V Leiden; prothrombin
mutation; protein S, protein C, and
antithrombin deficiencies)

Known hyperlipidemias

Valvular heart disease
a. Uncomplicated
b. Complicated§ (pulmonary hypertension, risk for atrial fibrillation,
history of subacute bacterial
endocarditis)

Initiation Continuation Comment: Concern exists about hypo-estrogenic effects
2
3
and reduced HDL levels, particularly among users of DMPA.
However, there is little concern about these effects with regard to POPs. The effects of DMPA might persist for some
time after discontinuation.
Initiation Continuation Comment: Concern exists about hypo-estrogenic effects
2
3
and reduced HDL levels, particularly among users of DMPA.
However, there is little concern about these effects with
regard to POPs. The effects of DMPA may persist for some
time after discontinuation.

Clarification: Routine screening is not appropriate because
of the rarity of the conditions and the high cost of screening.
Some types of hyperlipidemias are risk factors for vascular
disease.

Evidence: No direct evidence exists on the safety of POCs
among women with peripartum cardiomyopathy. Limited indirect evidence from noncomparative studies of women with
cardiac disease demonstrated few cases of hypertension,
thromoboembolism, and heart failure in women with cardiac
disease using POPs and DMPA (115,116).
Comment: Progestin-only implants might induce cardiac
arrhythmias in healthy women; women with peripartum cardiomyopathy have a high incidence of cardiac arrhythmias.

i. <6 mos
ii. ≥6 mos
b. Moderately or severely impaired
cardiac function (New York Heart
Association Functional Class III or
IV: patients with marked limitation
of activity or patients who should
be at complete rest) (114)

1
1
2

MMWR

June 18, 2010

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
POP

Condition

DMPA

Implants

Clarifications/Evidence/Comments

Initiation
3

Continuation
3

b. Severe thrombocytopenia

c. Immunosuppressive treatment
d. None of the above

2
2

Rheumatoid arthritis
a. On immunosuppressive therapy
b. Not on immunosuppressive
therapy

1
1

2/3
2

1
1

Evidence: Antiphospholipid antibodies are associated
with a higher risk for both arterial and venous thrombosis
(136,137).
Comment: Severe thrombocytopenia increases the risk for
bleeding. POCs might be useful in treating menorrhagia in
women with severe thrombocytopenia. However, given the
increased or erratic bleeding that may be seen on initiation
of DMPA and its irreversibility for 11–13 weeks after administration, initiation of this method in women with severe
thrombocytopenia should be done with caution.

Clarification: DMPA use among women on long-term
corticosteroid therapy with a history of, or with risk factors
for, nontraumatic fractures is classified as Category 3.
Otherwise, DMPA use for women with rheumatoid arthritis is
classified as Category 2.
Evidence: Limited evidence shows no consistent pattern of
improvement or worsening of rheumatoid arthritis with use
of oral contraceptives (138–143), progesterone (144), or
estrogen (145).

Neurologic Conditions
Headaches
a. Non-migrainous
(mild or severe)
b. Migraine
i. Without aura
rAge <35 yrs
rAge ≥35 yrs
ii. With aura, at any age

Initiation Continuation
1
1

1
1
2

2
2
3

Initiation
1

2
2
2

Continuation Initiation Continuation Clarification: Classification depends on accurate diagnosis
1
1
1
of severe headaches that are migrainous and headaches
that are not. Any new headaches or marked changes in
headaches should be evaluated. Classification is for women
without any other risk factors for stroke. Risk for stroke
increases with age, hypertension, and smoking.
2
2
2
Comment: Aura is a specific focal neurologic symptom.
2
2
2
For more information about this and other diagnostic
3
2
3
criteria, see: Headache Classification Subcommittee of the
International Headache Society. The international classification of headache disorders. 2nd Ed. Cephalalgia. 2004;24
(Suppl 1):1–150. http://www.i-h-s.org/upload/ct_clas/ihc_II_
main_no_print.pdf.
Concern exists that severe headaches might increase
with use of DMPA and implants. The effects of DMPA may
persist for some time after discontinuation.

Epilepsy§

Clarification: If a woman is taking anticonvulsants, refer
to the section on drug interactions. Certain anticonvulsants
lower POC effectiveness.

Clarification: The classification is based on data for women
with selected depressive disorders. No data on bipolar disorder or postpartum depression were available. A potential
exists for drug interactions between certain antidepressant
medications and hormonal contraceptives.

Depressive Disorders
Depressive disorders

Evidence: POC use did not increase depressive symptoms in women with depression compared with baseline
(146–149).

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
POP

Condition

DMPA

Implants

Clarifications/Evidence/Comments

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without heavy
bleeding

b. Heavy or prolonged bleeding
(includes regular and irregular
patterns)
Unexplained vaginal bleeding
(suspicious for serious condition)

Before evaluation

Comment: Irregular menstrual bleeding patterns are common among healthy women. POC use frequently induces an
irregular bleeding pattern. Implant use might induce irregular
bleeding patterns, especially during the first 3–6 months, but
these patterns may persist longer.
Clarification: Unusually heavy bleeding should raise the
suspicion of a serious underlying condition.
Clarification: If pregnancy or an underlying pathological
condition (such as pelvic malignancy) is suspected, it must
be evaluated and the category adjusted after evaluation.
Comment: POCs might cause irregular bleeding patterns,
which might mask symptoms of underlying pathology.
The effects of DMPA might persist for some time after
discontinuation.

Endometriosis

Benign ovarian tumors
(including cysts)

Severe dysmenorrhea

Cervical ectropion

Cervical intraepithelial neoplasia

Evidence: Among women with persistent HPV infection,
long-term DMPA use (≥5 years) might increase the risk for
carcinoma in situ and invasive carcinoma (150).

Cervical cancer (awaiting treatment)

Comment: Theoretical concern exists that POC use might
affect prognosis of the existing disease. While awaiting
treatment, women may use POCs. In general, treatment of
this condition can render a woman sterile.

Breast disease
a. Undiagnosed mass

Clarification: Evaluation should be pursued as early as
possible.

1
1

4
3

Comment: While awaiting treatment, women may use
POCs. In general, treatment of this condition renders a
woman sterile.

Ovarian cancer§

Comment: While awaiting treatment, women may use
POCs. In general, treatment of this condition can render a
woman sterile.

Uterine fibroids

Comment: POCs do not appear to cause growth of uterine
fibroids.

Gestational trophoblastic disease
a. Decreasing or undetectable
β–hCG levels
b. Persistently elevated β-hCG
levels or malignant disease§

b. Benign breast disease
c. Family history of cancer
d. Breast cancer§
i. Current
ii. Past and no evidence of
current disease for 5 years
Endometrial hyperplasia
Endometrial

cancer§

Comment: Breast cancer is a hormonally sensitive tumor,
and the prognosis for women with current or recent breast
cancer might worsen with POC use.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
Condition

POP

DMPA

Implants

Pelvic inflammatory disease (PID)
a. Past PID (assuming no current
risk factors for STIs)
i. With subsequent pregnancy
ii. Without subsequent
pregnancy
b. Current PID

Clarifications/Evidence/Comments

Comment: Whether POCs, like COCs, reduce the risk for
PID among women with STIs is unknown, but they do not
protect against HIV or lower genital tract STI.
1
1

1
1

Evidence: Evidence suggests a possible increased risk
for chlamydial cervicitis among DMPA users at high risk for
STIs. For other STIs, either evidence exists of no association between DMPA use and STI acquisition or evidence is
too limited to draw any conclusions. No evidence is available about other POCs (151–158)

High risk for HIV

Evidence: The balance of the evidence suggests no association between POC use and HIV acquisition, although
findings from studies of DMPA use conducted among higher
risk populations have been inconsistent (159–183).

HIV infection§

Evidence: Most studies suggest no increased risk for HIV
disease progression with hormonal contraceptive use,
as measured by changes in CD4 cell count, viral load, or
survival. Studies observing that women with HIV who use
hormonal contraception have increased risks for STIs are
generally consistent with reports among uninfected women.
One direct study found no association between hormonal
contraceptive use and increased risk for HIV transmission to
uninfected partners; several indirect studies reported mixed
results about whether hormonal contraception is associated
with increased risk for HIV-1 DNA or RNA shedding from the
genital tract (171,184–200).

AIDS§

Clarification: Drug interactions might exist between
hormonal contraceptives and ARV drugs; refer to the
section on drug interactions.

Evidence: Among women with uncomplicated schistosomiasis, limited evidence showed that DMPA use had no
adverse effects on liver function (201).

STIs
a. Current purulent cervicitis or
chlamydial infection or gonorrhea
b. Other STIs (excluding HIV and
hepatitis)
c. Vaginitis (including Trichomonas
vaginalis and bacterial vaginosis)
d. Increased risk for STIs

HIV/AIDS

Other Infections
Schistosomiasis
a. Uncomplicated

b. Fibrosis of liver§
(if severe, see cirrhosis)
Tuberculosis§
a. Nonpelvic
b. Pelvic
Malaria

Clarification: If a woman is taking rifampicin, refer to the
section on drug interactions. Rifampicin is likely to decrease
the effectiveness of some POCs.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
POP

DMPA

Implants

Clarifications/Evidence/Comments

Evidence: POCs had no adverse effects on serum lipid
levels in women with a history of gestational diabetes in 2
small studies. (202,203) Limited evidence is inconsistent
about the development of noninsulin-dependant diabetes
among users of POCs with a history of gestational diabetes
(204–207).

2
2

c. Nephropathy/retinopathy/
neuropathy§

d. Other vascular disease or
diabetes of >20 yrs’ duration§

Evidence: Among women with insulin- or noninsulin-dependent diabetes, limited evidence on use of POCs (POPs,
DMPA, LNG implant) suggests that these methods have
little effect on short-term or long-term diabetes control (e.g.,
glycosylated hemoglobin levels), hemostatic markers, or
lipid profile (208–211).
Comment: Concern exists about hypo-estrogenic effects
and reduced HDL levels, particularly among users of DMPA.
The effects of DMPA might persist for some time after
discontinuation. Some POCs might increase the risk for
thrombosis, although this increase is substantially less than
with COCs.
Comment: Concern exists about hypo-estrogenic effects
and reduced HDL levels, particularly among users of DMPA.
The effects of DMPA might persist for some time after
discontinuation. Some POCs might increase the risk for
thrombosis, although this increase is substantially less than
with COCs.

1
1
1

Condition

Endocrine Conditions
Diabetes
a. History of gestational disease

b. Nonvascular disease
i. Noninsulin-dependent
ii. Insulin-dependent§

Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Gastrointestinal Conditions
Inflammatory bowel disease (IBD)
(ulcerative colitis, Crohn disease)

Evidence: Risk for disease relapse among women with
IBD using oral contraceptives (most studies did not specify
formulation) did not increase significantly from that for
nonusers (212–216).
Comment: Absorption of POPs among women with IBD
might be reduced if the woman has substantial malabsorption caused by severe disease or small bowel surgery.
Women with IBD have a higher prevalence than the general
population of osteoporosis and osteopenia. Use of DMPA,
which has been associated with small changes in BMD,
might be of concern.

Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic

2
2
2
2

History of cholestasis
a. Pregnancy-related
b. Past COC–related

1
2

Viral hepatitis
a. Acute or flare
b. Carrier
c. Chronic

1
1
1

Comment: Theoretically, a history of COC-related cholestasis might predict subsequent cholestasis with POC use.
However, this has not been documented.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
POP

DMPA

Implants

Cirrhosis
a. Mild (compensated)
b. Severe§ (decompensated)

1
3

Liver tumors
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma§
b. Malignant§ (hepatoma)

2
3
3

Condition

Clarifications/Evidence/Comments

Evidence: Limited direct evidence suggests that hormonal
contraceptive use does not influence either progression or
regression of liver lesions among women with focal nodular
hyperplasia (217,218).
Comment: No evidence is available about hormonal contraceptive use among women with hepatocellular adenoma.
COC use in healthy women is associated with development
and growth of hepatocellular adenoma; whether other hormonal contraceptives have similar effects is not known.

Anemias
Thalassemia
Sickle cell

disease§

Iron deficiency anemia

Evidence: Among women with sickle cell disease, POC use
did not have adverse effects on hematologic parameters
and, in some studies, was beneficial with respect to clinical
symptoms (219–226).

Comment: Changes in the menstrual pattern associated
with POC use have little effect on hemoglobin levels.

Solid Organ Transplantation
Solid organ transplantaton§
a. Complicated: graft failure (acute
or chronic), rejection, cardiac
allograft vasculopathy
b. Uncomplicated

Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin, carbamazepine, barbiturates, primidone, topiramate,
oxcarbazepine)

Clarification: ARV drugs have the potential to either
decrease or increase the bioavailability of steroid hormones
in hormonal contraceptives. Limited data (Appendix M) suggest potential drug interactions between many ARV drugs
(particularly some NNRTIs and ritonavir-boosted protease
inhibitors) and hormonal contraceptives. These interactions
may alter the safety and effectiveness of both the hormonal
contraceptive and the ARV drug. Thus, if a woman on ARV
treatment decides to initiate or continue hormonal contraceptive use, the consistent use of condoms is recommended to both prevent HIV transmission and compensate for
any possible reduction in the effectiveness of the hormonal
contraceptive.

Clarification: Although the interaction of certain anticonvulsants with POPs and ETG implants is not harmful to
women, it is likely to reduce the effectiveness of POPs and
ETG implants. Whether increasing the hormone dose of
POPs alleviates this concern remains unclear. Use of other
contraceptives should be encouraged for women who are
long-term users of any of these drugs. Use of DMPA is a
Category 1 because its effectiveness is not decreased by
use of certain anticonvulsants.
Evidence: Use of certain anticonvulsants may decrease the
effectiveness of POCs (227–229)

b. Lamotrigine

Evidence: No drug interactions have been reported among
epileptic women taking lamotrigine and using POCs (230)

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for progestin-only contraceptives,*† including progestin-only pills, DMPA, and implants
Category
Condition
Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampicin or rifabutin therapy

POP

DMPA

Implants

1
1
1
3

1
1
1
1

1
1
1
2

Clarifications/Evidence/Comments

Clarification: Although the interaction of rifampicin or rifabutin with POPs and ETG implants is not harmful to women,
it is likely to reduce the effectiveness of POPs and ETG
implants. Use of other contraceptives should be encouraged
for women who are long-term users of any of these drugs.
Use of DMPA is a Category 1 because its effectiveness is
not decreased by use of rifampicin or rifabutin. Whether increasing the hormone dose of POPs alleviates this concern
remains unclear.

* Abbreviations: STI = sexually transmitted infection; HIV = human immunodeficiency virus; POC = progestin-only contraceptive; DMPA = depot medroxyprogesterone acetate;
BMD = bone mineral density; NET-EN = norethisterone enantate; BMI = body mass index; COC = combined oral contraceptive; HDL = high-density lipoprotein; POP = progestinonly pill; DVT = deep venous thrombosis; PE = pulmonary embolism; SLE = systemic lupus erythematosus; VTE = venous thromboembolism; MEC = Medical Eligibility Criteria;
hCG = human chorionic gonadotropin; HPV = human papillomavirus; PID = pelvic inflammatory disease; AIDS = acquired immunodeficiency syndrome; IBD = inflammatory
bowel disease; ARV = antiretroviral; LNG = levonorgestrel; NRTI = nucleoside reverse transcriptase inhibitor; NNRTI = non-nucleoside reverse transcriptase inhibitor; ETG =
etonogestrel.
† POCs do not protect against STI/HIV. If risk exists for STI/HIV (including during pregnancy or postpartum), the correct and consistent use of condoms is recommended, either
alone or with another contraceptive method. Consistent and correct use of the male latex condom reduces the risk for STIs and HIV transmission.
§ Condition that exposes a woman to increased risk as a result of unintended pregnancy.

References
1. Albertazzi P, Bottazzi M, Steel SA. Bone mineral density and depot
medroxyprogesterone acetate. Contraception 2006;73:577–83.
2. Banks E, Berrington A, Casabonne D. Overview of the relationship
between use of progestogen-only contraceptives and bone mineral
density. BJOG Br J Obstet Gynaecol 2001;108:1214–21.
3. Beksinska M, Smit J, Kleinschmidt I, Farley T, Mbatha F. Bone mineral
density in women aged 40–49 years using depot-medroxyprogesterone
acetate, norethisterone enanthate or combined oral contraceptives for
contraception. Contraception 2005;71:170–5.
4. Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral
density in adolescents using norethisterone enanthate, depot-medroxyprogesterone acetate or combined oral contraceptives for contraception.
Contraception 2007;75:438–43.
5. Berenson AB, Breitkopf CR, Grady JJ, Rickert VI, Thomas A. Eﬀects
of hormonal contraception on bone mineral density after 24 months of
use. Obstet Gynecol 2004;103:899–906.
6. Busen NH, Britt RB, Rianon N. Bone mineral density in a cohort of
adolescent women using depot medroxyprogesterone acetate for one to
two years. J Adolesc Health 2003;32:257–9.
7. Clark MK, Sowers M, Levy B, Nichols S. Bone mineral density loss and
recovery during 48 months in ﬁrst-time users of depot medroxyprogesterone acetate. Fertil Steril 2006;86:1466–74.
8. Cromer BA, Blair JM, Mahan JD, Zibners L, Naumovski Z. A prospective comparison of bone density in adolescent girls receiving depot
medroxyprogesterone acetate (Depo-Provera), levonorgestrel (Norplant),
or oral contraceptives. J Pediatr 1996;129:671–6.
9. Cromer BA, Stager M, Bonny A, et al. Depot medroxyprogesterone
acetate, oral contraceptives and bone mineral density in a cohort of
adolescent girls. J Adolesc Health 2004;35:434–41.
10. Cromer BA, Lazebnik R, Rome E, et al. Double-blinded randomized
controlled trial of estrogen supplementation in adolescent girls who
receive depot medroxyprogesterone acetate for contraception. Am J
Obstet Gynecol 2005;192:42-7.
11. Cromer BA, Bonny AE, Stager M, et al. Bone mineral density in
adolescent females using injectable or oral contraceptives: a 24-month
prospective study. Fertil Steril 2008.

12. Cundy T, Cornish J, Evans MC, Roberts H, Reid IR. Recovery of bone
density in women who stop using medroxyprogesterone acetate. BMJ
1994;308:247–8.
13. Cundy T, Cornish J, Roberts H, Elder H, Reid IR. Spinal bone density
in women using depot medroxyprogesterone contraception. Obstet
Gynecol 1998;92:569–73.
14. Cundy T, Cornish J, Roberts H, Reid IR. Menopausal bone loss in
long-term users of depot medroxyprogesterone acetate contraception.
Am J Obstet Gynecol 2002;186:978–83.
15. Cundy T, Ames R, Horne A, et al. A randomized controlled trial of
estrogen replacement therapy in long-term users of depot medroxyprogesterone acetate. J Clin Endocrinol Metab 2003;88:78–81.
16. Gbolade B, Ellis S, Murby B, Randall S, Kirkman R. Bone density in
long term users of depot medroxyprogesterone acetate. Br J Obstet
Gynaecol 1998;105:790–4.
17. Kaunitz AM, Miller PD, Rice VM, Ross D, McClung MR. Bone
mineral density in women aged 25–35 years receiving depot medroxyprogesterone acetate: recovery following discontinuation. Contraception
2006;74:90–9.
18. Kaunitz AM, Arias R, McClung M. Bone density recovery after depot
medroxyprogesterone acetate injectable contraception use. Contraception
2008;77:67–76.
19. Lappe JM, Stegman MR, Recker RR. The impact of lifestyle factors on
stress fractures in female Army recruits. Osteopor Int 2001;12:35–42.
20. Lara-Torre E, Edwards CP, Perlman S, Hertweck SP. Bone mineral density
in adolescent females using depot medroxyprogesterone acetate. J Pediatr
Adolesc Gynecol 2004;17:17–21.
21. Lopez LM, Grimes DA, Schulz KF, Curtis KM. Steroidal contraceptives: eﬀect on bone fractures in women. Cochrane Database Syst Rev
2006;CD006033.
22. McGough P, Bigrigg A. Eﬀect of depot medroxyprogesterone acetate
on bone density in a Scottish industrial city. Eur J Contracept Reprod
Health Care 2007;12:253–9.
23. Merki-Feld GS, Neﬀ M, Keller PJ. A 2-year prospective study on the
eﬀects of depot medroxyprogesterone acetate on bone mass-response
to estrogen and calcium therapy in individual users. Contraception
2003;67:79–86.

MMWR

24. Orr-Walker BJ, Evans MC, Ames RW, et al. The eﬀect of past use of
the injectable contraceptive depot medroxyprogesterone acetate on bone
mineral density in normal postmenopausal women. Clini Endocrinol
1998;49:615–8.
25. Ott SM, Scholes D, LaCroix AZ, et al. Eﬀects of contraceptive use on
bone biochemical markers in young women. J Clin Endocrinol Metab
2001;86:179–85.
26. Paiva LC, Pinto-Neto AM, Faundes A. Bone density among long-term
users of medroxyprogesterone acetate as a contraceptive. Contraception
1998;58:351–5.
27. Perrotti M, Bahamondes L, Petta C, Castro S. Forearm bone density in
long-term users of oral combined contraceptives and depot medroxyprogesterone acetate. Fertil Steril 2001;76:469–73.
28. Petitti DB, Piaggio G, Mehta S, Cravioto MC, Meirik O. Steroid
hormone contraception and bone mineral density: a cross-sectional
study in an international population. The WHO Study of Hormonal
Contraception and Bone Health. Obstet Gynecol 2000;95:736–44.
29. Rosenberg L, Zhang Y, Constant D, et al. Bone status after cessation of use of
injectable progestin contraceptives. Contraception 2007;76:425–31.
30. Scholes D, LaCroix AZ, Ott SM, Ichikawa LE, Barlow WE. Bone
mineral density in women using depot medroxyprogesterone acetate
for contraception. Obstet Gynecol 1999;93:233–8.
31. Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Injectable
hormone contraception and bone density: results from a prospective
study. Epidemiology 2002;13:581–7.
32. Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. The
association between depot medroxyprogesterone acetate contraception and bone mineral density in adolescent women. Contraception
2004;69:99–104.
33. Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Change in
bone mineral density among adolescent women using and discontinuing
depot medroxyprogesterone acetate contraception. Arch Pediatr Adolesc
Med 2005;159:139–44.
34. Shaarawy M, El-Mallah SY, Seoudi S, Hassan M, Mohsen IA. Eﬀects of
the long-term use of depot medroxyprogesterone acetate as hormonal
contraceptive on bone mineral density and biochemical markers of bone
remodeling. Contraception 2006;74:297–302.
35. Tang OS, Tang G, Yip P, Li B, Fan S. Long-term depot-medroxyprogesterone acetate and bone mineral density. Contraception 1999;59:25–9.
36. Tang OS, Tang G, Yip PS, Li B. Further evaluation on long-term
depot-medroxyprogesterone acetate use and bone mineral density: a
longitudinal cohort study. Contraception 2000;62:161–4.
37. Tharnprisarn W, Taneepanichskul S. Bone mineral density in adolescent
and young Thai girls receiving oral contraceptives compared with depot
medroxyprogesterone acetate: a cross-sectional study in young Thai
women. Contraception 2002;66:101–3.
38. Virutamasen P, Wangsuphachart S, Reinprayoon D, et al. Trabecular bone
in long-term depot-medroxyprogesterone acetate users. Asia-Oceania J
Obstet Gynaecol 1994;20:269–74.
39. Walsh JS, Eastell R, Peel NF. Eﬀects of depot medroxyprogesterone
acetate on bone density and bone metabolism before and after peak
bone mass: a case-control study. J Clin Endocrinol Metab 2008.
40. Wanichsetakul P, Kamudhamas A, Watanaruangkovit P, Siripakarn Y,
Visutakul P. Bone mineral density at various anatomic bone sites in
women receiving combined oral contraceptives and depot-medroxyprogesterone acetate for contraception. Contraception 2002;65:407–10.
41. Wetmore CM, Ichikawa L, LaCroix AZ, Ott SM, Scholes D. Association
between caﬀeine intake and bone mass among young women: potential eﬀect modiﬁcation by depot medroxyprogesterone acetate use.
Osteoporos Int 200819:519–27.
42. Bahamondes L, Perrotti M, Castro S, et al. Forearm bone density in users of Depo-Provera as a contraceptive method. Fertil Steril
1999;71:849–52.

June 18, 2010

43. Bahamondes L, Monteiro-Dantas C, Espejo-Arce X, et al. A prospective study of the forearm bone density of users of etonorgestreland levonorgestrel-releasing contraceptive implants. Hum Reprod
2006;21:466–70.
44. Bahamondes L, Espejo-Arce X, Hidalgo MM, et al. A cross-sectional
study of the forearm bone density of long-term users of levonorgestrelreleasing intrauterine system. Hum Reprod 2006;21:1316–9.
45. Beerthuizen R, van Beek A, Massai R, et al. Bone mineral density during long-term use of the progestagen contraceptive implant Implanon
compared to a non-hormonal method of contraception. Hum Reprod
2000;15:118–22.
46. Caird LE, Reid-Thomas V, Hannan WJ, Gow S, Glasier AF. Oral
progestogen-only contraception may protect against loss of bone mass
in breast-feeding women. Clin Endocrinol (Oxf ) 1994;41:739–45.
47. Di X, Li Y, Zhang C, Jiang J, Gu S. Eﬀects of levonorgestrel-releasing
subdermal contraceptive implants on bone density and bone metabolism.
Contraception 1999;60:161–6.
48. Diaz S, Reyes MV, Zepeda A, et al. Norplant((R)) implants and progesterone vaginal rings do not aﬀect maternal bone turnover and density
during lactation and after weaning. Hum Reprod 1999;14:2499–505.
49. Intaraprasert S, Taneepanichskul S, Theppisai U, Chaturachinda K. Bone
density in women receiving Norplant implants for contraception. J Med
Assoc Thai 1997;80:738–41.
50. Monteiro-Dantas C, Espejo-Arce X, Lui-Filho JF, et al. A three-year longitudinal evaluation of the forearm bone density of users of etonogestreland levonorgestrel-releasing contraceptive implants. Reprod Health
2007;4:11.
51. Naessen T, Olsson SE, Gudmundson J. Diﬀerential eﬀects on bone
density of progestogen-only methods for contraception in premenopausal
women. Contraception 1995;52:35–9.
52. Taneepanichskul S, Intaraprasert S, Theppisai U, Chaturachinda K. Bone
mineral density during long-term treatment with Norplant implants
and depot medroxyprogesterone acetate. A cross-sectional study of Thai
women. Contraception 1997;56:153–5.
53. Taneepanichskul S, Intaraprasert S, Theppisai U, Chaturachinda K.
Bone mineral density in long-term depot medroxyprogesterone acetate
acceptors. Contraception 1997;56:1–3.
54. Vanderjagt DJ, Sagay AS, Imade GE, Farmer SE, Glew RH. Eﬀect of
Norplant contraceptive on the bones of Nigerian women as assessed
by quantitative ultrasound and serum markers of bone turnover.
Contraception 2005;72:212–6.
55. Oﬃce on Women’s Health, US Department of Health and Human
Services. HHS blueprint for action on breastfeeding. Washington, DC:
US Department of Health and Human Services, Oﬃce on Women’s
Health; 2000.
56. Guiloﬀ E, Ibarrapo A, Zanartu J, et al. Eﬀect of contraception on lactation. Am J Obstet Gynecol 1974;118:42–5.
57. World Health Organization Special Programme of Research Development
and Research Training in human reproduction. Eﬀects of hormonal
contraceptives on milk volume and infant growth. Contraception
1984;30:505–22.
58. Heikkila M, Luukkainen T. Duration of breast-feeding and development of children after insertion of a levonorgestrel-releasing intrauterine
contraceptive device. Contraception 1982;25:279–92.
59. Giner VJ, Cortes G, V, Sotelo LA, Bondani G. Eﬀect of daily oral administration of 0.350 mg of norethindrone on lactation and on the composition of milk [in Spanish]. Ginecol Obstet Mex 1976;40:31–9.
60. Zacharias S, Aguilera E, Assenzo JR, Zanartu J. Eﬀects of hormonal and
nonhormonal contraceptives on lactation and incidence of pregnancy.
Contraception 1986;33:203–13.
61. Kamal I, Hefnawi F, Ghoneim M, Abdallah M, Abdel RS. Clinical,
biochemical, and experimental studies on lactation. V. Clinical
eﬀects of steroids on the initiation of lactation. Am J Obstet Gynecol
1970;108:655–8.

Vol. 59 / RR-4

Recommendations and Reports

62. Hannon PR, Duggan AK, Serwint JR, et al. The inﬂuence of medroxyprogesterone on the duration of breast-feeding in mothers in an urban
community. Arch Pediatr Adolesc Med 1997;151:490–6.
63. Halderman LD, Nelson AL. Impact of early postpartum administration
of progestin-only hormonal contraceptives compared with nonhormonal contraceptives on short-term breast-feeding patterns. Am J Obstet
Gynecol 2002;186:1250–6.
64. Narducci U, Piatti N. Use of Depo Provera as a contraceptive in the
puerperium [in Italian]. Minerva Ginecol 1973;25:107–11.
65. Melis GB, Strigini F, Fruzzetti F, et al. Norethisterone enanthate as
an injectable contraceptive in puerperal and non-puerperal women.
Contraception 1981;23:77–88.
66. Karim M, Ammar R, El-mahgoub S, et al. Injected progestogen and
lactation. Br Med J 1971;1:200–3.
67. Shaaban MM. Contraception with progestogens and progesterone during
lactation. J Steroid Biochem Mol Biol 1991;40:705–10.
68. Zanartu J, Aguilera E, Munoz-Pinto G. Maintenance of lactation by
means of continuous low-dose progestogen given post-partum as a
contraceptive. Contraception 1976;13:313–8.
69. McEwan JA, Joyce DN, Tothill AU, Hawkins DF. Early experience in contraception with a new progestogen. Contraception 1977;16:339–50.
70. McCann MF, Moggia AV, Higgins JE, Potts M, Becker C. The eﬀects of
a progestin-only oral contraceptive (levonorgestrel 0.03 mg) on breastfeeding. Contraception 1989;40:635–48.
71. West CP. The acceptability of a progestagen-only contraceptive during
breast-feeding. Contraception 1983;27:563–9.
72. Bjarnadottir RI, Gottfredsdottir H, Sigurdardottir K, Geirsson RT,
Dieben TO. Comparative study of the eﬀects of a progestogen-only
pill containing desogestrel and an intrauterine contraceptive device in
lactating women. BJOG 2001;108:1174–80.
73. Taneepanichskul S, Reinprayoon D, Thaithumyanon P, et al. Eﬀects
of the etonogestrel-releasing implant Implanon and a nonmedicated
intrauterine device on the growth of breast-fed infants. Contraception
2006;73:368–71.
74. Reinprayoon D, Taneepanichskul S, Bunyavejchevin S, et al. Eﬀects
of the etonogestrel-releasing contraceptive implant (Implanon(R)) on
parameters of breastfeeding compared to those of an intrauterine device.
Contraception 2000;62:239–46.
75. Seth U, Yadava HS, Agarwal N, Laumas KR, Hingorani V. Eﬀect of a
subdermal silastic implant containing norethindrone acetate on human
lactation. Contraception 1977;16:383–98.
76. Shaaban MM, Salem HT, Abdullah KA. Inﬂuence of levonorgestrel
contraceptive implants, NORPLANT, initiated early postpartum upon
lactation and infant growth. Contraception 1985;32:623–35.
77. Abdel-Aleem H, Abol-Oyoun SM, Shaaban MM, et al. The use of
nomegestrol acetate subdermal contraceptive implant, uniplant, during
lactation. Contraception 1996;54:281–6.
78. Croxatto HB, Diaz S, Peralta O, et al. Fertility regulation in nursing
women. II. Comparative performance of progesterone implants versus
placebo and copper T. Am J Obstet Gynecol 1982;144:201–8.
79. Diaz S, Peralta O, Juez G, et al. Fertility regulation in nursing women.
VI. Contraceptive eﬀectiveness of a subdermal progesterone implant.
Contraception 1984;30:311–25.
80. Sivin I, Diaz S, Croxatto HB, et al. Contraceptives for lactating women:
a comparative trial of a progesterone-releasing vaginal ring and the copper
T 380A IUD. Contraception 1997;55:225–32.
81. Massai R, Miranda P, Valdes P, et al. Preregistration study on the safety
and contraceptive eﬃcacy of a progesterone-releasing vaginal ring in
Chilean nursing women. Contraception 1999;60:9–14.
82. Shaamash AH, Sayed GH, Hussien MM, Shaaban MM. A comparative
study of the levonorgestrel-releasing intrauterine system Mirena(R) versus
the Copper T380A intrauterine device during lactation: breast-feeding
performance, infant growth and infant development. Contraception
2005;72:346–51.

83. WHO Special Programme of Research Development and Research
Training in Human Reproduction. Progestogen-only contraceptives
during lactation: II. Infant development. World Health Organization,
Task Force for Epidemiological Research on Reproductive Health; Special
Programme of Research, Development, and Research Training in Human
Reproduction. Contraception 1994;50:55–68.
84. WHO Special Programme of Research Development and Research
Training in Human Reproduction. Progestogen-only contraceptives
during lactation: I. Infant growth. World Health Organization Task
force for Epidemiological Research on Reproductive Health; Special
Programme of Research, Development and Research Training in Human
Reproduction. Contraception 1994;50:35–53.
85. Diaz S, Zepeda A, Maturana X, et al. Fertility regulation in nursing
women: IX. Contraceptive performance, duration of lactation, infant
growth, and bleeding patterns during use of progesterone vaginal rings,
progestin-only pills, Norplant(R) implants, and Copper T 380-A intrauterine devices. Contraception 1997;56:223–32.
86. Coutinho EM, Athayde C, Dantas C, Hirsch C, Barbosa I. Use of a
single implant of elcometrine (ST-1435), a nonorally active progestin, as a
long acting contraceptive for postpartum nursing women. Contraception
1999;59:115–22.
87. Massai MR, Diaz S, Quinteros E, et al. Contraceptive eﬃcacy and
clinical performance of Nestorone implants in postpartum women.
Contraception 2001;64:369–76.
88. Schiappacasse V, Diaz S, Zepeda A, Alvarado R, Herreros C. Health and
growth of infants breastfed by Norplant contraceptive implants users: a
six-year follow-up study. Contraception 2002;66:57–65.
89. Diaz S, Herreros C, Juez G, et al. Fertility regulation in nursing women:
VII. Inﬂuence of NORPLANT levonorgestrel implants upon lactation
and infant growth. Contraception 1985;32:53–74.
90. Massai R, Quinteros E, Reyes MV, et al. Extended use of a progesterone-releasing vaginal ring in nursing women: a phase II clinical trial.
Contraception 2005;72:352–7.
91. Jimenez J, Ochoa M, Soler MP, Portales P. Long-term follow-up of
children breast-fed by mothers receiving depot-medroxyprogesterone
acetate. Contraception 1984;30:523–33.
92. Abdulla KA, Elwan SI, Salem HS, Shaaban MM. Eﬀect of early postpartum use of the contraceptive implants, NORPLANT, on the serum
levels of immunoglobulins of the mothers and their breastfed infants.
Contraception 1985;32:261–6.
93. Shikary ZK, Betrabet SS, Toddywala WS, et al. Pharmacodynamic
eﬀects of levonorgestrel (LNG) administered either orally or subdermally
to early postpartum lactating mothers on the urinary levels of follicle
stimulating hormone (FSH), luteinizing hormone (LH) and testosterone
(T) in their breast-fed male infants. Contraception 1986;34:403–12.
94. Kurunmaki H. Contraception with levonorgestrel-releasing subdermal capsules, Norplant, after pregnancy termination. Contraception
1983;27:473–82.
95. Kurunmaki H, Toivonen J, Lähteenmäki PL, Luukkainen T. Immediate
postabortal contraception with Norplant: levonorgestrel, gonadotropin,
estradiol, and progesterone levels over two postaboral months and
return of fertility after removal of Norplant capsules. Contraception
1984;30:431-42.
96. Lahteenmaki P, Toivonen J, Lahteenmaki PL. Postabortal contraception with
norethisterone enanthate injections. Contraception 1983;27:553–62.
97. Ortayli N, Bulut A, Sahin T, Sivin I. Immediate postabortal contraception with the levonorgestrel intrauterine device, Norplant, and traditional
methods. Contraception 2001;63:309–14.
98. Bonny AE, Ziegler J, Harvey R, et al. Weight gain in obese and nonobese
adolescent girls initiating depot medroxyprogesterone, oral contraceptive
pills, or no hormonal contraceptive method. Arch Pediatr Adolesc Med
2006;160:40–5.

MMWR

99. Clark MK, Dillon JS, Sowers M, Nichols S. Weight, fat mass,
and central distribution of fat increase when women use depotmedroxyprogesterone acetate for contraception. Int J Obes (Lond)
2005;29:1252–8.
100. Jain J, Jakimiuk AJ, Bode FR, Ross D, Kaunitz AM. Contraceptive
eﬃcacy and safety of DMPA-SC. Contraception 2004;70:269–75.
101. Kozlowski KJ, Rickert VI, Hendon A, Davis P. Adolescents and
Norplant: preliminary findings of side effects. J Adolesc Health
1995;16:373–8.
102. Leiman G. Depo-medroxyprogesterone acetate as a contraceptive
agent: its eﬀect on weight and blood pressure. Am J Obstet Gynecol
1972;114:97–102.
103. Mangan SA, Larsen PG, Hudson S. Overweight teens at increased
risk for weight gain while using depot medroxyprogesterone acetate. J
Pediatr Adolesc Gynecol 2002;15:79–82.
104. Risser WL, Gefter LR, Barratt MS, Risser JM. Weight change in
adolescents who used hormonal contraception. J Adolesc Health
1999;24:433–6.
105. Westhoﬀ C, Jain JK, Milsom I, Ray A. Changes in weight with depot
medroxyprogesterone acetate subcutaneous injection 104 mg/0.65 mL
1. Contraception 2007;75:261–7.
106. Weiss HG, Nehoda H, Labeck B, et al. Pregnancies after adjustable
gastric banding. Obes Surg 2001;11:303–6.
107. Gerrits EG, Ceulemans R, van HR, Hendrickx L, Totte E. Contraceptive
treatment after biliopancreatic diversion needs consensus. Obes Surg
2003;13:378–82.
108. Victor A, Odlind V, Kral JG. Oral contraceptive absorption and sex
hormone binding globulins in obese women: eﬀects of jejunoileal
bypass. Gastroenterol Clin North Am 1987;16:483–91.
109. Andersen AN, Lebech PE, Sorensen TI, Borggaard B. Sex hormone levels and intestinal absorption of estradiol and D-norgestrel in women following bypass surgery for morbid obesity. Int J Obes 1982;6:91–6.
110. World Health Organization. Cardiovascular disease and use of oral and
injectable progestogen-only contraceptives and combined injectable
contraceptives. Results of an international, multicenter, case-control
study. Contraception 1998;57:315–24.
111. Heinemann LA, Assmann A, DoMinh T, et al. Oral progestogen-only
contraceptives and cardiovascular risk: results from the Transnational
Study on Oral Contraceptives and the Health of Young Women. Eur
J Contracept Reprod Health Care 1999;4:67–73.
112. Vasilakis C, Jick H, Mar Melero-Montes M. Risk of idiopathic
venous thromboembolism in users of progestogens alone. Lancet
1999;354:1610–1.
113. Sonmezer M, Atabekoglu C, Cengiz B, et al. Depot-medroxyprogesterone
acetate in anticoagulated patients with previous hemorrhagic corpus
luteum. European J Contracept Reprod Health Care 2005;10:9–14.
114. The Criteria Committee of the New York Heart Association.
Nomenclature and criteria for diagnosis of diseases of the heart and
great vessels. 9th ed. Boston, MA: Little, Brown & Co; 1994.
115. Avila WS, Grinberg M, Melo NR, Aristodemo PJ, Pileggi F.
Contraceptive use in women with heart disease [in Portuguese]. Arq
Bras Cardiol 1996;66:205–11.
116. Taurelle R, Ruet C, Jaupart F, Magnier S. Contraception using a
progestagen-only minipill in cardiac patients [in French]. Arch Mal
Coeur Vaiss 1979;72:98–106.
117. Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated with abnormal Pap results in systemic lupus erythematosus.
Rheumatology (Oxford) 2004;43:1386–9.

June 18, 2010

118. Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures
and breast cancer in a sample of women with systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1178–81.
119. Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin
gene mutation, and thrombosis risk in patients with antiphospholipid
antibodies. J Rheumatol 2002;29:1683–8.
120. Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional
Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. Arthritis Rheum
2001;44:2331–7.
121. Julkunen HA. Oral contraceptives in systemic lupus erythematosus:
side-eﬀects and inﬂuence on the activity of SLE. Scand J Rheumatol
1991;20:427–33.
122. Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women with
systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30.
123. Jungers P, Dougados M, Pelissier C, et al. Inﬂuence
Inﬂuence of oral contraceptive therapy on the activity of systemic lupus erythematosus. Arthritis
Rheum 1982;25:618–23.
124. Manzi S, Meilahn EN, Rairie JE, et al. Age-speciﬁc incidence rates of
myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study. Am J Epidemiol
1997;145:408–15.
125. McAlindon T, Giannotta L, Taub N, et al. Environmental factors
predicting nephristis in systemic lupus erythematosus. Ann Rheum
Dis 1993;52:720–4.
126. McDonald J, Stewart J, Urowitz MB, et al. Peripheral vascular disease in patients with systemic lupus erythematosus. Ann Rheum Dis
1992;51:56–60.
127. Mintz G, Gutierrez G, Deleze M, et al. Contraception with progestogens
in systemic lupus erythematosus. Contraception 1984;30:29–38.
128. Petri M. Musculoskeletal complications of systemic lupus erythematosus in the Hopkins Lupus Cohort: an update. Arthritis Care Res
1995;8:137–45.
129. Petri M, Kim MY, Kalunian KC, et al. Combined oral contraceptives in women with systemic lupus erythematosus. N Engl J Med
2005;353:2550–8.
130. Petri M. Lupus in Baltimore: evidence-based ‘clinical perarls’ from the
Hopkins Lupus Cohort. Lupus 2005;14:970–3.
131. Sanchez-Guerrero J, Uribe AG, Jimenez-Santana L, et al. A trial of
contraceptive methods in women with systemic lupus erythematosus.
N Engl J Med 2005;353:2539–49.
132. Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and
venous thrombosis after diagnosis of systemic lupus erythematosus.
Arthritis Rheum 2005;53:609–12.
133. Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrel-releasing intrauterine system in the management of menorrhagia in women
with hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–3.
134. Somers E, Magder LS, Petri M. Antiphospholipid antibodies and
incidence of venous thrombosis in a cohort of patients with systemic
lupus erythematosus. J Rheumatol 2002;29:2531–6.
135. Urowitz MB, Bookman AA, Koehler BE, et al. The bimodal mortality
pattern of systemic lupus erythematosus. Am J Med 1976;60:221–5.
136. Choojitarom K, Verasertniyom O, Totemchokchyakarn K, et al. Lupus
nephritis and Raynaud’s phenomenon are signiﬁcant risk factors for
vascular thrombosis in SLE patients with positive antiphospholipid
antibodies. Clini Rheumatol 2008;27:345–51.
137. Wahl DG, Guillemin F, de Maistre E, et al. Risk for venous thrombosis
related to antiphospholipid antibodies in systemic lupus erythematosus—a meta-analysis. Lupus 1997;6:467–73.

Vol. 59 / RR-4

Recommendations and Reports

138. Demers R, Blais JA, Pretty H. Rheumatoid arthritis treated by norethynodrel associated with mestranol: clinical aspects and laboratory
tests [in French]. Can Med Assoc J 1966;95:350–4.
139. Drossaers-Bakker KW, Zwinderman AH, Van ZD, Breedveld FC,
Hazes JM. Pregnancy and oral contraceptive use do not signiﬁcantly
inﬂuence outcome in long term rheumatoid arthritis. Ann Rheum Dis
2002;61:405–8.
140. Gilbert M, Rotstein J, Cunningham C, et al. Norethynodrel with mestranol in treatment of rheumatoid arthritis. JAMA 1964;190:235.
141. Gill D. Rheumatic complaints of women using anti-ovulatory drugs.
An evaluation. J Chronic Dis 1968;21:435–44.
142. Hazes JM, Dijkmans BA, Vandenbroucke JP, Cats A. Oral contraceptive treatment for rheumatoid arthritis: an open study in 10 female
patients. Br J Rheumatol 1989;28 Suppl 1:28–30.
143. Ostensen M, Aune B, Husby G. Eﬀect of pregnancy and hormonal
changes on the activity of rheumatoid arthritis. Scand J Rheumatol
1983;12:69–72.
144. Vignos PJ, Dorfman RI. Eﬀect of large doses of progesterone in rheumatoid arthritis. Am J Med Sci 1951;222:29–34.
145. Bijlsma JW, Huber-Bruning O, Thijssen JH. Eﬀect of oestrogen treatment on clinical and laboratory manifestations of rheumatoid arthritis.
Ann Rheum Dis 1987;46:777–9.
146. Cromer BA, Smith RD, Blair JM, Dwyer J, Brown RT. A prospective study of adolescents who choose among levonorgestrel implant
(Norplant), medroxyprogesterone acetate (Depo-Provera), or the
combined oral contraceptive pill as contraception. Pediatrics 1994;94
:687–94.
147. Gupta N, O’Brien R, Jacobsen LJ, et al. Mood changes in adolescents
using depo-medroxyprogesterone acetate for contraception: a prospective study. Am J Obstet Gynecol 2001;14:71–6.
148. Westoﬀ C, Truman C. Depressive symptoms and Depo-Provera.
Contraception 1998;57:237–40.
149. Westoﬀ C, Truman C, Kalmuss D, et al. Depressive symptoms and
Norplant contraceptive implants. Contraception 1998;57:241–5.
150. Smith JS. Cervical cancer and use of hormonal conraceptives: a systematic review. Lancet 2003;361:1159–67.
151. Baeten JM, Nyange PM, Richardson BA, et al. Hormonal contraception and risk of sexually transmitted disease acquisition: results from
a prospective study. Am J Obstet Gynecol 2001;185:380–5.
152. Giuliano AR, Papenfuss M, Abrahamsen M, et al. Human papillomavirus infection at the United States–Mexico border: implications for
cervical cancer prevention and control. Cancer Epidemiol Biomarkers
Prev 2001;10:1129–36.
153. Jacobson DL, Peralta L, Farmer M, et al. Relationship of hormonal
contraception and cervical ectopy as measured by computerized
planimetry to chlamydial infection in adolescents. Sex Transm Dis
2000;27:313–9.
154. Lavreys L, Chohan B, Ashley R, et al. Human herpesvirus 8: seroprevalence and correlates in prostitutes in Mombasa, Kenya. J Infect Dis
2003;187:359–63.
155. Morrison CS, Bright P, Wong EL, et al. Hormonal contraceptive use,
cervical ectopy, and the acquisition of cervical infections. Sex Transm
Dis 2004;31:561–7.
156. Moscicki AB, Hills N, Shiboski S, et al. Risks for incident human
papillomavirus infection and low-grade squamous intraepithelial lesion
development in young females. JAMA 2001;285:2995–3002.
157. Nsofor BI, Bello CS, Ekwempu CC. Sexually transmitted disease
among women attending a family planning clinic in Zaria, Nigeria.
Int J Gynaecol Obstet 1989;28:365–7.

158. Ruijs GJ, Kauer FM, van Gijssel PM, Schirm J, Schroder FP. Direct
immunoﬂuorescence for Chlamydia trachomatis on urogenital smears
for epidemiological purposes. Eur J Obstet Gyneco Reprod Biol
1988;27:289–97.
159. Aklilu M, Messele T, Tsegaye A, et al. Factors associated with HIV-1
infection among sex workers of Addis Ababa, Ethiopia. AIDS
2001;15:87–96.
160. Allen S, Seruﬁlira A, Gruber V, et al. Pregnancy and contraception use
among urban Rwandan women after HIV testing and counseling. Am
J Public Health 1993;83:705–10.
161. Baeten JM, Benki S, Chohan V, et al. Hormonal contraceptive use,
herpes simplex virus infection, and risk of HIV-1 acquisition among
Kenyan women. AIDS 2007;21:1771–7.
162. Bulterys M, Chao A, Habimana P, et al. Incident HIV-1 infection in a
cohort of young women in Butare, Rwanda. AIDS 1994;8:1585–91.
163. Carael M, Van de Perre PH, Lepage PH, et al. Human immunodeﬁciency virus transmission among heterosexual couples in Central Africa.
AIDS 1988;2:201–5.
164. Cohen CR, Duerr A, Pruithithada N, et al. Bacterial vaginosis and
HIV seroprevalence among female commercial sex workers in Chiang
Mai, Thailand. AIDS 1995;9:1093–7.
165. Criniti A, Mwachari CW, Meier AS, et al. Association of hormonal
contraception and HIV-seroprevalence in Nairobi, Kenya. AIDS
2003;17:2667–9.
166. Kapiga SH, Shao JF, Lwihula GK, Hunter DJ. Risk factors for HIV
infection among women in Dar-es-Salaam, Tanzania. J Acquir Immune
Deﬁc Syndr 1994;7:301–9.
167. Kapiga SH, Lyamuya EF, Lwihula GK, Hunter DJ. The incidence of
HIV infection among women using family planning methods in Dar
es Salaam, Tanzania. AIDS 1998;12:75–84.
168. Kiddugavu M, Makumbi F, Wawer MJ, et al. Hormonal contraceptive use and HIV-1 infection in a population-based cohort in Rakai,
Uganda. AIDS 2003;17:233–40.
169. Kilmarx PH, Limpakarnjanarat K, Mastro TD, et al. HIV-1 seroconversion in a prospective study of female sex workers in northern
Thailand: continued high incidence among brothel-based women.
AIDS 1998;12:1889–98.
170. Kleinschmidt I, Rees H, Delany S, et al. Injectable progestin contraceptive use and risk of HIV infection in a South African family planning
cohort. Contraception 2007;75:461–7.
171. Lavreys L, Chohan V, Overbaugh J, et al. Hormonal contraception and
risk of cervical infections among HIV-1-seropositive Kenyan women.
AIDS 2004;18:2179–84.
172. Limpakarnjanarat K, Mastro TD, Saisorn S, et al. HIV-1 and other
sexually transmitted infections in a cohort of female sex workers in
Chiang Rai, Thailand. Sex Transm Infect 1999;75:30–5.
173. Martin HL, Jr., Nyange PM, Richardson BA, et al. Hormonal contraception, sexually transmitted diseases, and risk of heterosexual
transmission of human immunodeﬁciency virus type 1. J Infect Dis
1998;178:1053–9.
174. Mati JK, Hunter DJ, Maggwa BN, Tukei PM. Contraceptive use and
the risk of HIV infection in Nairobi, Kenya. Int J Gynaecol Obstet
1995;48:61–7.
175. Morrison CS, Richardson BA, Mmiro F, et al. Hormonal contraception
and the risk of HIV acquisition. AIDS 2007;21:85–95.
176. Myer L, Denny L, Wright TC, Kuhn L. Prospective study of hormonal
contraception and women’s risk of HIV infection in South Africa. Int
J Epidemiol 2007;36:166–74.

MMWR

177. Nagachinta T, Duerr A, Suriyanon V, et al. Risk factors for HIV-1
transmission from HIV-seropositive male blood donors to their regular
female partners in northern Thailand. AIDS 1997;11:1765–72.
178. Nzila N, Laga M, Thiam MA, et al. HIV and other sexually
transmitted diseases among female prostitutes in Kinshasa. AIDS
1991;5:715–21.
179. Plourde PJ, Plummer FA, Pepin J, et al. Human immunodeﬁciency virus
type 1 infection in women attending a sexually transmitted diseases
clinic in Kenya [comment]. J Infect Dis 1992;166:86–92.
180. Rehle T, Brinkmann UK, Siraprapasiri T, et al. Risk factors of HIV-1
infection among female prostitutes in Khon Kaen, northeast Thailand.
Infection 1992;20:328–31.
181. Siraprapasiri T, Thanprasertsuk S, Rodklay A, et al. Risk factors for HIV
among prostitutes in Chiangmai, Thailand. AIDS 1991;5:579–82.
182. Taneepanichskul S, Phuapradit W, Chaturachinda K. Association of
contraceptives and HIV-1 infection in Thai female commercial sex
workers. Aust N Z J Obstet Gynaecol 1997;37:86–8.
183. Ungchusak K, Rehle T, Thammapornpilap P, et al. Determinants of
HIV infection among female commercial sex workers in northeastern
Thailand: results from a longitudinal study. J Acquir Immune Deﬁc
Syndr Hum Retrovirol 1996;12:500–7. Erratum in: J Acquir Immune
Deﬁc Syndr Hum Retrovirol 1998;18:192.
184. Allen S, Stephenson R, Weiss H, et al. Pregnancy, hormonal contraceptive use, and HIV-related death in Rwanda. J Womens Health (Larchmt
) 2007;16:1017–27.
185. Cejtin HE, Jacobson L, Springer G, et al. Eﬀect of hormonal contraceptive use on plasma HIV-1-RNA levels among HIV-infected women.
AIDS 2003;17:1702–4.
186. Clark RA, Kissinger P, Williams T. Contraceptive and sexually
transmitted diseases protection among adult and adolescent women
infected with human immunodeﬁciency virus. Int J STD AIDS
1996;7:439–42.
187. Clark RA, Theall KP, Amedee AM, et al. Lack of association between
genital tract HIV-1 RNA shedding and hormonal contraceptive use
in a cohort of Louisiana women. Sex Transm Dis 2007;34:870–2.
188. Clemetson DB, Moss GB, Willerford DM, et al. Detection of HIV
DNA in cervical and vaginal secretions. Prevalence and correlates among
women in Nairobi, Kenya. JAMA 1993;269:2860–4.
189. European Study Group on Heterosexual Transmission of HIV.
Comparison of female to male and male to female transmission of
HIV in 563 stable couples. BMJ 1992;304:809–13.
190. Kaul R, Kimani J, Nagelkerke NJ, et al. Risk factors for genital ulcerations in Kenyan sex workers. The role of human immunodeﬁciency
virus type 1 infection. Sex Transm Dis 1997;24:387–92.
191. Kilmarx PH, Limpakarnjanarat K, Kaewkungwal J, et al. Disease
progression and survival with human immunodeﬁciency virus type 1
subtype E infection among female sex workers in Thailand. J Infect
Dis 2000;181:1598–606.
192. Kovacs A, Wasserman SS, Burns D, et al. Determinants of HIV-1
shedding in the genital tract of women. Lancet 2001;358:1593–601.
193. Kreiss J, Willerford DM, Hensel M, et al. Association between cervical
inﬂammation and cervical shedding of human immunodeﬁciency virus
DNA. J Infect Dis 1994;170:1597-601.
194. Mostad SB, Overbaugh J, DeVange DM, et al. Hormonal contraception, vitamin A deﬁciency, and other risk factors for shedding of HIV-1
infected cells from the cervix and vagina. Lancet 1997;350:922–7.
195. Richardson BA, Otieno PA, Mbori-Ngacha D, et al. Hormonal contraception and HIV-1 disease progression among postpartum Kenyan
women. AIDS 2007;21:749–53.

June 18, 2010

196. Seck K, Samb N, Tempesta S, et al. Prevalence and risk factors of cervicovaginal HIV shedding among HIV-1 and HIV-2 infected women
in Dakar, Senegal. Sex Transm Infect 2001;77:190–3.
197. Stringer EM, Kaseba C, Levy J, et al. A randomized trial of the intrauterine contraceptive device vs hormonal contraception in women who
are infected with the human immunodeﬁciency virus. Am J Obstet
Gynecol 2007;197:144–8.
198. Taneepanichskul S, Intaraprasert S, Phuapradit W, Chaturachinda K.
Use of Norplant implants in asymptomatic HIV-1 infected women.
Contraception 1997;55:205–7.
199. Taneepanichskul S, Tanprasertkul C. Use of Norplant implants in the
immediate postpartum period among asymptomatic HIV-1-positive
mothers. Contraception 2001;64:39–41.
200. Wang CC, McClelland RS, Overbaugh J, et al. The eﬀect of hormonal contraception on genital tract shedding of HIV-1. AIDS
2004;18:205–9.
201. Tagy AH, Saker ME, Moussa AA, Kolgah A. The eﬀect of low-dose
combined oral contraceptive pills versus injectable contracetpive (Depot
Provera) on liver function tests of women with compensated bilharzial
liver ﬁbrosis. Contraception 2001;64:173–6.
202. Pyorala T, Vahapassi J, Huhtala M. The eﬀect of lynestrenol and norethindrone on the carbohydrate and lipid metabolism in subjects with
gestational diabetes. Ann Chir Gynaecol 1979;68:69–74.
203. Radberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies
in women with previous gestational diabetes during contraceptive
treatment: eﬀects on serum lipids and high density lipoproteins. Acta
Endocrinol (Copenh) 1982;101:134–9.
204. Xiang AH, Kawakubo M, Kjos SL, Buchanan TA. Long-acting
injectable progestin contraception and risk of type 2 diabetes in
Latino women with prior gestational diabetes mellitus. Diabetes Care
2006;29:613–7.
205. Xiang AH, Kawakubo M, Buchanan TA, Kjos SL. A longitudinal study
of lipids and blood pressure in relation to method of contraception in
Latino women with prior gestational diabetes mellitus. Diabetes Care
2007;30:1952–8.
206. Kjos SL, Peters RK, Xiang A, et al. Contraception and the risk of type
2 diabetes mellitus in Latina women with prior gestational diabetes
mellitus. JAMA 1998;280:533–8.
207. Nelson AL, Le MH, Musherraf Z, Vanberckelaer A. Intermediate-term
glucose tolerance in women with a history of gestational diabetes:
natural history and potential associations with breastfeeding and contraception. Am J Obstet Gynecol 2008;198:699–7.
208. Diab KM, Zaki MM. Contraception in diabetic women: comparative metabolic study of norplant, depot medroxyprogesterone acetate,
low dose oral contraceptive pill and CuT380A. J Obstet Gynecol Res
2000;26:17–26.
209. Lunt H, Brown LJ. Self-reported changes in capillary glucose and
insulin requirements during the menstrual cycle. Diabetic Med
1995;13:525–30.
210. Radberg T, Gustafson A, Skryten A, Karlsson K. Oral contraception
in diabetic women. A cross-over study on seum and high density
lipoprotein (HDL) lipids and diabetes control during progestogen
and combined estrogen/progestogen contraception. Horm Metab Res
1982;14:61–5.
211. Skouby SO, Molsted-Petersen L, Kuhl C, Bennet P. Oral contraceptives
in diabetic womne: metabolic eﬀects of four compounds with diﬀerent
estrogen/progestogen proﬁles. Fertil Steril 1986;46:858–64.

Vol. 59 / RR-4

Recommendations and Reports

212. Bitton A, Peppercorn MA, Antonioli DA, et al. Clinical, biological,
and histologic parameters as predictors of relapse in ulcerative colitis.
Gastroenterology 2001;120:13–20.
213. Cosnes J, Carbonnel F, Carrat F, Beaugerie L, Gendre JP. Oral contraceptive use and the clinical course of Crohn’s disease: a prospective
cohort study. Gut 1999;45:218–22.
214. Sutherland LR, Ramcharan S, Bryant H, Fick G. Eﬀect of oral contraceptive use on reoperation following surgery for Crohn’s disease. Dig
Dis Sci 1992;37:1377–82.
215. Timmer A, Sutherland LR, Martin F. Oral contraceptive use and
smoking are risk factors for relapse in Crohn’s disease. The Canadian
Mesalamine for Remission of Crohn’s Disease Study Group.
Gastroenterology 1998;114:1143–50.
216. Wright JP. Factors inﬂuencing ﬁrst relapse in patients with Crohn’s
disease. J Clin Gastroenterol 1992;15:12–6.
217. D’halluin V, Vilgrain V, Pelletier G, et al. Natural history of focal
nodular hyperplasia. A retrospective study of 44 cases [in French].
Gastroenterol Clin Biol 2001;25:1008–10.
218. Mathieu D, Kobeiter H, Maison P, et al. Oral contraceptive use and focal
nodular hyperplasia of the liver. Gastroenterology 2000;118:560–4.
219. Adadevoh BK, Isaacs WA. The eﬀect of megestrol acetate on sickling.
Am J Med Sci 1973;265:367–70.
220. Barbosa IC, Ladipo OA, Nascimento ML, et al. Carbohydrate
metabolism in sickle cell patients using subdermal implant containing
nomegesterol acetate (Uniplant). Contraception 2001;63:263–5.
221. de Abood M, de Castillo Z, Guerrero F, Espino M, Austin KL. Eﬀects
of Depo-Provera or Microgynon on the painful crises of sickle cell
anemia patients. Contraception 1997;56:313–6.

222. De Ceulaer K, Gruber C, Hayes R, Serjeant GR. Medroxyprogesterone
acetate and homozygous sickle-cell disease. Lancet 1982;2:229–31.
223. Howard RJ, Lillis C, Tuck SM. Contraceptives, counseling, and pregnancy in women with sickle cell disease. BMJ 1993;306:1735–7.
224. Ladipo OA, Falusi AG, Feldblum PJ, Osotimehin BO, Otolorin EO,
Ojengbede OA Norplant use by women with sickle cell disease. Int J
Gynaecol Obstet 1993;41:85–7.
225. Nascimento ML, Ladipo OA, Coutinho E. Nomogestrol acetate contraceptive implant use by women with sickle cell disease. Clin Pharmacol
Ther 1998;64:433–8.
226. Yoong WC, Tuck SM, Yardumian A. Red cell deformability in oral
contraceptive pill users with sickle cell anaemia. Br J Haematol
1999;104:868–70.
227. Odlind V, Olsson S-E. Enhanced metabolism of levonorgestrel
during phenytoin treatment in a woman with Norplant implants.
Contraception 1986;33:257–61.
228. Schindlbeck C, Janni W, Friese K. Failure of Implanon contraception
in a patient taking carbamazepine for epilepsia. Arch Gynecol Obstet
2006;273:255–6.
229. Shane-McWhorter L, Cerven JD, MacFarlane LL, Osborn C. Enhanced
metabolism of levonorgestrel during phenobarbital treatment and
resultant pregnancy. Pharmacotherapy 1998;18:1360–4.
230. Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens, reduces lamotrigine serum concentrations. Epilepsia
2005;46:1414–7.

MMWR

June 18, 2010

Appendix D
Classifications for Emergency Contraceptive Pills
Classiﬁcations for emergency contraceptive pills (ECPs) are
for both levonorgestrel and combined oral contraceptive pills.

ECPs do not protect against sexually transmitted infections
(STIs) or human immunodeﬁciency virus (HIV).

BOX. Categories for Classifying Emergency Contraceptive Pills

TABLE. Classifications for emergency contraceptive pills, including levonorgestrel contraceptive pills and combined oral
contraceptive pills*†
Condition

Category

Clarifications/Evidence/Comments

Not applicable

Clarification: Although this method is not indicated for a woman with a known or
suspected pregnancy, no harm to the woman, the course of her pregnancy, or the
fetus if ECPs are inadvertently used is known to exist.

Personal Characteristics and Reproductive History
Pregnancy

Breastfeeding
Past ectopic pregnancy
History of bariatric surgery§
a. Restrictive procedures: decrease storage capacity of the stomach (vertical banded gastroplasty, laparoscopic adjustable
gastric band, laparoscopic sleeve gastrectomy)
b. Malabsorptive procedures: decrease absorption of nutrients
and calories by shortening the functional length of the small
intestine (Roux-en-Y gastric bypass, biliopancreatic diversion)

Comment: Bariatric surgical procedures involving a malabsorptive component
have the potential to decrease oral contraceptive effectiveness, perhaps further
decreased by postoperative complications such as long-term diarrhea and/or
vomiting. Because of these malabsorptive concerns, an emergency IUD might be
more appropriate than ECPs.

History of severe cardiovascular complications§ (ischemic
heart disease, cerebrovascular attack, or other thromboembolic
conditions)

Comment: The duration of ECP use is less than that of regular use of COCs or
POPs and thus would be expected to have less clinical impact.

Angina pectoris

Comment: The duration of ECP use is less than that of regular use of COCs or
POPs and thus would be expected to have less clinical impact.

Cardiovascular Disease

Rheumatic Diseases
Rheumatoid arthritis
a. On immunosuppressive therapy
b. Not on immunosuppressive therapy

1
1

Neurologic Conditions
Migraine

Comment: The duration of ECP use is less than that of regular use of COCs or
POPs and thus would be expected to have less clinical impact.

Gastrointestinal Conditions
Inflammatory bowel disease (ulcerative colitis, Crohn disease)
Severe liver

disease§

(including jaundice)

1
2

Solid Organ Transplantation
Solid organ transplantation§
a. Complicated: graft failure (acute or chronic), rejection,
cardiac allograft vasculopathy
b. Uncomplicated

1
1

Comment: The duration of ECP use is less than that of regular use of COCs or
POPs and thus would be expected to have less clinical impact.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for emergency contraceptive pills, including levonorgestrel contraceptive pills and combined
oral contraceptive pills*†
Category

Clarifications/Evidence/Comments

Repeated ECP use

Clarification: Recurrent ECP use is an indication that the woman requires further
counseling about other contraceptive options. Frequently repeated ECP use may
be harmful for women with conditions classified as 2, 3, or 4 for CHC or POC use.

Rape

Comment: Use of ECPs in cases of rape has no restrictions.

Condition
Other

* Abbreviations: STI = sexually transmitted infection; HIV = human immunodeficiency virus; ECP, emergency contraceptive pill; IUD = intrauterine device; COC = combined oral
contraceptive; POP = progestin-only pill; CHC = combined hormonal contraceptive; POC = progestin-only contraceptive
† ECPs do not protect against STI/HIV. If risk exists for STI/HIV (including during pregnancy or postpartum), the correct and consistent use of condoms is recommended, either
alone or with another contraceptive method. Consistent and correct use of the male latex condom reduces the risk for STIs and HIV transmission.
§ Condition that exposes a woman to increased risk as a result of unintended pregnancy.

MMWR

June 18, 2010

Appendix E
Classifications for Intrauterine Devices
Classiﬁcations for intrauterine devices (IUDs) are for the
levonorgestrel-releasing (20 µg/24 hours) IUD and the copperbearing IUD (Box). IUDs do not protect against sexually

transmitted infections (STIs) or human immunodeﬁciency
virus (HIV).

BOX. Categories for Classifying Intrauterine Devices

LNG-IUD

Cu-IUD

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy

Clarification: The IUD is not indicated during pregnancy and
should not be used because of the risk for serious pelvic infection
and septic spontaneous abortion.

Age
a. Menarche to <20 yrs

Comment: Concern exists about both the risk for expulsion from
nulliparity and for STIs from sexual behaviour in younger age
groups.

c. ≥4 wks
d. Puerperal sepsis

1
4

Postabortion
a. First trimester
b. Second trimester

1
2

b. ≥20 yrs
Parity
a. Nulliparous

b Parous
Postpartum (breastfeeding or nonbreastfeeding women, including post-Cesarean
section)
a. <10 minutes after delivery of the
placenta
b. 10 minutes after delivery of the
placenta to <4 wks

c. Immediate postseptic abortion

Evidence: Data conflict about whether IUD use is associated
with infertility among nulliparous women, although well-conducted
studies suggest no increased risk (1–9).

Evidence: Immediate postpartum Cu-IUD insertion, particularly
when insertion occurs immediately after delivery of the placenta, is
associated with lower expulsion rates than is delayed postpartum
insertion up to 72 hours postpartum; no data exist that examine
times >72 hours postpartum. In addition, postplacental placement
at the time of Cesarean section has lower expulsion rates than
does postplacental vaginal insertions. Insertion complications of
perforation and infection are not increased by Cu-IUD placement
at any time during the postpartum period (10–23). No evidence is
available that compares different insertion times for the LNG-IUD.
Comment: Insertion of an IUD might substantially worsen the
condition.
Clarification: IUDs can be inserted immediately after first trimester spontaneous or induced abortion.
Evidence: Risk for complications from immediate versus delayed
insertion of an IUD after abortion did not differ. Expulsion was
greater when an IUD was inserted after a second trimester abortion than when inserted after a first trimester abortion. Safety or
expulsion for postabortion insertion of an LNG-IUD did not differ
from that of a Cu-IUD (24–37).
Comment: Insertion of an IUD might substantially worsen the
condition.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for intrauterine devices,*† including the LNG-IUD and the Cu-IUD
Category
LNG-IUD

Cu-IUD

Past ectopic pregnancy

History of pelvic surgery (see Postpartum,
including post-Cesarean section)

Condition

Smoking
a. Age <35 yrs
b. Age ≥35 yrs
i. <15 Cigarettes/day
ii. ≥15 Cigarettes/day

1
1

Obesity
a. ≥30 kg/m2 BMI
b. Menarche to <18 yrs and ≥30 kg/m2 BMI

1
1

History of bariatric surgery§
a. Restrictive procedures: decrease storage capacity of the stomach (vertical
banded gastroplasty, laparoscopic
adjustable gastric band, laparoscopic
sleeve gastrectomy)
b. Malabsorptive procedures: decrease
absorption of nutrients and calories
by shortening the functional length of
the small intestine (Roux-en-Y gastric
bypass, biliopancreatic diversion)

Clarifications/Evidence/Comments
Comment: The absolute risk for ectopic pregnancy is extremely
low because of the high effectiveness of IUDs. However, when a
woman becomes pregnant during IUD use, the relative likelihood
of ectopic pregnancy increases greatly.

Cardiovascular Disease
Multiple risk factors for arterial cardiovascular disease (such as older age,
smoking, diabetes, and hypertension)

Hypertension
For all categories of hypertension, classifications are based on the assumption that no other risk factors for cardiovascular disease exist. When multiple risk factors do exist,
risk for cardiovascular disease might increase substantially. A single reading of blood pressure level is not sufficient to classify a woman as hypertensive.
a. Adequately controlled hypertension
1
1
b. Elevated blood pressure levels (properly
taken measurements)
1
1
i. Systolic 140–159 mm Hg or diastolic
90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic
2
1
Comment: Theoretical concern exists about the effect of LNG on
≥100 mm Hg§
lipids. Use of Cu-IUDs has no restrictions.
c. Vascular disease
2
1
Comment: Theoretical concern exists about the effect of LNG on
lipids. Use of Cu-IUDs has no restrictions.
History of high blood pressure during
pregnancy (where current blood pressure is
measurable and normal)
Deep venous thrombosis (DVT)/
pulmonary embolism (PE)
a. History of DVT/PE, not on anticoagulant
therapy
i. Higher risk for recurrent DVT/PE (≥1
risk factors)

MMWR

June 18, 2010

TABLE. (Continued) Classifications for intrauterine devices,*† including the LNG-IUD and the Cu-IUD
Category
Condition

LNG-IUD

Cu-IUD

b. Acute DVT/PE

c. DVT/PE and established on anticoagulant therapy for at least 3 mos

Clarifications/Evidence/Comments
Evidence: No direct evidence exists on the use of POCs among
women with acute DVT/PE. Although findings on the risk for
venous thrombosis with the use of POCs in otherwise healthy
women are inconsistent, any small increased risk is substantially
less than that with COCs (38–40).
Evidence: No direct evidence exists on the use of POCs among
women with acute DVT/PE. Although findings on the risk for
venous thrombosis with the use of POCs in otherwise healthy
women are inconsistent, any small increased risk is substantially
less than that with COCs (38–40).
Evidence: Limited evidence indicates that insertion of the LNGIUD does not pose major bleeding risks in women on chronic
anticoagulant therapy. (41–44)
Comment: The LNG-IUD might be a useful treatment for menorrhagia in women on long-term chronic anticoagulation therapy.

i. Higher risk for recurrent DVT/PE (≥1
risk factors)

2
1
1

1
1
1

1
1

r ,OPXOUISPNCPQIJMJB
JODMVEJOH
antiphospholipid syndrome
r "DUJWFDBODFS NFUBTUBUJD
PO
therapy, or within 6 mos after
clinical remission), excluding nonmelanoma skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii. Lower risk for recurrent DVT/PE (no
risk factors)
d. Family history (first-degree relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged immobilization
f. Minor surgery without immobilization
Known thrombogenic mutations§ (e.g.,
factor V Leiden; prothrombin mutation;
protein S, protein C, and antithrombin
deficiencies)
Superficial venous thrombosis
a. Varicose veins
b. Superficial thrombophlebitis
Current and history of ischemic heart
disease§

Initiation

Continuation

Clarification: Routine screening is not appropriate because of the
rarity of the conditions and the high cost of screening.

Comment: Theoretical concern exists about the effect of LNG on
lipids. Use of Cu-IUDs has no restrictions.
1

Stroke§ (history of cerebrovascular
accident)

Comment: Theoretical concern exists about the effect of LNG on
lipids. Use of Cu-IUDs has no restrictions.

Known hyperlipidemias

Clarification: Routine screening is not appropriate because of the
rarity of the condition and the high cost of screening.

Valvular heart disease
a. Uncomplicated

Comment: According to the American Heart Association, administration of prophylactic antibiotics solely to prevent endocarditis
is not recommended for patients who undergo genitourinary tract
procedures, including insertion or removal of IUDs (45).
Comment: According to the American Heart Association, administration of prophylactic antibiotics solely to prevent endocarditis
is not recommended for patients who undergo genitourinary tract
procedures, including insertion or removal of IUDs (45).

b. Complicated§ (pulmonary hypertension, risk for atrial fibrillation, history of
subacute bacterial endocarditis)
Peripartum cardiomyopathy§
a. Normal or mildly impaired cardiac
function (New York Heart Association
Functional Class I or II: patients with no
limitation of activities or patients with
slight, mild limitation of activity) (46)
i. <6 mos
ii. ≥6 mos

2
2

Comment: IUD insertion might induce cardiac arrhythmias in
healthy women; women with peripartum cardiomyopathy have a
high incidence of cardiac arrhythmias.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for intrauterine devices,*† including the LNG-IUD and the Cu-IUD
Category
Condition

LNG-IUD

Cu-IUD

b. Moderately or severely impaired cardiac
function (New York Heart Association
Functional Class III or IV: patients with
marked limitation of activity or patients
who should be at complete rest) (46)

Clarifications/Evidence/Comments
Evidence: There is no direct evidence on the safety of IUDs
among women with peripartum cardiomyopathy. Limited indirect
evidence from noncomparative studies did not demonstrate any
cases of arrhythmia or infective endocarditis in women with cardiac disease who used IUDs (47,48).
Comment: IUD insertion might induce cardiac arrhythmias in
healthy women; women with peripartum cardiomyopathy have a
high incidence of cardiac arrhythmias.

Rheumatic Diseases
Systemic lupus erythematosus (SLE)§
Persons with SLE are at increased risk for ischemic heart disease, stroke, and VTE. Categories assigned to such conditions in the MEC should be the same for women
with SLE who have these conditions. For all categories of SLE, classifications are based on the assumption that no other risk factors for cardiovascular disease are present;
these classifications must be modified in the presence of such risk factors.
Many women with SLE can be considered good candidates for most contraceptive methods, including hormonal contraceptives (43,49–66).
Initiation
Continuation
3
1
1
Evidence: Antiphospholipid antibodies are associated with a
a. Positive (or unknown) antiphospholipid
antibodies
higher risk for both arterial and venous thrombosis (67,68).
b. Severe thrombocytopenia
2
3
2
Clarification: Severe thrombocytopenia increases the risk for
bleeding. The category should be assessed according to the
severity of thrombocytopenia and its clinical manifestations. In
women with very severe thrombocytopenia who are at risk for
spontaneous bleeding, consultation with a specialist and certain
pretreatments might be warranted.
Evidence: The LNG-IUD might be a useful treatment for menorrhagia in women with severe thrombocytopenia (43).
c. Immunosuppressive treatment
d. None of the above
Rheumatoid arthritis
a. On immunosuppressive therapy
b. Not on immunosuppressive therapy

2
2
Initiation
2

Continuation
1

2
1

1
1

Initiation
2

Continuation
1

Neurologic Conditions
Headaches
a. Non-migrainous (mild or severe)
b. Migraine
i. Without aura
r"HFZST
r"HFŜZST
ii. With aura, at any age

Initiation

Continuation

2
2
2

2
2
3

1
1
1

Epilepsy§

Clarification: Any new headaches or marked changes in headaches should be evaluated.

Comment: Aura is a specific focal neurologic symptom. For more
information about this and other diagnostic criteria, see: Headache
Classification Subcommittee of the International Headache
Society. The international classification of headache disorders.
2nd ed. Cephalalgia 2004;24(Suppl 1):1– 150. Available from
http://www.i-h-s.org/upload/ct_clas/ihc_II_main_no_print.pdf.

Depressive Disorders
Depressive disorders

Clarification: The classification is based on data for women with
selected depressive disorders. No data were available on bipolar
disorder or postpartum depression. Drug interactions potentially
can occur between certain antidepressant medications and hormonal contraceptives.

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without heavy bleeding
b. Heavy or prolonged bleeding (includes
regular and irregular patterns)

Initiation
1
1

Continuation
1
2

1
2

Clarification: Unusually heavy bleeding should raise suspicion of
a serious underlying condition.
Evidence: Evidence from studies examining the treatment effects
of the LNG-IUD among women with heavy or prolonged bleeding
reported no increase in adverse effects and found the LNG-IUD to
be beneficial in treating menorrhagia (69–76).

Unexplained vaginal bleeding (suspicion
for serious condition)
Before evaluation

Initiation
4

Continuation
2

Initiation
4

Clarification: If pregnancy or an underlying pathological condition
Continuation (such as pelvic malignancy) is suspected, it must be evaluated
and the category adjusted after evaluation. The IUD does not
2
need to be removed before evaluation.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for intrauterine devices,*† including the LNG-IUD and the Cu-IUD
Category
LNG-IUD

Cu-IUD

Endometriosis

Benign ovarian tumors (including cysts)

Severe dysmenorrhea

Comment: Dysmenorrhea might intensify with Cu-IUD use. LNGIUD use has been associated with reduction of dysmenorrhea.

Gestational trophoblastic disease
a. Decreasing or undetectable β–hCG
levels

Evidence: Limited evidence suggests that women using an IUD
after uterine evacuation for a molar pregnancy are not at greater
risk for postmolar trophoblastic disease than are women using
other methods of contraception (82–84).
Evidence: Limited evidence suggests that women using an IUD
after uterine evacuation for a molar pregnancy are not at greater
risk for postmolar trophoblastic disease than are women using
other methods of contraception (82–84)

Cervical ectropion

Cervical intraepithelial neoplasia

Condition

b. Persistently elevated β-hCG levels or
malignant disease§

Cervical cancer (awaiting treatment)

Initiation
4

Breast disease
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer
d. Breast cancer§
i. Current
ii. Past and no evidence of current
disease for 5 yrs
Endometrial hyperplasia

Endometrial cancer§

Continuation
2

Initiation
4

1
1
1

4
3

1
1

Continuation
2

Evidence: LNG-IUD use among women with endometriosis decreased dysmenorrhea, pelvic pain, and dyspareunia (77–81).

Comment: Theoretical concern exists that LNG-IUDs might
enhance progression of cervical intraepithelial neoplasia.
Continuation Comment: Concern exists about the increased risk for infection
and bleeding at insertion. The IUD most likely will need to be
2
removed at the time of treatment, but until then, the woman is at
risk for pregnancy.

2
1
1

Initiation
4

Clarifications/Evidence/Comments

Initiation
4

Comment: Breast cancer is a hormonally sensitive tumor.
Concerns about progression of the disease might be less with
LNG-IUDs than with COCs or higher-dose POCs.

Evidence: Among women with endometrial hyperplasia, no
adverse health events occurred with LNG-IUD use; most women
experienced disease regression (85–93).
Continuation Comment: Concern exists about the increased risk for infection,
perforation, and bleeding at insertion. The IUD most likely will
2
need to be removed at the time of treatment, but until then, the
woman is at risk for pregnancy.

Ovarian cancer§

Comment: Women with ovarian cancer who undergo fertility sparing treatment and need contraception may use an IUD.

Uterine fibroids

Evidence: Among women with uterine fibroids using an LNG-IUD,
most experienced improvements in serum levels of hemoglobin,
hematocrit, and ferritin (73,94–100) and menstrual blood loss
(73,75,94–101). Rates of LNG-IUD expulsion were higher in
women with uterine fibroids (11%) than in women without fibroids
(0%–3%); these findings were not statistically significant or significance testing was not conducted (75,101). Rates of expulsion
from noncomparative studies ranged from 0%–20% (94,96–100).
Comment: Women with heavy or prolonged bleeding should be
assigned the category for that condition.

Comment: An anatomic abnormality that distorts the uterine cavity might preclude proper IUD placement.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for intrauterine devices,*† including the LNG-IUD and the Cu-IUD
Category
LNG-IUD

Condition
Pelvic inflammatory disease (PID)
a. Past PID (assuming no known current
risk factors for STIs)

i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID

Initiation

Cu-IUD

Continuation

Initiation

Clarifications/Evidence/Comments

Continuation
Comment: IUDs do not protect against STI/HIV/PID. In women
at low risk for STIs, IUD insertion poses little risk for PID. Current
risk for STIs and desire for future pregnancy are relevant
considerations.

1
2
4

1
2
2

1
2
4

1
2
2

Clarification for continuation: Treat the PID using appropriate antibiotics. The IUD usually does not need to be removed if
the woman wishes to continue using it. Continued use of an IUD
depends on the woman’s informed choice and her current risk
factors for STIs and PID.
Evidence: Among IUD users treated for PID, clinical course did
not differ regardless of whether the IUD was removed or left in
place (102–104).

STIs
a. Current purulent cervicitis or chlamydial
infection or gonorrhea

Initiation
4

Continuation
2

Initiation
4

Continuation
2
Clarification for continuation: Treat the STI using appropriate antibiotics. The IUD usually does not need to be removed if
the woman wishes to continue using it. Continued use of an IUD
depends on the woman’s informed choice and her current risk
factors for STIs and PID.
Evidence: No evidence exists about whether IUD insertion among
women with STIs increases the risk for PID over that of women
with no IUD insertion. Among women who had an IUD inserted,
the absolute risk for subsequent PID was low among women with
STI at the time of insertion but greater than among women with no
STI at the time of IUD insertion (105–111).

b. Other STIs (excluding HIV and hepatitis)
c. Vaginitis (including Trichomonas
vaginalis and bacterial vaginosis)
d. Increased risk for STIs

2
2

2/3

Clarification for initiation: If a woman has a very high individual
likelihood of exposure to gonorrhea or chlamydial infection, the
condition is a Category 3.
Evidence: Using an algorithm to classify STI risk status among
IUD users, 1 study reported that 11% of women at high risk for
STIs experienced IUD-related complications compared with 5% of
those not classified as high risk (107).

HIV/AIDS
High risk for HIV

Initiation
2

Continuation
2

Initiation
2

HIV infection§

Evidence: Among IUD users, limited evidence shows no higher
risk for overall complications or for infectious complications in HIVinfected than in HIV-uninfected women. IUD use did not adversely
affect progression of HIV when compared with hormonal contraceptive use among HIV-infected women. Furthermore, IUD use
among HIV-infected women was not associated with increased
risk for transmission to sex partners (112,123–130).

AIDS§

Clarification for continuation: IUD users with AIDS should be
closely monitored for pelvic infection.

Clinically well on ARV therapy

Continuation
2
Evidence: Among women at risk for HIV, Cu-IUD use did not
increase risk for HIV acquisition (112–122).

Other Infections
Schistosomiasis
a. Uncomplicated
b. Fibrosis of the liver§ (if severe, see
cirrhosis)
Tuberculosis§
a. Nonpelvic
b. Pelvic
Malaria

1
1
Initiation
1
4

1
1
Continuation
1
3

Initiation
1
4

Continuation
1
3
Comment: Insertion of an IUD may substantially worsen the
condition.
1

MMWR

June 18, 2010

TABLE. (Continued) Classifications for intrauterine devices,*† including the LNG-IUD and the Cu-IUD
Category
LNG-IUD

Cu-IUD

2
2

1
1

2
2

1
1

1
1
1

Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic

2
2
2
2

1
1
1
1

History of cholestasis
a. Pregnancy-related
b. Past COC-related

1
2

1
1

Viral hepatitis
a. Acute or flare
b. Carrier
c. Chronic

1
1
1

Cirrhosis
a. Mild (compensated)
b. Severe§ (decompensated)

1
3

1
1

Thalassemia

Comment: Concern exists about an increased risk for blood loss
with Cu-IUDs.

Sickle cell disease§

Comment: Concern exists about an increased risk for blood loss
with Cu-IUDs.

Iron deficiency anemia

Comment: Concern exists about an increased risk for blood loss
with Cu-IUDs.

Condition

Clarifications/Evidence/Comments

Endocrine Conditions
Diabetes
a. History of gestational disease
b. Nonvascular disease
i. Noninsulin-dependent
ii. Insulin-dependent§
c. Nephropathy/retinopathy/neuropathy§
d. Other vascular disease or diabetes of
>20 yrs’ duration§
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Evidence: Limited evidence on the use of the LNG-IUD among
women with insulin-dependent or noninsulin-dependent diabetes
suggests that these methods have little effect on short-term or
long-term diabetes control (e.g., glycosylated hemoglobin levels),
hemostatic markers, or lipid profile (131,132).

Gastrointestinal Conditions
Inflammatory bowel disease (IBD)
(ulcerative colitis, Crohn disease)

Liver tumors
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma§

b. Malignant§ (hepatoma)

Evidence: Although two case reports described three women with
IBD who experienced exacerbation of disease 5 days–25 months
after LNG-IUD insertion (133,134), no comparative studies have
examined the safety of IUD use among women with IBD.

Comment: Concern exists that history of COC-related cholestasis
might predict subsequent cholestasis with LNG use. Whether risk
exists with use of LNG-IUD is unclear.

Comment: No evidence is available about hormonal contraceptive use in women with hepatocellular adenoma. COC use in
healthy women is associated with development and growth of
hepatocellular adenoma; whether other hormonal contraceptives
have similar effects is not known.

Anemias

Solid Organ Transplantation
Solid organ transplantation§
a. Complicated: graft failure (acute or
chronic), rejection, cardiac allograft
vasculopathy
b. Uncomplicated

Initiation
3

Continuation
2

Initiation
3

Continuation Evidence: No comparative studies have examined IUD use
among transplant patients. Four case reports of transplant
2
patients using IUDs provided inconsistent results, including beneficial effects and contraceptive failures (135–138).
2

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for intrauterine devices,*† including the LNG-IUD and the Cu-IUD
Category
LNG-IUD

Condition

Cu-IUD

Clarifications/Evidence/Comments

Drug Interactions
Antiretroviral (ARV) therapy
a. Nucleoside reverse transcriptase inhibitors (NRTIs)
b. Non-nucleoside reverse transcriptase
inhibitors (NNRTIs)
c. Ritonavir-boosted protease inhibitors

Initiation
2/3

Continuation
2

Initiation
2/3

2/3

Continuation Clarification: No known interaction exists between ARV therapy
and IUD use. However, AIDS as a condition is classified as
2
Category 3 for insertion and Category 2 for continuation unless
the woman is clinically well on ARV therapy, in which case, both
2
insertion and continuation are classified as Category 2 (see AIDS
condition).
2

Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin,
carbamazepine, barbiturates, primidone,
topiramate, oxcarbazepine)
b Lamotrigine

Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampicin or rifabutin therapy

1
1
1
1

Evidence: Limited evidence suggests use of certain anticonvulsants does not interfere with the contraceptive effectiveness of the
LNG-IUD (139).
Evidence: No drug interactions have been reported among epileptic women taking lamotrigine and using the LNG-IUD (140).

Evidence: One cross-sectional survey found that rifabutin had no
impact on the effectiveness of the LNG-IUD (139).

* Abbreviations: LNG-IUD = levonorgestrel-releasing intrauterine device; Cu-IUD = copper IUD; STI = sexually transmitted infection; HIV = human immunodeﬁciency virus; BMI =
body mass index; DVT = deep venous thrombosis; PE = pulmonary embolism; POC = progestin-only contraceptive; COC = combined oral contraceptive; SLE = systemic lupus
erythematosus; MEC = Medical Eligibility Criteria; hCG = human chorionic gonadotropin; PID = pelvic inﬂammatory disease; AIDS = acquired immunodeﬁciency syndrome;
ARV = antiretroviral; IBD = inﬂammatory bowel disease; NRTI = nucleoside reverse transcriptase inhibitor; NNRTI = non-nucleoside reverse transcriptase inhibitor.
† IUDs do not protect against STI/HIV. If risk exists for STI/HIV (including during pregnancy or postpartum), the correct and consistent use of condoms is recommended, either
alone or with another contraceptive method. Consistent and correct use of the male latex condom reduces the risk for STIs and HIV transmission
§ Condition that exposes a woman to increased risk as a result of unintended pregnancy.

References
1. Cramer DW, Schiﬀ I, Schoenbaum SC, Gibson M, Belisle S, Albrecht
B, et al. Tubal infertility and the intrauterine device. N Engl J Med
1985;312:941–7.
2. Daling JR, Weiss NS, Metch BJ, Chow WH, Soderstrom RM, Moore
DE, et al. Primary tubal infertility in relation to the use of an intrauterine
device. N Engl J Med 1985;312:937–41.
3. Daling JR, Weiss NS, Voigt LF, McKnight B, Moore DE. The intrauterine
device and primary tubal infertility. N Eng J Med 1992;326:203–4.
4. Delbarge W, Bátár I, Bafort M, Bonnivert J, Colmant C, Dhont M, et
al. Return to fertility in nulliparous and parous women after removal of
the GyneFix intrauterine contraceptive system. Eur J Contracept Reprod
Health Care 2002;7:24–30.
5. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after
discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304–14.
6. Hubacher D, et al. Use of copper intrauterine devices and the risk of tubal
infertility among nulligravid women. N Engl J Med 2001;345:561–7.
7. Skjeldestad FE, Bratt H. Return of fertility after use of IUDs (Nova-T,
MLCu250 and MLCu375). Adv Contracep 1987;3:139–45.
8. Urbach DR, Marrett LD, Kung R, Cohen MM. Association of performation of the appendix with female tubal infertility. Am J Epidemiol
2001;153:566–71.
9. Wilson JC. A prospective New Zealand study of fertility after removal of
copper intrauterine contraceptive devices for conception and because of
complications: a four-year study. Am J Obstet Gynecol 1989;160:391–6.
10. Thiery M, Vanderpas H, Delbeke L, Vankets H. Comparative performance
of 2 copper-wired IUDs (Ml-Cu-250 and T-Cu-200): immediate postpartum and interval insertion. Contracept Deliv Syst 1980;1:27–35.
11. Thiery M, Van Kets H, Van der PH, van Os W, Dombrowicz N. The
ML Cu250; clinical experience in Belgium and the Netherlands. Br J
Obstet Gynaecol 1982;89:51–3.
12. Brenner PF. A clinical trial of the Delta-T intrauterine device: immediate
postpartum insertion. Contraception 1983;28:135–47.

13. Chi IC, Wilkens L, Rogers S. Expulsions in immediate postpartum insertions of Lippes loop D and copper T IUDs and their counterpart Delta
devices—an epidemiological analysis. Contraception 1985;32:119–34.
14. Morrison C, Waszak C, Katz K, Diabate F, Mate EM. Clinical outcomes of two early postpartum IUD insertion programs in Africa.
Contraception 1996;53:17–21.
15. El-Shafei MM, Mashali A, Hassan EO, El-Boghdadi, El-Lakkany
N. Postpartum and postabortion intrauterine device insertion unmet
needs of safe reproductive health: three years experience of a Mansoura
University Hospital. Egypt Soc Obstet Gynecol 2000;26:253–62.
16. Muller ALL, Ramos JGL, Martins-Costa SH, et al. Transvaginal
ultrasonographic assessment of the expulsion rate of intrauterine
devices inserted in the immediate postpartum period: a pilot study.
Contraception 2005;72:192–5.
17. Zhou SW, Chi IC. Immediate postpartum IUD insertions in a Chinese
hospital—a two year follow-up. Int J Gynaecol Obstet 1991;35:157–64.
18. Bonilla Rosales F, Aguilar Zamudio ME, Cazares Montero Mde L,
Hernandez Ortiz ME, Luna Ruiz MA. Factors for expulsion of intrauterine device Tcu380A applied immediately postpartum and after a delayed
period [in Spanish]. Rev Med Inst Mex Seguro Soc 2005;43:5–10.
19. Lara R, Sanchez RA, Aznar R. Application of intreauterine device through
the incision of the Cesarean section [in Spanish]. Ginecol Obstet Mex
1989;57:23–7.
20. Welkovic S, Costa LO, Faundes A, de Alencar Ximenes R, Costa CF.
Post-partum bleeding and infection after post-placental IUD insertion.
Contraception 2001;63:155–8.
21. Celen S, Moroy P, Sucak A, Aktulay A, Danisman N. Clinical outcomes
of early postplacental insertion of intrauterine contraceptive devices.
Contraception 2004;69:279–82.
22. Eroglu K, Akkuzu G, Vural G, et al. Comparison of eﬃcacy and
complications of IUD insertion in immediate postplacental/early postpartum period with interval period: 1 year follow-up. Contraception
2006;74:376–81.

MMWR

23. Mishell DR, Jr., Roy S. Copper intrauterine contraceptive device event
rates following insertion 4 to 8 weeks post partum. Am J Obstet Gynecol
1982;143:29–35.
24. World Health Organization’s Special Programme of Research DaRTiHR.
Task Force on Intrauterine Devices for Fertility Regulation. IUD insertion following spontaneous abortion: a clinical trial of the TCu 220C,
Lippes loop D, and copper 7. Stud Fam Plann 1983;14:109–14.
25. World Health Organization’s Special Programme of Research DaRTiHR.
Task Force on Intrauterine Devices for Fertility Regulation. IUD insertion following termination of pregnancy: a clinical trial of the TCu 220C,
Lippes loop D, and copper 7. Stud Fam Plann 1983;14:99–108.
26. World Health Organization’s Special Programme of Research DaRTiHR.
Task Force on Intrauterine Devices for Fertility Regulation. The Alza T
IPCS 52, a longer acting progesterone IUD: safety and eﬃcacy compared
to the TCu220C and multiload 250 in two randomized multicentre
trials. Clin Reprod Fertil 1983;2:113–28.
27. El Tagy A, Sakr E, Sokal DC, Issa AH. Safety and acceptability of postabortal IUD insertion and the importance of counseling. Contraception
2003;67:229–34.
28. Gillett PG, Lee NH, Yuzpe AA, Cerskus I. A comparison of the eﬃcacy
and acceptability of the copper-7 intrauterine device following immediate or delayed insertion after ﬁrst-trimester therapeutic abortion. Fertil
Steril 1980;34:121–4.
29. Grimes D, Schulz K, Stanwood N. Immediate postabortal insertion of intrauterine devices. [update of Cochrane Database Syst Rev.
2000;(2):CD001777; PMID:10796820]. [Review]. Cochrane Database
Syst Rev 2002;CD001777.
30. Gupta I, Devi PK. Studies on immediate post-abortion copper ‘T’ device.
Indian J Med Res 1975;63:736–9.
31. Moussa A. Evaluation of postabortion IUD insertion in Egyptian women.
Contraception 2001;63:315–7.
32. Pakarinen P, Toivonen J, Luukkainen T. Randomized comparison of
levonorgestrel- and copper-releasing intrauterine systems immediately
after abortion, with 5 years’ follow-up. Contraception 2003;68:31–4.
33. Stanwood NL, Grimes DA, Schulz KF. Insertion of an intrauterine
contraceptive device after induced or spontaneous abortion: a review of
the evidence. BJOG 2001;108:1168–73.
34. Suvisaari J, Lahteenmaki P. Detailed analysis of menstrual bleeding
patterns after postmensstrual and postabortal insertion of a copper
IUD or a levonorgestrel-releasing intrauterine system. Contraception
1996;54:201–8.
35. Timonen H, Luukkainen T. Immediate postabortion insertion of the
copper-T (TCu-200) with eighteen months follow-up. Contraception
1974;9:153–60.
36. Tuveng JM, Skjeldestad FE, Iverson T. Postabortal insertion of IUD.
Adv Contracept 1986;2:387–92.
37. Zhang PZ. Five years experience with the copper T 200 in Shanghai—856
cases. Contraception 1980;22:561–71.
38. Cardiovascular disease and use of oral and injectable progestogenonly contraceptives and combined injectable contraceptives. Results
of an international, multicenter, case-control study. World Health
Organization Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Contraception 1998;57:315–24.
39. Heinemann LA, Assmann A, DoMinh T, et al. Oral progestogen-only
contraceptives and cardiovascular risk: results from the Transnational
Study on Oral Contraceptives and the Health of Young Women. Eur J
Contracept Reprod Health Care 1999;4:67–73.
40. Vasilakis C, Jick H, Mar Melero-Montes M. Risk of idiopathic
venous thromboembolism in users of progestogens alone. Lancet
1999;354:1610–1.
41. Kingman CE, Kadir RA, Lee CA, et al. The use of the levonorgestrelreleasing intrauterine system for treatment of menorrhagia in women
withinherited bleeding disorders. BJOG 2004;111:1425–8.

June 18, 2010

42. Pisoni CN, Cuadrado MJ, Khamashta MA, et al. Treatment of menorrhagia associated with oral anticoagulation: eﬃcacy and safety of
the levonorgestrel releasing intrauterine device (Mirena coil). Lupus
2006;15:877–80.
43. Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrel-releasing intrauterine system in the management of menorrhagia in women
with hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–3.
44. Lukes AS, Reardon B, Arepally G. Use of the levonorgestrel-releasing
intrauterine system in women with hemostatic disorders. Fertil Steril
2008;90:673–7.
45. Wilson W, Taubert KA, Gewitz M et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline
from the American Heart Association Rheumatic Fever, Endocarditis,
and Kawasaki Disease Committee, Council on Cardiovascular Disease
in the Young, and the Council on Clinical Cardiology, Council on
Cardiovascular Surgery and Anesthesia, and the Quality of Care and
Outcomes Research Interdisciplinary Working Group. Circulation.
2007;116:1736–1754.
46. The Criteria Committee of the New York Heart Association.
Nomenclature and criteria for diagnosis of diseases of the heart and
great vessels. 9th ed. Boston, MA: Little, Brown & Co; 1994.
47. Avila WS, Grinberg M, Melo NR, Aristodemo PJ, Pileggi F.
Contraceptive use in women with heart disease [in Portuguese]. Arq
Bras Cardiol 1996;66:205–11.
48. Suri V, Aggarwal N, Kaur R, et al. Safety of intrauterine contraceptive
device (copper T 200 B) in women with cardiac disease. Contraception
2008;78:315–8.
49. Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated with abnormal Pap results in systemic lupus erythematosus.
Rheumatology (Oxford) 2004;43:1386–9.
50. Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures
and breast cancer in a sample of women with systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1178–81.
51. Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin
gene mutation, and thrombosis risk in patients with antiphospholipid
antibodies. J Rheumatol 2002;29:1683–8.
52. Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham
risk factors fail to fully account for accelerated atherosclerosis in systemic
lupus erythematosus. Arthritis Rheum 2001;44:2331–7.
53. Julkunen HA. Oral contraceptives in systemic lupus erythematosus:
side-eﬀects and inﬂuence on the activity of SLE. Scand J Rheumatol
1991;20:427–33.
54. Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women
with systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30.
55 Jungers P, Dougados M, Pelissier C, et al. Inﬂuence of oral contraceptive
therapy on the activity of systemic lupus erythematosus. Arthritis Rheum
1982;25:618–23.
56. Manzi S, Meilahn EN, Rairie JE, et al. Age-speciﬁc incidence rates of
myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study. Am J Epidemiol
1997;145:408–15.
57. McAlindon T, Giannotta L, Taub N, et al. Environmental factors predicting nephristis in systemic lupus erythematosus. Ann Rheum Dis
1993;52:720–4.
58. McDonald J, Stewart J, Urowitz MB, et al. Peripheral vascular disease in patients with systemic lupus erythematosus. Ann Rheum Dis
1992;51:56–60.
59. Mintz G, Gutierrez G, Deleze M, et al. Contraception with progestogens
in systemic lupus erythematosus. Contraception 1984;30:29–38.
60. Petri M. Musculoskeletal complications of systemic lupus erythematosus in the Hopkins Lupus Cohort: an update. Arthritis Care Res
1995;8:137–45.
61. Petri M, Kim MY, Kalunian KC, et al. Combined oral contraceptives in women with systemic lupus erythematosus. N Engl J Med
2005;353:2550–8.

Vol. 59 / RR-4

Recommendations and Reports

62. Petri M. Lupus in Baltimore: evidence-based ‘clinical perarls’ from the
Hopkins Lupus Cohort. Lupus 2005;14:970–3.
63. Sanchez-Guerrero J, Uribe AG, Jimenez-Santana L, et al. A trial of
contraceptive methods in women with systemic lupus erythematosus.
N Eng J Med 2005;353:2539–49.
64. Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and venous
thrombosis after diagnosis of systemic lupus erythematosus. Arthritis
Rheum 2005;53:609–12.
65. Somers E, Magder LS, Petri M. Antiphospholipid antibodies and incidence of venous thrombosis in a cohort of patients with systemic lupus
erythematosus. J Rheumatol 2002;29:2531–6.
66. Urowitz MB, Bookman AA, Koehler BE, et al. The bimodal mortality
pattern of systemic lupus erythematosus. Am J Med 1976;60:221–5.
67. Choojitarom K, Verasertniyom O, Totemchokchyakarn K, et al. Lupus
nephritis and Raynaud’s phenomenon are signiﬁcant risk factors for
vascular thrombosis in SLE patients with positive antiphospholipid
antibodies. Clin Rheumatol 2008;27:345–51.
68. Wahl DG, Guillemin F, de Maistre E, et al. Risk for venous thrombosis
related to antiphospholipid antibodies in systemic lupus erythematosus—
a meta-analysis. Lupus 1997;6:467–73.
69. Barrington JW, Arunkalaivanan AS, bdel-Fattah M. Comparison between
the levonorgestrel intrauterine system (LNG-IUS) and thermal balloon
ablation in the treatment of menorrhagia. Eur J Obstet Gynecol Reprod
Biol 2003;108:72–4.
70. Gupta B, Mittal S, Misra R, Deka D, Dadhwal V. Levonorgestrel-releasing
intrauterine system vs. transcervical endometrial resection for dysfunctional
uterine bleeding. Int J Gynaecol Obstet 2006;95:261–6.
71. Hurskainen R, Teperi J, Rissanen P, et al. Quality of life and cost-eﬀectiveness of levonorgestrel-releasing intrauterine system versus hysterectomy
for treatment of menorrhagia: a randomised trial [see comment]. Lancet
2001;357:273–7.
72. Istre O, Trolle B. Treatment of menorrhagia with the levonorgestrel intrauterine system versus endometrial resection. Fertil Steril 2001;76:304–9.
73. Koh SC, Singh K. The eﬀect of levonorgestrel-releasing intrauterine
system use on menstrual blood loss and the hemostatic, ﬁbrinolytic/
inhibitor systems in women with menorrhagia. J Thromb Haemost
2007;5:133–8.
74. Lethaby AE, Cooke I, Rees M. Progesterone/progestogen releasing intrauterine systems versus either placebo or any other medication for heavy
menstrual bleeding. Cochrane Database Syst Rev 2000;CD002126.
75. Magalhaes J, Aldrighi JM, de Lima GR. Uterine volume and menstrual
patterns in users of the levonorgestrel-releasing intrauterine system
with idiopathic menorrhagia or menorrhagia due to leiomyomas.
Contraception 2007;75:193–8.
76. Stewart A, Cummins C, Gold L, Jordan R, Phillips W. The eﬀectiveness
of the levonorgestrel-releasing intrauterine system in menorrhagia: a
systematic review.
77. Fedele L, Bianchi S, Zanconato G, Portuese A, Raﬀaelli R. Use of a
levonorgestrel-releasing intrauterine device in the treatment of rectovaginal endometriosis. Fertil Steril 2001;75:485–8.
78. Lockhat FBE. The eﬀect of a levonorgestrel intrauterine system (LNGIUS) on symptomatic endometriosis. Fertil Steril 2002;77 Suppl
1:S24.
79. Petta CA, Ferriani RA, Abrao MS, et al. Randomized clinical trial of a
levonorgestrel-releasing intrauterine system and a depot GnRH analogue
for the treatment of chronic pelvic pain in women with endometriosis.
Hum Reprod 2005;20:1993–8.
80. Vercellini P, Aimi G, Panazza S, et al. A levonorgestrel-releasing intrauterine system for the treatment of dysmenorrhea associated with
endometriosis: a pilot study. Fertil Steril 1999;72:505–8.
81. Vercellini P, Frontino G, De Giorgi O, et al. Comparison of a levonorgestrel-releasing intrauterine device versus expectant management after
conservative surgery for symptomatic endometriosis: a pilot study. Fertil
Steril 2003;80:305–9.

82. Deicas RE, Miller DS, Rademaker AW, Lurain JR. The role of contraception in the development of postmolar trophoblastic tumour. Obstet
Gynecol 1991;78:221–6.
83. Adewole IF, Oladokun A, Fawole AO, Olawuyi JF, Adeleye JA. Fertility
regulatory methods and development of complications after evacuation
of complete hydatidiform mole. J Obstet Gynecol 2000;20:68–9.
84. Ho Yuen B, Burch P. Relationship of oral contraceptives and the intrauterine contraceptive devices to the regression of concentration of the
beta subunit of human chorionic gonadotropin and invasive complications after molar pregnancy. Am J Obstet Gynecoy 1983;145:214–7.
85. Haimovich S, Checa MA, Mancebo G, Fuste P, Carreras R. Treatment
of endometrial hyperplasia without atypia in peri- and postmenopausal women with a levonorgestrel intrauterine device. Menopause
2008;15:1002–7.
86. Varma R, Soneja H, Bhatia K, et al. The eﬀectiveness of a levonorgestrelreleasing intrauterine system (LNG-IUS) in the treatment of endometrial hyperplasia—a long-term follow-up study. Eur J Obstet Gynecol
Reprod Biol 2008;139:169–75.
87. Wheeler DT, Bristow RE, Kurman RJ. Histologic alterations in endometrial hyperplasia and well-diﬀerentiated carcinoma treated with
progestins. Am J Surg Pathol 2007;31:988–98.
88. Wildemeersch D, Janssens D, Pylyser K, et al. Management of
patients with non-atypical and atypical endometrial hyperplasia with
a levonorgestrel-releasing intrauterine system: long-term follow-up.
Maturitas 2007;57:210–3.
89. Clark TJ, Neelakantan D, Gupta JK. The management of endometrial
hyperplasia: an evaluation of current practice. Eur J Obstet Gynecol
Reprod Biol 2006;125:259–64.
90. Vereide AB, Arnes M, Straume B, Maltau JM, Orbo A. Nuclear
morphometric changes and therapy monitoring in patients with
endometrial hyperplasia: a study comparing eﬀects of intrauterine
levonorgestrel and systemic medroxyprogesterone. Gynecol Oncol
2003;91:526–33.
91. Perino A, Quartararo P, Catinella E, Genova G, Cittadini E. Treatment
of endometrial hyperplasia with levonorgestrel releasing intrauterine
devices. Acta Eur Fertil 1987;18:137–40.
92. Scarselli G, Mencaglia L, Tantini C, Colafranceschi M, Taddei G.
Hysteroscopic evaluation of intrauterine progesterone contraceptive
system as a treatment for abnormal uterine bleeding. Acta Eur Fertil
1984;15:279–82.
93. Orbo A, Arnes M, Hancke C, et al. Treatment results of endometrial
hyperplasia after prospective D-score classiﬁcation: a follow-up study
comparing eﬀect of LNG-IUD and oral progestins versus observation
only. Gynecol Oncol 2008;111:68–73.
94. Jindabanjerd K, Taneepanichskul S. The use of levonorgestrel–IUD
in the treatment of uterine myoma in Thai women. J Med Assoc Thai
2006;89 Suppl 4:S147–51.
95. Tasci Y, Caglar GS, Kayikcioglu F, Cengiz H, Yagci B, Gunes M.
Treatment of menorrhagia with the levonorgestrel releasing intrauterine
system: eﬀects on ovarian function and uterus. Arch Gynecol Obstet

2009;280:39–42
96. Rosa E Silva JC, de Sa Rosa e Silva AC, Candido dos Reis FJ, et al. Use
of a levonorgestrel-releasing intrauterine device for the symptomatic
treatment of uterine myomas. J Reprod Med 2005;50:613–7.
97. Mercorio F, De SR, Di Spiezio SA, et al. The eﬀect of a levonorgestrelreleasing intrauterine device in the treatment of myoma-related menorrhagia. Contraception 2003;67:277–80.

MMWR

98. Grigorieva V, Chen-Mok M, Tarasova M, Mikhailov A. Use of a
levonorgestrel-releasing intrauterine system to treat bledding related
to uterine leiomyomas. Fertil Steril 2003;79:1194–8.
99. Starczewski A, Iwanicki M. Intrauterine therapy with levonorgestrel
releasing IUD of women with hypermenorrhea secondary to uterine
ﬁbroids [in Polish]. Ginekol Pol 2000;71:1221-5.
100. Soysal S, Soysal ME. The eﬃcacy of levonorgestrel-releasing intrauterine
device in selected cases of myoma-related menorrhagia: a prospective
controlled trial. Gynecol Obstet Invest 2005;59:29–35.
101. Ikomi A, Mansell E, Spence-Jones C, Singer A. Treatment of menorrhagia with the levonorgestrel intrauterine system: can we learn from
our failures? J Obstet Gynaecol 2000;20:630–1.
102. Larsson B, Wennergren M. Investigation of a copper-intrauterine
device (Cu-IUD) for possible eﬀect on frequency and healing of pelvic
inﬂammatory disease. Contraception 1977;15:143–9.
103. Soderberg G, Lindgren S. Inﬂuence of an intrauterine device on the
course of an acute salpingitis. Contraception 1981;24:137–43.
104. Teisala K. Removal of an intrauterine device and the treatment of acute
pelvic inﬂammatory disease. Ann Med 1989;21:63–5.
105. Faúndes A, Telles E, Cristofoletti ML, Faúndes D, Castro S, Hardy E.
The risk of inadvertent intrauterine device insertion in women carriers of
endocervical Chlamydia trachomatis. Contraception 1998;58:105–9.
106. Ferraz do Lago R, Simões JA, Bahamondes L, et al. Follow-up of users
of intrauterine device with and without bacterial vaginosis and other
cervicovaginal infections. Contraception 2003;68:105–9.
107. Morrison CS, Sekadde-Kigondu C, Miller WC, Weiner DH, Sinei
SK. Use of sexually transmitted disease risk assessment algorithms
for selection of intrauterine device candidates. Contraception
1999;59:97–106.
108. Pap-Akeson M, Solheim F, Thorbert G, Akerlund M. Genital tract
infections associated with the intrauterine contraceptive device can be
reduced by inserting the threads into the uterine cavity. Br J Obstet
Gynaecol 1992;99:676–9.
109. Sinei SK, Schulz KF, Lamptey PR, Grimes DA, Mati JK, Rosenthal
SM, et al. Preventing IUDC-related pelvic infection: the eﬃcacy
of prophylactic doxycycline at insertion. Br J Obstet Gynaecol
1990;97:412–9.
110. Skjeldestad FE, Halvorsen LE, Kahn H, Nordbø SA, Saake K. IUD
users in Norway are at low risk of for genital C. trachomatis infection.
Contraception 1996;54:209–12.
111. Walsh TL, Bernstein GS, Grimes DA, Frezieres R, Bernstein L,
Coulson AH. Eﬀect of prophylactic antibiotics on morbidity associated with IUD insertion: results of a pilot randomized controlled trial.
Contraception 1994;50:319–27.
112. European Study Group on Heterosexual Transmission of HIV.
Comparison of female to male and male to female transmission of
HIV in 563 stable couples. BMJ 1992;304:809–13.
113. Carael M, Van de Perre PH, Lepage PH, et al. Human immunodeﬁciency virus transmission among heterosexual couples in Central Africa.
AIDS 1988;2:201–5.
114. Kapiga SH, Shao JF, Lwihula GK, Hunter DJ. Risk factors for HIV
infection among women in Dar-es-Salaam, Tanzania. J Acquir Immune
Deﬁc Syndr 1994;7:301–9.
115. Kapiga SH, Lyamuya EF, Lwihula GK, Hunter DJ. The incidence of
HIV infection among women using family planning methods in Dar
es Salaam, Tanzania. AIDS 1998;12:75–84.
116. Mann JM, Nzilambi N, Piot P, et al. HIV infection and associated risk factors in female prostitutes in Kinshasa, Zaire. AIDS
1998;2:249–54.

June 18, 2010

117. Martin HL, Jr., Nyange PM, Richardson BA, et al. Hormonal contraception, sexually transmitted diseases, and risk of heterosexual
transmission of human immunodeﬁciency virus type 1. J Infect Dis
1998;178:1053–9.
118. Mati JK, Hunter DJ, Maggwa BN, Tukei PM. Contraceptive use and
the risk of HIV infection in Nairobi, Kenya. Int J Gynaecol Obstet
1995;48:61–7.
119. Nicolosi A, Correa Leite ML, Musicco M, et al. The eﬃciency of
male-to-female and female-to-male sexual transmission of the human
immunodeﬁciency virus: a study of 730 stable couples. Italian Study
Group on HIV Heterosexual Transmission [comment]. Epidemiology
1994;5:570–5.
120. Plourde PJ, Plummer FA, Pepin J, et al. Human immunodeﬁciency virus
type 1 infection in women attending a sexually transmitted diseases
clinic in Kenya [comment]. J Infect Dis 1992;166:86–92.
121. Sinei SK, Fortney JA, Kigondu CS, et al. Contraceptive use and HIV
infection in Kenyan family planning clinic attenders. Int J STD AIDS
1996;7:65–70.
122. Spence MR, Robbins SM, Polansky M, Schable CA. Seroprevalence of
human immunodeﬁciency virus type I (HIV-1) antibodies in a familyplanning population. Sex Transm Dis 1991;18:143–5.
123. Morrison CS, Sekadde-Kigondu C, Sinei SK, et al. Is the intrauterine
device appropriate contraception for HIV-1–infected women? BJOG
2001;108:784–90.
124. Richardson BA, Morrison CS, Sekadde-Kigondu C, et al. Eﬀect of
intrauterine device use on cervical shedding of HIV-1 DNA. AIDS
1999;13:2091–7.
125. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D.
Complications of use of intrauterine devices among HIV-1–infected
women. Lancet 1998;351:1238–41.
126. Mostad SB, Overbaugh J, DeVange DM, et al. Hormonal contraception, vitamin A deﬁciency, and other risk factors for shedding of HIV-1
infected cells from the cervix and vagina. Lancet 1997;350:922–7.
127. Kovacs A, Wasserman SS, Burns D, et al. Determinants of HIV-1
shedding in the genital tract of women. Lancet 2001;358:1593–601.
128. Stringer EM, Kaseba C, Levy J, et al. A randomized trial of the intrauterine contraceptive device vs hormonal contraception in women who
are infected with the human immunodeﬁciency virus. Am J Obstet
Gynecol 2007;197:144–8.
129. Heikinheimo O, Lehtovirta P, Suni J, Paavonen J. The levonorgestrelreleasing intrauterine system (LNG-IUS) in HIV-infected women—
eﬀects on bleeding patterns, ovarian function and genital shedding of
HIV. Hum Reprod 2006;21:2857–61.
130. Lehtovirta P, Paavonen J, Heikinheimo O. Experience with the
levonorgestrel-releasing intrauterine system among HIV-infected
women. Contraception 2007;75:37–9.
131. Grigoryan OR, Grodnitskaya EE, Andreeva EN, et al. Contraception
in perimenopausal women with diabetes mellitus. Gynecol Endocrinol
2006;22:198–206.
132. Rogovskaya S, Rivera R, Grimes DA, et al. Eﬀect of a levonorgestrel
intrauterine system on women with type 1 diabetes: a randomized trial.
Obstet Gynecol 2005;105:811–5.
133. Cox M, Tripp J, Blacksell S. Clinical performance of the levonorgestrel
intrauterine system in routine use by the UK Family Planning and
Reproductive Health Research Network: 5-year report. J Fam Plann
Reprod Health Care 2002;28:73–7.
134. Wakeman J. Exacerbation of Crohn’s disease after insertion of a
levonorgestrel intrauterine system: a case report. J Fam Plann Reprod
Health Care 2003;29:154.

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Recommendations and Reports

135. Fong YF, Singh K. Eﬀect of the levonorgestrel-releasing intrauterine
system on uterine myomas in a renal transplant patient. Contraception
1999;60:51–3.
136. Zerner J, Doil KL, Drewry J, Leeber DA. Intrauterine contraceptive device failures in renal transplant patients. J Reprod Med
1981;26:99–102.
137. Lessan-Pezeshki M, Ghazizadeh S, Khatami MR, et al. Fertility and
contraceptive issues after kidney transplantation in women. Transplant
Proc 2004;36:1405–6.

138. O’Donnell D. Contraception in the female transplant recipient. Dialysis
& Transplantation 1986;15:610,612.
139. Bounds W, Guillebaud J. Observational series on women using the contraceptive Mirena concurrently with anti-epileptic and other enzymeinducing drugs. J Fam Plann Reprod Health Care 2002;28:78–80.
140. Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens, reduces lamotrigine serum concentrations. Epilepsia
2005;46:1414–7.

MMWR

June 18, 2010

Appendix F
Classifications for Copper Intrauterine Devices for
Emergency Contraception
A copper IUD (Cu-IUD) can be used within 5 days of
unprotected intercourse as an emergency contraceptive.
However, when the time of ovulation can be estimated, the
Cu-IUD can be inserted beyond 5 days after intercourse, if
necessary, as long as the insertion does not occur >5 days after
ovulation.

The eligibility criteria for interval Cu-IUD insertion also
apply for the insertion of Cu-IUDs as emergency contraception (Box). Cu-IUDs for emergency contraception do not
protect against sexually transmitted infections (STIs) or human
immunodeﬁciency virus (HIV).

BOX. Categories for Classifying Cu-IUDs as Emergency Contraception

TABLE. Classifications for copper intrauterine devices for emergency contraception*†
Condition

Category

Clarifications/Evidence/Comments

Pregnancy

Clarification: IUD use is not indicated during pregnancy and should not be used because
of the risk for serious pelvic infection and septic spontaneous abortion.

Rape
a. High risk for STI

Comment: IUDs do not protect against STI/HIV or PID. Among women with chlamydial
infection or gonorrhea, the potential increased risk for PID with IUD insertion should be
avoided. The concern is less for other STIs.

b. Low risk for STI

* Abbreviations: IUD = intrauterine device; Cu-IUD = copper IUD; STI = sexually transmitted infection; HIV = human immunodeficiency virus; PID = pelvic
inflammatory disease
† Cu-IUDs for emergency contraception do not protect against STI/HIV. If risk exists for STI/HIV (including during pregnancy or postpartum), the correct
and consistent use of condoms is recommended, either alone or with another contraceptive method. Consistent and correct use of the male latex condom
reduces the risk for STIs and HIV transmission.

Vol. 59 / RR-4

Recommendations and Reports

Appendix G
Classifications for Barrier Methods
Classiﬁcations for barrier contraceptive methods include
those for condoms, which include male latex condoms, male
polyurethane condoms, and female condoms; spermicides; and
diaphragm with spermicide or cervical cap (Box). Consistent
and correct use of the male latex condom reduces the risk for
STI/HIV transmission.

Women with conditions that make pregnancy an unacceptable risk should be advised that barrier methods for pregnancy
prevention may not be appropriate for those who cannot use
them consistently and correctly because of the relatively higher
typical-use failure rates of these methods.

BOX. Categories for Classifying Barrier Methods

Condom

Spermicide

Diaphragm/
cap

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy

Not
applicable

Age
a. Menarche to <40 yrs
b. ≥40 yrs

1
1

Parity
a. Nulliparous
b. Parous

1
1

1
2

Postpartum
a. <6 wks postpartum

b. ≥6 wks postpartum

1
1

Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic abortion

Not
Clarification: None of these methods are relevant for contraception during known
applicable pregnancy. However, for women who remain at risk for STI/HIV during pregnancy,
the correct and consistent use of condoms is recommended.

Not
Clarification: Diaphragm and cap are unsuitable until uterine involution is
applicable complete.
1

Past ectopic pregnancy

History of pelvic surgery

Smoking
a. Age <35 yrs
b. Age ≥35 yrs
i. <15 Cigarettes/day
ii. ≥15 Cigarettes/day

1
1

Obesity
a. ≥30 kg/m2 BMI
b. Menarche to <18 yrs and ≥30 kg/m2 BMI

1
1

Clarification: Risk for cervical cap failure is higher in parous women than in
nulliparous women.

Clarification: Diaphragm and cap are unsuitable until 6 weeks after second
trimester abortion.

Comment: Severe obesity might make diaphragm and cap placement difficult.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for barrier methods,*† including condoms, spermicides, and diaphragms/caps
Category
Condition
b. Malabsorptive procedures: decrease absorption of nutrients and calories by shortening the
functional length of the small intestine (Rouxen-Y gastric bypass, biliopancreatic diversion)

Condom

Spermicide

Diaphragm/
cap

1
1
1

Clarifications/Evidence/Comments

Cardiovascular Disease
Multiple risk factors for arterial cardiovascular
disease (such as older age, smoking, diabetes,
and hypertension)
Hypertension
a. Adequately controlled hypertension
b. Elevated blood pressure levels (properly taken
measurements)
i. Systolic 140–159 mm Hg or
diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic ≥100 mm
Hg§
c. Vascular disease
History of high blood pressure during
pregnancy (where current blood pressure is
measurable and normal)
Deep venous thrombosis (DVT)/pulmonary
embolism (PE)
a. History of DVT/PE, not on anticoagulant
therapy
i. Higher risk for recurrent DVT/PE (≥1 risk
factors)
r )JTUPSZPGFTUSPHFOBTTPDJBUFE%751&
r 1SFHOBODZBTTPDJBUFE%751&
r *EJPQBUIJD%751&
r ,OPXOUISPNCPQIJMJB
JODMVEJOHBOUJQIPTpholipid syndrome
r "DUJWFDBODFS NFUBTUBUJD
POUIFSBQZ
or within 6 mos after clinical remission),
excluding non-melanoma skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii. Lower risk for recurrent DVT/PE (no risk
factors)
b. Acute DVT/PE
c. DVT/PE and established on anticoagulant
therapy for at least 3 mos
i. Higher risk for recurrent DVT/PE (≥1 risk
factors)
r ,OPXOUISPNCPQIJMJB
JODMVEJOHBOUJQIPTpholipid syndrome
r "DUJWFDBODFS NFUBTUBUJD
POUIFSBQZ
or within 6 mos after clinical remission),
excluding non-melanoma skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii. Lower risk for recurrent DVT/PE (no risk
factors)
d. Family history (first-degree relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged immobilization
f. Minor surgery without immobilization
Known thrombogenic mutations§ (e.g., factor V
Leiden; prothrombin mutation; protein S, protein C,
and antithrombin deficiencies)

Clarification: Routine screening is not appropriate because of the rarity of the
conditions and the high cost of screening.

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for barrier methods,*† including condoms, spermicides, and diaphragms/caps
Category
Condom

Spermicide

Diaphragm/
cap

1
1
1

1
1

1
2

1
1
1

1
1

1
1
1

Unexplained vaginal bleeding
(suspicious for serious condition)
Before evaluation

Endometriosis

Benign ovarian tumors (including cysts)

Severe dysmenorrhea

Condition
Superficial venous thrombosis
a. Varicose veins
b. Superficial thrombophlebitis
Current and history of ischemic heart disease§
Stroke§ (history of cerebrovascular accident)
Known hyperlipidemias
Valvular heart disease
a. Uncomplicated
b. Complicated§ (pulmonary hypertension, risk for
atrial fibrillation, history of subacute bacterial
endocarditis)
Peripartum cardiomyopathy§
a. Normal or mildly impaired cardiac function
(New York Heart Association Functional Class
I or II: patients with no limitation of activities or
patients with slight, mild limitation of activity)
(1)
i. <6 mos
ii. ≥6 mos
b. Moderately or severely impaired cardiac function (New York Heart Association Functional
Class III or IV: patients with marked limitation
of activity or patients who should be at complete rest) (1)

Clarifications/Evidence/Comments

Clarification: Routine screening is not appropriate because of the rarity of the
conditions and the high cost of screening.

Rheumatic Diseases
Systemic lupus erythematosus§
a. Positive (or unknown) antiphospholipid
antibodies
b. Severe thrombocytopenia
c. Immunosuppressive treatment
d. None of the above
Rheumatoid arthritis
a. On immunosuppressive therapy
b. Not on immunosuppressive therapy

Neurologic Conditions
Headaches
a. Non-migrainous (mild or severe)
b. Migraine
i. Without aura
r "HFZST
r "HFŜZST
ii. With aura, at any age
Epilepsy§

Depressive Disorders
Depressive disorders

Reproductive Tract Infections and Disorders

Clarification: If pregnancy or an underlying pathological condition (such as pelvic
malignancy) is suspected, it must be evaluated and the category adjusted after
evaluation.

MMWR

June 18, 2010

TABLE. (Continued) Classifications for barrier methods,*† including condoms, spermicides, and diaphragms/caps
Category
Condom

Spermicide

Diaphragm/
cap

Gestational trophoblastic disease
a. Decreasing or undetectable β–hCG levels
b. Persistently elevated β-hCG levels or
malignant disease§

1
1

Cervical ectropion

Cervical intraepithelial neoplasia

Clarification: The cap should not be used. Diaphragm use has no restrictions.

Cervical cancer (awaiting treatment)

Clarification: The cap should not be used. Diaphragm use has no restrictions.

Condition

Clarifications/Evidence/Comments

Comment: Repeated and high-dose use of nonoxynol-9 can cause vaginal and
cervical irritation or abrasions.
Breast disease
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer
d. Breast cancer§
i. Current
ii. Past and no evidence of current disease
for 5 yrs

1
1
1

1
1

Endometrial hyperplasia

Endometrial cancer§

cancer§

Uterine fibroids

Anatomical abnormalities

Pelvic inflammatory disease (PID)
a. Past PID (assuming no current risk factors of
STIs)
i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID

1
1
1

1
1

Ovarian

STIs
a. Current purulent cervicitis or chlamydial infection or gonorrhea
b. Other STIs (excluding HIV and hepatitis)
c. Vaginitis (including Trichomonas vaginalis and
bacterial vaginosis)
d. Increased risk for STIs

Not
Clarification: The diaphragm cannot be used in certain cases of prolapse. Cap
applicable use is not appropriate for a woman with markedly distorted cervical anatomy.

HIV/AIDS
High risk for HIV

Evidence: Repeated and high-dose use of the spermicide nonoxynol-9 was associated with increased risk for genital lesions, which might increase the risk for
HIV infection (2).
Comment: Diaphragm use is assigned Category 4 because of concerns about
the spermicide, not the diaphragm.

HIV infection§

Comment: Use of spermicides and/or diaphragms (with spermicide) can disrupt
the cervical mucosa, which may increase viral shedding and HIV transmission to
uninfected sex partners.

AIDS§

Comment: Use of spermicides and/or diaphragms (with spermicide) can disrupt
the cervical mucosa, which may increase viral shedding and HIV transmission to
uninfected sex partners

Schistosomiasis
a. Uncomplicated
b. Fibrosis of liver§

1
1

Tuberculosis§
a. Nonpelvic
b. Pelvic

1
1

Other Infections

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Classifications for barrier methods,*† including condoms, spermicides, and diaphragms/caps
Category
Condom

Spermicide

Diaphragm/
cap

Malaria

History of toxic shock syndrome

Comment: Toxic shock syndrome has been reported in association with contraceptive sponge and diaphragm use.

Urinary tract infection

Comment: Use of diaphragms and spermicides might increase risk for urinary
tract infection.

1
1
1
1

1
1
1

Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic

1
1
1
1

History of cholestasis
a. Pregnancy-related
b. Past COC-related

1
1

Viral hepatitis
a. Acute or flare
b. Carrier
c. Chronic

1
1
1

Cirrhosis
a. Mild (compensated)
b. Severe§ (decompensated)

1
1

Liver tumors
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma§
b. Malignant§ (hepatoma)

1
1
1

Thalassemia

Sickle cell disease§

Iron deficiency anemia

Condition

Endocrine Conditions
Diabetes
a. History of gestational disease
b. Nonvascular disease
i. Noninsulin-dependent
ii. Insulin-dependent§
c. Nephropathy/retinopathy/neuropathy§
d. Other vascular disease or diabetes of >20 yrs’
duration§
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Gastrointestinal Conditions
Inflammatory bowel disease
(ulcerative colitis, Crohn disease)

Anemias

Solid Organ Transplantation
Solid organ transplantation§
a. Complicated: graft failure (acute or chronic),
rejection, cardiac allograft vasculopathy
b. Uncomplicated

Clarifications/Evidence/Comments

MMWR

June 18, 2010

TABLE. (Continued) Classifications for barrier methods,*† including condoms, spermicides, and diaphragms/caps
Category
Condition

Condom

Spermicide

Diaphragm/
cap

Clarifications/Evidence/Comments

Drug Interactions
Antiretroviral (ARV) therapy

Clarification: No drug interaction between ARV therapy and barrier method
use is known. However, HIV infection and AIDS are classified as Category 3 for
spermicides and diaphragms (see HIV/AIDS condition above).
1

Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampicin or rifabutin
therapy

1
1
1
1

Allergy to latex

a. Nucleoside reverse transcriptase inhibitors
(NRTIs)
b. Non-nucleoside reverse transcriptase
inhibitors (NNRTIs)
c. Ritonavir-boosted protease inhibitors
Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin, carbamazepine, barbiturates, primidone, topiramate,
oxcarbazepine)
b. Lamotrigine

Clarification: The condition of allergy to latex does not apply to plastic condoms/
diaphragms.

* Abbreviations: STI = sexually transmitted infection; HIV = human immunodeficiency virus; BMI, body mass index; DVT = deep venous thrombosis; PE = pulmonary embolism;
ARV = antiretroviral; hCG = human chorionic gonadotropin; PID = pelvic inflammatory disease; AIDS = acquired immunodeficiency syndrome; COC = combined oral contraceptive; NRTI = nucleoside reverse transcriptase inhibitor; NNRTI = non-nucleoside reverse transcriptase inhibitor.
† If risk exists for STI/HIV (including during pregnancy or postpartum), the correct and consistent use of condoms is recommended, either alone or with another contraceptive
method. Consistent and correct use of the male latex condom reduces the risk for STIs and HIV transmission. Women with conditions that make pregnancy an unacceptable
risk should be advised that barrier methods for pregnancy prevention may not be appropriate for those who cannot use them consistently and correctly because of the relatively
higher typical-use failure rates of these methods.
§ Condition that exposes a woman to increased risk as a result of unintended pregnancy.

References
1. The Criteria Committee of the New York Heart Association. Nomenclature
and criteria for diagnosis of diseses of the heart and great vessels. 9th ed.
Boston, MA: Little, Brown & Co; 1994.

2. Wilkinson D, Ramjee G, Tholandi M, Rutherford G. Nonoxynol-9 for
preventing vaginal acquisition of HIV infection by women from men.
Cochrane Database Syst Rev 2002;4:CD003939.

Vol. 59 / RR-4

Recommendations and Reports

Appendix H
Classifications for Fertility Awareness–Based Methods
Fertility awareness–based (FAB) methods of family planning
involve identifying the fertile days of the menstrual cycle,
whether by observing fertility signs such as cervical secretions
and basal body temperature or by monitoring cycle days (Box).
FAB methods can be used in combination with abstinence or
barrier methods during the fertile time. If barrier methods are
used, refer to Appendix G.
No medical conditions become worse because of use of FAB
methods. In general, FAB methods can be used without concern for health eﬀects to persons who choose them. However,
a number of conditions make their use more complex. The
existence of these conditions suggests that 1) use of these
methods should be delayed until the condition is corrected or
resolved or 2) persons using FAB methods will require special
counseling, and a more highly trained provider is generally
necessary to ensure correct use.
Women with conditions that make pregnancy an unacceptable risk should be advised that FAB methods might not be
appropriate for them because of the relatively higher typical-use
failure rates of these methods. FAB methods do not protect
against sexually transmitted infections (STIs) or human immunodeﬁciency virus (HIV).

Box. Definitions for terms associated with fertility awareness–
based methods

t Symptoms-based methods: FAB methods based on
observation of fertility signs (e.g., cervical secretions, basal
body temperature) such as the Cervical Mucus Method,
the Symptothermal Method, and the TwoDay Method.
t Calendar-based methods: FAB methods based on calendar calculations such as the Calendar Rhythm Method
and the Standard Days Method.
t Acccept (A): There is no medical reason to deny the particular FAB method to a woman in this circumstance.
t Caution (C): The method is normally provided in a
routine setting but with extra preparation and precautions. For FAB methods, this usually means that special
counselling might be needed to ensure correct use of the
method by a woman in this circumstance.
t Delay (D): Use of this method should be delayed until the
condition is evaluated or corrected. Alternative temporary
methods of contraception should be oﬀered.

TABLE. Fertility awareness–based methods,*† including symptoms-based and calendar-based methods
Category
Condition

Symptom-based Calendar-based
method
method

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy

Not applicable

Clarification: FAB methods are not relevant during pregnancy.

Life stage
a. Postmenarche
b. Perimenopause

Clarification: Menstrual irregularities are common in postmenarche and perimenopause and might complicate the use of FAB methods.
C
C

C
C

Breastfeeding
a. <6 wks postpartum
b. ≥6 wks

D
C

D
D

c. After menses begin

Comment: Use of FAB methods when breastfeeding might be less effective than
when not breastfeeding.
Comment: Women who are primarily breastfeeding and are amenorrheic are
unlikely to have sufficient ovarian function to produce detectable fertility signs and
hormonal changes during the first 6 months postpartum. However, the likelihood of
resumption of fertility increases with time postpartum and with substitution of breast
milk with other foods.
Comment: When the woman notices fertility signs, particularly cervical secretions, she can use a symptoms-based method. First postpartum menstrual cycles
in breastfeeding women vary significantly in length. Return to regularity takes
several cycles. When she has had at least 3 postpartum menses and her cycles are
regular again, she can use a calendar-based method. When she has had at least 4
postpartum menses and her most recent cycle lasted 26–32 days, she can use the
Standard Days Method. Before that time, a barrier method should be offered if the
woman plans to use a FAB method later.

MMWR

June 18, 2010

TABLE. (Continued) Fertility awareness–based methods,*† including symptoms-based and calendar-based methods
Category
Condition

Symptom-based Calendar-based
method
method

Postpartum (in nonbreastfeeding women)
a. <4 wks

Clarifications/Evidence/Comments

Comment: Postabortion women are likely to have sufficient ovarian function to
produce detectable fertility signs and/or hormonal changes; likelihood increases
with time postabortion. Women can start using calendar-based methods after they
have had at least 1 postabortion menses (e.g., women who before this pregnancy
had most cycles of 26–32 days can then use the Standard Days Method). Methods
appropriate for the postabortion period should be offered before that time.

Irregular vaginal bleeding

Comment: Presence of this condition makes FAB methods unreliable. Therefore,
barrier methods should be recommended until the bleeding pattern is compatible with proper method use. The condition should be evaluated and treated as
necessary.

Vaginal discharge

Comment: Because vaginal discharge makes recognition of cervical secretions
difficult, the condition should be evaluated and treated if needed before providing
methods based on cervical secretions.

C/D

Comment: Use of certain mood-altering drugs such as lithium, tricyclic antidepressants, and antianxiety therapies, and certain antibiotics and anti-inflammatory
drugs, might alter cycle regularity or affect fertility signs. The condition should be
carefully evaluated and a barrier method offered until the degree of effect has been
determined or the drug is no longer being used.

C
D

A
A

Comment: Elevated temperature levels might make basal body temperature difficult to interpret but have no effect on cervical secretions. Thus, use of a method
that relies on temperature should be delayed until the acute febrile disease abates.
Temperature-based methods are not appropriate for women with chronically elevated temperatures. In addition, some chronic diseases interfere with cycle regularity,
making calendar-based methods difficult to interpret.

b. ≥4 wks

Postabortion

Comment: Nonbreastfeeding women are not likely to have sufficient ovarian function to either require a FAB method or to have detectable fertility signs or hormonal
changes before 4 weeks postpartum. Although the risk for pregnancy is low, a
method appropriate for the postpartum period should be offered.
Comment: Nonbreastfeeding women are likely to have sufficient ovarian function
to produce detectable fertility signs and/or hormonal changes at this time; likelihood
increases rapidly with time postpartum. Women can use calendar-based methods
as soon as they have completed three postpartum menses. Methods appropriate for
the postpartum period should be offered before that time.

Reproductive Tract Infections and Disorders

Other
Use of drugs that affect cycle regularity,
hormones, and/or fertility signs

Diseases that elevate body temperature
a. Chronic diseases
b. Acute diseases

* Abbreviations: FAB = fertility awareness–based; A = accept; C = caution; D = delay; STI = sexually transmitted infection; HIV = human immunodeficiency infection.
† Fertility awareness–based methods do not protect against STI/HIV. If risk exists for STI/HIV (including during pregnancy or postpartum), the correct and consistent use of condoms
is recommended, either alone or with another contraceptive method. Consistent and correct use of the male latex condom reduces the risk for STIs and HIV transmission.

Vol. 59 / RR-4

Recommendations and Reports

Appendix I
Lactational Amenorrhea Method
The Bellagio Consensus provided the scientiﬁc basis for
deﬁning the conditions under which breastfeeding can be
used safely and eﬀectively for birth-spacing purposes, and
programmatic guidelines were developed for use of lactational amenorrhea in family planning (1,2). These guidelines
include the following three criteria, all of which must be met
to ensure adequate protection from an unplanned pregnancy:
1) amenorrhea; 2) fully or nearly fully breastfeeding, and 3)
<6 months postpartum.
The main indications for breastfeeding are to provide an ideal
food for the infant and protect against disease. No medical
conditions exist for which use of the lactational amenorrhea
method for contraception is restricted. However, breastfeeding might not be recommended for women or infants with
certain conditions.
Women with conditions that make pregnancy an unacceptable risk should be advised that the lactational amenorrhea method might not be appropriate for them because of
its relatively higher typical-use failure rates. The lactational
amenorrhea method does not protect against sexually transmitted infections (STIs) and human immunodeﬁciency virus
(HIV). If risk exists for STI/HIV (including during pregnancy
or postpartum), the correct and consistent use of condoms
is recommended, either alone or with another contraceptive
method. Consistent and correct use of the male latex condom
reduces the risk for STIs and HIV transmission.
HIV Infection
HIV can be transmitted from mother to infant through
breastfeeding. Therefore, in the United States, where replace-

ment feeding is aﬀordable, feasible, acceptable, sustainable,
and safe, breastfeeding for women with HIV is not recommended (3,4).
Other Medical Conditions
The American Academy of Pediatrics also recommends
against breastfeeding for women with active untreated tuberculosis disease, who are positive for human T-cell lymphotropic
virus types I or II, or who have herpes simplex lesions on a
breast (infant can feed from the other breast). In addition,
infants with classic galactosemia should not breastfeed (4).
Medication Used during Breastfeeding
To protect infant health, the American Academy of Pediatrics
does not recommend breastfeeding for women receiving certain
drugs, including diagnostic or therapeutic radioactive isotopes
or exposure to radioactive materials, antimetabolites or chemotherapeutic agents, and current use of drugs of abuse (4).
References
1. Kennedy KI, Rivera R, McNeilly AS. Consensus statement on the
use of breastfeeding as a family planning method. Contraception
1989;39:477–96.
2. Labbok M, Cooney K, Coly S. Guidelines: breastfeeding, family planning, and the Lactational Amenorrhea Method-LAM. Washington, DC:
Institute for Reproductive Health; 1994.
3. Perinatal HIV Guidelines Working Group. Public Health Service Task
Force recommendations for use of antiretroviral drugs in pregnant HIVinfected women for maternal health and interventions to reduce perinatal
HIV transmission in the United States. Rockville, MD: Public Health
Service Task Force; 2009.
4. Gartner LM, Morton J, Lawrence RA, et al. Breastfeeding and the use of
human milk. Pediatrics 2005;115:496–506.

MMWR

June 18, 2010

Appendix J
Coitus Interruptus (Withdrawal)
Coitus interruptus (CI), also known as withdrawal, is a traditional family planning method in which the man completely
removes his penis from the vagina, and away from the external
genitalia of the female partner, before he ejaculates. CI prevents
sperm from entering the woman’s vagina, thereby preventing
contact between spermatozoa and the ovum.
This method might be appropriate for couples
t who are highly motivated and able to use this method
eﬀectively;
t with religious or philosophical reasons for not using other
methods of contraception;
t who need contraception immediately and have entered
into a sexual act without alternative methods available;
t who need a temporary method while awaiting the start of
another method; or
t who have intercourse infrequently.

Some beneﬁts of CI are that the method, if used correctly,
does not aﬀect breastfeeding and is always available for primary
use or use as a back-up method. In addition, CI involves no
economic cost or use of chemicals. CI has no directly associated
health risks. CI does not protect against sexually transmitted
infections (STIs) and human immunodeﬁciency virus (HIV).
If risk exists for STI/HIV (including during pregnancy or
postpartum), the correct and consistent use of condoms is
recommended, either alone or with another contraceptive
method. Consistent and correct use of the male latex condom
reduces the risk for STIs and HIV transmission.
CI is unforgiving of incorrect use, and its eﬀectiveness
depends on the willingness and ability of the couple to use
withdrawal with every act of intercourse. Women with conditions that make pregnancy an unacceptable risk should be
advised that CI might not be appropriate for them because of
its relatively higher typical-use failure rates.

Vol. 59 / RR-4

Recommendations and Reports

Appendix K
Female and Male Sterilization
Tubal sterilization for women and vasectomy for men are
permanent, safe, and highly eﬀective methods of contraception.
In general, no medical conditions would absolutely restrict
a person’s eligibility for sterilization (with the exception of
known allergy or hypersensitivity to any materials used to
complete the sterilization method). However, certain conditions place a woman at high surgical risk; in these cases, careful
consideration should be given to the risks and beneﬁts of other
acceptable alternatives, including long-acting, highly eﬀective,
reversible methods and vasectomy. Female and male sterilization do not protect against sexually transmitted infections
(STIs) or human immunodeﬁciency virus (HIV). If risk exists
for STI/HIV (including during pregnancy or postpartum), the
correct and consistent use of condoms is recommended, either
alone or with another contraceptive method. Consistent and
correct use of the male latex condom reduces the risk for STIs
and HIV transmission.
Because these methods are intended to be irreversible, persons who choose sterilization should be certain that they want
to prevent pregnancy permanently. Most persons who choose

sterilization remain satisﬁed with their decision. However, a
small proportion of women regret this decision (1%–26% from
diﬀerent studies, with higher rates of regret reported by women
who were younger at sterilization) (1,2). Regret among men
about vasectomy has been reported to be approximately 5%
(3), similar to the proportion of women who report regretting
their husbands’ vasectomy (6%) (4). Therefore, all persons
should be appropriately counseled about the permanency of
sterilization and the availability of highly eﬀective, reversible
methods of contraception.
References
1. Peterson HB. Sterilization. Obstet Gynecol 2008;111:189–203.
2. Hillis SD, Marchbanks PA, Tylor LR, Peterson HB. Poststerilization regret:
ﬁndings from the United States Collaborative Review of Sterilization.
Obstet Gynecol 1999;93:889–95.
3. Ehn BE, Liljestrand J. A long-term follow-up of 108 vasectomized
men. Good counselling routines are important. Scand J Urol Nephrol
1995;29:477–81.
4. Jamieson DJ, Kaufman SC, Costello C, et al. A comparison of women’s
regret after vasectomy versus tubal sterilization. Obstet Gynecol
2002;99:1073–9.

MMWR

June 18, 2010

Appendix L
Summary of Classifications for Hormonal Contraceptive Methods and
Intrauterine Devices
Health-care providers can use the summary table as a quick
reference guide to the classiﬁcations for hormonal contraceptive methods and intrauterine contraception and to compare

classiﬁcations across these methods. See the full appendix for
each method for clariﬁcations to the numeric categories, as well
as for summaries of the evidence and additional comments.

BOX. Categories for Classifying Hormonal Contraceptives and IUDs

TABLE. Summary of classifications for hormonal contraceptive methods and intrauterine devices*
Condition

COC/P/R

POP

DMPA

Implants

LNG-IUD

Cu-IUD

Not applicable†

4†

Menarche to
<40 yrs = 1
≥40 yrs = 2

Menarche to
<18 yrs = 1
18–45 yrs = 1
>45 yrs = 1

Menarche to
<18 yrs = 2
18–45 yrs = 1
>45 yrs = 2

Menarche to
<18 yrs =1
18–45 yrs = 1
>45 yrs = 1

Menarche to
<20 yrs = 2
≥20 yrs = 1

Parity
a. Nulliparous
b. Parous

1
1

2
1

Breastfeeding
a. <1 mo postpartum
b. 1 mo to <6 mos
c. ≥6 mos postpartum

3†
2†
2†

2†
1†
1†

Postpartum
(nonbreastfeeding women)
a. <21 days
b. ≥21 days

3
1

1
1

1
4

Personal Characteristics and Reproductive History
Pregnancy
Age

Postpartum (breastfeeding or
nonbreastfeeding women, including
post-Cesarean section)
a. <10 min after delivery of the
placenta
b. 10 min after delivery of the placenta to <4 wks
c. ≥4 wks
d. Puerperal sepsis
Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic abortion

1†
1†
1†

1†
2
4

Past ectopic pregnancy

History of pelvic surgery (see postpartum, including Cesarean section)

3
4

1
1

Smoking
a. Age <35 yrs
b. Age ≥35 yrs
i. <15 Cigarettes/day
ii. ≥15 Cigarettes/day

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices*
Condition
Obesity
a. ≥30 kg/m2 BMI
b. Menarche to <18 yrs and
≥30 kg/m2 BMI
History of bariatric surgery§
a. Restrictive procedures: decrease
storage capacity of the stomach
(vertical banded gastroplasty, laparoscopic adjustable gastric band,
laparoscopic sleeve gastrectomy)
b. Malabsorptive procedures:
decrease absorption of nutrients
and calories by shortening the
functional length of the small intestine (Roux-en-Y gastric bypass,
biliopancreatic diversion)

COC/P/R

POP

DMPA

Implants

LNG-IUD

Cu-IUD

2
2

1
1

1
2

1
1

3/4†

2†

3†

2†

3†

1†

2†

1†

4†

3†

COCs: 3
P/R: 1

Cardiovascular Disease
Multiple risk factors for arterial
cardiovascular disease (such as
older age, smoking, diabetes, and
hypertension)
Hypertension
a. Adequately controlled
hypertension
b. Elevated blood pressure levels
(properly taken measurements)
i. Systolic 140–159 mm Hg or
diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or
diastolic ≥100 mm Hg§
c. Vascular disease
History of high blood pressure during pregnancy (where current blood
pressure is measurable and normal)
Deep venous thrombosis (DVT)/
pulmonary embolism (PE)
a. History of DVT/PE, not on
anticoagulant therapy
i. Higher risk for recurrent DVT/
PE (≥1 risk factors)
r )JTUPSZPGFTUSPHFO
associated DVT/PE
r 1SFHOBODZBTTPDJBUFE
DVT/PE
r *EJPQBUIJD%751&
r ,OPXOUISPNCPQIJMJB
including antiphospholipid
syndrome
r "DUJWFDBODFS NFUBTUBUJD
PO
therapy, or within 6 mos after
clinical remission), excluding
non-melanoma skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii.Lower risk for recurrent DVT/PE
(no risk factors)
b. Acute DVT/PE
c. DVT/PE and established on
anticoagulant therapy for at least 3
mos
i. Higher risk for recurrent DVT/
PE (≥1 risk factors)
r ,OPXOUISPNCPQIJMJB
including antiphospholipid
syndrome
r "DUJWFDBODFS NFUBTUBUJD
PO
therapy, or within 6 mos after
clinical remission), excluding
non-melanoma skin cancer
r )JTUPSZPGSFDVSSFOU%751&
ii. Lower risk for recurrent DVT/
PE (no risk factors)

MMWR

June 18, 2010

TABLE. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices*
Condition
d. Family history (first-degree
relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged
immobilization
f. Minor surgery without
immobilization
Known thrombogenic mutations§
(e.g. factor V Leiden; prothrombin
mutation; protein S, protein C, and
antithrombin deficiencies)
Superficial venous thrombosis
a. Varicose veins
b. Superficial thrombophlebitis
Current and history of ischemic
heart disease§

COC/P/R

POP

DMPA

Implants

LNG-IUD

Cu-IUD

4
2

2
1

1
1

4†

2†

1†

1
2

1
1

Initiation Continuation
4

Stroke§

(history of cerebrovascular
accident)

Initiation Continuation Initiation Continuation

Initiation Continuation
4

Known hyperlipidemias
Valvular heart disease
a. Uncomplicated
b. Complicated§ (pulmonary hypertension, risk for atrial fibrillation,
history of subacute bacterial
endocarditis)
Peripartum cardiomyopathy§
a. Normal or mildly impaired cardiac function (New York Heart
Association Functional Class I or
II: patients with no limitation of
activities or patients with slight,
mild limitation of activity) (1)
i. <6 mos
ii. ≥6 mos
b. Moderately or severely impaired
cardiac function (New York Heart
Association Functional Class III or
IV: patients with marked limitation
of activity or patients who should
be at complete rest) (1)

Initiation Continuation
2

2/3†

2†

2
2†

2†

1†

2
4

1
1

4
3
4

1
1
2

2
2
2

Initiation Continuation
3
3

Initiation Continuation
1
1

2
2
2

2†
2
2

2
2

1
1

Rheumatic Diseases
Systemic lupus erythematosus§
a. Positive (or unknown) antiphospholipid antibodies
b. Severe thrombocytopenia
c. Immunosuppressive treatment
d. None of the above
Rheumatoid arthritis
a. On immunosuppressive therapy
b. Not on immunosuppressive
therapy

3
2
2

2
2
2
2/3†
2

3†
2
1

2†
1
1

Initiation Continuation Initiation Continuation
2
1
2
1
1
1

1
1

Neurologic Conditions
Headaches
a. Non-migrainous (mild or severe)
b. Migraine
i. Without aura
r "HFZST
r "HF≥35 yrs
ii. With aura (at any age)
Epilepsy§

Initiation Continuation Initiation Continuation Initiation Continuation Initiation Continuation Initiation Continuation
1†
2†
1†
1†
1†
1†
1†
1†
1†
1†

2†
3†
4†

3†
4†
4†
1†

1†
1†
2†

2†
2†
3†
1†

2†
2†
2†

2†
2†
3†

2†
2†
2†

1†

If on treatment, see Drug Interactions section below

2†
2†
3†
1†

2†
2†
2†

2†
2†
3†
1

1†

1†
1†
1†
1

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices*
Condition

COC/P/R

POP

DMPA

Implants

LNG-IUD

Cu-IUD

1†

Initiation Continuation
1
1

1†

2†

Depressive Disorders
Depressive disorders

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without heavy
bleeding
b. Heavy or prolonged bleeding
(includes regular and irregular
patterns)

1†

2†

Unexplained vaginal bleeding (suspicious for serious condition)
Before evaluation

2†

3†

Endometriosis

Benign ovarian tumors (including
cysts)

Severe dysmenorrhea

Cervical ectropion

Cervical intraepithelial neoplasia

Gestational trophoblastic disease
a. Decreasing or undetectable ß-hCG
levels
b. Persistently elevated ß-hCG levels
or malignant disease§

Initiation Continuation Initiation Continuation

Cervical cancer (awaiting treatment)

Breast disease
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer
d. Breast cancer§
i. Current
ii. Past and no evidence of
current disease for 5 yrs
Endometrial hyperplasia

4†

2†

4†

2†

Initiation Continuation Initiation Continuation
2

2†
1
1

2
1
1

1
1
1

4
3

1
1

Endometrial cancer§

Initiation Continuation Initiation Continuation

Ovarian cancer§

Uterine fibroids

Anatomical abnormalities
a. Distorted uterine cavity (any congenital or acquired uterine abnormality distorting the uterine cavity
in a manner that is incompatible
with IUD insertion)
b. Other abnormalities (including
cervical stenosis or cervical lacerations) not distorting the uterine
cavity or interfering with IUD
insertion
Pelvic inflammatory disease (PID)
a. Past PID (assuming no current risk
factors of STIs)
i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID

1
1
1

Initiation Continuation Initiation Continuation
1
1
1
1
2
2
2
2
4
2†
4
2†

MMWR

June 18, 2010

TABLE. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices*
Condition

COC/P/R

POP

DMPA

Implants

2/3†

High risk for HIV

HIV infection§

AIDS§

1†

2†

STIs
a. Current purulent cervicitis or chlamydial infection or gonorrhea
b. Other STIs (excluding HIV and
hepatitis)
c. Vaginitis (including Trichomonas
vaginalis and bacterial vaginosis)
d. Increased risk for STIs

LNG-IUD

Cu-IUD

Initiation Continuation Initiation Continuation
4
2†
4
2†

HIV/AIDS
Initiation Continuation Initiation Continuation

Clinically well on ARV therapy

If on treatment, see Drug Interactions section below

Other Infections
Schistosomiasis
a. Uncomplicated
b. Fibrosis of the liver (if severe,
see Cirrhosis)§
Tuberculosis§
a. Nonpelvic
b. Pelvic

1
1

1†
1†

1
1

Initiation Continuation Initiation Continuation
1
1
1
1
4
3
4
3

If on treatment, see Drug Interactions section below
Malaria

2
2
3/4†

2
2
2

2
2
3

2
2
2

1
1
1

3/4†

1
1
1

2/3†

Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic

2
3
3
2

2
2
2
2

1
1
1
1

History of cholestasis
a. Pregnancy-related
b. Past COC-related

2
3

1
2

1
1

Initiation Continuation
3/4†
2
1
1
1
1

1
1
1

1
4

1
3

1
1

Endocrine Conditions
Diabetes
a. History of gestational disease
b. Nonvascular disease
i. Noninsulin-dependent
ii. Insulin-dependent§
c. Nephropathy/retinopathy/
neuropathy§
d. Other vascular disease or diabetes
of >20 yrs’ duration§
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Gastrointestinal Conditions
Inflammatory bowel disease (IBD)
(ulcerative colitis, Crohn disease)

Viral hepatitis
a. Acute or flare
b. Carrier
c. Chronic
Cirrhosis
a. Mild (compensated)
b. Severe§ (decompensated)

Vol. 59 / RR-4

Recommendations and Reports

TABLE. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices*
Condition

COC/P/R

POP

DMPA

Implants

LNG-IUD

Cu-IUD

2
4
4

2
3
3

1
1
1

Thalassemia

Sickle cell disease§

Iron-deficiency anemia

2†

1†

2†

2/3†

2†

2/3†

2†

3†

2†

2/3†

2†

2/3†

2†

Liver tumors
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma§
b. Malignant§ (hepatoma)

Anemias

Solid Organ Transplantation
Solid organ transplantation§
a. Complicated: graft failure (acute or
chronic), rejection, cardiac allograft
vasculopathy
b. Uncomplicated

Initiation Continuation Initiation Continuation
3
2
3
2

Drug Interactions
Antiretroviral therapy (see appendix M)
a. Nucleoside reverse transcriptase
inhibitors (NRTIs)
b. Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
c. Ritonavir-boosted protease
inhibitors

Initiation Continuation Initiation Continuation
2/3†
2†
2/3†
2†

Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin, carbamazepine, barbiturates, primidone, topiramate,
oxcarbazepine)
b. Lamotrigine

3†

2†

3†

Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampicin or rifabutin therapy

1
1
1
3†

1
1
1
1

1
1
1
2†

1
1
1
1

* Abbreviations: COC = combined oral contraceptive; P = combined hormonal contraceptive patch; R = combined hormonal vaginal ring; POP = progestin-only pill; DMPA = depot
medroxyprogesterone acetate; IUD = intrauterine device; LNG-IUD = levonorgestrel-releasing IUD; Cu-IUD = copper IUD; BMI = body mass index; DVT = deep venous thrombosis; PE = pulmonary embolism; hCG, = human chorionic gonadotropin; PID = pelvic inflammatory disease; STI = sexually transmitted infection; HIV = human immunodeficiency
virus; AIDS = acquired immunodeficiency syndrome; NRTI = nucleoside reverse transcriptase inhibitor; NNRTI = non-nucleoside reverse transcriptase.
† Consult the appendix for this contraceptive method for a clarification to this classification.
§ Condition that exposes a woman to increased risk as a result of unintended pregnancy.

Reference
1. The Criteria Committee of the New York Heart Association. Nomenclature
and criteria for diagnosis of diseases of the heart and great vessels. 9th ed.
Boston, MA: Little, Brown & Co.; 1994.

MMWR

June 18, 2010

Appendix M
Summary of Evidence Regarding Potential Drug Interactions between
Hormonal Contraception and Antiretroviral Therapies
Limited data from small, mostly unpublished studies suggest that some antiretroviral (ARV) therapies might alter the
pharmacokinetics of combined oral contraceptives (COCs).
Few studies have measured clinical outcomes. However, contraceptive steroid levels in the blood decrease substantially with
ritonavir-boosted protease inhibitors. Such decreases have the
potential to compromise contraceptive eﬀectiveness. Some of
the interactions between contraceptives and ARVs also have
led to increased ARV toxicity. For smaller eﬀects that occur
with non-nucleoside reverse transcriptase inhibitors, clinical
signiﬁcance is unknown, especially because studies have not
examined steady-state levels of contraceptive hormones. No
clinically signiﬁcant interactions have been reported between
contraceptive hormones and nucleoside reverse transcriptase
inhibitors.

Tables 1 and 2 summarize the evidence available about drug
interactions between ARV therapies and hormonal contraceptives. For up-to-date, detailed information about human
immunodeﬁciency virus (HIV) drug interactions, the following
resources might be helpful:
t Guidelines for the Use of Antiretroviral Agents in HIV1-Infected Adults and Adolescents from the DHHS
Panel on Antiretroviral Guidelines for Adults and
Adolescents. Available at http://aidsinfo.nih.gov/contentﬁles/AdultandAdolescentGL.pdf.
t HIV Drug Interactions website, University of Liverpool,
UK. Available at www.hiv-druginteractions.org.

TABLE 1. Drug interactions between COCs and ARV drugs*
Contraceptive effects†

ARV

ARV effects†

Nucleoside reverse transcriptase inhibitors (NRTIs)
Tenofovir disaproxil fumarate

EE ↔, NGM ↔ (1)

Tenofovir ↔ (1)

Zidovudine

No data

Zidovudine ↔ (2)
No change in viral load or CD4+ (2)

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Efavirenz

EE ↑ (3), EE ↔ (4), NGM ↓ (4), LNG ↓ (4)
Pregnancy rate 2.6/100 woman-years in 1
study in which up to 80% used hormonal
contraceptives (35% used COC) (5)

Efavirenz ↔ (3,4)

Etravirine

EE ↔, NET ↔ (6)

Etravirine ↑ (6)
Concurrent administration, generally safe and well tolerated
(6)

Nevirapine

EE ↔, NET ↔ (7)

Nevirapine ↔ (7)

Protease inhibitors and ritonavir-boosted protease inhibitors
Atazanavir/ritonavir

EE ↑, NET ↑ (8)

No data

Darunavir/ritonavir

EE ↓, NET ↔ (9)

Darunavir ↔ (9)

Fos-amprenavir/ritonavir

EE ↓ (10,11), NET ↓ (11)

Amprenavir ↔, ritonavir ↑, Elevated liver transaminases (10)

Indinavir§

EE ↔, NET ↔ (12)

No data

Lopinavir/ritonavir

EE ↓, NET ↔ (13)

No data

Nelfinavir

EE ↓, NET ↔ (14)

No data

Saquinavir§

No data

Saquinavir ↔ (15,16)

Tipranavir/ritonavir

EE↓ (17)

↑ Skin and musculoskeletal adverse events; possible drug
hypersensitivity reaction (17)

* Abbreviations: COC = combined oral contraceptive; ARV = antiretroviral; EE = ethinyl estradiol; NGM = norgestimate; NNRTI = non-nucleoside reverse
transcriptase inhibitor; LNG = levonorgestrel; NET = norethindrone.
† ↔, no change or change ≤30%; ↑, increase >30%; ↓, decrease >30%.
§ Saquinavir and indinavir are commonly given boosted by ritonavir, but there are no data on contraceptive interactions with the boosted regimens.

Vol. 59 / RR-4

Recommendations and Reports

TABLE 2. Drug interactions between DMPA and ARV drugs*
Contraceptive effects†

ARV

ARV effects†

Nucleoside reverse transcriptase inhibitors (NRTIs)
Zidovudine

No data

Zidovudine ↔ (2)
No change in viral load

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Efavirenz

MPA ↔ (18,19)
No ovulations during 3 cycles(18,19)

Efavirenz ↔ (18)
No change in viral load or CD4+, no grade 3- or 4-related adverse
events§ (20)

Pregnancy rate 2.6/100 woman-years in 1 study where
up to 80% used hormonal contraceptives (65% used
POIs) (5)
Nevirapine

MPA ↔ (18)
No ovulations during 3 cycles(18)

Nevirapine ↑ (18)
No change in viral load or CD4+, no grade 3- or 4-related adverse
events§ (20)

Protease inhibitors and ritonavir-boosted protease inhibitors
Nelfinavir

MPA ↔ (18)

Nelfinavir ↔ (18)
No change in viral load or CD4+, no grade 3- or 4-related adverse
events§ (20)

* Abbreviations: DMPA = depot medroxyprogesterone acetate; ARV = antiretroviral; NRTI = nucleoside reverse transcriptase inhibitor; NNRTI = non-nucleoside
reverse transcriptase; MPA = medroxyprogesterone acetate; POI = progestin-only injectables.
† ↔, no change or change ≤30%; ↑, increase > 30%.
§ The trial applied the standardized National Institutes of Health Division of AIDS Table for Grading Severity of Adult and Pediatric Adverse Events, 2004
(http://rcc.tech-res.com/Document/safetyandpharmacovigilance/DAIDS_AE_GradingTable_Clarification_August2009_Final.pdf). Grade 3 events are classified as severe. Severe events are defined as symptoms that limit activity or might require some assistance; require medical intervention or therapy; and
might require hospitalization. Grade 4 events are classified as life threatening. Life-threatening events include symptoms that result in extreme limitation
of activity and require substantial assistance; require substantial medical intervention and therapy; and probably require hospitalization or hospice.

References
1. Kearney BP, Isaacson E, Sayre J, Cheng AK. Tenofovir DF and oral
contraceptives: lack of a pharmacokinetic drug interaction [Abstract
A-1618]. In: Program and abstracts of the 43rd Interscience Conference on
Antimicrobial Agents and Chemotherapy, Chicago, IL, September 14–17,
2003. Washington, DC: American Society for Microbiology; 2003.
2. Aweeka FT, Rosenkranz SL, Segal Y, et al. The impact of sex and contraceptive therapy on the plasma and intracellular pharmacokinetics of
zidovudine. AIDS 2006;20:1833–41.
3. Joshi AS, Fiske WD, Benedek IH, et al. Lack of a pharmacokinetic
interaction between efavirenz (DMP 266) and ethinyl estradiol in healthy
female volunteers [Abstract 348]. 5th Conference on Retroviruses and
Opportunistic Infections, Chicago, IL, February 1–5, 1998.
4. Sevinsky H, Eley T, He B, et al. Eﬀect of efavirenz on the pharacokinetics
of ethinyl estradiol and norgestimate in healthy female subjects [Abstract
A958]. In: Program and abstracts of the 48th Interscience Conference on
Antimicrobial Agents and Chemotherapy, Washington, DC, October
25–28, 2008. Washington, DC: American Society for Microbiology;
2008.
5. Danel C, Moh R, Anzian A, et al. Tolerance and acceptability of an
efavirenz-based regimen in 740 adults (predominantly women) in West
Africa. J Acquir Immune Deﬁc Syndr 2006;42:29–35.
6. Scholler-Gyure M, Debroye C, Aharchi F, et al. No clinically relevant
eﬀect of TMC125 on the pharmacokinetics of oral contraceptives. 8th
International Congress on Drug Therapy in HIV Infection, Glasgow,
UK, November 12–16, 2006..
7. Mildvan D, Yarrish R, Marshak A, et al. Pharmacokinetic interaction
between nevirapine and ethinyl estradiol/norethindrone when administered concurrently to HIV-infected women. J Acquir Immune Deﬁc
Syndr 2002;29:471–7.

8. Zhang J, Chung E, Eley T et al. Eﬀect of atazanavir/ritonavir on the
pharmacokinetics of ethinyl estradiol and 17-deactyl-norgestimate in
healthy female subjects [Abstract A-1415]. In: Program and abstracts
of the 47th Interscience Conference on Antimicrobial Agents and
Chemotherapy, Chicago, IL, September 17–20, 2007. Washington,
DC: American Society for Microbiology; 2009.
9. Sekar V, Lefebvre E S-GSeal. Pharacokinetic interaction between
nevirapine and ethinyl estradiol, norethindrone, and TMC114, a new
protease inhibitor [Abstract A-368]. In: Program and abstracts of the 46th
Interscience Conference on Antimicrobial Agents and Chemotherapy,
San Francisco, CA, September 27–30, 2006. Washington, DC: American
Society for Microbiology; 2009.
10. Glaxo Smith Kline. Prescription medicines. Lexiva (fosamprenavir
calcium). Glaxo Smith Kline 2009. Available from http://us.gsk.com/
products/assets/us_lexiva.pdf. Accessed March 15, 2010.
11. Glaxo Smith Kline. Study APV10020. A phase I, open label, two period,
single-sequence, drug-drug interaction study comparing steady-state
plasma ethinyl estradiol and norethisterone pharmacokinetics following
administration of brevinor for 21 days with and without fosamprenavir
700 mg twice daily (BID) and ritonavir 100 mg (BID) for 21 days in
healthy adult female subjects. Glaxo Smith Kline 2009. Available from
http://www.gsk-clinicalstudyregister.com/ﬁles/pdf/23138.pdf. Accessed
March 15, 2010.
12. Merck & Company. Indinavir patient prescribing information. Merck
& Company 2009. Available from http://www.merck.com/product/usa/
pi_circulars/c/crixivan/crixivan_pi.pdf. Accessed March 15, 2010.
13. Abbott Laboratories. Lopinavir and ritonavir prescribing information,
2009. Abbott Laboratories 2009. Available from http://www.rxabbott.
com/pdf/kaletratabpi.pdf. Accessed March 15, 2010.
14. Agouron Pharmaceuticals. Viracept (Nelﬁnavir mesylate) prescribing
information, 2008. Agouron Pharmaceuticals 2009. Available from
http://us.gsk.com/products/assets/us_viracept.pdf. Accessed March 15,
2010.

MMWR

15. Mayer K, Poblete R, Hathaway B et al. Eﬃcacy, eﬀect of oral contraceptives, and adherence in HIV infected women receiving Fortovase
(Saquinavir) soft gel capsule (SQV-SGC; FTV) thrice (TID) and twice
(BID) daily regimens. XIII International AIDS Conference, 2000,
Durban, South Africa 2009.
16. Frohlich M, Burhenne J, Martin-Facklam M, et al. Oral contraception
does not alter single dose saquinavir pharmacokinetics in women. Br J
Clin Pharmacol 2004;57:244–52.
17. Food and Drug Administration. Highlights of prescribing information. Aptivus
(Tipranavir) Capsules. USFDA 2009. Available from http://www.accessdata.
fda.gov/drugsatfda_docs/label/2008/021814s005,022292lbl.pdf.

June 18, 2010

18. Cohn SE, Park JG, Watts DH, et al. Depo-medroxyprogesterone in
women on antiretroviral therapy: eﬀective contraception and lack of clinically signiﬁcant interactions. Clin Pharmacol Ther 2007;81:222–7.
19. Nanda K, Amaral E, Hays M, et al. Pharmacokinetic interactions between
depot medroxyprogesterone acetate and combination antiretroviral
therapy. Fertil Steril 2008;90:965–71.
20. Watts DH, Park JG, Cohn SE, et al. Safety and tolerability of depot
medroxyprogesterone acetate among HIV-infected women on antiretroviral therapy: ACTG A5093. Contraception 2008;77:84–90.

Abbreviations and Acronyms
A
AIDS
ARV
BMD
BMI
C
CDC
CHC
CI
COC
Cu-IUD
D
DMPA
DVT
ECP
EE
E-IUD
ETG
FAB
hCG
HDL
HIV
HPV

accept
acquired immunodeﬁciency syndrome
antiretroviral
bone mineral density
body mass index
caution
Centers for Disease Control and Prevention
combined hormonal contraceptive
coitus interruptus
combined oral contraceptive
copper intrauterine device
delayed
depot medroxyprogesterone acetate
deep venous thrombosis
emergency contraceptive pills
ethinyl estradiol
emergency intrauterine device
etonogestrel
fertility awareness–based methods
human chorionic gonadotropin
high-density lipoprotein
human immunodeﬁciency virus
human papillomavirus

IBD
IUS
IUD
LNG
LNG-IUD
MEC
NET-EN
NGM
NNRTI
NRTI
P
PE
PID
POC
POI
POP
R
SLE
STI
VTE
WHO

inﬂammatory bowel disease
intrauterine system
intrauterine device
levonorgestrel
levonorgestrel-releasing intrauterine device
Medical Eligibility Criteria
norethisterone enantate
norgestimate
non-nucleoside reverse transcriptase
inhibitor
nucleoside reverse transcriptase inhibitor
combined hormonal contraceptive patch
pulmonary embolism
pelvic inﬂammatory disease
progestin-only contraceptive
progestin-only injectable
progestin-only pill
combined hormonal vaginal ring
systemic lupus erythematosus
sexually transmitted infection
venous thromboembolism
World Health Organization

Vol. 59 / RR-4

Recommendations and Reports

U.S. Medical Eligibility Criteria for Contraceptive Use, 2010
Atlanta, GA, February 17–19, 2009
Chairpersons: Herbert B. Peterson, MD, University of North Carolina, Chapel Hill, North Carolina; Kathryn M. Curtis, PhD, Centers for Disease Control
and Prevention, Atlanta, Georgia.
CDC Steering Committee: Kathryn M. Curtis, PhD (Chair), Denise Jamieson, MD, John Lehnherr, Polly Marchbanks, PhD, Centers for Disease Control
and Prevention, Atlanta, Georgia.
Systematic Review Authors and Presenters: Sherry Farr, PhD, Suzanne Gaventa Folger, PhD, Melissa Paulen, MPH, Naomi Tepper, MD, Maura Whiteman,
PhD, Lauren Zapata, PhD, Centers for Disease Control and Prevention, Atlanta, Georgia; Kelly Culwell, MD, Nathalie Kapp, MD, World Health Organization,
Geneva, Switzerland; Catherine Cansino, MD, Johns Hopkins Bayview Medical Center, Baltimore, Maryland.
Invited Participants: Abbey Berenson, MD, University of Texas Medical Branch, Nassau Bay, Texas; Paul Blumenthal, MD, Stanford University, Palo Alto,
California (not able to attend); Willard Cates, Jr., MD, Family Health International, Research Triangle Park, North Carolina (not able to attend); Mitchell
Creinin, MD, University of Pittsburgh, Pittsburgh, Pennsylvania; Vanessa Cullins, MD, Planned Parenthood Federation of America, New York, New
York; Philip Darney, MD, University of California, San Francisco, California; Jennifer Dietrich, MD, Baylor College of Medicine, Houston, Texas; Linda
Dominguez, Southwest Women’s Health, Albuquerque, New Mexico; Melissa Gilliam, MD, The University of Chicago, Chicago, Illinois; Marji Gold, MD,
Albert Einstein College of Medicine, Bronx, New York; Alisa Goldberg, MD, Brigham and Women’s Hospital and Planned Parenthood of Massachusetts,
Boston, Massachusetts; David Grimes, MD, Family Health International, Research Triangle Park, North Carolina (not able to attend); Robert Hatcher, MD,
Emory University, Atlanta, Georgia; Stephen Heartwell, DrPH, Susan Thompson Buﬀett Foundation, Omaha, Nebraska; Andrew Kaunitz, MD, University
of Florida, Jacksonville, Florida; Uta Landy, PhD, University of California, San Francisco, California (not able to attend); Hal Lawrence, MD, American
College of Obstetricians and Gynecologists, Washington, DC; Ruth Lawrence, MD, American Academy of Pediatrics and University of Rochester, Rochester,
New York; Laura MacIsaac, MD, Albert Einstein School of Medicine, New York, New York; Trent MacKay, MD, National Institute of Child Health and
Human Development, National Institutes of Health, Bethesda, MD (not able to attend); Daniel Mishell, Jr, MD, University of Southern California, Los
Angeles, California; Mary Mitchell, American College of Obstetricians and Gynecologists, Washington, DC; Susan Moskosky, MS, US Department of
Health and Human Services, Rockville, Maryland; Patricia Murphy, DrPH, University of Utah, Salt Lake City, Utah; Kavita Nanda, MD, Family Health
International, Research Triangle Park, North Carolina; Jeﬀrey Peipert, MD, Washington University, St. Louis, Missouri; Michael Policar, MD, University
of California, San Francisco, California; Robert Rebar, MD, American Society of Reproductive Medicine, Birmingham, Alabama; Pablo Rodriquez, MD,
Providence, Rhode Island (not able to attend); John Santelli, MD, Columbia University, New York, New York (not able to attend); Sharon Schnare, MSN,
University of Washington, Seattle, Washington; David Soper, MD, University of South Carolina, Charleston, South Carolina; Lisa Soule, MD, Food and Drug
Administration, Silver Spring, Maryland; James Trussell, PhD, Princeton University, Princeton, New Jersey; Carolyn Westhoﬀ, MD, Columbia University,
New York, New York (not able to attend); Susan Wysocki, National Association of Nurse Practitioners in Women’s Health, Washington, DC; Mimi Zieman,
MD, Emory University, Atlanta, Georgia.
Consultants: Wendy Book, MD, Emory University, Atlanta, Georgia; Shinya Ito, Hospital for Sick Children, Toronto, Canada; Beth Jonas, MD, University
of North Carolina, Chapel Hill, North Carolina; Miriam Labbok, MD, University of North Carolina, Chapel Hill, North Carolina; Frederick Naftolin,
MD, New York University, New York, New York; Lubna Pal, Yale University, New Haven, Connecticut; Robin Rutherford, MD, Emory University, Atlanta,
Georgia; Roshan Shrestha, MD, Piedmont Hospital, Atlanta, Georgia; Kimberley Steele, MD, Johns Hopkins University, Baltimore, Maryland; Michael
Streiﬀ, MD, Johns Hopkins University, Baltimore, Maryland; Christine Wagner, PhD, University of Albany, Albany, New York; Joan Walker, MD, University
of Oklahoma, Oklahoma City, Oklahoma.
CDC Attendees: Janet Collins, PhD, Susan Hillis, PhD, Dmitry Kissin MD, Sam Posner, PhD, Natalya Revzina, MD, Cheryl Robbins, PhD, Lee Warner,
PhD.
This work was conducted within the Women’s Health and Fertility Branch (Maurizio Macaluso, Branch Chief ), in the Division of Reproductive Health (John
Lehnherr, Acting Director), National Center for Chronic Disease Prevention and Health Promotion (Ursula Bauer, Director).

MMWR

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ISSN: 1057-5987

Morbidity and Mortality Weekly Report
Recommendations and Reports / Vol. 62 / No. 5

June 21, 2013

U.S. Selected Practice Recommendations for
Contraceptive Use, 2013
Adapted from the World Health Organization Selected Practice
Recommendations for Contraceptive Use, 2nd Edition

Continuing Education Examination available at http://www.cdc.gov/mmwr/cme/conted.html.

U.S. Department of Health and Human Services
Centers for Disease Control and Prevention

Recommendations and Reports

CONTENTS

CONTENTS (Continued)

Introduction ............................................................................................................1

Appendix A: Summary Chart of U.S. Medical Eligibility Criteria for

Methods....................................................................................................................2
How To Use This Document ...............................................................................3
Summary of Changes from WHO SPR ............................................................4
Contraceptive Method Choice .........................................................................4

Contraceptive Use, 2010 .................................................................................. 47
Appendix B: When To Start Using Specific Contraceptive
Methods .............................................................................................................. 55
Appendix C: Examinations and Tests Needed Before Initiation of

Maintaining Updated Guidance ......................................................................4

Contraceptive Methods ................................................................................. 56

How To Be Reasonably Certain that a Woman Is Not Pregnant ............5

Appendix D: Routine Follow-Up After Contraceptive Initiation ........ 57

Intrauterine Contraception ................................................................................7

Appendix E: Management of Women with Bleeding Irregularities

Implants ................................................................................................................. 14
Injectables............................................................................................................. 17
Combined Hormonal Contraceptives ......................................................... 22

While Using Contraception .......................................................................... 58
Appendix F: Management of the IUD when a Cu-IUD or an LNG-IUD
User Is Found To Have Pelvic Inflammatory Disease ........................... 59

Progestin-Only Pills............................................................................................ 29
Standard Days Method..................................................................................... 33
Emergency Contraception .............................................................................. 34
Disclosure of Relationship

Female Sterilization ........................................................................................... 35
Male Sterilization ................................................................................................ 36
When Women Can Stop Using Contraceptives ....................................... 37
Conclusion ............................................................................................................ 37
Acknowledgment............................................................................................... 38
References............................................................................................................. 38

CDC, our planners, and our content experts wish to disclose
they have no financial interests or other relationships with
the manufacturers of commercial products, suppliers of commercial services, or commercial supporters. Planners have
reviewed content to ensure there is no bias. This document will
not include any discussion of the unlabeled use of a product
or a product under investigational use, with the exception
that some of the recommendations in this document might
be inconsistent with package labeling. CDC does not accept
commercial support.

Front cover photos, left to right: intrauterine device, oral contraceptive pills, diaphragm, syringe for injectable contraceptives, male condom, transdermal
contraceptive patch, etonogestrel implant, vaginal ring.
The MMWR series of publications is published by the Office of Surveillance, Epidemiology, and Laboratory Services, Centers for Disease Control and Prevention (CDC),
U.S. Department of Health and Human Services, Atlanta, GA 30333.
Suggested Citation: Centers for Disease Control and Prevention. [Title]. MMWR 2013;62(No. RR-#):[inclusive page numbers].

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William Schaffner, MD, Nashville, TN

Recommendations and Reports

U.S. Selected Practice Recommendations for Contraceptive Use, 2013
Adapted from the World Health Organization Selected Practice
Recommendations for Contraceptive Use, 2nd Edition
Prepared by
Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion

Summary
The U. S. Selected Practice Recommendations for Contraceptive Use 2013 (U.S. SPR), comprises recommendations that
address a select group of common, yet sometimes controversial or complex, issues regarding initiation and use of specific contraceptive
methods. These recommendations are a companion document to the previously published CDC recommendations U.S. Medical
Eligibility Criteria for Contraceptive Use, 2010 (U.S. MEC). U.S. MEC describes who can use various methods of contraception,
whereas this report describes how contraceptive methods can be used. CDC based these U.S. SPR guidelines on the global family
planning guidance provided by the World Health Organization (WHO). Although many of the recommendations are the same
as those provided by WHO, they have been adapted to be more specific to U.S. practices or have been modified because of new
evidence. In addition, four new topics are addressed, including the effectiveness of female sterilization, extended use of combined
hormonal methods and bleeding problems, starting regular contraception after use of emergency contraception, and determining
when contraception is no longer needed. The recommendations in this report are intended to serve as a source of clinical guidance
for health-care providers; health-care providers should always consider the individual clinical circumstances of each person seeking
family planning services. This report is not intended to be a substitute for professional medical advice for individual patients.
Persons should seek advice from their health-care providers when considering family planning options.

Introduction
Unintended pregnancy rates remain high in the United
States; approximately 50% of all pregnancies are unintended,
with higher proportions among adolescent and young women,
women who are racial/ethnic minorities, and women with lower
levels of education and income (1). Unintended pregnancies
increase the risk for poor maternal and infant outcomes (2)
and in 2002, resulted in $5 billion in direct medical costs in the
United States (3). Approximately half of unintended pregnancies
are among women who were not using contraception at the
time they became pregnant; the other half are among women
who became pregnant despite reported use of contraception
(4). Therefore, strategies to prevent unintended pregnancy
include assisting women at risk for unintended pregnancy and
their partners with choosing appropriate contraceptive methods
and helping women use methods correctly and consistently
to prevent pregnancy. In 2010, CDC first adapted global
guidance from the World Health Organization (WHO) to
help health-care providers counsel women, men, and couples
The material in this report originated in the National Center for
Chronic Disease Prevention and Health Promotion, Ursula Bauer,
PhD, Director; Division of Reproductive Health, Wanda Barfield,
MD, Director.
Corresponding preparer: Kathryn M. Curtis, PhD, Division of
Reproductive Health. Telephone: 770-488-5200; E-mail: [email protected].

about contraceptive method choice. The U.S. Medical Eligibility
Criteria for Contraceptive Use, 2010 (U.S. MEC), focuses on who
can safely use specific methods of contraception and provides
recommendations for the safety of contraceptive methods for
women with various medical conditions (e.g., hypertension and
diabetes) and characteristics (e.g., age, parity, and smoking status)
(Appendix A) (5). The recommendations in this new guide, U.S.
Selected Practice Recommendations for Contraceptive Use, 2013
(U.S. SPR), focuses on how contraceptive methods can be used
and provides recommendations on optimal use of contraceptive
methods for persons of all ages, including adolescents.
During the past 15 years, CDC has contributed to the
development and updating of the WHO global family planning
guidance. CDC has supported WHO by coordinating the
identification, critical appraisal, and synthesis of the scientific
evidence on which the WHO guidance is based. In 2002,
WHO published the first edition of the Selected Practice
Recommendations for Contraceptive Use (WHO SPR), which
presented evidence-based global guidance on how to use
contraceptive methods safely and effectively once they are
deemed to be medically appropriate. Since then, WHO has
regularly updated its guidance on the basis of new evidence,
and the document is now in its second edition (6), with an
additional update in 2008 (7). The WHO global guidance is
not intended for use directly by health-care providers; rather,
WHO intends for the guidance to be used by local or national
policy makers, family planning program managers, and the
MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

scientific community as a reference when they develop family
planning guidance at the country or program level (6). For
example, the United Kingdom adapted WHO SPR and in
2002 published the U.K. Selected Practice Recommendations
for Contraceptive Use for use by U.K. health-care providers (8).
CDC initiated a formal adaptation process to create U.S.
SPR, using both the second edition of WHO SPR (6) and the
2008 update (7) as the basis for the U.S. version. Although
much of the guidance is the same as the WHO guidance,
the recommendations are specific to U.S. family planning
practice. In addition, guidance on contraceptive methods not
available in the United States has been removed, and four
new topics for guidance have been added (the effectiveness
of female sterilization, extended use of combined hormonal
methods and bleeding problems, starting regular contraception
after use of emergency contraception, and determining when
contraception is no longer needed). This document contains
recommendations for health-care providers for the safe and
effective use of contraceptive methods and addresses provision of
contraceptive methods and management of side effects and other
problems with contraceptive method use. Although the term
woman is used throughout this report, these recommendations
refer to all females of reproductive age, including adolescents.
Adolescents are identified throughout this document as a special
population that might benefit from more frequent follow-up.
These recommendations are meant to serve as a source of
clinical guidance for health-care providers; health-care providers
should always consider the individual clinical circumstances
of each person seeking family planning services. This report is
not intended to be a substitute for professional medical advice
for individual patients; persons should seek advice from their
health-care providers when considering family planning options.

Methods
CDC initiated a process to adapt WHO SPR for the
United States. This adaptation process included four steps:
1) determining the scope of and process for the adaptation,
including an October 2010 meeting in which individual
feedback was solicited from a small group of partners and
experts; 2) preparing the systematic reviews of the evidence
during October 2010–September 2011 to be used for the
adaptation, including peer review; 3) convening a larger
meeting of experts in October 2011 to examine the evidence
and receive input on the recommendations; and 4) finalizing
recommendations by CDC.
During October 21–22, 2010, CDC convened a meeting of 10
partners and U.S. family planning experts in Atlanta, Georgia, to
discuss the scope of and process for a U.S. adaptation of WHO

MMWR / June 21, 2013 / Vol. 62 / No. 5

SPR. A list of participants is provided at the end of this report.
CDC identified the specific WHO recommendations that might
benefit from modification for the United States. Criteria used to
modify the WHO recommendations included the availability of
new scientific evidence or the context in which family planning
services are provided in the United States. CDC also identified
several WHO recommendations that needed additional specificity
to be useful for U.S. health-care providers, as well as the need for
additional recommendations not currently included in WHO
SPR. In addition, the meeting members discussed removing
recommendations that provide information about contraceptive
methods that are not available in the United States.
Representatives from CDC and WHO conducted systematic
reviews of the scientific evidence for each of the WHO
recommendations being considered for adaptation and for each
new topic being considered for addition to the guidance. The
purpose of these systematic reviews was to identify evidence
related to the common clinical challenges associated with the
recommendations. When no direct evidence was available,
indirect evidence and theoretical issues were considered. Standard
guidelines were followed for reporting systematic reviews (9,10),
and strength and quality of the evidence were graded using the
system of the U.S. Preventive Services Task Force (11). Each
complete systematic review was peer reviewed by two or three
experts before its use in the adaptation process. Peer reviewers,
who were identified from the list of persons scheduled to
participate in the October 2011 meeting, were asked to comment
on the search strategy, list of articles included in the reviews, and
the summary of findings. The systematic reviews were finalized
and provided to participants before the October 2011 meeting
and were published in May 2013 (12–30).
During October 4–7, 2011, CDC convened a meeting in
Atlanta, Georgia, of 36 experts who were invited to assist in
guideline development and provide their perspective on the
scientific evidence presented and the discussions on potential
recommendations that followed. The group included obstetrician/
gynecologists, pediatricians, family physicians, nurse-midwives,
nurse practitioners, epidemiologists, and others with research and
clinical practice expertise in contraceptive safety, effectiveness, and
management. All participants received all of the systematic reviews
before the meeting. During the meeting, the evidence from the
systematic review for each topic was presented, and participants
discussed the evidence and the translation of the scientific evidence
into recommendations that would meet the needs of U.S. healthcare providers. In particular, participants discussed whether and
how the U.S. context might be different from the global context
and whether these differences suggested any need for modifications
to the global guidance. CDC gathered the input from the experts
during the meeting and finalized the recommendations in this

Recommendations and Reports

report. The document was peer reviewed by meeting participants,
who were asked to comment on specific issues that were raised
during the meeting. Feedback also was received from an external
review panel, composed of health-care providers who had not
participated in the adaptation meetings. These providers were
asked to provide comments on the accuracy, feasibility, and clarity
of the recommendations, as well as to provide other comments.
Areas of research that need additional investigation also were
considered during the meeting (31).

How To Use This Document
The recommendations in this report are intended to
help health-care providers address issues related to use of
contraceptives, such as how to help a woman initiate use of a
contraceptive method, which examinations and tests are needed
before initiating use of a contraceptive method, what regular
follow-up is needed, and how to address problems that often
arise during use, including missed pills and side effects such as
unscheduled bleeding. Each recommendation addresses what
a woman or health-care provider can do in specific situations.
For situations in which certain groups of women might be
medically ineligible to follow the recommendations, comments
and reference to U.S. MEC are provided (5). The full U.S.
MEC recommendations and the evidence supporting those
recommendations were published in 2010 (5).
The information in this document is organized by
contraceptive method, and the methods generally are presented
in order of effectiveness, from highest to lowest. However, the
recommendations are not intended to provide guidance on
every aspect of provision and management of contraceptive
method use. Instead, they use the best available evidence
to address specific issues regarding common, yet sometimes
complex, clinical issues. Each contraceptive method section
generally includes information about initiation of the method,
regular follow-up, and management of problems with use (e.g.,
usage errors and side effects). Each section first provides the
recommendation and then includes a comments and evidence
section, which includes comments about the recommendations
and a brief summary of the scientific evidence on which the
recommendation is based.
Recommendations in this document are provided for
permanent methods of contraception, such as vasectomy
and female sterilization, as well as for reversible methods of
contraception, including the copper-containing intrauterine
device (Cu-IUD); levonorgestrel-releasing IUD (LNG-IUD);
the etonogestrel implant; progestin-only injectables; progestinonly pills (POPs); combined hormonal contraceptive methods

that contain both estrogen and a progestin, including combined
oral contraceptives (COCs), a transdermal contraceptive patch,
and a vaginal contraceptive ring; and the standard days method
(SDM). Recommendations also are provided for emergency
use of the Cu-IUD and emergency contraceptive pills (ECPs).
For each contraceptive method, recommendations are provided
on the timing for initiation of the method and indications for
when and for how long additional contraception, or a back-up
method, is needed. Many of these recommendations include
guidance that a woman can start a contraceptive method at any
time during her menstrual cycle if it is reasonably certain that
the woman is not pregnant. Guidance for health-care providers
on how to be reasonably certain that a woman is not pregnant
is provided.
For each contraceptive method, recommendations include the
examinations and tests needed before initiation of the method.
These recommendations apply to persons who are presumed to
be healthy. Those with known medical problems or other special
conditions might need additional examinations or tests before
being determined to be appropriate candidates for a particular
method of contraception. U.S. MEC might be useful in such
circumstances (5). Most women need no or very few examinations
or tests before initiating a contraceptive method. The following
classification system was developed by WHO and adopted by
CDC to categorize the applicability of the various examinations
or tests before initiation of contraceptive methods (6):
Class A: These tests and examinations are essential and
mandatory in all circumstances for safe and effective use of
the contraceptive method.
Class B: These tests and examinations contribute substantially
to safe and effective use, although implementation can be
considered within the public health context, service context, or
both. The risk for not performing an examination or test should
be balanced against the benefits of making the contraceptive
method available.
Class C: These tests and examinations do not contribute
substantially to safe and effective use of the contraceptive method.
These classifications focus on the relation of the examinations
or tests to safe initiation of a contraceptive method. They
are not intended to address the appropriateness of these
examinations or tests in other circumstances. For example,
some of the examinations or tests that are not deemed necessary
for safe and effective contraceptive use might be appropriate
for good preventive health care or for diagnosing or assessing
suspected medical conditions. Systematic reviews were
conducted for several different types of examinations and tests
to assess whether a screening test was associated with safe use
of contraceptive methods. Because no single convention exists
for screening panels for certain diseases, including diabetes,

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Recommendations and Reports

lipid disorders, and liver diseases, the search strategies included
broad terms for the tests and diseases of interest.
Summary charts and clinical algorithms that summarize
the guidance for the various contraceptive methods have been
developed for many of the recommendations, including when
to start using specific contraceptive methods (Appendix B),
examinations and tests needed before initiating the various
contraceptive methods (Appendix C), routine follow-up after
initiating contraception (Appendix D), management of bleeding
irregularities (Appendix E), and management of IUDs when
users are found to have pelvic inflammatory disease (PID)
(Appendix F). These summaries might be helpful to health-care
providers when managing family planning patients. Additional
tools are available on the U.S. SPR website (http://www.cdc.
gov/reproductivehealth/UnintendedPregnancy/USSPR.htm).

Summary of Changes from WHO SPR
Much of the guidance in U.S. SPR is the same or very similar
to the WHO SPR guidance. U.S. SPR includes new guidance
on the use of the combined contraceptive patch and vaginal
ring, as well as recommendations for four new topics:
t IPXUPTUBSUSFHVMBSDPOUSBDFQUJPOBGUFSUBLJOH&$1T
t NBOBHFNFOU PG CMFFEJOH JSSFHVMBSJUJFT BNPOH XPNFO
using extended or continuous combined hormonal
contraceptives (including pills, the patch, and the ring)
t XIFOBXPNBODBOSFMZPOGFNBMFTUFSJMJ[BUJPOGPSDPOUSBDFQUJPO
t XIFOBXPNBODBOTUPQVTJOHDPOUSBDFQUJWFTBOEOPUCF
at risk for unintended pregnancy
Adaptations to the WHO SPR recommendations include
1) changes to the length of the grace period for depot
medroxyprogesterone acetate (DMPA) reinjection, 2) differences
in some of the examinations and tests recommended before
contraceptive method initiation, 3) differences in some of the
recommendations for management of bleeding irregularities
because of new data and drug availability in the United States,
and 4) a modified missed pill algorithm to respond to concerns
of the CDC expert group and other reviewers that simplified
algorithms are preferable.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Contraceptive method effectiveness is critically important
in minimizing the risk for unintended pregnancy, particularly
among women for whom an unintended pregnancy would
pose additional health risks. The effectiveness of contraceptive
methods depends both on the inherent effectiveness of the
method itself and on how consistently and correctly it is used
(Table 1). Both consistent and correct use can vary greatly
with characteristics such as age, income, desire to prevent
or delay pregnancy, and culture. Methods that depend on
consistent and correct use by clients have a wide range of
effectiveness between typical and perfect users. IUDs and
implants are considered long-acting, reversible contraception
(LARC); these methods are highly effective because they do not
depend on regular compliance from the user. LARC methods
are appropriate for most women, including adolescents and
nulliparous women. All women should be counseled about
the full range and effectiveness of contraceptive options for
which they are medically eligible so that they can identify the
optimal method (Figure 1).
In choosing a method of contraception, the risk for human
immunodeficiency virus (HIV) infection and other sexually
transmitted diseases (STDs) also should be considered.
Although hormonal contraceptives and IUDs are highly
effective at preventing pregnancy, they do not protect against
STDs and HIV. Consistent and correct use of the male latex
condom reduces the risk for HIV infection and other STDs,
including chlamydial infection, gonorrhea, and trichomoniasis
(32). On the basis of a limited number of clinical studies, when
a male condom cannot be used properly to prevent infection,
a female condom should be considered (32). All patients,
regardless of contraceptive choice, should be counseled about
the use of condoms and the risk for STDs, including HIV
infection (32). Additional information about prevention
and treatment of STDs is available from the CDC Sexually
Transmitted Diseases Treatment Guidelines (32).

Maintaining Updated Guidance
As with any evidence-based guidance document, a key
challenge is keeping the recommendations up to date as new
scientific evidence becomes available. Working with WHO,
CDC uses the continuous identification of research evidence
(CIRE) system to ensure that WHO and CDC guidance is
based on the best available evidence and that a mechanism
is in place to update guidance when new evidence becomes
available (33). CDC will continue to work with WHO to
identify and assess all new relevant evidence and determine
whether changes in the recommendations are warranted. In

Recommendations and Reports

TABLE 1. Percentage of women experiencing an unintended pregnancy during the first year of typical use and the first year of perfect use of
contraception and the percentage continuing use at the end of the first year — United States
% of women experiencing an unintended pregnancy
within the first year of use
Method
No method¶
Spermicides**
Fertility awareness–based methods††
Standard days method
Two day method
Ovulation method
Symptothermal method
Withdrawal
Sponge
Parous women
Nulliparous women
Condom§§
Female
Male
Diaphragm***
Combined pill and progestin-only pill
Evra patch
NuvaRing
Depo-Provera
Intrauterine devices
Paragard (copper containing)
Mirena (levenorgestrel releasing)
Implanon
Female sterilization
Male sterilization
Lactational amenorrhea method†††

Typical use*

Perfect use†

% of women continuing use at 1 year§

85
28
24
—
—
—
—
22

85
18
—
5
4
3
0.4
4

—
42
47
—
—
—
—
46

24
12

20
9

36
—

21
18
12
9
9
9
6

5
2
6
0.3
0.3
0.3
0.2

41
43
57
67
67
67
56

0.8
0.2
0.05
0.5
0.15
—

0.6
0.2
0.05
0.5
0.10
—

78
80
84
100
100
—

Source: Adapted from Trussell J. Contraceptive failure in the United States. Contraception 2011;83:397–404.
* Among typical couples who initiate use of a method (not necessarily for the first time), the percentage who experience an accidental pregnancy during the first
year if they do not stop use for any other reason. Estimates of the probability of pregnancy during the first year of typical use for spermicides and the diaphragm
are taken from the 1995 National Survey of Family Growth (NSFG) corrected for underreporting of abortion; estimates for fertility awareness-based methods,
withdrawal, the male condom, the pill and Depo-Provera are taken from the 1995 and 2002 NSFG corrected for underreporting of abortion.
† Among couples who initiate use of a method (not necessarily for the first time) and who use it perfectly (both consistently and correctly), the percentage who
experience an accidental pregnancy during the first year if they do not stop use for any other reason.
§ Among couples attempting to avoid pregnancy, the percentage who continues to use a method for 1 year.
¶ The percentage becoming pregnant in the second and third columns are based on data from populations where contraception is not used and from women who
cease using contraception to become pregnant. Among such populations, approximately 89% become pregnant within 1 year. This estimate was lowered slightly
(to 85%) to represent the percentage who would become pregnant within 1 year among women not relying on reversible methods of contraception if they
abandoned contraception altogether.
** Foams, creams, gels, vaginal suppositories, and vaginal film.
†† The ovulation and two day methods are based on evaluation of cervical mucus. The standard days method avoids intercourse on cycle days 8–19. The symptothermal
method is a double-check method based on evaluation of cervical mucus to determine the first fertile day and evaluation of cervical mucus and temperature to
determine the last fertile day.
§§ Without spermicides.
*** With spermicidal cream or jelly.
††† This is a highly effective, temporary method of contraception. However, to maintain in effective protection against pregnancy, another method of contraception must
be used as soon as menstruation resumes, the frequency of duration of breastfeeds is reduced, bottle feeds are introduced, or the baby reaches age 6 months.

most cases, U.S. SPR will follow any updates in the WHO
guidance, which typically occurs every 3–4 years (or sooner
if warranted by new data). In addition, CDC will review any
interim WHO updates for their application in the United
States. CDC also will identify and assess any new literature
for the recommendations that are not included in the WHO
guidance and will completely review U.S. SPR every 3–4
years. Updates to the guidance can be found on the U.S.
SPR website (http://www.cdc.gov/reproductivehealth/
UnintendedPregnancy/USSPR.htm).

How To Be Reasonably Certain that a
Woman Is Not Pregnant
In most cases, a detailed history provides the most accurate
assessment of pregnancy risk in a woman who is about to start
using a contraceptive method. Several criteria for assessing
pregnancy risk are listed in the recommendation that follows.
These criteria are highly accurate (i.e., a negative predictive
value of 99%–100%) in ruling out pregnancy among women
who are not pregnant (34–37). Therefore, CDC recommends
that health-care providers use these criteria to assess pregnancy

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FIGURE 1. Effectiveness of family planning methods

Sources: Adapted from World Health Organization (WHO) Department of Reproductive Health and Research, Johns Hopkins Bloomberg School of Public Health/
Center for Communication Programs (CCP). Knowledge for health project. Family planning: a global handbook for providers (2011 update). Baltimore, MD; Geneva,
Switzerland: CCP and WHO; 2011; and Trussell J. Contraceptive failure in the United States. Contraception 2011;83:397–404.

status in a woman who is about to start using contraceptives
(Box 1). If a woman meets one of these criteria (and therefore
the health-care provider can be reasonably certain that she is
not pregnant), a urine pregnancy test might be considered
in addition to these criteria (based on clinical judgment),
bearing in mind the limitations of the accuracy of pregnancy
testing. If a woman does not meet any of these criteria, then
the health-care provider cannot be reasonably certain that she
is not pregnant, even with a negative pregnancy test. Routine
pregnancy testing for every woman is not necessary.
On the basis of clinical judgment, health-care providers
might consider the addition of a urine pregnancy test; however,
they should be aware of the limitations, including accuracy

MMWR / June 21, 2013 / Vol. 62 / No. 5

of the test relative to the time of last sexual intercourse,
recent delivery, or spontaneous or induced abortion. Routine
pregnancy testing for every woman is not necessary. If a woman
has had recent (i.e., within the last 5 days) unprotected sexual
intercourse, consider offering emergency contraception (either
a Cu-IUD or ECPs), if pregnancy is not desired.
Comments and Evidence Summary. The criteria for
determining whether a woman is pregnant depend on the
assurance that she has not ovulated within a certain amount of
time after her last menses, spontaneous or induced abortion, or
delivery. Among menstruating women, the timing of ovulation
can vary widely. During an average 28-day cycle, ovulation
generally occurs during days 9–20 (38). In addition, the

Recommendations and Reports

BOX 1. How To Be Reasonably Certain that a Woman Is Not Pregnant

A health-care provider can be reasonably certain that a
woman is not pregnant if she has no symptoms or signs
of pregnancy and meets any one of the following criteria:
t is ≤7 days after the start of normal menses
t has not had sexual intercourse since the start of last
normal menses
t has been correctly and consistently using a reliable
method of contraception
t is ≤7 days after spontaneous or induced abortion
t is within 4 weeks postpartum
t is fully or nearly fully breastfeeding (exclusively
breastfeeding or the vast majority [≥85%] of feeds are
breastfeeds),* amenorrheic, and <6 months
postpartum
* Source: Labbok M, Perez A, Valdez V, et al. The Lactational Amenorrhea
Method (LAM): a postpartum introductory family planning method with
policy and program implications. Adv Contracept 1994;10:93–109.

likelihood of ovulation is low from days 1–7 of the menstrual
cycle (39). After a spontaneous or an induced abortion,
ovulation can occur within 2–3 weeks and has been found
to occur as early as 8–13 days after the end of the pregnancy.
Therefore, the likelihood of ovulation is low ≤7 days after an
abortion (40–42). A recent systematic review reported that the
mean day of first ovulation among postpartum nonlactating
women occurred 45–94 days after delivery (43). In one study,
the earliest ovulation was reported at 25 days after delivery.
Among women who are within 6 months postpartum, are fully
or nearly fully breastfeeding, and are amenorrheic, the risk for
pregnancy is <2% (44).
Although pregnancy tests often are performed before
initiating contraception, the accuracy of qualitative urine
pregnancy tests varies depending on the timing of the test
relative to missed menses, recent sexual intercourse, or recent
pregnancy. The sensitivity of a pregnancy test is defined as
the concentration of human chorionic gonadotropin (hCG)
at which 95% of tests are positive. Most qualitative pregnancy
tests approved by the U.S. Food and Drug Administration
(FDA) report a sensitivity of 20–25 mIU/mL in urine (45–48)
However, pregnancy detection rates can vary widely because of
differences in test sensitivity and the timing of testing relative
to missed menses (47,49). Some studies have shown that an
additional 11 days past the day of expected menses are needed
to detect 100% of pregnancies using qualitative tests (46). In
addition, pregnancy tests cannot detect a pregnancy resulting
from recent sexual intercourse. Qualitative tests also might have
positive results for several weeks after termination of pregnancy

because hCG can be present for several weeks after delivery or
abortion (spontaneous or induced) (50–52).
For contraceptive methods other than IUDs, the benefits
of starting to use a contraceptive method likely exceed any
risk, even in situations in which the health-care provider is
uncertain whether the woman is pregnant. Therefore, the
health-care provider can consider having patients start using
contraceptive methods other than IUDs at any time, with
a follow-up pregnancy test in 2–4 weeks. The risks of not
starting to use contraception should be weighed against the
risks of initiating contraception use in a woman who might
be already pregnant. Most studies have shown no increased
risk for adverse outcomes, including congenital anomalies
or neonatal or infant death, among infants exposed in utero
to COCs (53–55). Studies also have shown no increased risk
for neonatal or infant death or developmental abnormalities
among infants exposed in utero to DMPA (54,56,57).
In contrast, for women who want to begin using an IUD
(Cu-IUD or LNG-IUD), in situations in which the healthcare provider is uncertain whether the woman is pregnant, the
woman should be provided with another contraceptive method
to use until the health-care provider is reasonably certain that
she is not pregnant and can insert the IUD. Pregnancies among
women with IUDs are at higher risk for complications such as
spontaneous abortion, septic abortion, preterm delivery, and
chorioamnionitis (58).
A systematic review identified four analyses of data
from three diagnostic accuracy studies that evaluated the
performance of the criteria listed above through use of a
pregnancy checklist compared with a urine pregnancy test
conducted concurrently (12). The performance of the checklist
to diagnose or exclude pregnancy varied, with sensitivity
of 55%–100% and specificity of 39%–89%. The negative
predictive value was consistent across studies at 99%–100%;
the pregnancy checklist correctly ruled out women who were
not pregnant. One of the studies assessed the added usefulness
of signs and symptoms of pregnancy and found that these
criteria did not substantially improve the performance of the
pregnancy checklist, although the number of women with signs
and symptoms was small (34) (Level of evidence: Diagnostic
accuracy studies, fair, direct).

Intrauterine Contraception
Three IUDs are available in the United States, the Cu-IUD
and two LNG-IUDs (containing a total of either 13.5 mg
or 52 mg levonorgestrel). Fewer than 1 woman out of 100
becomes pregnant in the first year of using IUDs (with typical
use) (59). IUDs are long acting, are reversible, and can be

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Recommendations and Reports

used by women of all ages, including adolescents, and both by
parous and nulliparous women. IUDs do not protect against
STDs; consistent and correct use of male latex condoms reduces
the risk for STDs, including HIV.

Initiation of Cu-IUDs
Timing
t 5IF$V*6%DBOCFJOTFSUFEBUBOZUJNFJGJUJTSFBTPOBCMZ
certain that the woman is not pregnant (Box 1).
t 5IF$V*6%BMTPDBOCFJOTFSUFEXJUIJOEBZTPGUIFGJSTU
act of unprotected sexual intercourse as an emergency
contraceptive. If the day of ovulation can be estimated, the
Cu-IUD also can be inserted >5 days after sexual intercourse
as long as insertion does not occur >5 days after ovulation.

Need for Back-Up Contraception
t /P BEEJUJPOBM DPOUSBDFQUJWF QSPUFDUJPO JT OFFEFE BGUFS
Cu-IUD insertion.

Special Considerations
Amenorrhea (Not Postpartum)
t Timing: The Cu-IUD can be inserted at any time if it is
reasonably certain that the woman is not pregnant (Box 1).
t Need for back-up contraception: No additional contraceptive
protection is needed.
Postpartum (Including After Cesarean Section)
t Timing: The Cu-IUD can be inserted at any time postpartum,
including immediately postpartum (U.S. MEC 1 or 2) (Box 2),
BOX 2. Categories of medical eligibility criteria for contraceptive use

U.S. MEC 1 = A condition for which there is no restriction
for the use of the contraceptive method.
U.S. MEC 2 = A condition for which the advantages of
using the method generally outweigh the theoretical or
proven risks.
U.S. MEC 3 = A condition for which the theoretical or
proven risks usually outweigh the advantages of using the
method.
U.S. MEC 4 = A condition that represents an unacceptable
health risk if the contraceptive method is used.
Abbreviations: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive
Use, 2010.
Source: CDC. U.S. medical eligibility criteria for contraceptive use.
MMWR 2010;59(No. RR-4).

MMWR / June 21, 2013 / Vol. 62 / No. 5

if it is reasonably certain that the woman is not pregnant
(Box 1). The Cu-IUD should not be inserted in a woman with
puerperal sepsis (U.S. MEC 4).
t Need for back-up contraception: No additional
contraceptive protection is needed.
Postabortion (Spontaneous or Induced)
t Timing: The Cu-IUD can be inserted within the first
7 days, including immediately postabortion (U.S. MEC 1
for first trimester abortion and U.S. MEC 2 for second
trimester abortion). The Cu-IUD should not be inserted
immediately after septic abortion (U.S. MEC 4).
t Need for back-up contraception: No additional
contraceptive protection is needed.
Switching from Another Contraceptive Method
t Timing: The Cu-IUD can be inserted immediately if it is
reasonably certain that the woman is not pregnant (Box 1).
Waiting for her next menstrual period is unnecessary.
t Need for back-up contraception: No additional
contraceptive protection is needed.
Comments and Evidence Summary. In situations in which
the health-care provider is not reasonably certain that the
woman is not pregnant, the woman should be provided with
another contraceptive method to use until the health-care
provider can be reasonably certain that she is not pregnant
and can insert the Cu-IUD.
A systematic review identified eight studies that suggested that
timing of Cu-IUD insertion in relation to the menstrual cycle in
nonpostpartum women had little effect on long-term outcomes
(rates of continuation, removal, expulsion, or pregnancy) or on
short-term outcomes (pain at insertion, bleeding at insertion, or
immediate expulsion) (13) (Level of evidence: II-2, fair, direct).

Initiation of LNG-IUDs
Timing of LNG-IUD Insertion
t 5IF-/(*6%DBOCFJOTFSUFEBUBOZUJNFJGJUJTSFBTPOBCMZ
certain that the woman is not pregnant (Box 1).

Need for Back-Up Contraception
t *GUIF-/(*6%JTJOTFSUFEXJUIJOUIFGJSTUEBZTTJODF
menstrual bleeding started, no additional contraceptive
protection is needed.
t *GUIF-/(*6%JTJOTFSUFEEBZTTJODFNFOTUSVBMCMFFEJOH
started, the woman needs to abstain from sexual intercourse
or use additional contraceptive protection for the next 7 days.

Recommendations and Reports

Special Considerations
Amenorrhea (Not Postpartum)
t Timing: The LNG-IUD can be inserted at any time if it is
reasonably certain that the woman is not pregnant (Box 1).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Including After Cesarean Section)
t Timing: The LNG-IUD can be inserted at any time,
including immediately postpartum (U.S. MEC 1 or 2) if
it is reasonably certain that the woman is not pregnant
(Box 1). The LNG-IUD should not be inserted in a
woman with puerperal sepsis (U.S. MEC 4).
t Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (60), no
additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycle needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >7 days since menstrual bleeding
began, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postabortion (Spontaneous or Induced)
t Timing: The LNG-IUD can be inserted within the first
7 days, including immediately postabortion (U.S. MEC 1
for first-trimester abortion and U.S. MEC 2 for secondtrimester abortion). The LNG-IUD should not be inserted
immediately after a septic abortion (U.S. MEC 4).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days unless the
IUD is placed at the time of a surgical abortion.
Switching from Another Contraceptive Method
t Timing: The LNG-IUD can be inserted immediately if it
is reasonably certain that the woman is not pregnant (Box 1).
Waiting for her next menstrual period is unnecessary.
t Need for back-up contraception: If it has been >7 days
since menstrual bleeding began, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
t Switching from a Cu-IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle
and it has been >5 days since menstrual bleeding started,

theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A
health-care provider can consider providing ECPs at the
time of LNG-IUD insertion.
Comments and Evidence Summary. In situations in which
the health-care provider is uncertain whether the woman might
be pregnant, the woman should be provided with another
contraceptive method to use until the health-care provider
can be reasonably certain that she is not pregnant and can
insert the LNG-IUD. If a woman needs to use additional
contraceptive protection when switching to an LNG-IUD
from another contraceptive method, consider continuing her
previous method for 7 days after LNG-IUD insertion. No
direct evidence was found regarding the effects of inserting
LNG-IUDs on different days of the cycle on short- or longterm outcomes (13).

Examinations and Tests Needed Before
Initiation of a Cu-IUD or an LNG-IUD
Among healthy women, few examinations or tests are needed
before initiation of an IUD (Table 2). Bimanual examination
and cervical inspection are necessary before IUD insertion. A
baseline weight and BMI measurement might be useful for
monitoring IUD users over time. If a woman has not been
screened for STDs according to STD screening guidelines,
screening can be performed at the time of insertion. Women
with known medical problems or other special conditions
might need additional examinations or tests before being
determined to be appropriate candidates for a particular
method of contraception. U.S. MEC might be useful in such
circumstances (5).
Comments and Evidence Summary. Weight (BMI):
Obese women can use IUDs (U.S. MEC 1) (5); therefore,
screening for obesity is not necessary for the safe initiation
of IUDs. However, measuring weight and calculating BMI
(weight [kg] / height [m]2) at baseline might be helpful for
monitoring any changes and counseling women who might
be concerned about weight change perceived to be associated
with their contraceptive method.
Bimanual examination and cervical inspection: Bimanual
examination and cervical inspection are necessary before IUD
insertion to assess uterine size and position and to detect any
cervical or uterine abnormalities that might indicate infection
or otherwise prevent IUD insertion (61,62).
STDs: Women should be routinely screened for chlamydial
infection and gonorrhea according to national screening
guidelines. The CDC Sexually Transmitted Diseases Treatment
Guidelines provide information on screening eligibility, timing,
and frequency of screening and on screening for persons

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Recommendations and Reports

TABLE 2. Classification of examinations and tests needed before IUD
insertion
Class*
Examination or test
Examinations
Blood pressure
Weight (BMI) (weight [kg]/
height [m]2)
Clinical breast examination
Bimanual examination and
cervical inspection
Laboratory tests
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology
(Papanicolaou smear)
STD screening with
laboratory tests
HIV screening with laboratory
tests

Coppercontaining IUD

Levonorgestrelreleasing IUD

C
—†

C
A

C
C
C
C
C
C

—§

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
IUD = intrauterine device; STD = sexually transmitted disease; U.S. MEC = U.S.
Medical Eligibility Criteria for Contraceptive Use, 2010.
* Class A: essential and mandatory in all circumstances for safe and effective
use of the contraceptive method. Class B: contributes substantially to safe
and effective use, but implementation may be considered within the public
health and/or service context; the risk of not performing an examination or
test should be balanced against the benefits of making the contraceptive
method available. Class C: does not contribute substantially to safe and
effective use of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for any
methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 2). However,
measuring weight and calculating BMI at baseline might be helpful for monitoring
any changes and counseling women who might be concerned about weight
change perceived to be associated with their contraceptive method.
§ Most women do not require additional STD screening at the time of IUD
insertion if they have already been screened according to CDC’s STD Treatment
Guidelines (available at http://www.cdc.gov/std/treatment). If a woman has
not been screened according to guidelines, screening can be performed at
the time of IUD insertion, and insertion should not be delayed. Women with
purulent cervicitis or current chlamydial infection or gonorrhea should not
undergo IUD insertion (U.S. MEC 4). Women who have a very high individual
likelihood of STD exposure (e.g., those with a currently infected partner)
generally should not undergo IUD insertion (U.S. MEC 3). For these women,
IUD insertion should be delayed until appropriate testing and treatment occur.

with risk factors (32). If STD screening guidelines have been
followed, most women do not need additional STD screening
at the time of IUD insertion. If a woman has not been screened
according to guidelines, screening can be performed at the time
of IUD insertion and insertion should not be delayed. Women
with purulent cervicitis or current chlamydial infection or
gonorrhea should not undergo IUD insertion (U.S. MEC 4).
Women who have a very high individual likelihood of STD
exposure (e.g., those with a currently infected partner) generally
should not undergo IUD insertion (U.S. MEC 3) (5). For these
women, IUD insertion should be delayed until appropriate

MMWR / June 21, 2013 / Vol. 62 / No. 5

testing and treatment occur. A systematic review did not
identify any evidence regarding women who were screened
versus not screened for STDs before IUD insertion (14).
Although women with STDs at the time of IUD insertion
have a higher risk for PID, the overall rate of PID among all
IUD users is low (63,64).
Hemoglobin: Women with iron-deficiency anemia can use
the LNG-IUD (U.S. MEC 1) (5); therefore, screening for
anemia is not necessary for safe initiation of the LNG-IUD.
Women with iron-deficiency anemia generally can use the
Cu-IUD (U.S. MEC 2). Measurement of hemoglobin before
initiation of Cu-IUDs is not necessary because of the minimal
change in hemoglobin among women with and without anemia
using Cu-IUDs. A systematic review identified four studies that
provided direct evidence for changes in hemoglobin among
women with anemia who received Cu-IUDs (30). Evidence
from one randomized trial (65) and one prospective cohort
study (66) showed no significant changes in hemoglobin
among Cu-IUD users with anemia, whereas two prospective
cohort studies (67,68) showed a statistically significant decrease
in hemoglobin levels during 12 months of follow-up; however,
the magnitude of the decrease was small and most likely not
clinically significant. The systematic review also identified 21
studies that provided indirect evidence by examining changes
in hemoglobin among healthy women receiving Cu-IUDs
(69–89), which generally showed no clinically significant
changes in hemoglobin levels with up to 5 years of follow-up
(Level of evidence: I to II-2, fair, direct).
Liver enzymes: Women with liver disease can use the
Cu-IUD (U.S. MEC 1) (5); therefore, screening for liver
disease is not necessary for the safe initiation of the Cu-IUD.
Although women with certain liver diseases generally should
not use the LNG-IUD (U.S. MEC 3) (5), screening for liver
disease before initiation of the LNG-IUD is not necessary
because of the low prevalence of these conditions and the
high likelihood that women with liver disease already would
have had the condition diagnosed. A systematic review did
not identify any evidence regarding outcomes among women
who were screened versus not screened with liver enzyme tests
before initiation of hormonal contraceptive use (14). The
prevalence of liver disorders among women of reproductive
age is low. In 2008, among adults aged 18–44 years, the
percentage with liver disease (not further specified) was 1.0%
(90). In 2009, the incidence of acute hepatitis A, B, or C
among women was <1 per 100,000 population (91). During
1998–2007, the incidence of liver carcinoma among women
was approximately 3 per 100,000 population (92). Because
estrogen and progestins are metabolized in the liver, the use
of hormonal contraceptives among women with liver disease

Recommendations and Reports

might, theoretically, be a concern. The use of hormonal
contraceptives, specifically COCs and POPs, does not affect
disease progression or severity in women with hepatitis,
cirrhosis, or benign focal nodular hyperplasia (93,94), although
evidence is limited, and no evidence exists for the LNG-IUD.
Clinical breast examination: Women with breast disease
can use the Cu-IUD (U.S. MEC 1) (5); therefore, screening
for breast disease is not necessary for the safe initiation of
the Cu-IUD. Although women with current breast cancer
should not use the LNG-IUD (U.S. MEC 4) (5), screening
asymptomatic women with a clinical breast examination
before inserting an IUD is not necessary because of the low
prevalence of breast cancer among women of reproductive
age. A systematic review did not identify any evidence
regarding outcomes among women who were screened versus
not screened with a breast examination before initiation of
hormonal contraceptives (15). The incidence of breast cancer
among women of reproductive age in the United States is low.
In 2009, the incidence of breast cancer among women aged
20–49 years was approximately 72 per 100,000 women (95).
Cervical cytology: Although women with cervical cancer
should not undergo IUD insertion (U.S. MEC 4) (5),
screening asymptomatic women with cervical cytology before
IUD insertion is not necessary because of the high rates of
cervical screening, low incidence of cervical cancer in the
United States, and high likelihood that a woman with cervical
cancer already would have had the condition diagnosed. A
systematic review did not identify any evidence regarding
outcomes among women who were screened versus not
screened with cervical cytology before initiation of IUDs (14).
Cervical cancer is rare in the United States, with an incidence
rate of 8.1 per 100,000 women per year during 2004–2008
(95). The incidence and mortality rates from cervical cancer
have declined dramatically in the United States, largely because
of cervical cytology screening (96). Overall screening rates for
cervical cancer in the United States are high; among women
aged 22–30 years, approximately 87% reported having cervical
cytology screening within the last 3 years (97).
HIV screening: Although women with acquired
immunodeficiency syndrome (AIDS) who are not clinically
well should generally not undergo IUD insertion (U.S. MEC 3)
(5), HIV screening is not necessary before IUD insertion
because of the high likelihood that a woman in the United
States with such an advanced stage of disease already would
have had the condition diagnosed. A systematic review did
not identify any evidence regarding outcomes among women
who were screened versus not screened for HIV infection
before IUD insertion (14). Limited evidence suggests that
IUDs are not associated with disease progression, increased

infection, or other adverse health effects among women with
HIV infection (98).
Other screening: Women with hypertension, diabetes,
hyperlipidemia, or thrombogenic mutations can use
(U.S. MEC 1) or generally can use (U.S. MEC 2) IUDs (5).
Therefore, screening for these conditions is not necessary for
the safe initiation of IUDs.

Provision of Prophylactic Antibiotics at the
Time of IUD Insertion
t 1SPQIZMBDUJDBOUJCJPUJDTBSFHFOFSBMMZOPUSFDPNNFOEFE
for Cu-IUD or LNG-IUD insertion.
Comments and Evidence Summary. Theoretically,
IUD insertion could induce bacterial spread and lead to
complications such as PID or infective endocarditis. A
metaanalysis was conducted of randomized controlled
trials examining antibiotic prophylaxis versus placebo or
no treatment for IUD insertion (99). Use of prophylaxis
reduced the frequency of unscheduled return visits but did not
significantly reduce the incidence of PID or premature IUD
discontinuation. Although the risk for PID was higher within
the first 20 days after insertion, the incidence of PID was low
among all women who had IUDs inserted (63). In addition,
the American Heart Association recommends that the use of
prophylactic antibiotics solely to prevent infective endocarditis
is not needed for genitourinary procedures (100). Studies have
not demonstrated a conclusive link between genitourinary
procedures and infective endocarditis or a preventive benefit
of prophylactic antibiotics during such procedures (100).

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

– Assess any changes in health status, including
medications, that would change the appropriateness of
the IUD for safe and effective continued use on the
basis of U.S. MEC (e.g., category 3 and 4 conditions
and characteristics).
– Consider performing an examination to check for the
presence of the IUD strings.
– Consider assessing weight changes and counseling women
who are concerned about weight changes perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. Evidence from a
systematic review about the effect of a specific follow-up visit
schedule on IUD continuation is very limited and of poor
quality. The evidence did not suggest that greater frequency of
visits or earlier timing of the first follow-up visit after insertion
improves continuation of use (16) (Level of evidence: II-2,
poor, direct). Evidence from four studies from a systematic
review on the incidence of PID among IUD initiators, or
IUD removal as a result of PID, suggested that the incidence
of PID did not differ between women using Cu-IUDs and
those using DMPA, COCs, or LNG-IUDs (17) (Level of
evidence: I to II-2, good, indirect). Evidence on the timing of
PID after IUD insertion is mixed. Although the rate of PID
was generally low, the largest study suggested that the rate of
PID was significantly higher in the first 20 days after insertion
(63) (Level of evidence: I to II-3, good to poor, indirect).

Bleeding Irregularities with Cu-IUD Use
t #FGPSF $V*6% JOTFSUJPO
QSPWJEF DPVOTFMJOH BCPVU
potential changes in bleeding patterns during Cu-IUD
use. Unscheduled spotting or light bleeding, as well as
heavy or prolonged bleeding, is common during the first
3–6 months of Cu-IUD use, is generally not harmful,
and decreases with continued Cu-IUD use.
t *GDMJOJDBMMZJOEJDBUFE
DPOTJEFSBOVOEFSMZJOHHZOFDPMPHJDBM
problem, such as Cu-IUD displacement, an STD,
pregnancy, or new pathologic uterine conditions (e.g.,
polyps or fibroids), especially in women who have already
been using the Cu-IUD for a few months or longer and
who have developed a new onset of heavy or prolonged
bleeding. If an underlying gynecological problem is found,
treat the condition or refer for care.
t *GBOVOEFSMZJOHHZOFDPMPHJDBMQSPCMFNJTOPUGPVOEBOE
the woman requests treatment, the following treatment
option can be considered during days of bleeding:
– Nonsteroidal antiinflammatory drugs (NSAIDs) for
short-term treatment (5–7 days)

MMWR / June 21, 2013 / Vol. 62 / No. 5

t *GCMFFEJOHQFSTJTUTBOEUIFXPNBOGJOETJUVOBDDFQUBCMF
counsel her on alternative contraceptive methods, and
offer another method if it is desired.
Comments and Evidence Summary. During contraceptive
counseling and before insertion of the Cu-IUD, information
about common side effects such as unscheduled spotting or
light bleeding or heavy or prolonged menstrual bleeding,
especially during the first 3–6 months of use, should be
discussed (70). These bleeding irregularities are generally
not harmful. Enhanced counseling about expected bleeding
patterns and reassurance that bleeding irregularities are
generally not harmful has been shown to reduce method
discontinuation in clinical trials with other contraceptives (i.e.,
DMPA) (101,102).
Evidence is limited on specific drugs, doses, and durations
of use for effective treatments for bleeding irregularities with
Cu-IUD use; therefore, although this document includes
general recommendations for treatments to consider, evidence
for specific regimens is lacking.
A systematic review identified 11 articles that examined
various therapeutic treatments for heavy menstrual bleeding,
prolonged menstrual bleeding, or both among women using
Cu-IUDs (18). Nine studies examined the use of various oral
NSAIDs for the treatment of heavy or prolonged menstrual
bleeding among Cu-IUD users and compared them to either
a placebo or a baseline cycle. Three of these trials examined
the use of indomethacin (103–105), another three examined
mefenamic acid (106–108), and another three examined
flufenamic acid (103,104,109). Other NSAIDs used in the
reported trials included alclofenac (103,104), suprofen (110),
and diclofenac sodium (111). All but one NSAID study (107)
demonstrated statistically significant or notable reductions in
mean total menstrual blood loss with NSAID use. One study
among 19 Cu-IUD users with heavy bleeding suggested that
treatment with oral tranexamic acid can significantly reduce
mean blood loss during treatment compared with placebo
(111). Data regarding the overall safety of tranexamic acid
are limited; an FDA warning states that tranexamic acid
is contraindicated in women with active thromboembolic
disease or with a history or intrinsic risk for thrombosis
or thromboembolism (112,113). Treatment with aspirin
demonstrated no statistically significant change in mean blood
loss among women whose pretreatment menstrual blood loss
was >80 mL or 60–80 mL; treatment resulted in a significant
increase among women whose pretreatment menstrual
blood loss was <60 mL (114). One study examined the use
of a synthetic form of vasopressin, intranasal desmopressin
(300 µg/day), for the first 5 days of menses for three treatment
cycles and found a significant reduction in mean blood loss

Recommendations and Reports

compared with baseline (106) (Level of evidence: I to II-3,
poor to fair, direct). Only one small study examined treatment
of spotting with three separate NSAIDs and did not observe
improvements in spotting in any of the groups (103) (Level
of evidence: I, poor, direct).

are generally not harmful has been shown to reduce method
discontinuation in clinical trials with other hormonal
contraceptives (i.e., DMPA) (101,102). No direct evidence
was found regarding therapeutic treatments for bleeding
irregularities during LNG-IUD use.

Bleeding Irregularities (Including
Amenorrhea) with LNG-IUD Use

Management of the IUD when a Cu-IUD or
an LNG-IUD User Is Found To Have PID

t #FGPSF -/(*6% JOTFSUJPO
QSPWJEF DPVOTFMJOH BCPVU
potential changes in bleeding patterns during LNG-IUD
use. Unscheduled spotting or light bleeding is expected
during the first 3–6 months of LNG-IUD use, is generally
not harmful, and decreases with continued LNG-IUD
use. Over time, bleeding generally decreases with LNGIUD use, and many women experience only light
menstrual bleeding or amenorrhea. Heavy or prolonged
bleeding, either unscheduled or menstrual, is uncommon
during LNG-IUD use.

Irregular Bleeding (Spotting, Light Bleeding, or
Heavy or Prolonged Bleeding)
t *GDMJOJDBMMZJOEJDBUFE
DPOTJEFSBOVOEFSMZJOHHZOFDPMPHJDBM
problem, such as LNG-IUD displacement, an STD,
pregnancy, or new pathologic uterine conditions (e.g.,
polyps or fibroids). If an underlying gynecological problem
is found, treat the condition or refer for care.
t *GCMFFEJOHQFSTJTUTBOEUIFXPNBOGJOETJUVOBDDFQUBCMF
counsel her on alternative contraceptive methods, and
offer another method if it is desired.

Amenorrhea
t "NFOPSSIFB EPFT OPU SFRVJSF BOZ NFEJDBM USFBUNFOU
Provide reassurance.
– If a woman’s regular bleeding pattern changes abruptly
to amenorrhea, consider ruling out pregnancy if
clinically indicated.
t *GBNFOPSSIFBQFSTJTUTBOEUIFXPNBOGJOETJUVOBDDFQUBCMF
counsel her on alternative contraceptive methods, and
offer another method if it is desired
Comments and Evidence Summary. During contraceptive
counseling and before insertion of the LNG-IUD, information
about common side effects such as unscheduled spotting
or light bleeding, especially during the first 3–6 months of
use, should be discussed. Approximately half of LNG-IUD
users are likely to experience amenorrhea or oligomenorrhea
by 2 years of use (115). These bleeding irregularities are
generally not harmful. Enhanced counseling about expected
bleeding patterns and reassurance that bleeding irregularities

t 5SFBUUIF1*%BDDPSEJOHUPUIF$%$Sexually Transmitted
Diseases Treatment Guidelines (32).
t 1SPWJEFDPNQSFIFOTJWFNBOBHFNFOUGPS45%T
JODMVEJOH
counseling about condom use.
t 5IF*6%EPFTOPUOFFEUPCFSFNPWFEJNNFEJBUFMZJGUIF
woman needs ongoing contraception.
t 3FBTTFTT UIF XPNBO JO o IPVST *G OP DMJOJDBM
improvement occurs, continue antibiotics and consider
removal of the IUD.
t *G UIF XPNBO XBOUT UP EJTDPOUJOVF VTF
SFNPWF UIF *6%
sometime after antibiotics have been started to avoid the potential
risk for bacterial spread resulting from the removal procedure.
t *G UIF *6% JT SFNPWFE
DPOTJEFS &$1T JG BQQSPQSJBUF
Counsel the woman on alternative contraceptive methods,
and offer another method if it is desired.
t "TVNNBSZPG*6%NBOBHFNFOUJOXPNFOXJUI1*%JT
provided (Appendix F).
Comments and Evidence Summary. Treatment outcomes
do not generally differ between women with PID who retain
the IUD and those who have the IUD removed; however,
appropriate antibiotic treatment and close clinical follow-up
are necessary.
A systematic review identified four studies that included
women using copper or nonhormonal IUDs who developed
PID and compared outcomes between women who had the
IUD removed or did not (19). One randomized trial showed
that women with IUDs removed had longer hospitalizations
than those who did not, although no differences in PID
recurrences or subsequent pregnancies were observed (116).
Another randomized trial showed no differences in laboratory
findings among women who removed the IUD compared
with those who did not (117). One prospective cohort study
showed no differences in clinical or laboratory findings during
hospitalization; however, the IUD removal group had longer
hospitalizations (118). One randomized trial showed that
the rate of recovery for most clinical signs and symptoms
was higher among women who had the IUD removed than
among women who did not (119). No evidence was found
regarding women using LNG-IUDs (Level of evidence: I to
II-2, fair, direct).

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Management of the IUD when a Cu-IUD or
an LNG-IUD User Is Found To Be Pregnant
t &WBMVBUFGPSQPTTJCMFFDUPQJDQSFHOBODZ
t "EWJTF UIF XPNBO UIBU TIF IBT BO JODSFBTFE SJTL GPS
spontaneous abortion (including septic abortion that
might be life threatening) and of preterm delivery if the
IUD is left in place. The removal of the IUD reduces these
risks but might not decrease the risk to the baseline level
of a pregnancy without an IUD.
– If she does not want to continue the pregnancy, counsel
her about options.
– If she wants continue the pregnancy, advise her to seek
care promptly if she has heavy bleeding, cramping, pain,
abnormal vaginal discharge, or fever.

IUD Strings Are Visible or Can Be Retrieved Safely
from the Cervical Canal
t "EWJTFUIFXPNBOUIBUUIF*6%TIPVMECFSFNPWFEBT
soon as possible.
– If the IUD is to be removed, remove it by pulling on
the strings gently.
– Advise the woman that she should return promptly if
she has heavy bleeding, cramping, pain, abnormal
vaginal discharge, or fever.
t *GTIFDIPPTFTUPLFFQUIF*6%
BEWJTFIFSUPTFFLDBSF
promptly if she has heavy bleeding, cramping, pain,
abnormal vaginal discharge, or fever.

IUD Strings Are Not Visible and Cannot Be
Retrieved Safely
t *G VMUSBTPOPHSBQIZ JT BWBJMBCMF
DPOTJEFS QFSGPSNJOH PS
referring for ultrasound examination to determine the
location of the IUD. If the IUD cannot be located, it might
have been expelled or have perforated the uterine wall.
t *GVMUSBTPOPHSBQIZJTOPUQPTTJCMFPSUIF*6%JTEFUFSNJOFE
by ultrasound to be inside the uterus, advise the woman
to seek care promptly if she has heavy bleeding, cramping,
pain, abnormal vaginal discharge, or fever.
Comments and Evidence Summary. Removing the IUD
improves the pregnancy outcome if the IUD strings are visible
or the device can be retrieved safely from the cervical canal.
Risks for spontaneous abortion, preterm delivery, and infection
are substantial if the IUD is left in place.
Theoretically, the fetus might be affected by hormonal
exposure from an LNG-IUD; however, whether this exposure
increases the risk for fetal abnormalities is unknown.
A systematic review identified nine studies suggesting that
women who did not remove their IUDs during pregnancy
were at greater risk for adverse pregnancy outcomes (including

MMWR / June 21, 2013 / Vol. 62 / No. 5

spontaneous abortion, septic abortion, preterm delivery, and
chorioamnionitis) compared with women who had their IUDs
removed or who did not have an IUD (58). Cu-IUD removal
decreased risks but not to the baseline risk for pregnancies
without an IUD. One case series examined LNG-IUDs.
When they were not removed, eight in 10 pregnancies ended
in spontaneous abortions (Level of evidence: II-2, fair, direct).

Implants
The etonogestrel implant, a single rod with 68 mg of
etonogestrel, is available in the United States. Fewer than 1
woman out of 100 become pregnant in the first year of use of
the etonogestrel implant with typical use (59). The implant is
long acting, is reversible, and can be used by women of all ages,
including adolescents. The implant does not protect against
STDs; consistent and correct use of male latex condoms reduces
the risk for STDs, including HIV.

Initiation of Implants
Timing
t 5IFJNQMBOUDBOCFJOTFSUFEBUBOZUJNFJGJUJTSFBTPOBCMZ
certain that the woman is not pregnant (Box 1).

Need for Back-Up Contraception
t *G UIF JNQMBOU JT JOTFSUFE XJUIJO UIF GJSTU EBZT TJODF
menstrual bleeding started, no additional contraceptive
protection is needed.
t *GUIFJNQMBOUJTJOTFSUFEEBZTTJODFNFOTUSVBMCMFFEJOH
started, the woman needs to abstain from sexual intercourse
or use additional contraceptive protection for the next 7 days.

Special Considerations
Amenorrhea (Not Postpartum)
t Timing: The implant can be inserted at any time if it is
reasonably certain that the woman is not pregnant (Box 1).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Breastfeeding)
t Timing: The implant can be inserted at any time (U.S.
MEC 2 if <1 month postpartum and U.S. MEC 1 if ≥1
month postpartum) if it is reasonably certain that the
woman is not pregnant (Box 1).
t Need for back-up contraception: If the woman is <6 months
postpartum, amenorrheic, and fully or nearly fully breastfeeding
(exclusively breastfeeding or the vast majority [≥85%] of feeds

Recommendations and Reports

are breastfeeds) (60), no additional contraceptive protection is
needed. Otherwise, a woman who is ≥21 days postpartum and
has not experienced return of her menstrual cycle needs to
abstain from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >5 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postpartum (Not Breastfeeding)
t Timing: The implant can be inserted at any time, including
immediately postpartum (U.S. MEC 1) if it is reasonably
certain that the woman is not pregnant (Box 1).
t Need for back-up contraception: A woman who is
≥21 days postpartum and has not experienced return of
her menstrual cycle needs to abstain from sexual
intercourse or use additional contraceptive protection for
the next 7 days. If her menstrual cycles have returned and
it has been >5 days since menstrual bleeding started, she
needs to abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postabortion (Spontaneous or Induced)
t Timing: The implant can be inserted within the first 7 days,
including immediately after the abortion (U.S. MEC 1).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days unless the
implant is placed at the time of a surgical abortion.
Switching from Another Contraceptive Method
t Timing: The implant can be inserted immediately if it is
reasonably certain that the woman is not pregnant (Box 1).
Waiting for her next menstrual period is unnecessary.
t Need for back-up contraception: If it has been >5 days
since menstrual bleeding started, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days after insertion.
t Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle and
it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A healthcare provider may consider any of the following options:
– Advise the woman to retain the IUD for at least 7 days
after the implant is inserted and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 7 days before removing
the IUD and switching to the new method.
– Advise the woman to use ECPs at the time of IUD removal.

Comments and Evidence Summary. In situations in which
the health-care provider is uncertain whether the woman might
be pregnant, the benefits of starting the implant likely exceed
any risk; therefore, starting the implant should be considered
at any time, with a follow-up pregnancy test in 2–4 weeks.
If a woman needs to use additional contraceptive protection
when switching to an implant from another contraceptive
method, consider continuing her previous method for 7 days
after implant insertion. No direct evidence was found regarding
the effects of starting the etonogestrel implant at different
times of the cycle.

Class*
C
—†
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
STD = sexually transmitted disease; U.S. MEC = U.S. Medical Eligibility Criteria for
Contraceptive Use, 2010.
* Class A: essential and mandatory in all circumstances for safe and effective
use of the contraceptive method. Class B: contributes substantially to safe and
effective use, but implementation may be considered within the public health
and/or service context; the risk of not performing an examination or test should
be balanced against the benefits of making the contraceptive method
available. Class C: does not contribute substantially to safe and effective use
of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for
any methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 2). However,
measuring weight and calculating BMI at baseline might be helpful for
monitoring any changes and counseling women who might be concerned about
weight change perceived to be associated with their contraceptive method.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Comments and Evidence Summary. Weight (BMI): Obese
women can use implants (U.S. MEC 1) (5); therefore, screening
for obesity is not necessary for the safe initiation of implants.
However, measuring weight and calculating BMI at baseline
might be helpful for monitoring any changes and counseling
women who might be concerned about weight change perceived
to be associated with their contraceptive method.
Bimanual examination and cervical inspection: A pelvic
examination is not necessary before initiation of implants
because it would not facilitate detection of conditions for which
implant use would be unsafe. Women with current breast cancer
should not use implants (U.S. MEC 4); women with certain
liver diseases generally should not use implants (U.S. MEC 3)
(5). However, none of these conditions are likely to be detected
by pelvic examination (120). A systematic review identified
two case-control studies that compared delayed and immediate
pelvic examination before initiation of hormonal contraceptives,
specifically oral contraceptives or DMPA (15). No differences in
risk factors for cervical neoplasia, incidence of STDs, incidence
of abnormal Papanicolaou smears, or incidence of abnormal
wet mounts were observed. No evidence was found regarding
implants (Level of evidence: II-2 fair, direct).
Liver enzymes: Although women with certain liver diseases
generally should not use implants (U.S. MEC 3) (5), screening
for liver disease before initiation of implants is not necessary
because of the low prevalence of these conditions and the
high likelihood that women with liver disease already would
have had the condition diagnosed. A systematic review did
not identify any evidence regarding outcomes among women
who were screened versus not screened with liver enzyme
tests before initiation of hormonal contraceptives (14). The
prevalence of liver disorders among women of reproductive
age is low. In 2008, the percentage of adults aged 18–44
years with liver disease (not further specified) was 1.0%
(90). In 2009, the incidence of acute hepatitis A, B, or C
among women was <1 per 100,000 population (91). During
1998–2007, the incidence of liver carcinoma among women
was approximately 3 per 100,000 population (92). Because
estrogen and progestins are metabolized in the liver, the use
of hormonal contraceptives among women with liver disease
might, theoretically, be a concern. The use of hormonal
contraceptives, specifically COCs and POPs, does not affect
disease progression or severity in women with hepatitis,
cirrhosis, or benign focal nodular hyperplasia (93,94), although
evidence is limited and no evidence exists for implants.
Clinical breast examination: Although women with
current breast cancer should not use implants (U.S. MEC 4)
(5), screening asymptomatic women with a clinical breast

MMWR / June 21, 2013 / Vol. 62 / No. 5

examination before initiating an implant is not necessary
because of the low prevalence of breast cancer among women
of reproductive age (15–49 years). A systematic review did not
identify any evidence regarding outcomes among women who
were screened versus not screened with a breast examination
before initiation of hormonal contraceptives (15). The
incidence of breast cancer among women of reproductive age
in the United States is low. In 2009, the incidence of breast
cancer among women aged 20–49 years was approximately 72
per 100,000 women (95).
Other screening: Women with hypertension, diabetes,
hyperlipidemia, anemia, thrombogenic mutations, cervical
intraepithelial neoplasia, cervical cancer, STDs, or HIV infection
can use (U.S. MEC 1) or generally can use (U.S. MEC 2)
implants (5); therefore, screening for these conditions is not
necessary for the safe initiation of implants.

Routine Follow-Up After Implant Insertion
These recommendations address when routine follow-up is
needed for safe and effective continued use of contraception
for healthy women. The recommendations refer to general
situations and might vary for different users and different
situations. Specific populations that might benefit from more
frequent follow-up visits include adolescents, those with certain
medical conditions or characteristics, and those with multiple
medical conditions.
t "EWJTFBXPNBOUPSFUVSOBUBOZUJNFUPEJTDVTTTJEFFGGFDUT
or other problems, if she wants to change the method being
used, and when it is time to remove or replace the
contraceptive method. No routine follow-up visit is required.
t "UPUIFSSPVUJOFWJTJUT
IFBMUIDBSFQSPWJEFSTTFFJOHJNQMBOU
users should do the following:
– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including
medications, that would change the appropriateness of
the implant for safe and effective continued use based
on U.S. MEC (e.g., category 3 and 4 conditions and
characteristics).
– Consider assessing weight changes and counseling women
who are concerned about weight changes perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. A systematic review
did not identify any evidence regarding whether a routine
follow-up visit after initiating an implant improves correct or
continued use (16).

Recommendations and Reports

Bleeding Irregularities (Including
Amenorrhea) During Implant Use
t #FGPSF JNQMBOU JOTFSUJPO
QSPWJEF DPVOTFMJOH BCPVU
potential changes in bleeding patterns during implant use.
Unscheduled spotting or light bleeding is common with
implant use, and some women experience amenorrhea.
These bleeding changes are generally not harmful and
might or might not decrease with continued implant use.
Heavy or prolonged bleeding, unscheduled or menstrual,
is uncommon during implant use.

Irregular Bleeding (Spotting, Light Bleeding, or
Heavy or Prolonged Bleeding)
t *GDMJOJDBMMZJOEJDBUFE
DPOTJEFSBOVOEFSMZJOHHZOFDPMPHJDBM
problem, such as interactions with other medications, an
STD, pregnancy, or new pathologic uterine conditions
(e.g., polyps or fibroids). If an underlying gynecological
problem is found, treat the condition or refer for care.
t *GBOVOEFSMZJOHHZOFDPMPHJDQSPCMFNJTOPUGPVOEBOE
the woman wants treatment, the following treatment
options during days of bleeding can be considered:
– NSAIDS for short-term treatment (5–7 days)
– Hormonal treatment (if medically eligible) with lowdose COCs or estrogen for short-term treatment
(10–20 days)
t *G JSSFHVMBS CMFFEJOH QFSTJTUT BOE UIF XPNBO GJOET JU
unacceptable, counsel her on alternative methods, and
offer another method if it is desired.

Amenorrhea
t "NFOPSSIFB EPFT OPU SFRVJSF BOZ NFEJDBM USFBUNFOU
Provide reassurance.
– If a woman’s regular bleeding pattern changes abruptly
to amenorrhea, consider ruling out pregnancy if
clinically indicated.
t *GBNFOPSSIFBQFSTJTUTBOEUIFXPNBOGJOETJUVOBDDFQUBCMF
counsel her on alternative contraceptive methods, and
offer another method if it is desired.
Comments and Evidence Summary. During contraceptive
counseling and before insertion of the implant, information
about common side effects, such as unscheduled spotting or
light bleeding and amenorrhea, especially during the first
year of use should be discussed. A pooled analysis of data
from 11 clinical trials indicate that a significant proportion of
etonogestrel implant users had relatively little bleeding: 22%
of women experienced amenorrhea and 34% experienced
infrequent spotting, although 7% reported frequent bleeding
and 18% reported prolonged bleeding (121). Unscheduled
bleeding or amenorrhea is generally not harmful. Enhanced

counseling about expected bleeding patterns and reassurance
that bleeding irregularities are generally not harmful has been
shown to reduce discontinuation in clinical trials with other
hormonal contraceptives (i.e., DMPA) (101,102).
A systematic review and four newly published studies
examined several medications for the treatment of bleeding
irregularities with primarily LNG contraceptive implants
(122–126). Two small studies found significant cessation of
bleeding within 7 days of start of treatment among women
taking oral celecoxib (200 mg) daily for 5 days or oral
mefenamic acid (500 mg) 3 times daily for 5 days compared
with placebo (124,125). Differences in bleeding cessation
were not found among women with etonogestrel implants
taking mifepristone but were found when women with the
implants combined mifepristone with either ethinyl estradiol
or doxycycline (126,127). Doxycycline alone or in combination
with ethinyl estradiol did not improve bleeding cessation
among etonogestrel implant users (126). Among LNG implant
users, mifepristone reduced the number of bleeding or spotting
days but only after 6 months of treatment (128). Evidence
also suggests that estrogen (129–131), daily COCs (129),
levonorgestrel pills (130), tamoxifen (132), or tranexamic
acid (133) can reduce the number of bleeding or spotting
days during treatment among levonorgestrel implant users. In
one small study, vitamin E was found to significantly reduce
the mean number of bleeding days after the first treatment
cycle; however, another larger study reported no significant
differences in length of bleeding and spotting episodes with
vitamin E treatment (134,135). Use of aspirin did not result
in a significant difference in median length of bleeding or
bleeding and spotting episodes after treatment (134). One
study among implant users reported a reduction in number of
bleeding days after initiating ibuprofen; however, another trial
did not demonstrate any significant differences in the number
of spotting and bleeding episodes with ibuprofen compared
with placebo (123,130).

Injectables
Progestin-only injectable contraceptives (DMPA, 150 mg
intramuscularly or 104 mg subcutaneously) are available in
the United States; the only difference between these two
formulations is the route of administration. Approximately 6
out of 100 women will become pregnant in the first year of use
of DMPA with typical use (59). DMPA is reversible and can
be used by women of all ages, including adolescents. DMPA
does not protect against STDs; consistent and correct use of
male latex condoms reduces the risk for STDs, including HIV.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Initiation of Injectables
Timing
t 5IFGJSTU%.1"JOKFDUJPODBOCFHJWFOBUBOZUJNFJGJUJT
reasonably certain that the woman is not pregnant (Box 1).

Need for Back-Up Contraception
t *G%.1"JTTUBSUFEXJUIJOUIFGJSTUEBZTTJODFNFOTUSVBM
bleeding started, no additional contraceptive protection
is needed.
t *G%.1"JTTUBSUFEEBZTTJODFNFOTUSVBMCMFFEJOHTUBSUFE
the woman needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.

Special Considerations
Amenorrhea (Not Postpartum)
t Timing: The first DMPA injection can be given at any
time if it is reasonably certain that the woman is not
pregnant (Box 1).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Breastfeeding)
t Timing: The first DMPA injection can be given at any
time, including immediately postpartum (U.S. MEC 2 if
<1 month postpartum and U.S. MEC 1 if ≥1 month
postpartum) if it is reasonably certain that the woman is
not pregnant (Box 1).
t Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (60), no
additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycle needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >7 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postpartum (Not Breastfeeding)
t Timing: The first DMPA injection can be given at any
time, including immediately postpartum (U.S. MEC 1)
if it is reasonably certain that the woman is not pregnant
(Box 1).
t Need for back-up contraception: A woman who is
≥21 days postpartum and has not experienced return of
her menstrual cycle needs to abstain from sexual

MMWR / June 21, 2013 / Vol. 62 / No. 5

intercourse or use additional contraceptive protection for
the next 7 days. If her menstrual cycles have returned and
it has been >7 days since menstrual bleeding started, she
needs to abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postabortion (Spontaneous or Induced)
t Timing: The first DMPA injection can be given within
the first 7 days, including immediately postabortion
(U.S. MEC 1).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days unless the
injection is given at the time of a surgical abortion.
Switching from Another Contraceptive Method
t Timing: The first DMPA injection can be given
immediately if it is reasonably certain that the woman is
not pregnant (Box 1). Waiting for her next menstrual
period is unnecessary.
t Need for back-up contraception: If it has been >7 days
since menstrual bleeding started, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
t Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle and
it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A healthcare provider may consider any of the following options:
– Advise the women to retain the IUD for at least 7 days
after the injection and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 7 days before removing
the IUD and switching to the new method.
– Advise the woman to use ECPs at the time of IUD removal.
Comments and Evidence Summary. In situations in which
the health-care provider is uncertain whether the woman might
be pregnant, the benefits of starting DMPA likely exceed
any risk; therefore, starting DMPA should be considered at
any time, with a follow-up pregnancy test in 2–4 weeks. If a
woman needs to use additional contraceptive protection when
switching to DMPA from another contraceptive method,
consider continuing her previous method for 7 days after
DMPA injection.
A systematic review identified eight articles examining
DMPA initiation on different days of the menstrual cycle (20).
Evidence from two studies with small samples indicated that
DMPA injections given up to day 7 of the menstrual cycle
inhibited ovulation; when DMPA was administered after

Recommendations and Reports

day 7, ovulation occurred in some women. Cervical mucus
was of poor quality (i.e., not favorable for sperm penetration)
in 90% of women within 24 hours of the injection (Level
of evidence: II-2, fair) (136–138). Studies found that use of
another contraceptive method until DMPA could be initiated
(bridging option) did not help women initiate DMPA and was
associated with more unintended pregnancies than immediate
receipt of DMPA (139–143) (Level of evidence: I to II-3, fair
to poor, indirect).

Class*
C
—†
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; DMPA = depot medroxyprogesterone
acetate; HIV = human immunodeficiency virus; STD = sexually transmitted
disease; U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use, 2010.
* Class A: essential and mandatory in all circumstances for safe and effective
use of the contraceptive method. Class B: contributes substantially to safe and
effective use, but implementation may be considered within the public health
and/or service context; the risk of not performing an examination or test should
be balanced against the benefits of making the contraceptive method
available. Class C: does not contribute substantially to safe and effective use
of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for
any methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 2). However,
measuring weight and calculating BMI at baseline might be helpful for
monitoring any changes and counseling women who might be concerned about
weight change perceived to be associated with their contraceptive method.

the safe initiation of DMPA. However, measuring weight and
calculating BMI at baseline might be helpful for monitoring
any changes and counseling women who might be concerned
about weight change perceived to be associated with their
contraceptive method. (See guidance on follow-up for DMPA
users for evidence on weight gain with DMPA use.)
Bimanual examination and cervical inspection: Pelvic
examination is not necessary before initiation of DMPA
because it does not facilitate detection of conditions for
which DMPA would be unsafe. Although women with
current breast cancer should not use DMPA (U.S. MEC 4),
and women with severe hypertension, heart disease, vascular
disease, migraine headaches with aura, or certain liver diseases
generally should not use DMPA (U.S. MEC 3) (5), none of
these conditions are likely to be detected by pelvic examination
(120). A systematic review identified two case-control studies
that compared delayed versus immediate pelvic examination
before initiation of hormonal contraceptives, specifically oral
contraceptives or DMPA (15). No differences in risk factors for
cervical neoplasia, incidence of STDs, incidence of abnormal
Papanicolaou smears, or incidence of abnormal wet mounts
were observed (Level of evidence: II-2, fair, direct).
Blood pressure: Women with hypertension generally can
use DMPA (U.S. MEC 2), with the exception of women with
severe hypertension or vascular disease, who generally should
not use DMPA (U.S. MEC 3) (5). Screening for hypertension
before initiation of DMPA is not necessary because of the
low prevalence of undiagnosed severe hypertension and the
high likelihood that women with these conditions already
would have had them diagnosed. A systematic review did
not identify any evidence regarding outcomes among women
who were screened versus not screened with a blood pressure
measurement before initiation of progestin-only contraceptives
(21). The prevalence of undiagnosed hypertension among
women of reproductive age is low. During 1999–2008 among
women aged 20–44 years in the United States, the percentage
with diagnosed hypertension was 7.8%, and the percentage
with undiagnosed hypertension was 1.9% (144).
Glucose: Although women with complicated diabetes
generally should not use DMPA (U.S. MEC 3) (5), screening
for diabetes before initiation of DMPA is not necessary because
of the low prevalence of undiagnosed diabetes and the high
likelihood that women with complicated diabetes would
already have had the condition diagnosed. A systematic review
did not identify any evidence regarding outcomes among
women who were screened versus not screened with glucose
measurement before initiation of hormonal contraceptives
(14). The prevalence of diabetes among women of reproductive
age is low. During 1999–2008 among women aged 20–44 years

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

in the United States, the percentage with diagnosed diabetes
was 3% and the percentage with undiagnosed diabetes was
0.5% (144). Although hormonal contraceptives can have some
adverse effects on glucose metabolism in healthy and diabetic
women, the overall clinical effect is minimal (145–151).
Liver enzymes: Although women with certain liver diseases
generally should not use DMPA (U.S. MEC 3) (5), screening
for liver disease before initiation of DMPA is not necessary
because of the low prevalence of these conditions and the high
likelihood that women with liver disease already would have
had the condition diagnosed. A systematic review did not
identify any evidence regarding outcomes among women who
were screened versus not screened with liver enzyme tests before
initiation of hormonal contraceptives (14). The prevalence of
liver disorders among women of reproductive age is low. In 2008
among adults aged 18–44 years, the percentage with liver disease
(not further specified) was 1.0% (90). In 2009, the incidence of
acute hepatitis A, B, or C among women was <1 per 100,000
population (91). During 1998–2007, the incidence of liver
carcinoma among women was approximately 3 per 100,000
population (92). Because estrogen and progestins are metabolized
in the liver, the use of hormonal contraceptives among women
with liver disease might, theoretically, be a concern. The use of
hormonal contraceptives, specifically COCs and POPs, does not
affect disease progression or severity in women with hepatitis,
cirrhosis, or benign focal nodular hyperplasia (93,94), although
evidence is limited and no evidence exists for DMPA.
Clinical breast examination: Although women with current
breast cancer should not use DMPA (U.S. MEC 4) (5), screening
asymptomatic women with a clinical breast examination before
initiating DMPA is not necessary because of the low prevalence
of breast cancer among women of reproductive age. A systematic
review did not identify any evidence regarding outcomes
among women who were screened versus not screened with
a clinical breast examination before initiation of hormonal
contraceptives (15). The incidence of breast cancer among
women of reproductive age in the United States is low. In 2009,
the incidence of breast cancer among women aged 20–49 years
was approximately 72 per 100,000 women (95).
Other screening: Women with hyperlipidemia, anemia,
thrombogenic mutations, cervical intraepithelial neoplasia,
cervical cancer, HIV infection, or other STDs can use
(U.S. MEC 1) or generally can use (U.S. MEC 2) DMPA (5);
therefore, screening for these conditions is not necessary for
the safe initiation of DMPA.

Routine Follow-Up After Injectable
Initiation
These recommendations address when routine follow-up
is recommended for safe and effective continued use of
contraception for healthy women. The recommendations refer
to general situations and might vary for different users and
different situations. Specific populations that might benefit
from more frequent follow-up visits include adolescents, those
with certain medical conditions or characteristics, and those
with multiple medical conditions.
t "EWJTFBXPNBOUPSFUVSOBUBOZUJNFUPEJTDVTTTJEFFGGFDUT
or other problems, if she wants to change the method
being used, and when it is time for reinjection. No routine
follow-up visit is required.
t "U PUIFS SPVUJOF WJTJUT
IFBMUIDBSF QSPWJEFST TFFJOH
injectable users should do the following:
– Assess the woman’s satisfaction with her contraceptive method
and whether she has any concerns about method use.
– Assess any changes in health status, including
medications, that would change the appropriateness of
the injectable for safe and effective continued use based
on U.S. MEC (e.g., category 3 and 4 conditions and
characteristics).
– Consider assessing weight changes and counseling women
who are concerned about weight changes perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. Although no evidence
exists regarding whether a routine follow-up visit after initiating
DMPA improves correct or continued use, monitoring weight
or BMI change over time is important for DMPA users.
A systematic review identified a limited body of evidence that
examined whether weight gain in the few months after DMPA
initiation predicted future weight gain (17). Two studies found
significant differences in weight gain or BMI at follow-up
periods ranging from 12 to 36 months between early weight
gainers (i.e., those who gained >5% of their baseline body
weight within 6 months after initiation) and those who were
not early weight gainers (152,153). The differences between
groups were more pronounced at 18, 24, and 36 months
than at 12 months. One study found that most adolescent
DMPA users who had gained >5% of their baseline weight by
3 months gained even more weight by 12 months (154) (Level
of evidence: II-2, fair, to II-3, fair, direct).

Timing of Repeat Injections
Reinjection Interval
t 1SPWJEFSFQFBU%.1"JOKFDUJPOTFWFSZNPOUIT XFFLT

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Special Considerations
Early Injection
t 5IFSFQFBU%.1"JOKFDUJPODBOCFHJWFOFBSMZXIFOOFDFTTBSZ
Late Injection
t 5IFSFQFBU%.1"JOKFDUJPODBOCFHJWFOVQUPXFFLT
late (15 weeks from the last injection) without requiring
additional contraceptive protection.
t *GUIFXPNBOJTXFFLTMBUF XFFLTGSPNUIFMBTUJOKFDUJPO

for a repeat DMPA injection, she can have the injection if it is
reasonably certain that she is not pregnant (Box 1). She needs to
abstain from sexual intercourse or use additional contraceptive
protection for the next 7 days. She might consider the use of
emergency contraception if appropriate.
Comments and Evidence Summary. There are no time
limits on early injections; injections can be given when
necessary (e.g., when a woman cannot return at the routine
interval). WHO has extended the time that a woman can
have a late reinjection (i.e., grace period) for DMPA use from
2 weeks to 4 weeks on the basis of data from one study showing
low pregnancy rates through 4 weeks; however, the CDC
expert group did not consider the data to be generalizable to
the United States because a large proportion of women in the
study were breastfeeding. Therefore, U.S. SPR recommends
a grace period of 2 weeks.
A systematic review identified 12 studies evaluating time to
pregnancy or ovulation after the last injection of DMPA (155).
Although pregnancy rates were low during the 2-week interval
following the reinjection date and for 4 weeks following the
reinjection date, data were sparse and one study included a
large proportion of breastfeeding women (156–158). Studies
also indicated a wide variation in time to ovulation after the
last DMPA injection, with the majority ranging from 15 to
49 weeks from the last injection (159–167) (Level of evidence:
II-2, fair, direct).

Bleeding Irregularities (Including
Amenorrhea) During Injectable Use
t #FGPSF %.1" JOJUJBUJPO
QSPWJEF DPVOTFMJOH BCPVU
potential changes in bleeding patterns during DMPA use.
Amenorrhea and unscheduled spotting or light bleeding
is common with DMPA use, and heavy or prolonged
bleeding can occur with DMPA use. These bleeding
irregularities are generally not harmful and might decrease
with continued DMPA use.

Unscheduled Spotting or Light Bleeding
t *GDMJOJDBMMZJOEJDBUFE
DPOTJEFSBOVOEFSMZJOHHZOFDPMPHJDBM
problem, such as interactions with other medications, an
STD, pregnancy, or new pathologic uterine conditions
(e.g., polyps or fibroids). If an underlying gynecological
problem is found, treat the condition or refer for care.
t *GBOVOEFSMZJOHHZOFDPMPHJDQSPCMFNJTOPUGPVOEBOE
the woman wants treatment, the following treatment
option during days of bleeding can be considered:
– NSAIDs for short-term treatment (5–7 days)
t *G VOTDIFEVMFE TQPUUJOH PS MJHIU CMFFEJOH QFSTJTUT BOE UIF
woman finds it unacceptable, counsel her on alternative
contraceptive methods, and offer another method if it is desired.

Heavy or Prolonged Bleeding
t *GDMJOJDBMMZJOEJDBUFE
DPOTJEFSBOVOEFSMZJOHHZOFDPMPHJDBM
problem, such as interactions with other medications, an
STD, pregnancy, or new pathologic uterine conditions
(such as fibroids or polyps). If an underlying gynecologic
problem is identified, treat the condition or refer for care.
t *GBOVOEFSMZJOHHZOFDPMPHJDQSPCMFNJTOPUGPVOEBOE
the woman wants treatment, the following treatment
options during days of bleeding can be considered:
– NSAIDS for short-term treatment (5–7 days)
– Hormonal treatment (if medically eligible) with lowdose COCs or estrogen for short-term treatment
(10–20 days)
t *GIFBWZPSQSPMPOHFECMFFEJOHQFSTJTUTBOEUIFXPNBOGJOET
it unacceptable, counsel her on alternative contraceptive
methods, and offer another method if it is desired.

Amenorrhea
t "NFOPSSIFB EPFT OPU SFRVJSF BOZ NFEJDBM USFBUNFOU
Provide reassurance.
– If a woman’s regular bleeding pattern changes abruptly
to amenorrhea, consider ruling out pregnancy if
clinically indicated.
t *GBNFOPSSIFBQFSTJTUTBOEUIFXPNBOGJOETJUVOBDDFQUBCMF
counsel her on alternative contraceptive methods, and
offer another method if it is desired.
Comments and Evidence Summary. During contraceptive
counseling and before initiation of DMPA, information
about common side effects such as irregular bleeding should
be discussed. Unscheduled bleeding or spotting is common
with DMPA use (168). Additionally, amenorrhea is common
after ≥1 years of continuous use (168,169). These bleeding
irregularities are generally not harmful. Enhanced counseling
among DMPA users detailing expected bleeding patterns and

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

reassurance that these irregularities generally are not harmful
has been shown to reduce DMPA discontinuation in clinical
trials (101,102).
A systematic review, as well as two additional studies,
examined the treatment of bleeding irregularities during
DMPA use (122,170,171). Two small studies found significant
cessation of bleeding within 7 days of starting treatment
among women taking valdecoxib for 5 days or mefenamic
acid for 5 days compared with placebo (172,173). Treatment
with ethinyl estradiol was found to stop bleeding better
than placebo during the treatment period, although rates
of discontinuation were high, and safety outcomes were not
examined (174). In one small study among DMPA users who
had been experiencing amenorrhea for 2 months, treatment
with COCs was found to alleviate amenorrhea better than
placebo (175). No studies examined the effects of aspirin on
bleeding irregularities among DMPA users.

Combined Hormonal Contraceptives
Combined hormonal contraceptives contain both estrogen
and a progestin and include 1) COCs (various formulations),
2) a transdermal contraceptive patch (which releases 150 µg
of norelgestromin and 20 µg ethinyl estradiol daily), and
3) a vaginal contraceptive ring (which releases 120 µ g
etonogestrel and 15 µg ethinyl estradiol daily). Approximately
9 out of 100 women become pregnant in the first year of use
with combined hormonal contraceptives with typical use (59).
These methods are reversible and can be used by women of all
ages. Combined hormonal contraceptives are generally used for
21–24 consecutive days, followed by 4–7 hormone-free days
(either no use or placebo pills). These methods are sometimes
used for an extended period with infrequent or no hormonefree days. Combined hormonal contraceptives do not protect
against STDs; consistent and correct use of male latex condoms
reduces the risk for STDs, including HIV.

Initiation of Combined Hormonal
Contraceptives
Timing
t $PNCJOFE IPSNPOBM DPOUSBDFQUJWFT DBO CF JOJUJBUFE BU
any time if it is reasonably certain that the woman is not
pregnant (Box 1).

Need for Back-Up Contraception
t *GDPNCJOFEIPSNPOBMDPOUSBDFQUJWFTBSFTUBSUFEXJUIJO
the first 5 days since menstrual bleeding started, no
additional contraceptive protection is needed.

MMWR / June 21, 2013 / Vol. 62 / No. 5

t *GDPNCJOFEIPSNPOBMDPOUSBDFQUJWFTBSFTUBSUFEEBZT
since menstrual bleeding started, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.

Special Considerations
Amenorrhea (Not Postpartum)
t Timing: Combined hormonal contraceptives can be
started at any time if it is reasonably certain that the
woman is not pregnant (Box 1).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Breastfeeding)
t Timing: Combined hormonal contraceptives can be started
when the woman is medically eligible to use the method (176)
and if it is reasonably certain that she is not pregnant. (Box 1).
– Postpartum women who are breastfeeding should not use
combined hormonal contraceptives during the first
3 weeks after delivery (U.S. MEC 4) because of concerns
about increased risk for venous thromboembolism and
generally should not use combined hormonal contraceptives
during the fourth week postpartum (U.S. MEC 3) because
of concerns about potential effects on breastfeeding
performance. Postpartum, breastfeeding women with
other risk factors for venous thromboembolism generally
should not use combined hormonal contraceptives 4–6
weeks after delivery (U.S. MEC 3).
t Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (60), no
additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycle needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >5 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postpartum (Not Breastfeeding)
t Timing: Combined hormonal contraceptives can be started
when the woman is medically eligible (176) and if it is
reasonably certain that she is not pregnant (Box 1).
– Postpartum women should not use combined hormonal
contraceptives during the first 3 weeks after delivery
(U.S. MEC 4) because of concerns about increased risk

Recommendations and Reports

for venous thromboembolism. Postpartum women with
other risk factors for venous thromboembolism
generally should not use combined hormonal
contraceptives 3–6 weeks after delivery (U.S. MEC 3).
t Need for back-up contraception: A woman who is ≥21
days postpartum and whose menstrual cycles have not
returned needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days. If
her menstrual cycles have returned and it has been >5 days
since menstrual bleeding started, she needs to abstain from
sexual intercourse or use additional contraceptive
protection for the next 7 days.
Postabortion (Spontaneous or Induced)
t Timing: Combined hormonal contraceptives can be started
within the first 7 days after first or second trimester abortion,
including immediately postabortion (U.S. MEC 1).
t Need for back-up contraception: She needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days unless combined hormonal
contraceptives are started at the time of a surgical abortion.
Switching from Another Contraceptive Method
t Timing: Combined hormonal contraceptives can be
started immediately if it is reasonably certain that the
woman is not pregnant (Box 1). Waiting for her next
menstrual period is unnecessary.
t Need for back-up contraception: If it has been >5 days
since menstrual bleeding started, she needs to abstain from
sexual intercourse or use additional contraceptive
protection for the next 7 days.
t Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle and
it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A healthcare provider may consider any of the following options:
– Advise the women to retain the IUD for at least 7 days
after combined hormonal contraceptives are initiated
and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 7 days before removing
the IUD and switching to the new method.
– Advise the woman to use ECPs at the time of IUD removal.
Comments and Evidence Summary. In situations in which
the health-care provider is uncertain whether the woman
might be pregnant, the benefits of starting combined hormonal
contraceptives likely exceed any risk; therefore, starting
combined hormonal contraceptives should be considered at
any time, with a follow-up pregnancy test in 2–4 weeks. If a

woman needs to use additional contraceptive protection when
switching to combined hormonal contraceptives from another
contraceptive method, consider continuing her previous method
for 7 days after starting combined hormonal contraceptives.
A systematic review of 18 studies examined the effects of
starting combined hormonal contraceptives on different days
of the menstrual cycle (22). Overall, the evidence suggested
that pregnancy rates did not differ by the timing of combined
hormonal contraceptive initiation (143,177–179) (Level of
evidence: I to II-3, fair, indirect). The more follicular activity that
occurred before starting COCs, the more likely ovulation was to
occur; however, no ovulations occurred when COCs were started
at a follicle diameter of 10 mm (mean cycle day 7.6) or when the
ring was started at 13 mm (median cycle day 11) (180–189) (Level
of evidence: I to II-3, fair, indirect). Bleeding patterns and other
side effects did not vary with the timing of combined hormonal
contraceptive initiation (177,178,190–194) (Level of evidence:
I to II-2, good to poor, direct). Although continuation rates of
combined hormonal contraceptives were initially improved by
the “quick start” approach (i.e., starting on the day of the visit),
the advantage disappeared over time (178,179,190–195) (Level
of evidence: I to II-2, good to poor, direct).

Examinations and Tests Needed Before
Initiation of Combined Hormonal
Contraceptives
Among healthy women, few examinations or tests are
needed before initiation of combined hormonal contraceptives
(Table 5). Blood pressure should be measured before initiation
of combined hormonal contraceptives. Baseline weight
and BMI measurements might be useful for monitoring
combined hormonal contraceptive users over time. Women
with known medical problems or other special conditions
might need additional examinations or tests before being
determined to be appropriate candidates for a particular
method of contraception. U.S. MEC might be useful in such
circumstances (5).
Comments and Evidence Summary. Blood pressure:
Women who have more severe hypertension (systolic pressure
of ≥160 mm Hg or diastolic pressure of ≥100 mm Hg)
or vascular disease should not use combined hormonal
contraceptives (U.S. MEC 4), and women who have less
severe hypertension (systolic pressure of 140–159 mm Hg or
diastolic pressure of 90–99 mm Hg) or adequately controlled
hypertension generally should not use combined hormonal
contraceptives (U.S. MEC 3) (5). Therefore, blood pressure
should be measured before initiating combined hormonal
contraceptives. If access to health care is limited, blood pressure
measurements may be obtained in nonclinical settings, such as

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

TABLE 5. Classification of examinations and tests needed before
combined hormonal contraceptive initiation
Examination or laboratory test

Class*

Examination
Blood pressure
Weight (BMI) (weight [kg]/height [m]2)
Clinical breast examination
Bimanual examination and cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou smear)
STD screening with laboratory tests
HIV screening with laboratory tests

A†
—§
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
STD = sexually transmitted disease; U.S. MEC = U.S. Medical Eligibility Criteria for
Contraceptive Use, 2010.
* Class A: essential and mandatory in all circumstances for safe and effective
use of the contraceptive method. Class B: contributes substantially to safe and
effective use, but implementation may be considered within the public health
and/or service context; the risk of not performing an examination or test should
be balanced against the benefits of making the contraceptive method
available. Class C: does not contribute substantially to safe and effective use
of the contraceptive method.
† In cases in which access to health care might be limited, the blood pressure
measurement can be obtained by the woman in a nonclinical setting (e.g.,
pharmacy or fire station) and self-reported to the provider.
§ Weight (BMI) measurement is not needed to determine medical eligibility for
any methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 2). However,
measuring weight and calculating BMI at baseline might be helpful for
monitoring any changes and counseling women who might be concerned about
weight change perceived to be associated with their contraceptive method.

pharmacies or fire stations, and reported by the woman to her
provider. Evidence suggests that cardiovascular outcomes are
worse among women who did not have their blood pressure
measured before initiating COCs.
A systematic review identified six articles from three studies
that reported cardiovascular outcomes among women who had
blood pressure measurements and women who did not have
blood pressure measurements before initiating COCs (21).
Three case-control studies showed that women who did not
have blood pressure measurements before initiating COCs
had a higher risk for acute myocardial infarction than women
who did have blood pressure measurements (196–198). Two
case-control studies showed that women who did not have
blood pressure measurements before initiating COCs had
a higher risk for ischemic stroke than women who did have
blood pressure measurements (199,200). One case-control
study showed no difference in the risk for hemorrhagic stroke
among women who initiated COCs regardless of whether their
blood pressure was measured (201). Studies that examined
hormonal contraceptive methods other than COCs were not
identified (Level of evidence: II-2, fair, direct).

MMWR / June 21, 2013 / Vol. 62 / No. 5

Weight (BMI): Obese women generally can use combined
hormonal contraceptives (U.S. MEC 2) (5); therefore,
screening for obesity is not necessary for the safe initiation
of combined hormonal contraceptives. However, measuring
weight and calculating BMI at baseline might be helpful for
monitoring any changes and counseling women who might
be concerned about weight change perceived to be associated
with their contraceptive method.
Bimanual examination and cervical inspection: Pelvic
examination is not necessary before initiation of combined
hormonal contraceptives because it does not facilitate detection
of conditions for which hormonal contraceptives would be
unsafe. Women with certain conditions such as current breast
cancer, severe hypertension or vascular disease, heart disease,
migraine headaches with aura, and certain liver diseases, as well
as women aged ≥35 years who smoke ≥15 cigarettes per day,
should not use (U.S. MEC 4) or generally should not use (U.S.
MEC 3) combined hormonal contraceptives (5); however, none
of these conditions are likely to be detected by pelvic examination
(120). A systematic review identified two case-control studies
that compared delayed and immediate pelvic examination
before initiation of hormonal contraceptives, specifically oral
contraceptives or DMPA (15). No differences in risk factors for
cervical neoplasia, incidence of STDs, incidence of abnormal
Papanicolaou smears, or incidence of abnormal wet mounts were
found (Level of evidence: II-2 fair, direct).
Glucose: Although women with complicated diabetes
should not use (U.S. MEC 4) or generally should not use
(U.S. MEC 3) combined hormonal contraceptives, depending
on the severity of the condition (5), screening for diabetes
before initiation of hormonal contraceptives is not necessary
because of the low prevalence of undiagnosed diabetes and the
high likelihood that women with complicated diabetes already
would have had the condition diagnosed. A systematic review
did not identify any evidence regarding outcomes among
women who were screened versus not screened with glucose
measurement before initiation of hormonal contraceptives
(14). The prevalence of diabetes among women of reproductive
age is low. During 1999–2008 among women aged 20–44 years
in the United States, the percentage with diagnosed diabetes
was 3% and the percentage with undiagnosed diabetes was
0.5% (144). Although hormonal contraceptives can have some
adverse effects on glucose metabolism in healthy and diabetic
women, the overall clinical effect is minimal (145–151).
Lipids: Although some women with hyperlipidemias
generally should not use combined hormonal contraceptives
(U.S. MEC 2/3, depending on the type and severity of the
hyperlipidemia and presence of other cardiovascular risk
factors) (5), screening for hyperlipidemia before initiation of

Recommendations and Reports

hormonal contraceptives is not necessary because of the low
prevalence of undiagnosed disease in women of reproductive
age and the low likelihood of clinically significant changes
with use of hormonal contraceptives. A systematic review
did not identify any evidence regarding outcomes among
women who were screened versus not screened with lipid
measurement before initiation of hormonal contraceptives
(14). The prevalence of hyperlipidemia among women of
reproductive age is low. During 1999–2008 among women
aged 20–44 years in the United States, approximately 10%
had hypercholesterolemia, defined as total cholesterol
≥ 240 mg/dL or currently taking lipid-lowering medications,
and the prevalence of undiagnosed hypercholesterolemia was
approximately 2% (144). Studies have shown mixed results
about the effects of hormonal methods on lipid levels, and the
clinical significance of these changes is unclear (202–204). In
addition, women with abnormal lipid levels at baseline were
not found to have increased risk for adverse changes to their
lipid profile when using hormonal methods (202).
Liver enzymes: Although women with certain liver
diseases should not use (U.S. MEC 4) or generally should
not use (U.S. MEC 3) combined hormonal contraceptives
(5), screening for liver disease before initiation of combined
hormonal contraceptives is not necessary because of the low
prevalence of these conditions and the high likelihood that
women with liver disease already would have had the condition
diagnosed. A systematic review did not identify any evidence
regarding outcomes among women who were screened versus
not screened with liver enzyme tests before initiation of
hormonal contraceptives (14). The prevalence of liver disorders
among women of reproductive age is low. In 2008 among
adults aged 18–44 years, the percentage with liver disease (not
further specified) was 1.0% (90). In 2009, the incidence of
acute hepatitis A, B, or C among women was <1 per 100,000
population (91). During 1998–2007, the incidence of liver
carcinoma among women was approximately 3 per 100,000
population (92). Because estrogen and progestins are
metabolized in the liver, the use of hormonal contraceptives
among women with liver disease might, theoretically, be a
concern. The use of hormonal contraceptives, specifically
COCs and POPs, does not affect disease progression or severity
in women with hepatitis, cirrhosis, or benign focal nodular
hyperplasia (93,94), although evidence is limited; no evidence
exists for other types of combined hormonal contraceptives.
Thrombogenic mutations: Women with thrombogenic
mutations should not use combined hormonal contraceptives
(U.S. MEC 4) (5) because of the increased risk for venous
thromboembolism (205). However, studies have shown
that universal screening for thrombogenic mutations before

initiating COCs is not cost-effective because of the rarity of
the conditions and the high cost of screening (206–208).
Clinical breast examination: Although women with
current breast cancer should not use combined hormonal
contraceptives (U.S. MEC 4) (5), screening asymptomatic
women with a clinical breast examination before initiating
combined hormonal contraceptives is not necessary because
of the low prevalence of breast cancer among women of
reproductive age. A systematic review did not identify any
evidence regarding outcomes among women who were
screened versus not screened with a breast examination before
initiation of hormonal contraceptives (15). The incidence of
breast cancer among women of reproductive age in the United
States is low. In 2009, the incidence of breast cancer among
women aged 20–49 years was approximately 72 per 100,000
women (95).
Other screening: Women with anemia, cervical intraepithelial
neoplasia, cervical cancer, HIV infection, or other STDs can
use (U.S. MEC 1) or generally can use (U.S. MEC 2) combined
hormonal contraceptives (5); therefore, screening for these
conditions is not necessary for the safe initiation of combined
hormonal contraceptives.

Number of Pill Packs that Should Be
Provided at Initial and Return Visits
t "UUIFJOJUJBMBOESFUVSOWJTJUT
QSPWJEFPSQSFTDSJCFVQUPB
1-year supply of COCs (e.g., 13 28-day pill packs),
depending on the woman’s preferences and anticipated use.
t "XPNBOTIPVMECFBCMFUPPCUBJO$0$TFBTJMZJOUIF
amount and at the time she needs them.
Comments and Evidence Summary. The more pill packs
given up to 13 cycles, the higher the continuation rates.
Restricting the number of pill packs distributed or prescribed
can result in unwanted discontinuation of the method and
increased risk for pregnancy.
A systematic review of the evidence suggested that providing
a greater number of pill packs was associated with increased
continuation (23). Studies that compared provision of one
versus 12 packs, one versus 12 or 13 packs, or three versus seven
packs found increased continuation of pill use among women
provided with more pill packs (209–211). However, one study
found that there was no difference in continuation when patients
were provided one and then three packs versus four packs all at
once (212). In addition to continuation, a greater number of
pills packs provided was associated with fewer pregnancy tests,
fewer pregnancies, and lower cost per client. However, a greater
number of pill packs (i.e., 13 packs versus three packs) also was
associated with increased pill wastage in one study (210) (Level
of evidence: I to II-2, fair, direct).

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Routine Follow-Up After Combined
Hormonal Contraceptive Initiation
These recommendations address when routine follow-up
is recommended for safe and effective continued use of
contraception for healthy women. The recommendations refer
to general situations and might vary for different users and
different situations. Specific populations that might benefit
from more frequent follow-up visits include adolescents, those
with certain medical conditions or characteristics, and those
with multiple medical conditions.
t "EWJTFBXPNBOUPSFUVSOBUBOZUJNFUPEJTDVTTTJEFFGGFDUT
or other problems or if she wants to change the method
being used. No routine follow-up visit is required.
t "UPUIFSSPVUJOFWJTJUT
IFBMUIDBSFQSPWJEFSTTFFJOHDPNCJOFE
hormonal contraceptive users should do the following:
– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including
medications, that would change the appropriateness of
combined hormonal contraceptives for safe and
effective continued use based on U.S. MEC (e.g.,
category 3 and 4 conditions and characteristics).
– Assess blood pressure.
– Consider assessing weight changes and counseling women
who are concerned about weight changes perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. No evidence exists
regarding whether a routine follow-up visit after initiating combined
hormonal contraceptives improves correct or continued use.
Monitoring blood pressure is important for combined hormonal
contraceptive users. Health-care providers might consider
recommending women obtain blood pressure measurements in
nonclinical settings (e.g., pharmacy or fire station).
A systematic review identified five studies that examined the
incidence of hypertension among women who began using
a COC versus those who started a nonhormonal method
of contraception or a placebo (17). Few women developed
hypertension after initiating COCs, and studies examining
increases in blood pressure after COC initiation found mixed
results. No studies were identified that examined changes in
blood pressure among patch or vaginal ring users (Level of
evidence: I, fair, to II-2, fair, indirect).

Late or Missed Doses and Side Effects from
Combined Hormonal Contraceptive Use
For the following recommendations, a dose is considered
late when <24 hours have elapsed since the dose should have

MMWR / June 21, 2013 / Vol. 62 / No. 5

been taken. A dose is considered missed if ≥24 hours have
elapsed since the dose should have been taken. For example,
if a COC pill was supposed to have been taken on Monday at
9:00 a.m. and is taken at 11:00 a.m., the pill is late; however,
by Tuesday morning at 11:00 a.m., Monday’s 9:00 a.m. pill
has been missed and Tuesday’s 9:00 a.m. pill is late. For COCs,
the recommendations only apply to late or missed hormonally
active pills and not to placebo pills. Recommendations are
provided for late or missed pills (Figure 2), the patch (Figure 3),
and the ring (Figure 4).
Comments and Evidence Summary. Inconsistent or
incorrect use of combined hormonal contraceptives is a major
cause of combined hormonal contraceptive failure. Extending
the hormone-free interval is considered to be a particularly risky
time to miss combined hormonal contraceptives. Seven days of
continuous combined hormonal contraceptive use is deemed
necessary to reliably prevent ovulation. The recommendations
reflect a balance between simplicity and precision of science.
Women who frequently miss COCs or experience other usage
errors with combined hormonal patch or combined vaginal
ring should consider an alternative contraceptive method
that is less dependent on the user to be effective (e.g., IUD,
implant, or injectable).
A systematic review identified 36 studies that examined
measures of contraceptive effectiveness of combined hormonal
contraceptives during cycles with extended hormone-free
intervals, shortened hormone-free intervals, or deliberate
nonadherence on days not adjacent to the hormone-free
interval (24). Most of the studies examined COCs (188,213–
240), two examined the combined hormonal patch (234,241),
and six examined the combined vaginal ring (185,242–246).
No direct evidence on the effect of missed pills on the risk
for pregnancy was found. Studies of women deliberately
extending the hormone-free interval up to 14 days found
wide variability in the amount of follicular development and
occurrence of ovulation (216,219,221,222,224,225,227–230);
in general, the risk for ovulation was low, and among women
who did ovulate, cycles were usually abnormal. In studies of
women who deliberately missed pills on various days during
the cycle not adjacent to the hormone-free interval, ovulation
occurred infrequently (214,220–222,230,231,233,234).
Studies comparing 7-day hormone-free intervals with shorter
hormone-free intervals found lower rates of pregnancy
(213,217,226,232) and significantly greater suppression of
ovulation (215,225,236–238,240) among women with shorter
intervals in all but one study (235), which found no difference.
Two studies that compared 30-µg ethinyl estradiol pills with
20-µg ethinyl estradiol pills showed more follicular activity
when 20-µg ethinyl estradiol pills were missed (216,219). In

Recommendations and Reports

FIGURE 2. Recommended actions after late or missed combined oral contraceptives

If one hormonal pill is late:
(<24 hours since a pill
should have been taken)

If one hormonal pill has been
missed: (24 to <48 hours since a
pill should have been taken)

tTake the late or missed pill as
soon as possible.
tContinue taking the remaining
pills at the usual time (even if it
means taking two pills on the
same day).
tNo additional contraceptive
protection is needed.
tEmergency contraception is not
usually needed but can be
considered if hormonal pills
were missed earlier in the cycle
or in the last week of the
previous cycle.

studies examining the combined vaginal ring, three studies
found that nondeliberate extension of the hormone-free
interval for 24 to <48 hours from the scheduled period
did not increase the risk for pregnancy (242,243,245); one
study found that ring insertion after a deliberately extended
hormone-free interval that allowed a 13-mm follicle to develop
interrupted ovarian function and further follicular growth
(185); and one study found that inhibition of ovulation was
maintained after deliberately forgetting to remove the ring
for up to 2 weeks after normal ring use (246). In studies
examining the combined hormonal patch, one study found
that missing 1–3 consecutive days before patch replacement
(either wearing one patch 3 days longer before replacement
or going 3 days without a patch before replacing the next
patch) on days not adjacent to the patch-free interval resulted
in little follicular activity and low risk for ovulation (234),
and one pharmacokinetic study found that serum levels of

If two or more consecutive hormonal
pills have been missed: (≥48 hours since
a pill should have been taken)
tTake the most recent missed pill as
soon as possible. (Any other missed
pills should be discarded.)
tContinue taking the remaining pills at
the usual time (even if it means taking
two pills on the same day).
tUse back-up contraception (e.g.,
condoms) or avoid sexual intercourse
until hormonal pills have been taken
for 7 consecutive days.
tIf pills were missed in the last week of
hormonal pills (e.g., days 15–21 for
28-day pill packs):
— Omit the hormone-free interval by
finishing the hormonal pills in the
current pack and starting a new
pack the next day.
— If unable to start a new pack
immediately, use back-up
contraception (e.g., condoms) or
avoid sexual intercourse until
hormonal pills from a new pack
have been taken for 7 consecutive
days.
t&NFSHFODZDPOUSBDFQUJPOTIPVMECF
considered if hormonal pills were
missed during the first week and
unprotected sexual intercourse
occurred in the previous 5 days.
t&NFSHFODZDPOUSBDFQUJPONBZBMTP
be considered at other times as
appropriate.

ethinyl estradiol and progestin norelgestromin remained within
reference ranges after extending patch wear for 3 days (241).
No studies were found on extending the patch-free interval. In
studies that provide indirect evidence on the effects of missed
combined hormonal contraception on surrogate measures of
pregnancy, how differences in surrogate measures correspond
to pregnancy risk is unclear (Level of evidence: I, good, indirect
to II-3, poor, direct).

Vomiting or Severe Diarrhea While Using COCs
Certain steps should be taken by women who experience
vomiting or severe diarrhea while using COCs (Figure 5).
Comments and Evidence Summary. Theoretically, the
contraceptive effectiveness of COCs might be decreased because
of vomiting or severe diarrhea. Because of the lack of evidence
that addresses vomiting or severe diarrhea while using COCs,
these recommendations are based on the recommendations
MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

FIGURE 3. Recommended actions after delayed application or detachment with combined hormonal patch
Delayed application or detachment* for <48
hours since a patch should have been applied
or reattached

Delayed application or detachment* for ≥48
hours since a patch should have been applied
or reattached

t"QQMZBOFXQBUDIBTTPPOBTQPTTJCMF *G
detachment occured <24 hours since the
QBUDIXBTBQQMJFE
USZUPSFBQQMZUIFQBUDI
PSSFQMBDFXJUIBOFXQBUDI

t,FFQUIFTBNFQBUDIDIBOHFEBZ
t/PBEEJUJPOBMDPOUSBDFQUJWFQSPUFDUJPOJT
OFFEFE
t&NFSHFODZDPOUSBDFQUJPOJTOPUVTVBMMZ
needed but can be considered if delayed
application or detachment occurred earlier
JOUIFDZDMFPSJOUIFMBTUXFFLPGUIF

QSFWJPVTDZDMF

t"QQMZBOFXQBUDIBTTPPOBTQPTTJCMF
t,FFQUIFTBNFQBUDIDIBOHFEBZ
t6TFCBDLVQDPOUSBDFQUJPO FH
DPOEPNT

or avoid sexual intercourse until a patch has
CFFOXPSOGPSDPOTFDVUJWFEBZT
t*GUIFEFMBZFEBQQMJDBUJPOPSEFUBDINFOU
PDDVSSFEJOUIFUIJSEQBUDIXFFL
0NJUUIFIPSNPOFGSFFXFFLCZ

öOJTIJOHUIFUIJSEXFFLPGQBUDIVTF
LFFQJOHUIFTBNFQBUDIDIBOHFEBZ

BOETUBSUJOHBOFXQBUDIJNNFEJBUFMZ
*GVOBCMFUPTUBSUBOFXQBUDI

JNNFEJBUFMZ
VTFCBDLVQ

DPOUSBDFQUJPO FH
DPOEPNT
PSBWPJE
TFYVBMJOUFSDPVSTFVOUJMBOFXQBUDIIBT
CFFOXPSOGPSDPOTFDVUJWFEBZT
t&NFSHFODZDPOUSBDFQUJPOTIPVMECF

considered if the delayed application or
EFUBDINFOUPDDVSSFEXJUIJOUIFöSTUXFFL
of patch use and unprotected sexual
JOUFSDPVSTFPDDVSSFEJOUIFQSFWJPVTEBZT
t&NFSHFODZDPOUSBDFQUJPONBZBMTPCF
DPOTJEFSFEBUPUIFSUJNFTBTBQQSPQSJBUF

* If detachment takes place but the woman is unsure when the detachment occurred, consider the patch to have been detached for ≥48 hours since a patch should
have been applied or reattached.

for missed COCs. No evidence was found on the effects of
vomiting or diarrhea on measures of contraceptive effectiveness
including pregnancy, follicular development, hormone levels,
or cervical mucus quality.

Unscheduled Bleeding with Extended or
Continuous Use of Combined
Hormonal Contraceptives
t #FGPSFJOJUJBUJPOPGDPNCJOFEIPSNPOBMDPOUSBDFQUJWFT
provide counseling about potential changes in bleeding
patterns during extended or continuous combined
hormonal contraceptive use. (Extended contraceptive use
is defined as a planned hormone-free interval after at least
two contiguous cycles. Continuous contraceptive use is
defined as uninterrupted use of hormonal contraception
without a hormone-free interval [247].)
t 6OTDIFEVMFETQPUUJOHPSCMFFEJOHJTDPNNPOEVSJOHUIF
first 3–6 months of extended or continuous combined
hormonal contraceptive use. It is generally not harmful
and decreases with continued combined hormonal
contraceptive use.

MMWR / June 21, 2013 / Vol. 62 / No. 5

t *GDMJOJDBMMZJOEJDBUFE
DPOTJEFSBOVOEFSMZJOHHZOFDPMPHJDBM
problem, such as inconsistent use, interactions with other
medications, cigarette smoking, an STD, pregnancy, or
new pathologic uterine conditions (e.g., polyps or
fibroids). If an underlying gynecological problem is found,
treat the condition or refer for care.
t *GBOVOEFSMZJOHHZOFDPMPHJDBMQSPCMFNJTOPUGPVOEBOE
the woman wants treatment, the following treatment
option can be considered:
– Advise the woman to discontinue combined hormonal
contraceptive use (i.e., a hormone-free interval) for 3–4
consecutive days; a hormone-free interval is not
recommended during the first 21 days of using the
continuous or extended combined hormonal
contraceptive method. A hormone-free interval also is
not recommended more than once per month because
contraceptive effectiveness might be reduced.
t *GVOTDIFEVMFETQPUUJOHPSCMFFEJOHQFSTJTUTBOEUIFXPNBO
finds it unacceptable, counsel her on alternative contraceptive
methods, and offer another method if it is desired.
Comments and Evidence Summary. During contraceptive
counseling and before initiating extended or continuous

Recommendations and Reports

FIGURE 4. Recommended actions after delayed insertion or reinsertion with combined vaginal ring
Delayed insertion of a new ring or delayed
reinsertion* of a current ring for <48 hours
since a ring should have been inserted

Delayed insertion of a new ring or delayed
reinsertion* for ≥48 hours since a ring should
have been inserted

t*OTFSUSJOHBTTPPOBTQPTTJCMF
t,FFQUIFSJOHJOVOUJMUIFTDIFEVMFESJOH
SFNPWBMEBZ
t/PBEEJUJPOBMDPOUSBDFQUJWFQSPUFDUJPOJT
OFFEFE
t&NFSHFODZDPOUSBDFQUJPOJTOPUVTVBMMZ
needed but can be considered if delayed
insertion or reinsertion occurred earlier in
UIFDZDMFPSJOUIFMBTUXFFLPGUIFQSFWJPVT
DZDMF

t*OTFSUSJOHBTTPPOBTQPTTJCMF
t,FFQUIFSJOHJOVOUJMUIFTDIFEVMFESJOH
SFNPWBMEBZ
t6TFCBDLVQDPOUSBDFQUJPO FH
DPOEPNT

or avoid sexual intercourse until a ring has
CFFOXPSOGPSDPOTFDVUJWFEBZT
t*GUIFSJOHSFNPWBMPDDVSSFEJOUIFUIJSE
week of ring use:
0NJUUIFIPSNPOFGSFFXFFLCZ

finishing the third week of ring use and
TUBSUJOHBOFXSJOHJNNFEJBUFMZ
*GVOBCMFUPTUBSUBOFXSJOH

JNNFEJBUFMZ
VTFCBDLVQDPOUSBDFQUJPO
FH
DPOEPNT
PSBWPJETFYVBM

intercourse until a new ring has been
XPSOGPSDPOTFDVUJWFEBZT
t&NFSHFODZDPOUSBDFQUJPOTIPVMECF

considered if the delayed insertion or
reinsertion occurred within the first week of
SJOHVTFBOEVOQSPUFDUFETFYVBMJOUFSDPVSTF
PDDVSSFEJOUIFQSFWJPVTEBZT
t&NFSHFODZDPOUSBDFQUJPONBZBMTPCF
DPOTJEFSFEBUPUIFSUJNFTBTBQQSPQSJBUF

* If removal takes place but the woman is unsure of how long the ring has been removed, consider the ring to have been removed for ≥48 hours since a ring should
have been inserted or reinserted.

combined hormonal contraceptives, information about
common side effects such as unscheduled spotting or bleeding,
especially during the first 3–6 months of use, should be
discussed (248). These bleeding irregularities are generally
not harmful and usually improve with persistent use of the
hormonal method. To avoid unscheduled spotting or bleeding,
counseling should emphasize the importance of correct use and
timing; for users of contraceptive pills, emphasize consistent
pill use. Enhanced counseling about expected bleeding patterns
and reassurance that bleeding irregularities are generally not
harmful has been shown to reduce method discontinuation in
clinical trials with DMPA (101,102).
A systematic review identified three studies with small study
populations that addressed treatments for unscheduled bleeding
among women using extended or continuous combined
hormonal contraceptives (25). In two separate randomized
clinical trials in which women were taking either contraceptive
pills or using the contraceptive ring continuously for 168 days,
women assigned to a hormone-free interval of 3 or 4 days
reported improved bleeding. Although they noted an initial
increase in flow, this was followed by an abrupt decrease 7–8
days later with eventual cessation of flow 11–12 days later.

These findings were compared with women who continued to
use their method without a hormone-free interval, in which a
greater proportion reported either treatment failure or fewer
days of amenorrhea (249,250). In another randomized trial of
66 women with unscheduled bleeding among women using 84
days of hormonally active contraceptive pills, oral doxycycline
(100 mg twice daily) initiated the first day of bleeding and
taken for 5 days did not result in any improvement in bleeding
compared with placebo (251) (Level of evidence: I, fair, direct).

Progestin-Only Pills
POPs contain only a progestin and no estrogen and are
available in the United States. Approximately 9 out of 100
women become pregnant in the first year of use with POPs
with typical use (59). POPs are reversible and can be used
by women of all ages. POPs do not protect against STDs;
consistent and correct use of male latex condoms reduces the
risk for STDs, including HIV.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

FIGURE 5. Recommended steps after vomiting or diarrhea while using combined oral contraceptives
Vomiting or diarrhea (for any
reason, for any duration) that
occurs within 24 hours after
taking a hormonal pill

Vomiting or diarrhea, for any
reason, continuing for 24 to <48
hours after taking any hormonal
pill

tTaking another hormonal pill
(redose) is unnecessary.
tContinue taking pills daily at the
usual time (if possible, despite
discomfort).
tNo additional contraceptive
protection is needed.
tEmergency contraception is not
usually needed but can be
considered as appropriate.

Initiation of POPs
Timing
t 101TDBOCFTUBSUFEBUBOZUJNFJGJUJTSFBTPOBCMZDFSUBJO
that the woman is not pregnant (Box 1).

Need for Back-Up Contraception
t *G101TBSFTUBSUFEXJUIJOUIFGJSTUEBZTTJODFNFOTUSVBM
bleeding started, no additional contraceptive protection
is needed.
t *G101TBSFTUBSUFEEBZTTJODFNFOTUSVBMCMFFEJOHTUBSUFE
the woman needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 2 days.

Special Considerations
Amenorrhea (Not Postpartum)
t Timing: POPs can be started at any time if it is reasonably
certain that the woman is not pregnant (Box 1).

MMWR / June 21, 2013 / Vol. 62 / No. 5

Vomiting or diarrhea, for any reason,
continuing for ≥48 hours after taking any
hormonal pill

tContinue taking pills daily at the usual
time (if possible, despite discomfort).
tUse back-up contraception (e.g.,
condoms) or avoid sexual intercourse
until hormonal pills have been taken
for 7 consecutive days after vomiting or
diarrhea has resolved.
tIf vomiting or diarrhea occurred in the
last week of hormonal pills (e.g., days
15–21 for 28-day pill packs):
— Omit the hormone-free interval by
finishing the hormonal pills in the
current pack and starting a new
pack the next day.
— If unable to start a new pack
immediately, use back-up
contraception (e.g., condoms) or
avoid sexual intercourse until
hormonal pills from a new pack
have been taken for 7 consecutive
days.
t&NFSHFODZDPOUSBDFQUJPOTIPVMECF
considered if vomiting or diarrhea
occurred within the first week of a new
pill pack and unprotected sexual
intercourse occurred in the previous 5
days.
t&NFSHFODZDPOUSBDFQUJPONBZBMTPCF
considered at other times as
appropriate.

t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 2 days.
Postpartum (Breastfeeding)
t Timing: POPs can be started at any time, including
immediately postpartum (U.S. MEC 2 if <1 month postpartum
and U.S. MEC 1 if ≥1 month postpartum) if it is reasonably
certain that the woman is not pregnant (Box 1).
t Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (60), no
additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycles needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 2 days. If her menstrual cycles have

Recommendations and Reports

returned and it has been >5 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 2 days.
Postpartum (Not Breastfeeding)
t Timing: POPs can be started at any time, including
immediately postpartum (U.S. MEC 1), if it is reasonably
certain that the woman is not pregnant (Box 1).
t Need for back-up contraception: Women who are
≥21 days postpartum and whose menstrual cycles have
not returned need to abstain from sexual intercourse or
use additional contraceptive protection for the next 2 days.
If her menstrual cycles have returned and it has been >5
days since menstrual bleeding started, she needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 2 days.
Postabortion (Spontaneous or Induced)
t Timing: POPs can be started within the first 7 days,
including immediately postabortion (U.S. MEC 1).
t Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 2 days unless POPs
are started at the time of a surgical abortion.

Unlike COCs, POPs inhibit ovulation in about half of cycles,
although the rates vary widely by individual (252). Peak serum
steroid levels are reached about 2 hours after administration,
followed by rapid distribution and elimination, such that by
24 hours after administration, serum steroid levels are near
baseline (252). Therefore, taking POPs at approximately
the same time each day is important. An estimated 48
hours of POP use has been deemed necessary to achieve the
contraceptive effects on cervical mucus (252). If a woman needs
to use additional contraceptive protection when switching to
POPs from another contraceptive method, consider continuing
her previous method for 2 days after starting POPs. No direct
evidence was found regarding the effects of starting POPs at
different times of the cycle.

Switching from Another Contraceptive Method
t Timing: POPs can be started immediately if it is reasonably
certain that the woman is not pregnant (Box 1). Waiting
for her next menstrual period is unnecessary.
t Need for back-up contraception: If it has been >5 days
since menstrual bleeding started, she needs to abstain from
sexual intercourse or use additional contraceptive
protection for the next 2 days.
t Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle and
it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A healthcare provider may consider any of the following options:
– Advise the women to retain the IUD for at least 2 days
after POPs are initiated and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 2 days before removing
the IUD and switching to the new method.
– Advise the woman to use ECPs at the time of IUD removal.
Comments and Evidence Summary. In situations in which
the health-care provider is uncertain whether the woman might
be pregnant, the benefits of starting POPs likely exceed any
risk; therefore, starting POPs should be considered at any time,
with a follow-up pregnancy test in 2–4 weeks.

TABLE 6. Classification of examinations and tests needed before POP
initiation
Examination or laboratory test
Examination
Blood pressure
Weight (BMI) (weight [kg]/height [m]2)
Clinical breast examination
Bimanual examination and cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou smear)
STD screening with laboratory tests
HIV screening with laboratory tests

Class*
C
—†
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
POP = progestin-only pill; STD = sexually transmitted disease; U.S. MEC = U.S.
Medical Eligibility Criteria for Contraceptive Use, 2010.
* Class A: essential and mandatory in all circumstances for safe and effective
use of the contraceptive method. Class B: contributes substantially to safe and
effective use, but implementation may be considered within the public health
and/or service context; the risk of not performing an examination or test should
be balanced against the benefits of making the contraceptive method
available. Class C: does not contribute substantially to safe and effective use
of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for
any methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 2). However,
measuring weight and calculating BMI at baseline might be helpful for
monitoring any changes and counseling women who might be concerned about
weight change perceived to be associated with their contraceptive method.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

for a particular method of contraception. U.S. MEC might
be useful in such circumstances (5).
Comments and Evidence Summary. Weight (BMI): Obese
women can use POPs (U.S. MEC 1) (5); therefore, screening
for obesity is not necessary for the safe initiation of POPs.
However, measuring weight and calculating BMI at baseline
might be helpful for monitoring any changes and counseling
women who might be concerned about weight change
perceived to be associated with their contraceptive method.
Bimanual examination and cervical inspection: Pelvic
examination is not necessary before initiation of POPs because
it does not facilitate detection of conditions for which POPs
would be unsafe. Women with current breast cancer should
not use POPs (U.S. MEC 4), and women with certain liver
diseases generally should not use POPs (U.S. MEC 3) (5);
however, neither of these conditions are likely to be detected
by pelvic examination (120). A systematic review identified
two case-control studies that compared delayed versus
immediate pelvic examination before initiation of hormonal
contraceptives, specifically oral contraceptives or DMPA (15).
No differences in risk factors for cervical neoplasia, incidence
of STDs, incidence of abnormal Papanicolaou smears, or
incidence of abnormal wet mounts were observed (Level of
evidence: II-2 fair, direct).
Liver enzymes: Although women with certain liver diseases
generally should not use POPs (U.S. MEC 3) (5), screening
for liver disease before initiation of POPs is not necessary
because of the low prevalence of these conditions and the
high likelihood that women with liver disease already would
have had the condition diagnosed. A systematic review did
not identify any evidence regarding outcomes among women
who were screened versus not screened with liver enzyme
tests before initiation of hormonal contraceptives (14). The
prevalence of liver disorders among women of reproductive
age is low. In 2008 among U.S. adults aged 18–44 years,
the percentage with liver disease (not further specified) was
1.0% (90). In 2009, the incidence of acute hepatitis A, B,
or C among women was <1 per 100,000 population (91).
During 1998–2007, the incidence of liver carcinoma among
women was approximately 3 per 100,000 population (92).
Because estrogen and progestins are metabolized in the liver,
the use of hormonal contraceptives among women with liver
disease might, theoretically, be a concern. The use of hormonal
contraceptives, specifically COCs and POPs, does not affect
disease progression or severity in women with hepatitis,
cirrhosis, or benign focal nodular hyperplasia (93,94).
Clinical breast examination: Although women with current
breast cancer should not use POPs (U.S. MEC 4) (5), screening
asymptomatic women with a clinical breast examination

MMWR / June 21, 2013 / Vol. 62 / No. 5

before initiating POPs is not necessary because of the low
prevalence of breast cancer among women of reproductive age.
A systematic review did not identify any evidence regarding
outcomes among women who were screened versus not
screened with a clinical breast examination before initiation of
hormonal contraceptives (15). The incidence of breast cancer
among women of reproductive age in the United States is low.
In 2009, the incidence of breast cancer among women ages
20–49 was approximately 72 per 100,000 women (95).
Other screening: Women with hypertension, diabetes,
hyperlipidemia, anemia, thrombogenic mutations, cervical
intraepithelial neoplasia, cervical cancer, STDs, or HIV
infection can use (U.S. MEC 1) or generally can use (U.S.
MEC 2) POPs (5); therefore, screening for these conditions
is not necessary for the safe initiation of POPs.

Number of Pill Packs that Should Be
Provided at Initial and Return Visits
t "UUIFJOJUJBMBOESFUVSOWJTJUT
QSPWJEFPSQSFTDSJCFVQUPB
1-year supply of POPs (e.g., 13 28-day pill packs),
depending on the woman’s preferences and anticipated use.
t " XPNBO TIPVME CF BCMF UP PCUBJO 101T FBTJMZ JO UIF
amount and at the time she needs them.
Comments and Evidence Summary. The more pill packs
given up to 13 cycles, the higher the continuation rates.
Restricting the number of pill packs distributed or prescribed
can result in unwanted discontinuation of the method and
increased risk for pregnancy.
A systematic review of the evidence suggested that providing
a greater number of pill packs was associated with increased
continuation (23). Studies that compared provision of one
versus 12 packs, one versus 12 or 13 packs, or three versus
seven packs found increased continuation of pill use among
women provided with more pill packs (209–211). However,
one study found that there was no difference in continuation
when patients were provided one and then three packs versus
four packs all at once (212). In addition to continuation, a
greater number of pill packs provided was associated with fewer
pregnancy tests, fewer pregnancies, and lower cost per client.
However, a greater number of pill packs (13 packs versus three
packs) also was associated with increased pill wastage in one
study (210) (Level of evidence: I to II-2, fair, direct).

Recommendations and Reports

different situations. Specific populations that might benefit
from more frequent follow-up visits include adolescents, those
with certain medical conditions or characteristics, and those
with multiple medical conditions.
t "EWJTFBXPNBOUPSFUVSOBUBOZUJNFUPEJTDVTTTJEFFGGFDUT
or other problems or if she wants to change the method
being used. No routine follow-up visit is required.
t "UPUIFSSPVUJOFWJTJUT
IFBMUIDBSFQSPWJEFSTTFFJOH101
users should do the following:
– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including medications,
that would change the appropriateness of POPs for safe
and effective continued use based on U.S. MEC (e.g.,
category 3 and 4 conditions and characteristics).
– Consider assessing weight changes and counseling women
who are concerned about weight changes perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. No evidence was
found regarding whether a routine follow-up visit after
initiating POPs improves correct or continued use.

Missed POPs
For the following recommendations, a dose is considered
missed if it has been >3 hours since it should have been taken.
t 5BLFPOFQJMMBTTPPOBTQPTTJCMF
t $POUJOVFUBLJOHQJMMTEBJMZ
POFFBDIEBZ
BUUIFTBNFUJNF
each day, even if it means taking two pills on the same day.
t 6TFCBDLVQDPOUSBDFQUJPO FH
DPOEPNT
PSBWPJETFYVBM
intercourse until pills have been taken correctly, on time,
for 2 consecutive days.
t &NFSHFODZ DPOUSBDFQUJPO TIPVME CF DPOTJEFSFE JG UIF
woman has had unprotected sexual intercourse.
Comments and Evidence Summary. Inconsistent or
incorrect use of oral contraceptive pills is a major reason for oral
contraceptive failure. Unlike COCs, POPs inhibit ovulation
in about half of cycles, although this rate varies widely by
individual (252). Peak serum steroid levels are reached about
2 hours after administration, followed by rapid distribution
and elimination, such that by 24 hours after administration,
serum steroid levels are near baseline (252). Therefore, taking
POPs at approximately the same time each day is important.
An estimated 48 hours of POP use was deemed necessary to
achieve the contraceptive effects on cervical mucus (252).
Women who frequently miss POPs should consider an
alternative contraceptive method that is less dependent on
the user to be effective (e.g., IUD, implant, or injectable).

No evidence was found regarding the effects of missed POPs
available in the United States on measures of contraceptive
effectiveness including pregnancy, follicular development,
hormone levels, or cervical mucus quality.

Vomiting or Severe Diarrhea (for any
Reason or Duration) that Occurs Within
3 Hours After Taking a Pill
t 5BLFBOPUIFSQJMMBTTPPOBTQPTTJCMF JGQPTTJCMF
EFTQJUF
discomfort).
t $POUJOVFUBLJOHQJMMTEBJMZ
POFFBDIEBZ
BUUIFTBNFUJNF
each day.
t 6TFCBDLVQDPOUSBDFQUJPO FH
DPOEPNT
PSBWPJETFYVBM
intercourse until 2 days after vomiting or diarrhea has resolved.
t &NFSHFODZ DPOUSBDFQUJPO TIPVME CF DPOTJEFSFE JG UIF
woman has had unprotected sexual intercourse.
Comments and Evidence Summary. Theoretically, the
contraceptive effectiveness of POPs might be decreased because
of vomiting or severe diarrhea. Because of the lack of evidence
to address this question, these recommendations are based on
the recommendations for missed POPs. No evidence was found
regarding the effects of vomiting or diarrhea on measures of
contraceptive effectiveness, including pregnancy, follicular
development, hormone levels, or cervical mucus quality.

Standard Days Method
SDM is a method based on fertility awareness; users must
avoid unprotected sexual intercourse on days 8–19 of the
menstrual cycle (253). Approximately 5 out of 100 women
become pregnant in the first year of use with perfect (i.e.,
correct and consistent) use of SDM (253); effectiveness based
on typical use is not available for this method but is expected
to be lower than that for perfect use. SDM is reversible and can
be used by women of all ages. SDM does not protect against
STDs; consistent and correct use of male latex condoms reduces
the risk for STDs, including HIV.

Use of SDM Among Women with Various
Menstrual Cycle Durations
Menstrual Cycles of 26–32 Days
t 5IFTFXPNFONBZVTFUIFNFUIPE
t 1SPWJEFBCBSSJFSNFUIPEPGDPOUSBDFQUJPOGPSQSPUFDUJPO
on days 8–19 if she wants one.
t *GTIFIBTVOQSPUFDUFETFYVBMJOUFSDPVSTFEVSJOHEBZTo
consider the use of emergency contraception if appropriate.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Two or More Menstrual Cycles of <26 or >32 Days
Within Any 1 Year of SDM Use
t "EWJTF UIF XPNBO UIBU UIF NFUIPE NJHIU OPU CF
appropriate for her because of a higher risk for pregnancy.
Help her consider another method.
Comments and Evidence Summary. The probability of
pregnancy is increased when the menstrual cycle is outside the
range of 26–32 days, even if unprotected sexual intercourse is
avoided on days 8–19. A study of 7,600 menstrual cycles, including
information on cycle length and signs of ovulation, concluded that
the theoretical effectiveness of SDM is greatest for women with
cycles of 26–32 days, that the method is still effective for women
who occasionally have a cycle outside this range, and that it is
less effective for women who consistently have cycles outside this
range. Information from daily hormonal measurements shows
that the timing of the 6-day fertile window varies greatly, even
among women with regular cycles (39,254,255).

Emergency Contraception
Emergency contraception consists of methods that can be
used by women after sexual intercourse to prevent pregnancy.
Emergency contraception methods have varying ranges
of effectiveness depending on the method and timing of
administration. Four options are available in the United States:
the Cu-IUD and three types of ECPs.

Types of Emergency Contraception
Intrauterine Device

t *OBEEJUJPO
XIFOUIFEBZPGPWVMBUJPODBOCFFTUJNBUFE
the Cu-IUD can be inserted beyond 5 days after sexual
intercourse, as long as insertion does not occur >5 days
after ovulation.
ECPs
t &$1TTIPVMECFUBLFOBTTPPOBTQPTTJCMFXJUIJOEBZTPG
unprotected sexual intercourse.
Comments and Evidence Summary. Cu-IUDs are highly
effective as emergency contraception (256) and can be
continued as regular contraception. UPA and levonorgestrel
ECPs have similar effectiveness when taken within 3 days after
unprotected sexual intercourse; however, UPA has been shown
to be more effective than the levonorgestrel formulation 3–5
days after unprotected sexual intercourse (257). The combined
estrogen and progestin regimen is less effective than UPA
or levonorgestrel and also is associated with more frequent
occurrence of side effects (nausea and vomiting) (258). The
levonorgestrel formulation might be less effective than UPA
among obese women (257).
Two studies of UPA use found consistent decreases in
pregnancy rates when administered within 120 hours of
unprotected sexual intercourse (257,259). Five studies found
that the levonorgestrel and combined regimens decreased risk
for pregnancy through the fifth day after unprotected sexual
intercourse; however, rates of pregnancy were slightly higher
when ECPs were taken after 3 days (260–264). A meta-analysis
of levonorgestrel ECPs found that pregnancy rates were low
when administered within 4 days after unprotected sexual
intercourse but increased at 4–5 days (265) (Level of evidence:
I to II-2, good to poor, direct).

t $V*6%

Advance Provision of ECPs

ECPs
t 6MJQSJTUBMBDFUBUF 61"
JOBTJOHMFEPTF NH

t -FWPOPSHFTUSFMJOBTJOHMFEPTF NH
PSBTBTQMJUEPTF
(1 dose of 0.75 mg of levonorgestrel followed by a second
dose of 0.75 mg of levonorgestrel 12 hours later)
t $PNCJOFEFTUSPHFOBOEQSPHFTUJOJOEPTFT :V[QFSFHJNFO
1 dose of 100 µg of ethinyl estradiol plus 0.50 mg of
levonorgestrel followed by a second dose of 100 µg of ethinyl
estradiol plus 0.50 mg of levonorgestrel 12 hours later)

Initiation of Emergency Contraception
Timing
Cu-IUD
t 5IF$V*6%DBOCFJOTFSUFEXJUIJOEBZTPGUIFGJSTUBDUPG
unprotected sexual intercourse as an emergency contraceptive.

MMWR / June 21, 2013 / Vol. 62 / No. 5

t "OBEWBODFTVQQMZPG&$1TNBZCFQSPWJEFETPUIBU&$1T
will be available when needed and can be taken as soon as
possible after unprotected sexual intercourse.
Comments and Evidence Summary. A systematic review
identified 17 studies that reported on safety or effectiveness of
advance ECPs in adult or adolescent women (26). Any use of
ECPs was two to seven times greater among women who received
an advance supply of ECPs. However, a summary estimate
(relative risk = 0.97; 95% confidence interval = 0.77–1.22) of
five randomized controlled trials did not indicate a significant
reduction in unintended pregnancies at 12 months with
advance provision of ECPs. In the majority of studies among
adults or adolescents, patterns of regular contraceptive use,
pregnancy rates, and incidence of STDs did not vary between
those who received advance ECPs and those who did not.
Although available evidence supports the safety of advance

Recommendations and Reports

provision of ECPs, effectiveness of advance provision of ECPs
in reducing pregnancy rates at the population level has not been
demonstrated (Level of evidence: I to II-3, good to poor, direct).

Initiation of Regular Contraception
After ECPs
UPA
t "OZ SFHVMBS DPOUSBDFQUJWF NFUIPE DBO CF TUBSUFE
immediately after the use of UPA.
t 5IFXPNBOOFFETUPBCTUBJOGSPNTFYVBMJOUFSDPVSTFPS
use barrier contraception for 14 days or until her next
menses, whichever comes first.
t "EWJTFUIFXPNBOUPIBWFBQSFHOBODZUFTUJGTIFEPFTOPU
have a withdrawal bleed within 3 weeks.

Levonorgestrel and Combined Estrogen and
Progestin ECPs
t "OZ SFHVMBS DPOUSBDFQUJWF NFUIPE DBO CF TUBSUFE
immediately after the use of levonorgestrel or combined
estrogen and progestin ECPs.
t 5IFXPNBOOFFETUPBCTUBJOGSPNTFYVBMJOUFSDPVSTFPS
use barrier contraception for 7 days.
t "EWJTFUIFXPNBOUPIBWFBQSFHOBODZUFTUJGTIFEPFTOPU
have a withdrawal bleed within 3 weeks.
Comments and Evidence Summary. Data on when a
woman can start regular contraception after ECPs are limited
to expert opinion and product labeling (27). Theoretically,
the effectiveness of systemic hormonal contraception might
be decreased when administered concurrently or in close
succession because of the antiprogestin properties of UPA
(266,267); these theoretical concerns do not exist for combined
estrogen and progestin or levonorgestrel formulations of
ECPs. The resumption or initiation of regular hormonal
contraception after ECP use involves consideration of the
risk for pregnancy if ECPs fail and the risks for unintended
pregnancy if contraception initiation is delayed until the
subsequent menstrual cycle. If a woman is planning to initiate
contraception after the next menstrual period after ECP
use, the cycle in which ECPs are used might be shortened,
prolonged, or involve unscheduled bleeding.

Prevention and Management of Nausea
and Vomiting with ECP Use
Nausea and Vomiting
t -FWPOPSHFTUSFM BOE 61" &$1T DBVTF MFTT OBVTFB BOE
vomiting than combined estrogen and progestin ECPs.

t 3PVUJOF VTF PG BOUJFNFUJDT CFGPSF UBLJOH &$1T JT OPU
recommended. Pretreatment with antiemetics may be
considered depending on availability and clinical judgment.
Vomiting Within 3 Hours of Taking ECPs
t "OPUIFSEPTFPG&$1TIPVMECFUBLFOBTTPPOBTQPTTJCMF
Use of an antiemetic should be considered.
Comments and Evidence Summary. Many women do
not experience nausea or vomiting when taking ECPs, and
predicting which women will experience nausea or vomiting
is difficult. Although routine use of antiemetics before taking
ECPs is not recommended, antiemetics are effective in some
women and can be offered when appropriate. Health-care
providers who are deciding whether to offer antiemetics to
women taking ECPs should consider the following: 1) women
taking combined estrogen and progestin ECPs are more
likely to experience nausea and vomiting than those who
take levonorgestrel or UPA ECPs; 2) evidence indicates that
antiemetics reduce the occurrence of nausea and vomiting in
women taking combined estrogen and progestin ECPs; and
3) women who take antiemetics might experience other side
effects from the antiemetics.
A systematic review examined incidence of nausea and
vomiting with different ECP regimens and effectiveness of
antinausea drugs in reducing nausea and vomiting with ECP
use (28). The levonorgestrel regimen was associated with
significantly less nausea than a nonstandard dose of UPA
(50 mg) and the standard combined estrogen and progestin
regimen (268–270). Use of the split-dose levonorgestrel
showed no differences in nausea and vomiting compared
with the single-dose levonorgestrel (260,261,263,271) (Level
of evidence: I, good-fair, indirect). Two trials of antinausea
drugs, meclizine and metoclopramide, taken before combined
estrogen and progestin ECPs, reduced the severity of nausea
(272,273). Significantly less vomiting occurred with meclizine
but not metoclopramide (Level of evidence: I, good-fair,
direct). No direct evidence was found regarding the effects of
vomiting after taking ECPs.

Female Sterilization
Laparoscopic, abdominal, and hysteroscopic methods of
female sterilization are available in the United States, and
some of these procedures can be performed in an outpatient
procedure or office setting. Fewer than 1 out of 100 women
become pregnant in the first year after female sterilization
(59). Because these methods are intended to be irreversible,
all women should be appropriately counseled about the
permanency of sterilization and the availability of highly

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

effective, long-acting, reversible methods of contraception.
Female sterilization does not protect against STDs; consistent
and correct use of male latex condoms reduces the risk for
STDs, including HIV.

When Hysteroscopic Sterilization Is
Reliable for Contraception
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contraception, a hysterosalpingogram (HSG) must be
performed 3 months after the sterilization procedure to
confirm bilateral tubal occlusion.
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from sexual intercourse or use additional contraceptive
protection until she has confirmed bilateral tubal occlusion.

When Laparoscopic and Abdominal
Approches Are Reliable for Contraception
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immediately after laparoscopic and abdominal approaches.
No additional contraceptive protection is needed.
Comments and Evidence Summary. HSG confirmation
is necessary to confirm bilateral tubal occlusion after
hysteroscopic sterilization. The inserts for the hysteroscopic
sterilization system available in the United States are placed
bilaterally into the fallopian tubes and require 3 months
for adequate fibrosis and scarring leading to bilateral tubal
occlusion. After hysteroscopic sterilization, advise the woman
to correctly and consistently use an effective method of
contraception while awaiting confirmation. If compliance
with another method might be a problem, a woman and her
health-care provider may consider DMPA injection at the time
of sterilization to ensure adequate contraception for 3 months.
Unlike laparoscopic and abdominal sterilizations, pregnancy
risk beyond 7 years of follow-up has not been studied among
women who received hysteroscopic sterilization.
Pregnancy risk with at least 10 years of follow-up has
been studied among women who received laparoscopic and
abdominal sterilizations (274,275). Although these methods
are highly effective, pregnancies can occur many years after
the procedure, and the risk for pregnancy is higher among
younger women (274,276).
A systematic review was conducted to identify studies that
reported whether pregnancies occurred after hysteroscopic
sterilization (29). Twenty-four studies were identified that
reported whether pregnancies occurred after hysteroscopic
sterilization and found that very few pregnancies occurred
among women with confirmed bilateral tubal occlusion;
however, few studies include long-term follow-up, and

MMWR / June 21, 2013 / Vol. 62 / No. 5

none with follow-up for >7 years. Among women who had
successful bilateral placement, most pregnancies that occurred
after hysteroscopic sterilization were in women who did
not have confirmed bilateral tubal occlusion at 3 months,
either because of lack of follow up or misinterpretation of
HSG results (277–279). Some pregnancies occurred within
3 months of placement, including among women who were
already pregnant at the time of the procedure, women who
did not use alternative contraception, or women who had
failures of alternative contraception (277,278,280–283).
Although these studies generally demonstrated high rates of
bilateral placement, some pregnancies occurred as a result
of lack of bilateral placement identified on later imaging
(277,278,280,281,283,284). Most pregnancies occurred after
deviations from FDA directions, which include placement in
the early follicular phase of the menstrual cycle, imaging at
3 months to document proper placement, and use of effective
alternative contraception until documented occlusion (Level
of evidence: II-3, fair, direct).

Male Sterilization
Male sterilization, or vasectomy, is one of the few
contraceptive methods available to men and can be performed
in an outpatient procedure or office setting. Fewer than 1
woman out of 100 becomes pregnant in the first year after
her male partner undergoes sterilization (59). Because male
sterilization is intended to be irreversible, all men should be
appropriately counseled about the permanency of sterilization
and the availability of highly effective, long-acting, reversible
methods of contraception for women. Male sterilization does
not protect against STDs; consistent and correct use of male
latex condoms reduces the risk for STDs, including HIV.

When Vasectomy Is Reliable for
Contraception
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a vasectomy to ensure the procedure was successful.
t 5IFNBOTIPVMECFBEWJTFEUIBUIFTIPVMEVTFBEEJUJPOBM
contraceptive protection or abstain from sexual intercourse
until he has confirmation of vasectomy success by
postvasectomy semen analysis.

Other Postprocedure Recommendations
t 5IFNBOTIPVMESFGSBJOGSPNFKBDVMBUJPOGPSBQQSPYJNBUFMZ
1 week after the vasectomy to allow for healing of surgical
sites and, after certain methods of vasectomy, occlusion
of the vas.

Recommendations and Reports

Comments and Evidence Summary. The Vasectomy
Guideline Panel of the American Urological Association
performed a systematic review of key issues concerning the
practice of vasectomy (285). All English-language publications
on vasectomy published during 1949–2011 were reviewed. For
more information, see the American Urological Association
Vasectomy Guidelines (available at http://www.auanet.org/
education/vasectomy.cfm).
Motile sperm disappear within a few weeks after vasectomy
(286–289). The time to azoospermia varies widely in different
studies; however, by 12 weeks after the vasectomy, 80% of men
have azoospermia, and almost all others have rare nonmotile
sperm (defined as ≤100,000 nonmotile sperm per milliliter)
(285). The number of ejaculations after vasectomy is not a
reliable indicator of when azoospermia or rare nonmotile sperm
will be achieved (285). Once azoospermia or rare nonmotile
sperm has been achieved, patients can rely on the vasectomy for
contraception, although not with 100% certainty. The risk for
pregnancy after a man has achieved postvasectomy azoospermia
is approximately one in 2,000 (290–294).
A median of 78% (range 33%–100%) of men return for
a single postvasectomy semen analysis (285). In the largest
cohorts that appear typical of North American vasectomy
practice, approximately two thirds of men (55%–71%) return
for at least one postvasectomy semen analysis (291,295–299).
Assigning men an appointment after their vasectomy might
improve compliance with follow-up (300).

When Women Can Stop Using
Contraceptives
t $POUSBDFQUJWFQSPUFDUJPOJTTUJMMOFFEFEGPSXPNFOBHFE
>44 years if the woman wants to avoid pregnancy.
Comments and Evidence Summary. The age at which
a woman is no longer at risk for pregnancy is not known.
Although uncommon, spontaneous pregnancies occur
among women aged >44 years. Both the American College
of Obstetricians and Gynecologists and the North American
Menopause Society recommend that women continue
contraceptive use until menopause or age 50–55 years
(301,302). The median age of menopause is approximately 51
years in North America (301) but can vary from ages 40 to 60
years (303). The median age of definitive loss of natural fertility
is 41 years but can range up to age 51 years (304,305). No
reliable laboratory tests are available to confirm definitive loss
of fertility in a woman. The assessment of follicle-stimulating
hormone levels to determine when a woman is no longer fertile
might not be accurate (301).

Health-care providers should consider the risks for becoming
pregnant in a woman of advanced reproductive age, as well as any
risks of continuing contraception until menopause. Pregnancies
among women of advanced reproductive age are at higher
risk for maternal complications, such as hemorrhage, venous
thromboembolism, and death, and fetal complications, such
as spontaneous abortion, stillbirth, and congenital anomalies
(306–308). Risks associated with continuing contraception,
in particular risks for acute cardiovascular events (venous
thromboembolism, myocardial infarction, or stroke) or breast
cancer, also are important to consider. U.S. MEC states that
on the basis of age alone, women aged >45 years can use POPs,
implants, the LNG-IUD, or the Cu-IUD (U.S. MEC 1) (5).
Women aged >45 years generally can use combined hormonal
contraceptives and DMPA (U.S. MEC 2) (5). However, women
in this age group might have chronic conditions or other risk
factors that might render use of hormonal contraceptive methods
unsafe; U.S. MEC might be helpful in guiding the safe use of
contraceptives in these women.
The incidence of venous thromboembolism was higher
among oral contraceptive users aged ≥45 years compared with
younger oral contraceptive users in two studies (309–311);
however, an interaction between hormonal contraception
and increased age compared with baseline risk was not
demonstrated (309,310) or was not examined (311). The
relative risk for myocardial infarction was higher among all
oral contraceptive users than in nonusers, although a trend of
increased relative risk with increasing age was not demonstrated
(312,313). No studies were found regarding the risk for stroke
in COC users aged ≥45 years (Level of evidence: II-2, good
to poor, direct).
A pooled analysis by the Collaborative Group on Hormonal
Factors and Breast Cancer in 1996 (314) found small increased
relative risks for breast cancer among women aged ≥45 years
whose last use of combined hormonal contraceptives was <5
years previously and for those whose last use was 5–9 years
previously. Seven more recent studies suggested small but
nonsignificant increased relative risks for breast carcinoma
in situ or breast cancer among women who had used oral
contraceptives or DMPA when they were aged ≥40 years
compared with those who had never used either method
(315–321) (Level of evidence: II-2, fair, direct).

Conclusion
Women, men, and couples have increasing numbers of safe
and effective choices for contraceptive methods, including LARC
methods such as IUDs and implants, to reduce the risk for
unintended pregnancy. However, with these expanded options

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

comes the need for evidence-based guidance to help health-care
providers offer quality family planning care to their patients,
including choosing the most appropriate contraceptive method
for individual circumstances and using that method correctly,
consistently, and continuously to maximize effectiveness.
Removing unnecessary barriers can help patients access and
successfully use contraceptive methods. Several medical barriers
to initiating and continuing contraceptive methods might exist,
such as unnecessary screening examinations and tests before
starting the method (e.g., a pelvic examination before initiation
of COCs), inability to receive the contraceptive on the same
day as the visit (e.g., waiting for test results that might not be
needed or waiting until the woman’s next menstrual period to
start use), and difficulty obtaining continued contraceptive
supplies (e.g., restrictions on number of pill packs dispensed
at one time). Removing unnecessary steps, such as providing
prophylactic antibiotics at the time of IUD insertion or requiring
unnecessary follow-up procedures, also can help patients access
and successfully use contraception.
Most women can start most contraceptive methods at
any time, and few examinations or tests, if any, are needed
before starting a contraceptive method. Routine follow-up
for most women includes assessment of her satisfaction with
the contraceptive method, concerns about method use, and
changes in health status or medications that could affect
medical eligibility for continued use of the method. Because
changes in bleeding patterns are one of the major reasons
for discontinuation of contraception, recommendations are
provided for the management of bleeding irregularities with
various contraceptive methods. In addition, because women
and health-care providers can be confused about the procedures
for missed pills and dosing errors with the contraceptive patch
and ring, the instructions are streamlined for easier use. ECPs
and emergency use of the Cu-IUD are important options for
women, and recommendations on using these methods, as
well as starting regular contraception after use of emergency
contraception, are provided. Male and female sterilization are
highly effective methods of contraception for men, women, and
couples who have completed childbearing; for men undergoing
vasectomy and women undergoing a hysteroscopic sterilization
procedure, additional contraceptive protection is needed until
the success of the procedure can be confirmed.
CDC is committed to working with partners at the federal,
national, and local levels to disseminate, implement, and
evaluate the recommendations in U.S. SPR so that the
information reaches health-care providers. Strategies for
dissemination and implementation include collaborating
with other federal agencies and professional and service
organizations to widely distribute the recommendations
through presentations, electronic distribution, newsletters, and

MMWR / June 21, 2013 / Vol. 62 / No. 5

other publications; development of provider tools and job aids
to assist providers in implementing the new recommendations;
and training activities for students, as well as for continuing
education. CDC will conduct a survey of family planning
health-care providers before and after release of this report
to assess attitudes and practices related to contraceptive
use. Results from this survey will assist CDC in evaluating
the impact of these recommendations on the provision
of contraceptives in the United States. Finally, CDC will
continually monitor new scientific evidence and will update
these recommendations as warranted by new evidence. Updates
to the recommendations, as well as provider tools and other
resources, are available on the CDC U.S. SPR website (http://
www.cdc.gov/reproductivehealth/UnintendedPregnancy/
USSPR.htm).
Acknowledgment
This report is based, in part, on the work of the Promoting Family
Planning Team, Department of Reproductive Health and Research,
World Health Organization, and its development of the Selected
Practice Recommendations for Contraceptive Use.
References
1. Finer LB, Zolna MR. Unintended pregnancy in the United States:
incidence and disparities, 2006. Contraception 2011;84:478–85.
2. Gipson JD, Koenig MA, Hindin MJ. The effects of unintended
pregnancy on infant, child, and parental health: a review of the literature.
Stud Fam Plann 2008;39:18–38.
3. Trussell J. The cost of unintended pregnancy in the United States.
Contraception 2007;75:168–70.
4. Finer LB, Henshaw SK. Disparities in rates of unintended pregnancy in
the United States, 1994 and 2001. Perspect Sex Reprod Health
2006;38:90–6.
5. CDC. U.S. medical eligibility criteria for contraceptive use. MMWR
2010;59(No. RR-4).
6. World Health Organization. Selected practice recommendations for
contraceptive use. Second ed. Geneva: World Health Organization; 2004.
7. World Health Organization. Selected practice recommendations for
contraceptive use. 2008 update. Geneva, Switzerland: World Health
Organization; 2008. Available at http://whqlibdoc.who.int/hq/2008/
WHO_RHR_08.17_eng.pdf.
8. Faculty of Sexual and Reproductive Health Care. UK Selected Practice
Recommendations for Contraceptive Use. London, England: Faculty of
Sexual and Reproductive Health Care; 2002. Available at http://www.
fsrh.org/pdfs/SelectedPracticeRecommendations2002.pdf.
9. Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items
for systematic reviews and meta-analyses: the PRISMA statement. Int J
Surg 2010;8:336–41.
10. Stroup DF, Berlin JA, Morton SC, et al. Meta-analysis of observational
studies in epidemiology: a proposal for reporting. Meta-analysis Of
Observational Studies in Epidemiology (MOOSE) group. JAMA
2000;283:2008–12.
11. Harris RP, Helfand M, Woolf SH, et al. Current methods of the US
Preventive Services Task Force: a review of the process. Am J Prev Med
2001;20(Suppl):21–35.
12. Tepper NK, Marchbanks PA, Curtis KM. Use of a checklist to rule out
pregnancy: a systematic review. Contraception 2013;87:661–5.

Recommendations and Reports

13. Whiteman MK, Tyler CP, Folger SG, Gaffield ME, Curtis KM. When
can a woman have an intrauterine device inserted? A systematic review.
Contraception 2013;87:666–73.
14. Tepper NK, Steenland MW, Marchbanks PA, Curtis KM. Laboratory
screening prior to initiating contraception: a systematic review.
Contraception 2013;87:645–9.
15. Tepper NK, Curtis KM, Steenland MW, Marchbanks PA. Physical
examination prior to initiating hormonal contraception: a systematic
review. Contraception 2013;87:650–4.
16. Steenland MW, Zapata LB, Brahmi D, Marchbanks PA, Curtis KM. The
effect of follow-up visits or contacts after contraceptive initiation on
method continuation and correct use. Contraception 2013;87:625–30.
17. Steenland MW, Zapata LB, Brahmi D, Marchbanks PA, Curtis KM.
Appropriate follow up to detect potential adverse events after initiation
of select contraceptive methods: a systematic review. Contraception
2013;87:611–24.
18. Godfrey EM, Folger SG, Jeng G, Jamieson DJ, Curtis KM. Treatment
of bleeding irregularities in women with copper-containing IUDs: a
systematic review. Contraception 2013;87:549–66.
19. Tepper NK, Steenland MW, Gaffield ME, Marchbanks PA, Curtis KM.
Retention of intrauterine devices in women who acquire pelvic inflammatory
disease: a systematic review. Contraception 2013;87:655–60.
20. Kapp N, Gaffield ME. Initiation of progestogen-only injectables on
different days of the menstrual cycle and its effect on contraceptive
effectiveness and compliance: a systematic review. Contraception
2013;87:576–82.
21. Tepper NK, Curtis KM, Steenland MW, Marchbanks PA. Blood pressure
measurement prior to initiating hormonal contraception: a systematic
review. Contraception 2013;87:631–8.
22. Brahmi D, Curtis KM. When can a woman start combined hormonal
contraceptives (CHCs)? A systematic review. Contraception 2013;
87:524–38.
23. Steenland MW, Rodriguez MI, Marchbanks PA, Curtis KM. How does
the number of oral contraceptive pill packs dispensed or prescribed affect
continuation and other measures of consistent and correct use? A
systematic review. Contraception 2013;87:605–10.
24. Zapata LB, Steenland MW, Brahmi D, Marchbanks PA, Curtis KM.
Effect of missed combined hormonal contraceptives on contraceptive
effectiveness: a systematic review. Contraception 2013;87:685–700.
25. Godfrey EM, Whiteman MK, Curtis KM. Treatment of unscheduled
bleeding in women using extended- or continuous-use combined hormonal
contraception: a systematic review. Contraception 2013;87:567–75.
26. Rodriguez MI, Curtis KM, Gaffield ML, Jackson E, Kapp N. Advance
supply of emergency contraception: a systematic review. Contraception
2013;87:590–601.
27. Salcedo J, Rodriguez MI, Curtis KM, Kapp N. When can a woman
resume or initiate contraception after taking emergency contraceptive
pills? A systematic review. Contraception 2013;87:602–4.
28. Rodriguez MI, Godfrey EM, Warden M, Curtis KM. Prevention and
management of nausea and vomiting with emergency contraception: a
systematic review. Contraception 2013;87:583–9.
29. Cleary TP, Tepper NK, Cwiak C, et al. Pregnancies after hysteroscopic
sterilization: a systematic review. Contraception 2013;87:539–48.
30. Tepper NK, Steenland MW, Marchbanks PA, Curtis KM. Hemoglobin
measurement prior to initiating copper intrauterine devices: a systematic
review. Contraception 2013;87:639–44.
31. Folger SG, Jamieson DJ, Godfrey EM, Zapata LB, Curtis KM. Evidencebased guidance on selected practice recommendations for contraceptive
use: identification of research gaps. Contraception 2013;87:517–23.
32. CDC. Sexually transmitted diseases treatment guidelines. MMWR
2010;59(No. RR-12).
33. Mohllajee AP, Curtis KM, Flanagan RG, Rinehart W, Gaffield ML,
Peterson HB. Keeping up with evidence a new system for WHO’s evidencebased family planning guidance. Am J Prev Med 2005;28:483–90.

34. Stanback J, Nakintu N, Qureshi Z, Nasution M. Does assessment of
signs and symptoms add to the predictive value of an algorithm to rule
out pregnancy? J Fam Plann Reprod Health Care 2006;32:27–9.
4UBOCBDL+
/BOEB,
3BNJSF[:
3PVOUSFF8
$BNFSPO4#7BMJEBUJPO
of a job aid to rule out pregnancy among family planning clients in
Nicaragua. Rev Panam Salud Publica 2008;23:116–8.
36. Stanback J, Qureshi Z, Sekadde-Kigondu C, Gonzalez B, Nutley T.
Checklist for ruling out pregnancy among family-planning clients in
primary care. Lancet 1999;354:566.
37. Torpey K, Mwenda L, Kabaso M, et al. Excluding pregnancy among
women initiating antiretroviral therapy: efficacy of a family planning
job aid. BMC Public Health 2010;10:249.
38. Cole LA, Ladner DG, Byrn FW. The normal variabilities of the menstrual
cycle. Fertil Steril 2009;91:522–7.
39. Wilcox AJ, Dunson D, Baird DD. The timing of the “fertile window”
in the menstrual cycle: day specific estimates from a prospective study.
BMJ 2000;321:1259–62.
40. Donnet ML, Howie PW, Marnie M, Cooper W, Lewis M. Return of
ovarian function following spontaneous abortion. Clin Endocrinol (Oxf)
1990;33:13–20.
41. Lahteenmaki P. Postabortal contraception. Ann Med 1993;25:185–9.
42. Stoddard A, Eisenberg DL. Controversies in family planning: timing of
ovulation after abortion and the conundrum of postabortion intrauterine
device insertion. Contraception 2011;84:119–21.
43. Jackson E, Glasier A. Return of ovulation and menses in postpartum, nonlactating women: a systematic review. Obstet Gynecol 2011;117:657–62.
44. Kennedy KI, Rivera R, McNeilly AS. Consensus statement on the use of
breastfeeding as a family planning method. Contraception 1989;39:477–96.
45. Food and Drug Administration. 510(k) premarket notification. Silver
Spring, MD: Food and Drug Administration; 2013. Available at http://
www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMN/pmn.cfm.
46. Cervinski MA, Gronowski AM. Reproductive-endocrine point-of-care testing:
current status and limitations. Clin Chem Lab Med 2010;48:935–42.
47. Cole LA. Human chorionic gonadotropin tests. Expert Rev Mol Diagn
2009;9:721–47.
48. Eichner SF, Timpe EM. Urinary-based ovulation and pregnancy: pointof-care testing. Ann Pharmacother 2004;38:325–31.
49. Wilcox AJ, Baird DD, Dunson D, McChesney R, Weinberg CR. Natural
limits of pregnancy testing in relation to the expected menstrual period.
JAMA 2001;286:1759–61.
,PSIPOFO +
"MGUIBO )
:MPTUBMP 1
7FMEIVJT +
4UFONBO 6)
Disappearance of human chorionic gonadotropin and its alpha- and
beta-subunits after term pregnancy. Clin Chem 1997;43:2155–63.
51. Reyes FI, Winter JS, Faiman C. Postpartum disappearance of chorionic
gonadotropin from the maternal and neonatal circulations. Am J Obstet
Gynecol 1985;153:486–9.
52. Steier JA, Bergsjo P, Myking OL. Human chorionic gonadotropin in
maternal plasma after induced abortion, spontaneous abortion, and
removed ectopic pregnancy. Obstet Gynecol 1984;64:391–4.
53. Bracken MB. Oral contraception and congenital malformations in
offspring: a review and meta-analysis of the prospective studies. Obstet
Gynecol 1990;76:552–7.
54. Gray RH, Pardthaisong T. In utero exposure to steroid contraceptives
and survival during infancy. Am J Epidemiol 1991;134:804–11.
55. Pardthaisong T, Gray RH. In utero exposure to steroid contraceptives
and outcome of pregnancy. Am J Epidemiol 1991;134:795–803.
56. Jaffe B, Harlap S, Baras M, et al. Long-term effects of MPA on human
progeny: intellectual development. Contraception 1988;37:607–19.
1BSEUIBJTPOH 5
:FODIJU $
(SBZ 3 5IF MPOHUFSN HSPXUI BOE
development of children exposed to Depo-Provera during pregnancy or
lactation. Contraception 1992;45:313–24.
58. Brahmi D, Steenland MW, Renner RM, Gaffield ME, Curtis KM.
Pregnancy outcomes with an IUD in situ: a systematic review.
Contraception 2012;85:131–9.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

59. Trussell J. Contraceptive failure in the United States. Contraception
2011;83:397–404.
60. Labbok M, Perez A, Valdes V, et al. The Lactational Amenorrhea Method
(LAM): a postpartum introductory family planning method with policy
and program implications. Adv Contracept 1994;10:93–109.
61. Teva Women’s Health. ParaGard physicians prescribing information.
Sellersville, PA: Teva Women’s Health; 2013. Available at http://www.
paragard.com/images/ParaGard_info.pdf.
62. Bayer HealthCare Pharmaceuticals. Mirena physicians prescribing
information. Wayne, NJ: Bayer HealthCare Pharmaceuticals; 2013.
Available at http://www.berlex.com/html/products/pi/Mirena_PI.pdf.
63. Farley TM, Rosenberg MJ, Rowe PJ, Chen JH, Meirik O. Intrauterine
devices and pelvic inflammatory disease: an international perspective.
Lancet 1992;339:785–8.
64. Mohllajee AP, Curtis KM, Peterson HB. Does insertion and use of an
intrauterine device increase the risk of pelvic inflammatory disease among
women with sexually transmitted infection? A systematic review.
Contraception 2006;73:145–53.
65. Rivera R, Almonte H, Arreola M, et al. The effects of three different
regimens of oral contraceptives and three different intrauterine devices
on the levels of hemoglobin, serum iron and iron binding capacity in
anemic women. Contraception 1983;27:311–27.
66. Effects of contraceptives on hemoglobin and ferritin. Task Force for
Epidemiological Research on Reproductive Health, United Nations
Development Programme/United Nations Population Fund/World Health
Organization/World Bank Special Programme of Research, Development
and Research Training in Human Reproduction, World Health
Organization, Geneva, Switzerland. Contraception 1998;58:262–73.
67. Calzolari E, Guglielmo R, Viola F, Migliore L. Hematological parameters
and iron therapy in women with IUDs: experimental study. Minerva
Ginecol 1981;33:355–62.
68. Hassan EO, El-Husseini M, El-Nahal N. The effect of 1-year use of the
CuT 380A and oral contraceptive pills on hemoglobin and ferritin levels.
Contraception 1999;60:101–5.
69. Andersson K, Odlind V, Rybo G. Levonorgestrel-releasing and copperreleasing (Nova T) IUDs during five years of use: a randomized
comparative trial. Contraception 1994;49:56–72.
70. Andrade AT, Pizarro E, Shaw STJ, Souza JP, Belsey EM, Rowe PJ.
Consequences of uterine blood loss caused by various intrauterine
contraceptive devices in South American women. World Health
Organization Special Programme of Research, Development and Research
Training in Human Reproduction. Contraception 1988;38:1–18.
71. Blum M, Ariel J, Zacharowitch D. Ferritin, a faithful reflection of iron
deficiency in IUD wearers with mild vaginal spotting. Adv Contracept
1991;7:39–42.
72. El-sheikha Z, Hamza A, Mahmoud M. Menstrual blood loss of TCu-380
A and TCu-200 B IUDs. Popul Sci 1990;9:55–62.
73. Gallegost AJ, Aznar R, Merino G, Guizer E. Intrauterine devices and
menstrual blood loss: a comparative study of eight devices during the
first six months of use. Contraception 1978;17:153–61.
74. Gao J, Zeng S, Sun BL, et al. Menstrual blood loss, haemoglobin and
ferritin concentration of Beijing women wearing steel ring, VCu 200,
and TCu 220c IUDs. Contraception 1986;34:559–71.
75. Goh TH, Hariharan M. Effect of laparoscopic sterilization and insertion
of Multiload Cu 250 and Progestasert IUDs on serum ferritin levels.
Contraception 1983;28:329–36.
76. Goh TH, Hariharan M, Tan CH. A longitudinal study of serum iron
indices and haemoglobin concentration following copper-IUD insertion.
Contraception 1980;22:389–95.
77. Guillebaud J, Bonnar J, Morehead J, Matthews A. Menstrual blood-loss
with intrauterine devices. Lancet 1976;1:387–90.
78. Haugan T, Skjeldestad FE, Halvorsen LE, Kahn H. A randomized trial
on the clinical performance of Nova T380 and Gyne T380 Slimline
copper IUDs. Contraception 2007;75:171–6.

MMWR / June 21, 2013 / Vol. 62 / No. 5

79. Kivijarvi A, Timonen H, Rajamaki A, Gronroos M. Iron deficiency in
women using modern copper intrauterine devices. Obstet Gynecol
1986;67:95–8.
80. Larsson B, Hamberger L, Rybo G. Influence of copper intrauterine
contraceptive devices (Cu-7-IUD) on the menstrual blood-loss. Acta
Obstet Gynecol Scand 1975;54:315–8.
81. Larsson G, Milsom I, Jonasson K, Lindstedt G, Rybo G. The long-term
effects of copper surface area on menstrual blood loss and iron status in
women fitted with an IUD. Contraception 1993;48:471–80.
82. Malmqvist R, Petersohn L, Bengtsson LP. Menstrual bleeding with
copper-covered intrauterine contraceptive devices. Contraception
1974;9:627–33.
83. Milsom I, Andersson K, Jonasson K, Lindstedt G, Rybo G. The influence
of the Gyne-T 380S IUD on menstrual blood loss and iron status.
Contraception 1995;52:175–9.
84. Milsom I, Rybo G, Lindstedt G. The influence of copper surface area
on menstrual blood loss and iron status in women fitted with an IUD.
Contraception 1990;41:271–81.
85. Piedras J, Cordova MS, Perez-Toral MC, Lince E, Garza-Flores J.
Predictive value of serum ferritin in anemia development after insertion
of T Cu 220 intrauterine device. Contraception 1983;27:289–97.
86. Sivin I, Alvarez F, Diaz J, et al. Intrauterine contraception with copper
and with levonorgestrel: a randomized study of the TCu 380Ag and
levonorgestrel 20 mcg/day devices. Contraception 1984;30:443–56.
87. Sivin I. Two years of intrauterine contraception with levonorgestrel and
with copper: a randomized comparison of the TCu 380Ag and
levonorgestrel 20 mcg/day devices. Contraception 1987;35:245–55.
88. Tchai BS, Kim SW, Han JH, Im MW. Menstrual blood loss, iron
nutriture, and the effects of Alza-T IPCS 52, T-Cu 220C and Lippes
Loop D in Korean women. Seoul J Med 1987;28:51–9.
89. Wright EA, Kapu MM, Isichei UP. Zinc depletion and menorrhagia in
Nigerians using copper T-200 intrauterine device. Trace Elem Med
1989;6:147–9.
90. Pleis JR, Lucas JW, Ward BW. Summary health statistics for U.S. adults:
National Health Interview Survey, 2008. Vital Health Stat 10
2009;10:1–157.
91. CDC. Viral hepatitis surveillance, United States, 2009. Atlanta, GA: CDC;
2011. Available at http://www.cdc.gov/hepatitis/Statistics/2009Surveillance/
PDFs/2009HepSurveillanceRpt.pdf.
92. Kohler BA, Ward E, McCarthy BJ, et al. Annual report to the nation
on the status of cancer, 1975–2007, featuring tumors of the brain and
other nervous system. J Natl Cancer Inst 2011;103:714–36.
93. Kapp N, Curtis KM. Hormonal contraceptive use among women with
liver tumors: a systematic review. Contraception 2009;80:387–90.
94. Kapp N, Tilley IB, Curtis KM. The effects of hormonal contraceptive
use among women with viral hepatitis or cirrhosis of the liver: a
systematic review. Contraception 2009;80:381–6.
95. National Cancer Institute. National Cancer Institute at the National
Institutes for Health [homepage]. Bethesda, MD: National Cancer
Institute. Available at http://www.cancer.gov.
96. Watson M, Saraiya M, Benard V, et al. Burden of cervical cancer in the
United States, 1998–2003. Cancer 2008;113(Suppl):2855–64.
97. CDC. Cervical cancer screening among women aged 18-30 years—
United States, 2000–2010. MMWR 2013;61:1038–42.
98. Curtis KM, Nanda K, Kapp N. Safety of hormonal and intrauterine
methods of contraception for women with HIV/AIDS: a systematic
review. AIDS 2009;23(Suppl 1):S55–67.
99. Grimes DA, Schulz KF. Prophylactic antibiotics for intrauterine device
insertion: a metaanalysis of the randomized controlled trials.
Contraception 1999;60:57–63.

Recommendations and Reports

100. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective
endocarditis: guidelines from the American Heart Association: a
guideline from the American Heart Association Rheumatic Fever,
Endocarditis, and Kawasaki Disease Committee, Council on
$BSEJPWBTDVMBS %JTFBTF JO UIF :PVOH
BOE UIF $PVODJM PO $MJOJDBM
Cardiology, Council on Cardiovascular Surgery and Anesthesia, and
the Quality of Care and Outcomes Research Interdisciplinary Working
Group. Circulation 2007;116:1736–54.
101. Canto De Cetina TE, Canto P, Ordonez Luna M. Effect of counseling
to improve compliance in Mexican women receiving depotmedroxyprogesterone acetate. Contraception 2001;63:143–6.
102. Lei ZW, Wu SC, Garceau RJ, et al. Effect of pretreatment counseling on
discontinuation rates in Chinese women given depo-medroxyprogesterone
acetate for contraception. Contraception 1996;53:357–61.
103. Toppozada M, Anwar M, Abdel Rahman H, Gaweesh S. Control of
IUD-induced bleeding by three non-steroidal anti-inflammatory drugs.
Contracept Deliv Syst 1982;3:117–25.
5PQQP[BEB.
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&M"ZZBU."
,IBNJT:.BOBHFNFOUPG
uterine bleeding by PGs or their synthesis inhibitors. Adv Prostaglandin
Thromboxane Res 1980;8:1459–63.
105. Wu S, Wang C, Cheng W, et al. Randomized multi-center study of
baofuxin for treatment of bleeding side-effect induced by IUD. Reprod
Contracept 2000;11:152–7.
106. Mercorio F, De Simone R, Di Carlo C, et al. Effectiveness and mechanism
of action of desmopressin in the treatment of copper intrauterine devicerelated menorrhagia: a pilot study. Hum Reprod 2003;18:2319–22.
107. Pedron N, Lozano M, Aznar R. Treatment of hypermenorrhea with mefenamic
acid in women using IUDs. Contracept Deliv Syst 1982;3:135–9.
108. Pizarro E, Mehech G, Hidalgo M, Munoz G, Romero C. Effect of
meclofenamic acid on menstruation in hypermenorrheic women using
intrauterine devices. Rev Chil Obstet Ginecol 1988;53:43–56.
109. Chinese National IUD Research Working Group. Prevention and treatment
of IUD-induced menorrhagia with antifibrinolytic and antiprostaglandin
drugs. Zhonghua Fu Chan Ke Za Zhi 1987;22:291–4, 312.
110. Di Lieto A, Catalano D, Miranda L, Paladini A. Action of a prostaglandin
synthetase inhibitor on IUD associated uterine bleeding. Clin Exp Obstet
Gynecol 1987;14:41–4.
:MJLPSLBMB 0
7JJOJLLB - $PNQBSJTPO CFUXFFO BOUJGJCSJOPMZUJD BOE
antiprostaglandin treatment in the reduction of increased menstrual blood
loss in women with intrauterine contraceptive devices. Br J Obstet Gynaecol
1983;90:78–83.
112. Food and Drug Administration. FDA prescribing information. Cyklokapron:
USBOFYBNJDBDJEJOKFDUJPO/FX:PSL
/FX:PSL"WBJMBCMFBUhttp://
www.accessdata.fda.gov/drugsatfda_docs/label/2011/019281s030lbl.pdf.
113. Food and Drug Administration. FDA prescribing information. Lysteda:
tranexamic acid tablets. Parsippany, New Jersey; 2011. Available at http://
www.accessdata.fda.gov/drugsatfda_docs/label/2011/022430s002lbl.pdf.
114. Pedron N, Lozano M, Gallegos AJ. The effect of acetylsalicylic acid on menstrual
blood loss in women with IUDs. Contraception 1987;36:295–303.
115. Hidalgo M, Bahamondes L, Perrotti M, Diaz J, Dantas-Monteiro C, Petta C.
Bleeding patterns and clinical performance of the levonorgestrel-releasing
intrauterine system (Mirena) up to two years. Contraception 2002;
65:129–32.
116. Larsson B, Wennergren M. Investigation of a copper-intrauterine device
(Cu-IUD) for possible effect on frequency and healing of pelvic
inflammatory disease. Contraception 1977;15:143–9.
117. Soderberg G, Lindgren S. Influence of an intrauterine device on the
course of an acute salpingitis. Contraception 1981;24:137–43.

118. Teisala K. Removal of an intrauterine device and the treatment of acute
pelvic inflammatory disease. Ann Med 1989;21:63–5.
119. Altunyurt S, Demir N, Posaci C. A randomized controlled trial of coil
removal prior to treatment of pelvic inflammatory disease. Eur J Obstet
Gynecol Reprod Biol 2003;107:81–4.
120. Stewart FH, Harper CC, Ellertson CE, Grimes DA, Sawaya GF, Trussell
J. Clinical breast and pelvic examination requirements for hormonal
contraception: current practice vs evidence. JAMA 2001;285:2232–9.
121. Mansour D, Korver T, Marintcheva-Petrova M, Fraser IS. The effects
of Implanon on menstrual bleeding patterns. Eur J Contracept Reprod
Health Care 2008;13(Suppl 1):13–28.
122. Abdel-Aleem H, D’Arcangues C, Vogelsong K, Gulmezoglu AM.
Treatment of vaginal bleeding irregularities induced by progestin only
contraceptives. Cochrane Database Syst Rev 2007;CD003449.
123. Archer DF, Philput CB, Levine AS, et al. Effects of ethinyl estradiol
and ibuprofen compared to placebo on endometrial bleeding, cervical
mucus and the postcoital test in levonorgestrel subcutaneous implant
users. Contraception 2008;78:106–12.
124. Buasang K, Taneepanichskul S. Efficacy of celecoxib on controlling irregular
uterine bleeding secondary to Jadelle use. J Med Assoc Thai 2009;92:301–7.
125. Phaliwong P, Taneepanichskul S. The effect of mefenamic acid on
controlling irregular uterine bleeding second to Implanon use. J Med Assoc
Thai 2004;87(Suppl 3):S64–8.
126. Weisberg E, Hickey M, Palmer D, et al. A randomized controlled trial
of treatment options for troublesome uterine bleeding in Implanon users.
Hum Reprod 2009;24:1852–61.
127. Weisberg E, Hickey M, Palmer D, et al. A pilot study to assess the effect of
three short-term treatments on frequent and/or prolonged bleeding compared
to placebo in women using Implanon. Hum Reprod 2006;21:295–302.
128. Cheng L, Zhu H, Wang A, Ren F, Chen J, Glasier A. Once a month
administration of mifepristone improves bleeding patterns in women using
subdermal contraceptive implants releasing levonorgestrel. Hum Reprod
2000;15:1969–72.
129. Alvarez-Sanchez F, Brache V, Thevenin F, Cochon L, Faundes A. Hormonal
treatment for bleeding irregularities in Norplant implant users. Am J Obstet
Gynecol 1996;174:919–22.
130. Diaz S, Croxatto HB, Pavez M, Belhadj H, Stern J, Sivin I. Clinical assessment
of treatments for prolonged bleeding in users of Norplant implants.
Contraception 1990;42:97–109.
131. Witjaksono J, Lau TM, Affandi B, Rogers PA. Oestrogen treatment for
increased bleeding in Norplant users: preliminary results. Hum Reprod
1996;11(Suppl 2):109–14.
132. Abdel-Aleem H, Shaaban OM, Amin AF, Abdel-Aleem AM. Tamoxifen
treatment of bleeding irregularities associated with Norplant use.
Contraception 2005;72:432–7.
133. Phupong V, Sophonsritsuk A, Taneepanichskul S. The effect of tranexamic
acid for treatment of irregular uterine bleeding secondary to Norplant use.
Contraception 2006;73:253–6.
134. D’Arcangues C, Piaggio G, Brache V, et al. Effectiveness and acceptability
of vitamin E and low-dose aspirin, alone or in combination, on Norplantinduced prolonged bleeding. Contraception 2004;70:451–62.
135. Subakir SB, Setiadi E, Affandi B, Pringgoutomo S, Freisleben HJ.
Benefits of vitamin E supplementation to Norplant users–in vitro and
in vivo studies. Toxicology 2000;148:173–8.
136. Petta C, Faundes A, Dunson T, Ramos M, DeLucio M, Faundes D.
Timing of onset of contraceptive effectiveness in Depo-Provera users.
II. Effects on ovarian function. Fertil Steril 1998;70:817–20.

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Recommendations and Reports

137. Petta C, Faundes A, Dunson T, Ramos M, DeLucio M, Faundes D.
Timing of onset of contraceptive effectiveness in Depo-Provera users:
Part I. Changes in cervical mucus. Fertil Steril 1998;69:252–7.
138. Siriwongse T, Snidvongs W, Tantayaporn P, Leepipatpaiboon S. Effect
of depo-medroxyprogesterone acetate on serum progesterone levels when
administered on various cycle days. Contraception 1982;26:487–93.
139. Balkus J, Miller L. Same-day administration of depot-medroxyprogesterone
acetate injection: a retrospective chart review. Contraception 2005;
71:395–8.
140. Morroni C, Grams M, Tiezzi L, Westhoff C. Immediate monthly combination
contraception to facilitate initiation of the depot medroxyprogesterone acetate
contraceptive injection. Contraception 2004;70:19–23.
141. Nelson A, Katz T. Initiation and continuation rates seen in 2-year experience
with Same Day injections of DMPA. Contraception 2007;75:84–7.
142. Rickert V, Tiezzi L, Lipshutz J, Leon J, Vaughan R, Westhoff C. Depo
Now: preventing unintended pregnancies among adolescents and young
adults. J Adolesc Health 2007;40:22–8.
143. Sneed R, Westhoff C, Morroni C, Tiezzi L. A prospective study of
immediate initiation of depo medroxyprogesterone acetate contraceptive
injection. Contraception 2005;71:99–103.
144. Cox S, Dietz P, Bowman B, Posner S. Prevalence of chronic conditions among
women of reproductive age. Third National Summit on Preconception
Health and Health Care; Tampa, FL.
145. Diab KM, Zaki MM. Contraception in diabetic women: comparative
metabolic study of Norplant, depot medroxyprogesterone acetate, low
dose oral contraceptive pill and CuT380A. J Obstet Gynaecol Res
2000;26:17–26.
146. Garg SK, Chase HP, Marshall G, Hoops SL, Holmes DL, Jackson WE.
Oral contraceptives and renal and retinal complications in young women
with insulin-dependent diabetes mellitus. JAMA 1994;271:1099–102.
147. Grigoryan OR, Grodnitskaya EE, Andreeva EN, Chebotnikova TV,
Melnichenko GA. Use of the NuvaRing hormone-releasing system in
late reproductive-age women with type 1 diabetes mellitus. Gynecol
Endocrinol 2008;24:99–104.
148. Kahn HS, Curtis KM, Marchbanks PA. Effects of injectable or
implantable progestin-only contraceptives on insulin-glucose metabolism
and diabetes risk. Diabetes Care 2003;26:216–25.
149. Lopez LM, Grimes DA, Schulz KF. Steroidal contraceptives: effect on
carbohydrate metabolism in women without diabetes mellitus.
Cochrane Database Syst Rev 2009;CD006133.
150. Rogovskaya S, Rivera R, Grimes DA, et al. Effect of a levonorgestrel
intrauterine system on women with type 1 diabetes: a randomized trial.
Obstet Gynecol 2005;105:811–5.
151. Troisi RJ, Cowie CC, Harris MI. Oral contraceptive use and glucose
metabolism in a national sample of women in the united states. Am J
Obstet Gynecol 2000;183:389–95.
152. Bonny A, Secic M, Cromer B. Early weight gain related to later weight
gain in adolescents on depot medroxyprogesterone acetate. Obstet Gynecol
2011;117:793–7.
-F:
3BINBO.
#FSFOTPO"&BSMZXFJHIUHBJOQSFEJDUJOHMBUFSXFJHIU
gain among depot medroxyprogesterone acetate users. Obstet Gynecol
2009;114:279–84.
154. Risser WL. Weight change in adolescents who used hormonal contraception.
J Adolesc Health 1999;24:433–6.
155. Paulen ME, Curtis KM. When can a woman have repeat progestogenonly injectables—depot medroxyprogesterone acetate or norethisterone
enantate? Contraception 2009;80:391–408.

MMWR / June 21, 2013 / Vol. 62 / No. 5

156. Pardthaisong T. Return of fertility after use of the injectable contraceptive
Depo Provera: up-dated data analysis. J Biosoc Sci 1984;16:23–34.
157. Schwallie PC, Assenzo JR. The effect of depo-medroxyprogesterone acetate
on pituitary and ovarian function, and the return of fertility following its
discontinuation: a review. Contraception 1974;10:181–202.
158. Steiner MJ, Kwok C, Stanback J, et al. Injectable contraception: what should
the longest interval be for reinjections? Contraception 2008;77:410–4.
159. Bassol S, Garza-Flores J, Cravioto MC, et al. Ovarian function following
a single administration of depo-medroxyprogesterone acetate (DMPA)
at different doses. Fertil Steril 1984;42:216–22.
160. Fotherby K, Koetsawang S, Mathrubutham M. Pharmacokinetic study
of different doses of Depo Provera. Contraception 1980;22:527–36.
161. Fotherby K, Saxena BN, Shrimanker K, et al. A preliminary pharmacokinetic
and pharmacodynamic evaluation of depot-medroxyprogesterone acetate
and norethisterone oenanthate. Fertil Steril 1980;34:131–9.
162. Garza-Flores J, Cardenas S, Rodriguez V, Cravioto MC, Diaz-Sanchez V,
Perez-Palacios G. Return to ovulation following the use of long-acting injectable
contraceptives: a comparative study. Contraception 1985;31:361–6.
163. Jain J, Dutton C, Nicosia A, Wajszczuk C, Bode FR, Mishell DR Jr.
Pharmacokinetics, ovulation suppression and return to ovulation
following a lower dose subcutaneous formulation of Depo-Provera.
Contraception 2004;70:11–8.
164. Lan PT, Aedo AR, Landgren BM, Johannisson E, Diczfalusy E. Return
of ovulation following a single injection of depo-medroxyprogesterone
acetate: a pharmacokinetic and pharmacodynamic study. Contraception
1984;29:1–18.
165. Ortiz A, Hirol M, Stanczyk FZ, Goebelsmann U, Mishell DR. Serum
medroxyprogesterone acetate (MPA) concentrations and ovarian function
following intramuscular injection of depo-MPA. J Clin Endocrinol Metab
1977;44:32–8.
166. Saxena BN, Dusitsin N, Tankeyoon M, Chaudhury RR. Return of
ovulation after the cessation of depot-medroxy progesterone acetate
treatment in Thai women. J Med Assoc Thai 1980;63:66–9.
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ovulation by a new subcutaneous depot medroxyprogesterone acetate
(104 mg/0.65 mL) contraceptive formulation in Asian women. Clin
Ther 2004;26:1845–54.
168. Hubacher D, Lopez L, Steiner MJ, Dorflinger L. Menstrual pattern changes
from levonorgestrel subdermal implants and DMPA: systematic review
and evidence-based comparisons. Contraception 2009;80:113–8.
169. Arias RD, Jain JK, Brucker C, Ross D, Ray A. Changes in bleeding
patterns with depot medroxyprogesterone acetate subcutaneous
injection 104 mg. Contraception 2006;74:234–8.
170. Dempsey A, Roca C, Westhoff C. Vaginal estrogen supplementation during
Depo-Provera initiation: a randomized controlled trial. Contraception
2010;82:250–5.
171. Harel Z, Biro F, Kollar L, Riggs S, Flanagan P, Vaz R. Supplementation
with vitamin C and/or vitamin B(6) in the prevention of Depo-Provera
side effects in adolescents. J Pediatr Adolesc Gynecol 2002;15:153–8.
172. Nathirojanakun P, Taneepanichskul S, Sappakitkumjorn N. Efficacy
of a selective COX-2 inhibitor for controlling irregular uterine bleeding
in DMPA users. Contraception 2006;73:584–7.
173. Tantiwattanakul P, Taneepanichskul S. Effect of mefenamic acid on
controlling irregular uterine bleeding in DMPA users. Contraception
2004;70:277–9.

Recommendations and Reports

174. Said S, Sadek W, Rocca M, et al. Clinical evaluation of the therapeutic
effectiveness of ethinyl oestradiol and oestrone sulphate on prolonged
bleeding in women using depot medroxyprogesterone acetate for
contraception. World Health Organization, Special Programme of Research,
Development and Research Training in Human Reproduction, Task Force
on Long-acting Systemic Agents for Fertility Regulation. Hum Reprod
1996;11(Suppl 2):1–13.
175. Sadeghi-Bazargani H, Ehdaeivand F, Arshi S, Eftekhar H, Sezavar H,
Amanati L. Low-dose oral contraceptive to re-induce menstrual bleeding
in amenorrheic women on DMPA treatment: a randomized clinical trial.
Med Sci Monit 2006;12:CR420–5.
176. CDC. Update to CDC’s U.S. Medical Eligibility Criteria for Contraceptive
Use, 2010: Revised recommendations for the use of contraceptive methods
during the postpartum period. MMWR 2011;60:878–83.
177. Westhoff C, Morroni C, Kerns J, Murphy PA. Bleeding patterns after
immediate vs. conventional oral contraceptive initiation: a randomized,
controlled trial. Fertil Steril 2003;79:322–9.
178. Westhoff C, Heartwell S, Edwards S, et al. Initiation of oral contraceptives
using a quick start compared with a conventional start—A randomized
controlled trial. Obstet Gynecol 2007;109:1270–6.
179. Edwards SM, Zieman M, Jones K, Diaz A, Robilotto C, Westhoff C. Initiation
of oral contraceptives—start now! J Adolesc Health 2008;43:432–6.
180. Baerwald AR, Olatunbosun OA, Pierson RA. Ovarian follicular development
is initiated during the hormone-free interval of oral contraceptive use.
Contraception 2004;70:371–7.
181. Baerwald AR, Pierson RA. Ovarian follicular development during the use
of oral contraception: a review. J Obstet Gynaecol Can 2004;26:19–24.
182. Duijkers IJM, Klipping C, Verhoeven CHJ, Dieben TOM. Ovarian
function with the contraceptive vaginal ring or an oral contraceptive:
a randomized study. Human Reproduction 2004;19):2668–73.
183. Killick S, Eyong E, Elstein M. Ovarian follicular development in oral
contraceptive cycles. Fertil Steril 1987;48:409–13.
184. Molloy BG, Coulson KA, Lee JM, Watters JK. “Missed pill” conception:
fact or fiction? Br Med J (Clin Res Ed) 1985;290:1474–5.
185. Mulders TM, Dieben TO, Bennink HJ. Ovarian function with a novel
combined contraceptive vaginal ring. Hum Reprod 2002;17:2594–9.
186. Schwartz JL, Creinin MD, Pymar HC, Reid L. Predicting risk of ovulation
in new start oral contraceptive users. Obstet Gynecol 2002;99:177–82.
187. Sitavarin S, Jaisamrarn U, Taneepanichskul S. A randomized trial on
the impact of starting day on ovarian follicular activity in very low dose
oral contraceptive pills users. J Med Assoc Thai 2003;86:442–8.
188. Smith SK, Kirkman RJ, Arce BB, McNeilly AS, Loudon NB, Baird DT.
The effect of deliberate omission of Trinordiol or Microgynon on the
hypothalamo-pituitary-ovarian axis. Contraception 1986;34:513–22.
189. Taylor DR, Anthony FW, Dennis KJ. Suppression of ovarian function by
Microgynon 30 in day 1 and day 5 “starters.” Contraception 1986;
33:463–71.
190. Lara-Torre E, Schroeder B. Adolescent compliance and side effects with Quick
Start initiation of oral contraceptive pills. Contraception 2002;66:81–5.
191. Murthy AS, Creinin MD, Harwood B, Schreiber CA. Same-day initiation
of the transdermal hormonal delivery system (contraceptive patch) versus
traditional initiation methods. Contraception 2005;72:333–6.
192. Westhoff C, Osborne L, Schafer J, Morroni C. Bleeding patterns after
immediate initiation of an oral compared with a vaginal hormonal
contraceptive. Obstet Gynecol 2005;106:89–96.
:FTIBZB"
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contraception: effect on the incidence of breakthrough bleeding and
compliance. Eur J Contracept Reprod Health Care 1998;3:121–3.

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of oral contraception: the effect on the incidence of breakthrough
bleeding and compliance in women. Eur J Contracept Reprod Health
Care 1996;1:263–5.
195. Westhoff C, Kerns J, Morroni C, Cushman LF, Tiezzi L, Murphy PA.
Quick start: novel oral contraceptive initiation method. Contraception
2002;66:141–5.
196. Acute myocardial infarction and combined oral contraceptives: results
of an international multicentre case-control study. WHO Collaborative
Study of Cardiovascular Disease and Steroid Hormone Contraception.
Lancet 1997;349:1202–9.
197. Dunn N, Thorogood M, Faragher B, et al. Oral contraceptives and
myocardial infarction: results of the MICA case-control study. BMJ
1999;318:1579–83.
198. Lewis MA, Heinemann LA, Spitzer WO, MacRae KD, Bruppacher R. The
use of oral contraceptives and the occurrence of acute myocardial infarction in
young women. Results from the Transnational Study on Oral Contraceptives
BOEUIF)FBMUIPG:PVOH8PNFO$POUSBDFQUJPOo
199. Ischaemic stroke and combined oral contraceptives: results of an international,
multicentre, case-control study. WHO Collaborative Study of Cardiovascular
Disease and Steroid Hormone Contraception. Lancet 1996;348:498–505.
200. Heinemann LA, Lewis MA, Spitzer WO, Thorogood M, GuggenmoosHolzmann I, Bruppacher R. Thromboembolic stroke in young women. A
European case-control study on oral contraceptives. Transnational Research
(SPVQ PO 0SBM $POUSBDFQUJWFT BOE UIF )FBMUI PG :PVOH 8PNFO
Contraception 1998;57:29–37.
201. Haemorrhagic stroke, overall stroke risk, and combined oral contraceptives:
results of an international, multicentre, case-control study. WHO
Collaborative Study of Cardiovascular Disease and Steroid Hormone
Contraception. Lancet 1996;348:505–10.
202. Berenson AB, Rahman M, Wilkinson G. Effect of injectable and oral
contraceptives on serum lipids. Obstet Gynecol 2009;114:786–94.
203. Dilbaz B, Ozdegirmenci O, Caliskan E, Dilbaz S, Haberal A. Effect of
etonogestrel implant on serum lipids, liver function tests and hemoglobin
levels. Contraception 2010;81:510–4.
204. Nelson A. Combined oral contraceptives. In: Hatcher RA, Trussel J, Nelson
A, Cates W Jr, Stewart FH, Kowal D, eds. Contraceptive technology. 19th
FE/FX:PSL
/:"SEFOU.FEJB
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205. Mohllajee AP, Curtis KM, Martins SL, Peterson HB. Does use of hormonal
contraceptives among women with thrombogenic mutations increase their
risk of venous thromboembolism? A systematic review. Contraception
2006;73:166–78.
206. Wu O, Robertson L, Twaddle S, et al. Screening for thrombophilia in
high-risk situations: systematic review and cost-effectiveness analysis. The
Thrombosis: Risk and Economic Assessment of Thrombophilia Screening
(TREATS) study. Health technology assessment (Winchester, England)
2006;10:1–110.
207. Blickstein D, Blickstein I. Oral contraception and thrombophilia. Curr
Opin Obstet Gynecol 2007;19:370–6.
208. Wu O, Greer IA. Is screening for thrombophilia cost-effective? Curr
Opin Hematol 2007;14:500–3.
209. Foster D, Hulett D, Bradsberry M, Darney P, Policar M. Number of
oral contraceptive pill packages dispensed and subsequent unintended
pregnancies. Obstet Gynecol 2011;117:566–72.
210. Foster D, Parvataneni R, de Bocanegra H, Lewis C, Bradsberry M,
Darney P. Number of oral contraceptive pill packages dispensed, method
continuation, and costs. Obstet Gynecol 2006;108:1107–14.

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Recommendations and Reports

211. White KO, Westhoff C. The effect of pack supply on oral contraceptive
pill continuation: a randomized controlled trial. Obstet Gynecol 2011;
118:615–22.
212. Chin Quee D, Cuthbertson C, Janowitz B. Over-the-counter pill
provision: evidence from Jamaica. Stud Fam Plann 2006;37:99–110.
213. Anttila L, Kunz M, Marr J. Bleeding pattern with drospirenone 3
mg+ethinyl estradiol 20 mcg 24/4 combined oral contraceptive compared
with desogestrel 150 mcg+ethinyl estradiol 20 mcg 21/7 combined oral
contraceptive. Contraception 2009;80:445–51.
214. Chowdhury V, Joshi UM, Gopalkrishna K, Betrabet S, Mehta S, Saxena
BN. ‘Escape’ ovulation in women due to the missing of low dose combination
oral contraceptive pills. Contraception 1980;22:241–7.
215. Christin-Maitre S, Serfaty D, Chabbert-Buffet N, Ochsenbein E, Chassard
D, Thomas JL. Comparison of a 24-day and a 21-day pill regimen for the
novel combined oral contraceptive, nomegestrol acetate and 17beta-estradiol
(NOMAC/E2): a double-blind, randomized study. Hum Reprod
2011;26:1338–47.
216. Creinin MD, Lippman JS, Eder SE, Godwin AJ, Olson W. The effect of
extending the pill-free interval on follicular activity: triphasic norgestimate/35
micro g ethinyl estradiol versus monophasic levonorgestrel/20 micro g
ethinyl estradiol. Contraception 2002;66:147–52.
217. Dinger J, Minh TD, Buttmann N, Bardenheuer K. Effectiveness of
oral contraceptive pills in a large U.S. cohort comparing progestogen
and regimen. Obstet Gynecol 2011;117:33–40.
218. Elomaa K, Lahteenmaki P. Ovulatory potential of preovulatory sized follicles
during oral contraceptive treatment. Contraception 1999;60:275–9.
219. Elomaa K, Rolland R, Brosens I, et al. Omitting the first oral contraceptive
pills of the cycle does not automatically lead to ovulation. Am J Obstet
Gynecol 1998;179:41–6.
220. Endrikat J, Wessel J, Rosenbaum P, Dusterberg B. Plasma concentrations
of endogenous hormones during one regular treatment cycle with a lowdose oral contraceptive and during two cycles with deliberate omission
of two tablets. Gynecol Endocrinol 2004;18:318–26.
221. Hamilton CJ, Hoogland HJ. Longitudinal ultrasonographic study of the
ovarian suppressive activity of a low-dose triphasic oral contraceptive during
correct and incorrect pill intake. Am J Obstet Gynecol 1989;161:1159–62.
222. Hedon B, Cristol P, Plauchut A, et al. Ovarian consequences of the transient
interruption of combined oral contraceptives. Int J Fertil 1992;37:270–6.
223. Killick SR. Ovarian follicles during oral contraceptive cycles: their
potential for ovulation. Fertil Steril 1989;52:580–2.
224. Killick SR, Bancroft K, Oelbaum S, Morris J, Elstein M. Extending
the duration of the pill-free interval during combined oral contraception.
Adv Contracept 1990;6:33–40.
225. Klipping C, Duijkers I, Trummer D, Marr J. Suppression of ovarian
activity with a drospirenone-containing oral contraceptive in a 24/4
regimen. Contraception 2008;78:16–25.
226. Klipping C, Marr J. Effects of two combined oral contraceptives
containing ethinyl estradiol 20 microg combined with either
drospirenone or desogestrel on lipids, hemostatic parameters and
carbohydrate metabolism. Contraception 2005;71:409–16.
227. Landgren BM, Csemiczky G. The effect of follicular growth and luteal
function of “missing the pill.” A comparison between a monophasic and a
triphasic combined oral contraceptive. Contraception 1991;43:149–59.
228. Landgren BM, Diczfalusy E. Hormonal consequences of missing the pill
during the first two days of three consecutive artificial cycles. Contraception
1984;29:437–46.
229. Letterie GS. A regimen of oral contraceptives restricted to the periovulatory
period may permit folliculogenesis but inhibit ovulation. Contraception
1998;57:39–44.

MMWR / June 21, 2013 / Vol. 62 / No. 5

230. Letterie GS, Chow GE. Effect of “missed” pills on oral contraceptive
effectiveness. Obstet Gynecol 1992;79:979–82.
231. Morris SE, Groom GV, Cameron ED, Buckingham MS, Everitt JM, Elstein
M. Studies on low dose oral contraceptives: plasma hormone changes in relation
to deliberate pill (‘Microgynon 30’) omission. Contraception 1979;20:61–9.
232. Nakajima ST, Archer DF, Ellman H. Efficacy and safety of a new 24-day
oral contraceptive regimen of norethindrone acetate 1 mg/ethinyl estradiol
20 micro g (Loestrin 24 Fe). Contraception 2007;75:16–22.
233. Nuttall ID, Elstein M, McCafferty E, Seth J, Cameron ED. The effect of
ethinyl estradiol 20 mcg and levonorgestrel 250 mcg on the pituitaryovarian function during normal tablet-taking and when tablets are missed.
Contraception 1982;26:121–35.
234. Pierson RA, Archer DF, Moreau M, Shangold GA, Fisher AC, Creasy
GW. Ortho Evra/Evra versus oral contraceptives: follicular development
and ovulation in normal cycles and after an intentional dosing error.
Fertil Steril 2003;80:34–42.
235. Rible RD, Taylor D, Wilson ML, Stanczyk FZ, Mishell DR Jr. Follicular
development in a 7-day versus 4-day hormone-free interval with an oral
contraceptive containing 20 mcg ethinyl estradiol and 1 mg norethindrone
acetate. Contraception 2009;79:182–8.
236. Schlaff WD, Lynch AM, Hughes HD, Cedars MI, Smith DL. Manipulation
of the pill-free interval in oral contraceptive pill users: the effect on follicular
suppression. Am J Obstet Gynecol 2004;190:943–51.
237. Spona J, Elstein M, Feichtinger W, et al. Shorter pill-free interval in combined
oral contraceptives decreases follicular development. Contraception
1996;54:71–7.
238. Sullivan H, Furniss H, Spona J, Elstein M. Effect of 21-day and 24-day
oral contraceptive regimens containing gestodene (60 microg) and ethinyl
estradiol (15 microg) on ovarian activity. Fertil Steril 1999;72:115–20.
239. Wang E, Shi S, Cekan SZ, Landgren BM, Diczfalusy E. Hormonal
consequences of “missing the pill.” Contraception 1982;26:545–66.
240. Willis SA, Kuehl TJ, Spiekerman AM, Sulak PJ. Greater inhibition of
the pituitary–ovarian axis in oral contraceptive regimens with a shortened
hormone-free interval. Contraception 2006;74:100–3.
241. Abrams LS, Skee DM, Natarajan J, et al. Pharmacokinetics of norelgestromin
and ethinyl estradiol delivered by a contraceptive patch (Ortho Evra/Evra)
under conditions of heat, humidity, and exercise. J Clin Pharmacol
2001;41:1301–9.
242. Ahrendt HJ, Nisand I, Bastianelli C, et al. Efficacy, acceptability and
tolerability of the combined contraceptive ring, NuvaRing, compared
with an oral contraceptive containing 30 microg of ethinyl estradiol
and 3 mg of drospirenone. Contraception 2006;74:451–7.
243. Bjarnadottir RI, Tuppurainen M, Killick SR. Comparison of cycle control
with a combined contraceptive vaginal ring and oral levonorgestrel/ethinyl
estradiol. Am J Obstet Gynecol 2002;186:389–95.
244. Brucker C, Karck U, Merkle E. Cycle control, tolerability, efficacy and
acceptability of the vaginal contraceptive ring, NuvaRing: results of
clinical experience in Germany. Eur J Contracept Reprod Health Care
2008;13:31–8.
245. Dieben TO, Roumen FJ, Apter D. Efficacy, cycle control, and user
acceptability of a novel combined contraceptive vaginal ring. Obstet
Gynecol 2002;100:585–93.
246. Mulders TM, Dieben TO. Use of the novel combined contraceptive vaginal
ring NuvaRing for ovulation inhibition. Fertil Steril 2001;75:865–70.
247. Guilbert E, Boroditsky R, Black A, et al. Canadian Consensus Guideline
on Continuous and Extended Hormonal Contraception, 2007. J Obstet
Gynaecol Can 2007;29(Suppl 2):S1–32.

Recommendations and Reports

248. Wiegratz I, Stahlberg S, Manthey T, et al. Effect of extended-cycle
regimen with an oral contraceptive containing 30 mcg ethinylestradiol
and 2 mg dienogest on bleeding patterns, safety, acceptance and
contraceptive efficacy. Contraception 2011;84:133–43.
249. Sulak PJ, Kuehl TJ, Coffee A, Willis S. Prospective analysis of occurrence
and management of breakthrough bleeding during an extended oral
contraceptive regimen. Am J Obstet Gynecol 2006;195:935–41.
250. Sulak PJ, Smith V, Coffee A, Witt I, Kuehl AL, Kuehl TJ. Frequency
and management of breakthrough bleeding with continuous use of the
transvaginal contraceptive ring: a randomized controlled trial. Obstet
Gynecol 2008;112:563–71.
251. Kaneshiro B, Edelman A, Carlson N, Morgan K, Nichols M, Jensen J.
Treatment of unscheduled bleeding in continuous oral contraceptive users
with doxycycline: a randomized controlled trial. Obstet Gynecol 2010;
115:1141–9.
252. McCann MF, Potter LS. Progestin-only oral contraception: a comprehensive
review. Contraception 1994;50:S1–195.
253. Arevalo M, Jennings V, Sinai I. Efficacy of a new method of family
planning: the Standard Days Method. Contraception 2002;65:333–8.
254. Arevalo M, Sinai I, Jennings V. A fixed formula to define the fertile
window of the menstrual cycle as the basis of a simple method of natural
family planning. Contraception 1999;60:357–60.
255. Wilcox AJ, Dunson DB, Weinberg CR, Trussell J, Baird DD. Likelihood
of conception with a single act of intercourse: providing benchmark rates for
assessment of post-coital contraceptives. Contraception 2001;63:211–5.
256. Cleland K, Zhu H, Goldstuck N, Cheng L, Trussell J. The efficacy of
intrauterine devices for emergency contraception: a systematic review
of 35 years of experience. Hum Reprod 2012;27:1994–2000.
257. Glasier AF, Cameron ST, Fine PM, et al. Ulipristal acetate versus
levonorgestrel for emergency contraception: a randomised noninferiority trial and meta-analysis. Lancet 2010;375:555–62.
258. Raymond E, Taylor D, Trussell JMJS. Minimum effectiveness of the
levonorgestrel regimen of emergency contraception. Contraception
2004;69:79–81.
259. Fine P, Mathe H, Ginde S, Cullins V, Morfesis J, Gainer E. Ulipristal
acetate taken 48–120 hours after intercourse for emergency contraception.
Obstet Gynecol 2010;115:257–63.
260. Dada OA, Godfrey EM, Piaggio G, von Hertzen H. A randomized, doubleblind, noninferiority study to compare two regimens of levonorgestrel for
emergency contraception in Nigeria. Contraception 2010;82:373–8.
261. Ngai SW, Fan S, Li S, et al. A randomized trial to compare 24 h versus
12 h double dose regimen of levonorgestrel for emergency contraception.
Hum Reprod 2005;20:307–11.
262. Ellertson C, Evans M, Ferden S, et al. Extending the time limit for
TUBSUJOHUIF:V[QFSFHJNFOPGFNFSHFODZDPOUSBDFQUJPOUPIPVST
Obstet Gynecol 2003;101:1168–71.
263. Von Hertzen H, Piaggio G, Ding J, et al. Low dose mifepristone and
two regimens of levonorgestrel for emergency contraception: a WHO
multicentre randomised trial. Lancet 2002;360:1803–10.
264. Rodrigues I, Grou F, Joly J. Effectiveness of emergency contraceptive
pills between 72 and 120 hours after unprotected sexual intercourse.
Am J Obstet Gynecol 2001;184:531–7.
265. Piaggio G, Kapp N, von Hertzen H. Effect on pregnancy rates of the delay
in the administration of levonorgestrel for emergency contraception: a
combined analysis of four WHO trials. Contraception 2011;84:35–9.
266. Watson Pharma Inc. Prescribing Information for Ella. 2010. Morristown, NJ.
267. Emergency contraceptive pills. Medical and service delivery guidelines. 2012.
Available at http://www.cecinfo.org/custom-content/uploads/2013/03/
Medical-and-Service-Delivery-Guidelines-English-2012.pdf.

268. Creinin MD, Schlaff W, Archer DF, et al. Progesterone receptor
modulator for emergency contraception - A randomized controlled trial.
Obstet Gynecol 2006;108:1089–97.
269. Farajkhoda T, Khoshbin A, Enjezab B, Bokaei M, Zarchi MK. Assessment
of two emergency contraceptive regimens in Iran: levonorgestrel versus
UIF:V[QF/JHFS+$MJO1SBDUo
270. Ho PC, Kwan MSW. A prospective randomized comparison of
MFWPOPSHFTUSFM XJUI UIF:V[QF SFHJNFO JO QPTUDPJUBM DPOUSBDFQUJPO
Hum Reprod 1993;8:389–92.
271. Arowojolu AO, Okewole IA, Adekunle AO. Comparative evaluation of
the effectiveness and safety of two regimens of levonorgestrel for emergency
contraception in Nigerians. Contraception 2002;66:269–73.
272. Raymond EG, Creinin MD, Barnhart KT, Lovvorn AE, Rountree RW,
Trussell J. Meclizine for prevention of nausea associated with use of emergency
contraceptive pills: a randomized trial. Obstet Gynecol 2000;95:271–7.
273. Ragan RE, Rock RW, Buck HW. Metoclopramide pretreatment attenuates
emergency contraceptive-associated nausea. Am J Obstet Gynecol
2003;188:330–3.
274. Peterson HB, Xia Z, Hughes JM, Wilcox LS, Tylor LR, Trussell J. The risk
of pregnancy after tubal sterilization: findings from the U.S. Collaborative
Review of Sterilization. Am J Obstet Gynecol 1996;174:1161–8, 8–70.
275. Peterson HB. Sterilization. Obstet Gynecol 2008;111:189–203.
276. Lawrie TA, Nardin JM, Kulier R, Boulvain M. Techniques for the
interruption of tubal patency for female sterilisation. Cochrane Database
Syst Rev 2011; (2):CD003034.
277. Veersema S, Vleugels MP, Moolenaar LM, Janssen CA, Brolmann HA.
Unintended pregnancies after Essure sterilization in the Netherlands.
Fertil Steril 2010;93:35–8.
278. Levy B, Levie MD, Childers ME. A summary of reported pregnancies after
hysteroscopic sterilization. J Minim Invasive Gynecol 2007;14:271–4.
279. Legendre G, Levaillant JM, Faivre E, Deffieux X, Gervaise A, Fernandez H.
3D ultrasound to assess the position of tubal sterilization microinserts. Hum
Reprod 2011;26:2683–9.
280. Duffy S, Marsh F, Rogerson L, et al. Female sterilisation: a cohort
controlled comparative study of ESSURE versus laparoscopic sterilisation.
BJOG 2005;112:1522–8.
281. Levie MD, Chudnoff SG. Prospective analysis of office-based hysteroscopic
sterilization. J Minim Invasive Gynecol 2006;13:98–101.
282. Arjona JE, Mino M, Cordon J, Povedano B, Pelegrin B, Castelo-Branco
C. Satisfaction and tolerance with office hysteroscopic tubal sterilization.
Fertil Steril 2008;90:1182–6.
283. Grosdemouge I, Engrand JB, Dhainault C, et al. La pratique francaise
de la pose des implants de sterilisation tubaire Essure. Gynecol Obstet
Fertil 2009;37:389–95.
284. Shavell VI, Abdallah ME, Diamond MP, Berman JM. Placement of a
permanent birth control device at a university medical center. J Reprod
Med 2009;54:218–22.
285. American Urological Association. Vasectomy guideline 2012. Available
at http://www.auanet.org/education/vasectomy.cfm.
286. Bedford J, Zelikovsky G. Viability of spermatozoa in the human
ejaculate after vasectomy. Fertil Steril 1979;32:460–3.
287. Edwards I. Earlier testing after vasectomy, based on the absence of
motile sperm. Fertil Steril 1993;59:431–6.
288. Jouannet P, David G. Evolution of the properties of semen immediately
following vasectomy. Fertil Steril 1978;29:435–41.
289. Labrecque M, Hays M, Chen-Mok M, Barone M, Sokal D. Frequency
and patterns of early recanalization after vasectomy. BMC Urol 2006;6:25.
290. Philp T, Guillebaud J, Budd D. Complications of vasectomy: review of
16,000 patients. Br J Urol 1984;56:745–8.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

291. Alderman PM. The lurking sperm. A review of failures in 8879
vasectomies performed by one physician. JAMA 1988;259:3142–4.
292. Black T, Francome C. The evolution of the Marie Stopes electrocautery
no-scalpel vasectomy procedure. J Fam Plann Reprod Health Care
2002;28:137–8.
293. Davies AH, Sharp RJ, Cranston D, Mitchell RG. The long-term outcome
following “special clearance” after vasectomy. Br J Urol 1990;66:211–2.
294. Philp T, Guillebaud J, Budd D. Late failure of vasectomy after two
documented analyses showing azoospermic semen. Br Med J (Clin Res Ed)
1984;289:77–9.
295. Belker A, Sexter M, Sweitzer S, Raff M. The high rate of noncompliance
for post-vasectomy semen examination: medical and legal considerations.
J Urol 1990;144:284–6.
296. Chawla A, Bowles B, Zini A. Vasectomy follow-up: clinical significance
of rare nonmotile sperm in postoperative semen analysis. Urology
2004;64:1212–5.
297. Labrecque M, Bedard L, Laperriere L. Efficacy and complications
associated with vasectomies in two clinics in the Quebec region. Can
Fam Physician 1998;44:1860–6.
298. Labrecque M, Nazerali H, Mondor M, Fortin V, Nasution M.
Effectiveness and complications associated with 2 vasectomy occlusion
techniques. J Urol 2002;168:2495–8.
299. Maatman TJ, Aldrin L, Carothers GG. Patient noncompliance after
vasectomy. Fertil Steril 1997;68:552–5.
300. Dhar NB, Jones JS, Bhatt A, Babineau D. A prospective evaluation of
the impact of scheduled follow-up appointments with compliance rates
after vasectomy. BJU Int 2007;99:1094–7.
301. Hillard PJ, Berek JS, Barss VA, et al. Guidelines for women’s health care:
a resource manual. 3rd ed. Washington, DC: American College of
Obstetricians and Gynecologists; 2007.
302. The North American Menopause Society. Prescription hormonal
therapies. Menopause practice: a clinician’s guide. 4th ed. 2010.
303. Te Velde ER, Pearson PL. The variability of female reproductive ageing.
Hum Reprod Update 2002;8:141–54.
304. Broekmans FJ, Soules MR, Fauser BC. Ovarian aging: mechanisms
and clinical consequences. Endocr Rev 2009;30:465–93.
305. Wood JW. Fecundity and natural fertility in humans. Oxf Rev Reprod
Biol 1989;11:61–109.
306. Bateman BT, Simpson LL. Higher rate of stillbirth at the extremes of
reproductive age: a large nationwide sample of deliveries in the United
States. Am J Obstet Gynecol 2006;194:840–5.
307. Berg CJ, Callaghan WM, Syverson C, Henderson Z. Pregnancy-related
mortality in the United States, 1998 to 2005. Obstet Gynecol 2010;
116:1302–9.

MMWR / June 21, 2013 / Vol. 62 / No. 5

308. Balasch J, Gratacós E. Delayed childbearing: effects on fertility and the
outcome of pregnancy. Curr Opin Obstet Gynecol 2012;24:187–93.
309. Lidegaard O, Lokkegaard E, Svendsen AL, Agger C. Hormonal
contraception and risk of venous thromboembolism: national follow-up
study. BMJ 2009;339:b2890.
310. Lidegaard O, Nielsen LH, Skovlund CW, Skjeldestad FE, Lokkegaard
E. Risk of venous thromboembolism from use of oral contraceptives
containing different progestogens and oestrogen doses: Danish cohort
study, 2001–9. BMJ 2011;343:d6423.
311. Nightingale AL, Lawrenson RA, Simpson EL, Williams TJ, MacRae
KD, Farmer RD. The effects of age, body mass index, smoking and
general health on the risk of venous thromboembolism in users of
combined oral contraceptives. Eur J Contracept Reprod Health Care
2000;5:265–74.
312. Slone D, Shapiro S, Kaufman DW, Rosenberg L, Miettinen OS, Stolley
PD. Risk of myocardial infarction in relation to current and discontinued
use of oral contraceptives. N Engl J Med 1981;305:420–4.
313. Tanis BC, van den Bosch MA, Kemmeren JM, et al. Oral contraceptives
and the risk of myocardial infarction. N Engl J Med 2001;345:1787–93.
314. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer
and hormonal contraceptives: collaborative reanalysis of individual data
on 53 297 women with breast cancer and 100 239 women without breast
cancer from 54 epidemiological studies. Lancet 1996;347:1713–27.
315. Gill JK, Press MF, Patel AV, Bernstein L. Oral contraceptive use and
risk of breast carcinoma in situ (United States). Cancer Causes Control
2006;17:1155–62.
316. Kumle M, Weiderpass E, Braaten T, Persson I, Adami HO, Lund E. Use
of oral contraceptives and breast cancer risk: the Norwegian-Swedish
Women’s Lifestyle and Health Cohort Study. Cancer Epidemiol
Biomarkers Prev 2002;11:1375–81.
317. Marchbanks PA, McDonald JA, Wilson HG, et al. Oral contraceptives
and the risk of breast cancer. N Engl J Med 2002;346:2025–32.
318. Newcomb PA, Longnecker MP, Storer BE, et al. Recent oral contraceptive
use and risk of breast cancer (United States). Cancer Causes Control
1996;7:525–32.
319. Rosenberg L, Palmer JR, Rao RS, et al. Case-control study of oral contraceptive
use and risk of breast cancer. Am J Epidemiol 1996;143:25–37.
3PTFOCFSH-
;IBOH:
$PPHBO1'
4USPN#-
1BMNFS+3"DBTFDPOUSPM
study of oral contraceptive use and incident breast cancer. Am J Epidemiol
2009;169:473–9.
321. Shapiro S, Rosenberg L, Hoffman M, et al. Risk of breast cancer in relation
to the use of injectable progestogen contraceptives and combined estrogen/
progestogen contraceptives. Am J Epidemiol 2000;151:396–403.

Recommendations and Reports

Appendix A
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010
Key:
1. No restriction (method can be used)
2. Advantages generally outweigh theoretical or proven
risks
3. Theoretical or proven risks usually outweigh the
advantages
4. Unacceptable health risk (method not to be used)

Condition

Sub-condition

Combined
pill, patch,
ring

I
Age

Anatomic
abnormalities

Anemias

Updated June 2012. This summary sheet only contains
a subset of the recommendations from the US MEC.
For complete guidance, see: http://www.cdc.gov/
reproductivehealth/unintendedpregnancy/USMEC.htm.
Most contraceptive methods do not protect against sexually
transmitted infections (STIs). Consistent and correct use of
the male latex condom reduces the risk of STIs and HIV.

Progestinonly pill

Injection

Implant

LNG-IUD Copper-IUD

Menarche to
<40=1

Menarche to
<18=1

Menarche to
<18=2

Menarche to
<18=1

Menarche to
<20=2

>40=2

18-45=1

>20=1

>45=1

>45=2

>45=1

a) Distorted uterine
cavity

b) Other
abnormalities

a) Thalassemia

b) Sickle cell disease†

c) Iron-deficiency
anemia

Benign ovarian tumors

(including cysts)

Breast disease

a) Undiagnosed mass

b) Benign breast
disease

c) Family history of
cancer

d) Breast cancer†
i) current

a) < 1 month
postpartum

b) 1 month or more
postpartum

Awaiting treatment

ii) past and no
evidence of
current disease for
5 years
Breastfeeding
(see also Postpartum)

Cervical cancer

Cervical ectropion

4
1

Cervical
intraepithelial
neoplasia

See table footnotes on page 54.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix A (Continued)
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010

Condition

Sub-condition

Combined
pill, patch,
ring

I
Cirrhosis

DVT/PE

Progestinonly pill

Injection

Implant

LNG-IUD Copper-IUD

a) Mild
(compensated)

b) Severe†
(decompensated)

i) higher risk for
recurrent DVT/PE

ii) lower risk for
recurrent DVT/PE

i) higher risk for
recurrent DVT/PE

ii) lower risk for
recurrent DVT/PE

d) Family history
(first-degree relatives)

(i) with prolonged
immobilization

(ii) without
prolonged
immobilization

a) History of
DVT/PE, not
on anticoagulant
therapy

b) Acute DVT/PE
c) DVT/PE and
established on
anticoagulant
therapy for at least 3
months

e) Major surgery

f ) Minor
surgery without
immobilization
Depressive disorders
See table footnotes on page 54.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix A (Continued)
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010

Condition

Sub-condition

Combined
pill, patch,
ring

I
Diabetes mellitus

a) History of
gestational diabetes
mellitus only

Progestinonly pill

Injection

Implant

LNG-IUD Copper-IUD

(i) non-insulin
dependent

(ii) insulin
dependent†

c) Nephropathy/
retinopathy/
neuropathy†

3/4*

d) Other vascular
disease or diabetes of
>20 years’ duration†

3/4*

Endometrial cancer†

Endometrial
hyperplasia

b) Non-vascular
disease

Endometriosis

2
1

(i) treated by
cholecystectomy

(ii) medically
treated

(see also Drug
Interactions)

Gallbladder disease

a) Symptomatic

Headaches

2
1

Epilepsy†

Gestational
trophoblastic disease

(iii) current

b) Asymptomatic

a) Decreasing or
undetectable ß-hCG
levels

b) Persistently
elevated ß-hCG
levels or malignant
disease†

a) Non-migrainous

i) without aura,
age <35

ii) without aura,
age >35

iii) with aura, any
age

b) Migraine

See table footnotes on page 54.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix A (Continued)
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010

Condition

Sub-condition

Combined
pill, patch,
ring

I
History of bariatric surgery†

a) Restrictive
procedures
b) Malabsorptive
procedures

History of cholestasis

Progestinonly pill

Injection

Implant

LNG-IUD Copper-IUD

COCs: 3

P/R: 1

a) Pregnancy-related

b) Past COC-related

History of high blood pressure
during pregnancy

History of pelvic surgery

HIV

High risk

HIV infected
(see also Drug
Interactions)†

AIDS (see also Drug
Interactions) †

Clinically well on
therapy
Hyperlipidemias
Hypertension

If on treatment, see Drug Interactions
2/3*

(i) systolic 140159 or diastolic
90-99

(ii) systolic ≥160
or diastolic ≥100†

a) Adequately
controlled
hypertension
b) Elevated blood
pressure levels
(properly taken
measurements)

c) Vascular disease

Inflammatory bowel disease

(Ulcerative colitis,
Crohn’s disease)

2/3*

Ischemic heart
disease†

Current and
history of

Liver tumors

a) Benign

ii) Hepatocellular
adenoma†

See table footnotes on page 54.

i) Focal nodular
hyperplasia

b) Malignant†
Malaria

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix A (Continued)
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010

Condition

Sub-condition

Combined
pill, patch,
ring

Progestinonly pill

Injection

Implant

LNG-IUD Copper-IUD

Multiple risk factors for arterial
cardiovascular disease

(such as older age,
smoking, diabetes
and hypertension)

3/4*

Obesity

a) >30 kg/m2 BMI

b) Menarche to
<18 years and
>30 kg/m2 BMI

Ovarian cancer†
Parity

a) Nulliparous

b) Parous

(i) with
subsequent
pregnancy

(ii) without
subsequent
pregnancy

Past ectopic
pregnancy
Pelvic inflammatory disease

a) Past, (assuming no
current risk factors
of STIs)

b) Current
Peripartum

cardiomyopathy†

Postabortion

Postpartum
(see also Breastfeeding)

a) Normal or mildly
impaired cardiac
function
(i) <6 months

(ii) >6 months

b) Moderately or
severely impaired
cardiac function

a) First trimester

b) Second trimester

c) Immediately postseptic abortion

a) <21 days

b) 21 days to
42 days
(i) with other risk
factors for VTE
(ii) without other
risk factors for
VTE
c) >42 days

See table footnotes on page 54.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix A (Continued)
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010

Condition

Sub-condition

Combined
pill, patch,
ring

I
Postpartum (in breastfeeding
or non-breastfeeding women,
including post-cesarean
section)

Schistosomiasis

Smoking

Solid organ
transplantation†
Stroke†

LNG-IUD Copper-IUD

C
1

b) 10 minutes after
delivery of the
placenta to
< 4 weeks

c) >4 weeks

d) Puerperal sepsis

NA*

a) On
immunosuppressive
therapy

2/3*

b) Not on
immunosuppressive
therapy

4*
2

4*
1

a) Uncomplicated

b) Fibrosis of the
liver†

a) Current purulent
cervicitis or
chlamydial infection
or gonorrhea

b) Other STIs
(excluding HIV and
hepatitis)

c) Vaginitis
(including
trichomonas
vaginalis and
bacterial vaginosis)

d) Increased risk of
STIs

2/3*

a) Age <35

b) Age >35, <15
cigarettes/day

c) Age >35, >15
cigarettes/day

a) Complicated

b) Uncomplicated

History of
cerebrovascular
accident

See table footnotes on page 54.

Implant

Severe dysmenorrhea
STIs

Injection

a) <10 minutes after
delivery of the
placenta

Pregnancy
Rheumatoid
arthritis

Progestinonly pill

MMWR / June 21, 2013 / Vol. 62 / No. 5

3
3

Recommendations and Reports

Appendix A (Continued)
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010

Condition

Sub-condition

Combined
pill, patch,
ring

I
Superficial venous thrombosis

Systemic lupus
erythematosus†

Progestinonly pill

Injection

Implant

LNG-IUD Copper-IUD

a) Varicose veins

b) Superficial
thrombophlebitis

a) Positive (or
unknown)
antiphospholipid
antibodies

b) Severe
thrombocytopenia

c)
Immunosuppressive
treatment

d) None of the above
Thrombogenic
mutations†

Thyroid disorders

Simple goiter/
hyperthyroid/
hypothyroid

Tuberculosis†
(see also Drug
Interactions)

a) Non-pelvic

b) Pelvic

Unexplained vaginal bleeding

(suspicious for
serious condition)
before evaluation

Uterine fibroids
Valvular heart
disease

a) Uncomplicated
Complicated†

Vaginal bleeding
patterns

a) Irregular pattern
without heavy
bleeding

b) Heavy or
prolonged bleeding

Viral hepatitis

a) Acute or flare
b) Carrier/Chronic

3/4*

See table footnotes on page 54.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix A (Continued)
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2010

Condition

Sub-condition

Combined
pill, patch,
ring

Progestinonly pill

Injection

Implant

LNG-IUD Copper-IUD

Drug Interactions
Antiretroviral therapy

Anticonvulsant therapy

Antimicrobial therapy

a) Nucleoside
reverse transcriptase
inhibitors

2/3*

b) Non-nucleoside
reverse transcriptase
inhibitors

2/3*

c) Ritonavir-boosted
protease inhibitors

2/3*

a) Certain
anticonvulsants
(phenytoin,
carbamazepine,
barbiturates,
primidone,
topiramate,
oxcarbazepine)

b) Lamotrigine

a) Broad spectrum
antibiotics

b) Antifungals

c) Antiparasitics

d) Rifampicin or
rifabutin therapy

Abbreviations: AIDS = acquired immunodeficiency syndrome; BMI = body mass index; C = continuation of contraceptive method; COC = combined oral
contraceptive; Cu-IUD = copper-containing intrauterine device; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HIV = human
immunodeficiency virus; I = initiation of contraceptive method; LNG-IUD = levonorgestrel-releasing intrauterine device; NA = not applicable;
PE = pulmonary embolism; STI = sexually transmitted infection; VTE = venous thromboembolism.
Source: Modified from CDC. Summary chart of U.S. medical eligibility criteria for contraceptive use. Atlanta, GA: CDC; 2012. (Available at http://www.
cdc.gov/reproductivehealth/UnintendedPregnancy/USMEC.htm.)
* Please see the complete guidance for a clarification to this classification: www.cdc.gov/reproductivehealth/unintendedpregnancy/USMEC.htm.
† Condition that exposes a woman to increased risk as a result of unintended pregnancy.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix B
When To Start Using Specific Contraceptive Methods

Contraceptive method

When to start (if the provider is
reasonably certain that the woman is
not pregnant)

Copper-containing IUD

Anytime

Not needed

Levonorgestrel-releasing IUD

Anytime

If >7 days after menses started, use
Bimanual examination and cervical
back-up method or abstain for 7 days. inspection†

Implant

Anytime

If >5 days after menses started, use
None
back-up method or abstain for 7 days.

Injectable

Anytime

If >7 days after menses started, use
None
back-up method or abstain for 7 days.

Combined hormonal contraceptive

Anytime

If >5 days after menses started, use
Blood pressure measurement
back-up method or abstain for 7 days.

Progestin-only pill

Anytime

If >5 days after menses started, use
None
back-up method or abstain for 2 days.

Additional contraception
(i.e., back-up) needed

Examinations or tests needed
before initiation*
Bimanual examination and cervical
inspection†

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus; IUD = intrauterine device; STD = sexually transmitted disease; U.S. MEC = U.S. Medical
Eligibility Criteria for Contraceptive Use, 2010.
* Weight (BMI) measurement is not needed to determine medical eligibility for any methods of contraception because all methods can be used (U.S. MEC 1) or generally
can be used (U.S. MEC 2) among obese women (Box 2). However, measuring weight and calculating BMI (weight [kg]/height [m]2) at baseline might be helpful for
monitoring any changes and counseling women who might be concerned about weight change perceived to be associated with their contraceptive method.
† Most women do not require additional STD screening at the time of IUD insertion if they have already been screened according to CDC’s STD Treatment Guidelines
(available at http://www.cdc.gov/std/treatment). If a woman has not been screened according to guidelines, screening can be performed at the time of IUD insertion,
and insertion should not be delayed. Women with purulent cervicitis or current chlamydial infection or gonorrhea should not undergo IUD insertion (U.S. MEC 4).
Women who have a very high individual likelihood of STD exposure (e.g., those with a currently infected partner) generally should not undergo IUD insertion
(U.S. MEC 3) (Box 2). For these women, IUD insertion should be delayed until appropriate testing and treatment occurs.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix C
Examinations and Tests Needed Before Initiation of Contraceptive Methods
The examinations or tests noted apply to women who are
presumed to be healthy. Those with known medical problems
or other special conditions might need additional examinations
or tests before being determined to be appropriate candidates
for a particular method of contraception. The U.S. Medical
Eligibility Criteria for Contraceptive Use, 2010 (U.S. MEC),
might be useful in such circumstances (5). The following
classification was considered useful in differentiating the
applicability of the various examinations or tests:
Class A: essential and mandatory in all circumstances for
safe and effective use of the contraceptive method.
Class B: contributes substantially to safe and effective use,
but implementation may be considered within the public
health and/or service context; risk of not performing an
examination or test should be balanced against the benefits
of making the contraceptive method available.

Class C: does not contribute substantially to safe and
effective use of the contraceptive method.
These classifications focus on the relationship of the
examinations or tests to safe initiation of a contraceptive
method. They are not intended to address the appropriateness
of these examinations or tests in other circumstances. For
example, some of the examinations or tests that are not deemed
necessary for safe and effective contraceptive use might be
appropriate for good preventive health care or for diagnosing
or assessing suspected medical conditions.
No examinations or tests are needed before initiating
condoms or spermicides. A bimanual examination is necessary
for diaphragm fitting. A bimanual examination and cervical
inspection are needed for cervical cap fitting.

TABLE. Examinations and tests needed before initiation of contraceptive methods
Contraceptive method and class
Examination or test
Examination
Blood pressure
Weight (BMI) (weight [kg]/
height [m]2)
Clinical breast examination
Bimanual examination and
cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology
(Papanicolaou smear)
STD screening with laboratory
tests
HIV screening with laboratory
tests

Cu-IUD and
LNG-IUD

Implant

Injectable

CHC

POP

Condom

Diaphragm or
cervical cap

Spermicide

C
—†

A*
—†

C
—†

C
C

C
A

C
C

C
A§

C
C

C
C
C
C
C
C

—¶

Abbreviations: BMI = body mass index; CHC = combined hormonal contraceptive; Cu-IUD = copper-containing intrauterine device; DMPA = depot medroxyprogesterone
acetate; HIV = human immunodeficiency virus; LNG-IUD = levonorgestrel-releasing intrauterine device; POP = progestin-only pill; STD = sexually transmitted disease;
U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use, 2010.
* In cases in which access to health care might be limited, the blood pressure measurement can be obtained by the woman in a nonclinical setting (e.g., pharmacy
or fire station) and self-reported to the provider.
† Weight (BMI) measurement is not needed to determine medical eligibility for any methods of contraception because all methods can be used (U.S. MEC 1) or generally
can be used (U.S. MEC 2) among obese women (Box 2). However, measuring weight and calculating BMI at baseline might be helpful for monitoring any changes
and counseling women who might be concerned about weight change perceived to be associated with their contraceptive method.
§ A bimanual examination (not cervical inspection) is needed for diaphragm fitting.
¶ Most women do not require additional STD screening at the time of IUD insertion if they have already been screened according to CDC’s STD Treatment Guidelines
(available at http://www.cdc.gov/std/treatment). If a woman has not been screened according to guidelines, screening can be performed at the time of IUD insertion
and insertion should not be delayed. Women with purulent cervicitis or current chlamydial infection or gonorrhea should not undergo IUD insertion (U.S. MEC 4).
Women who have a very high individual likelihood of STD exposure (e.g., those with a currently infected partner) generally should not undergo IUD insertion
(U.S. MEC 3). For these women, IUD insertion should be delayed until appropriate testing and treatment occurs.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix D
Routine Follow-Up After Contraceptive Initiation
These recommendations address when routine follow-up
is recommended for safe and effective continued use of
contraception for healthy women. The recommendations refer
to general situations and might vary for different users and

TABLE. Routine follow-up after contraceptive initiation
Contraceptive method
Action

Cu-IUD or LNG-IUD

Implant

Injectable

CHC

POP

Assess any changes in health status, including medications, that
would change the method’s appropriateness for safe and
effective continued use based on U.S. MEC (i.e., category 3 and 4
conditions and characteristics) (Box 2).

Consider performing an examination to check for the presence of
IUD strings.

—

Consider assessing weight changes and counseling women who
are concerned about weight change perceived to be associated
with their contraceptive method.

Measure blood pressure.

—

General follow-up
Advise women to return at any time to discuss side effects or other
problems or if they want to change the method. Advise women
using IUDs, implants, or injectables when the IUD or implant
needs to be removed or when a reinjection is needed. No routine
follow-up visit is required.
Other routine visits
Assess the woman’s satisfaction with her current method and
whether she has any concerns about method use.

Abbreviations: CHC = combined hormonal contraceptive; Cu-IUD = copper-containing intrauterine device; HIV = human immunodeficiency virus; IUD = intrauterine
device; LNG-IUD = levonorgestrel-releasing intrauterine device; POP = progestin-only pill; U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use, 2010.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix E
Management of Women with Bleeding Irregularities While Using Contraception

If bleeding persists, or if the woman requests it, medical treatment can be considered.*

Cu-IUD
users

LNG-IUD
users†

For unscheduled
spotting or light
bleeding or for heavy
or prolonged bleeding:
tNSAIDs (5–7 days
of treatment)

Implant
users†

For unscheduled
spotting or light
bleeding or heavy/
prolonged bleeding:
tNSAIDs (5–7 days
of treatment)
tHormonal treatment
(if medically eligible)
with COCs or
estrogen (10–20 days
of treatment)

Injectable
(DMPA) users

For unscheduled
spotting or light
bleeding:
tNSAIDs (5–7 days
of treatment)

For heavy or
prolonged bleeding:
tNSAIDs (5–7 days of
treatment)
tHormonal treatment
(if medically eligible)
with COCs or estrogen
(10–20 days of
treatment)

CHC users (extended or
continuous regimen)

Hormone-free interval
for 3–4 consecutive days

Not recommended during
the first 21 days of
extended or continuous
CHC use

Not recommended more
than once per month
because contraceptive
effectiveness might be
reduced

If bleeding disorder persists or woman finds it unacceptable

Counsel on alternative methods and offer another method, if desired.

Abbreviations: CHC = combined hormonal contraceptive; COC = combined oral contraceptive; Cu-IUD = copper-containing intrauterine device; DMPA = depot
medroxyprogesterone acetate; LNG-IUD = levonorgestrel-releasing intrauterine device; NSAIDs = nonsteroidal antiinflammatory drugs.
* If clinically warranted, evaluate for underlying condition. Treat the condition or refer for care.
† Heavy or prolonged bleeding, either unscheduled or menstrual, is uncommon.

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

Appendix F
Management of the IUD when a Cu-IUD or an LNG-IUD User Is Found To Have
Pelvic Inflammatory Disease
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Abbreviations: Cu-IUD = copper-containing IUD; IUD = intrauterine device; LNG-IUD = levonorgestrel-releasing IUD; PID = pelvic inflammatory disease.
* Treat according to CDC’s STD Treatment Guidelines (available at http://www.cdc.gov/std/treatment).

MMWR / June 21, 2013 / Vol. 62 / No. 5

Recommendations and Reports

U.S. Selected Practice Recommendations for Contraceptive Use Participants
CDC Steering Committee
Kathryn M. Curtis, PhD (Chair), Denise J. Jamieson, MD, Polly A. Marchbanks, PhD, Naomi K. Tepper, MD, CDC, Atlanta, Georgia.
Invited Meeting Participants,
October 21–22, 2010, Atlanta, Georgia
Herbert B. Peterson, MD, University of North Carolina, Chapel Hill, North Carolina (Chair); Abbey Berenson, MD, University of Texas Medical Branch,
Nassau Bay, Texas; Philip Darney, MD, University of California, San Francisco, California; David Eisenberg, MD, Washington University, St. Louis,
Missouri; Paula Hillard, MD, Stanford University, Palo Alto, California; Andrew Kaunitz, MD, University of Florida, Jacksonville, Florida; Trent MacKay,
MD, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland; Mary Mitchell, American College
of Obstetricians and Gynecologists, Washington, DC; Michael Policar, MD, University of California, San Francisco, California; Sarah Prager, University of
Washington, Seattle, Washington.
Systematic Review Presenters and Authors
Meeting, October 4–7, 2011, Atlanta, Georgia
Kathryn M. Curtis, PhD, Suzanne G. Folger, PhD, Emily M. Godfrey, MD, Denise J. Jamieson, MD, Gary Jeng, PhD, Polly A. Marchbanks, PhD, Sarah
Murtaza, MPH, Maria W. Steenland, MPH, Naomi K. Tepper, MD, Crystal P. Tyler, PhD, Maura K. Whiteman, PhD, Lauren B. Zapata, PhD, CDC, Atlanta,
Georgia; Dalia Brahmi, MD, Ipas, Carrboro, NC; Nathalie Kapp, MD, Mary Lyn E. Gaffield, PhD, Maria I. Rodriguez, MD, World Health Organization,
Geneva, Switzerland; Tara P. Cleary, MD, Carrie Cwiak, MD, Emory University, Atlanta, Georgia; Jennifer Salcedo, MD, University of California, Los Angeles,
California; Ira Sharlip, MD, American Urological Association and University of California, San Francisco, California.
Invited Meeting Participants,
October 4–7, 2011, Atlanta, Georgia
Willard Cates, Jr., MD, FHI360, Research Triangle Park, North Carolina (Chair); Herbert B. Peterson, MD, University of North Carolina, Chapel Hill, North
Carolina (Chair); Rebecca Allen, MD, American Society for Reproductive Medicine and Brown University, Providence, Rhode Island; Abbey Berenson, MD,
University of Texas Medical Branch, Nassau Bay, Texas; Paul Blumenthal, MD, Stanford University, Palo Alto, California; Mitchell Creinin, MD, University
PG$BMJGPSOJB
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College of Medicine, Houston, Texas; Linda Dominguez, Southwest Women’s Health, Albuquerque, New Mexico; Alison Edelman, MD, Oregon Health
Sciences University, Portland, Oregon; David Eisenberg, MD, Washington University, St. Louis, Missouri; Melissa Gilliam, MD, The University of Chicago,
$IJDBHP
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Planned Parenthood of Massachusetts, Boston, Massachusetts; Robert Hatcher, MD, Emory University, Atlanta, Georgia; Mark Hathaway, MD, Association
for Reproductive Health Professionals and Washington Hospital Center, Washington, DC; Stephen Heartwell, DrPH, Susan Thompson Buffett Foundation,
Omaha, Nebraska; Paula Hillard, MD, Stanford University, Palo Alto, California; Andrew Kaunitz, MD, University of Florida, Jacksonville, Florida; Hal
Lawrence, MD, American College of Obstetricians and Gynecologists, Washington, DC; Laura MacIsaac, MD, Albert Einstein School of Medicine, New
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Mitchell, American College of Obstetricians and Gynecologists, Washington, DC; Susan Moskosky, MS, U.S. Department of Health and Human Services,
Rockville, Maryland; Patricia Murphy, DrPH, University of Utah, Salt Lake City, Utah; Kavita Nanda, MD, FHI360, Research Triangle Park, North Carolina;
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Michael Policar, MD, University of California, San Francisco, California; Sarah Prager, University of Washington, Seattle, Washington; Ira Sharlip, MD,
American Urological Association and University of California, San Francisco, California; David Soper, MD, University of South Carolina, Charleston, South
Carolina; Lisa Soule, MD, Food and Drug Administration, Silver Spring, Maryland; Maria Trent, MD, Johns Hopkins University, Baltimore, Maryland;
+BNFT5SVTTFMM
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Emory University, Atlanta, Georgia.
External Reviewers
Courtney Benedict, MSN, Planned Parenthood Federation of America, Sonoma, California; Gale Burstein, MD, Erie County Department of Health, Buffalo,
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MSN, University of Washington, Seattle, Washington.

MMWR / June 21, 2013 / Vol. 62 / No. 5

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Morbidity and Mortality Weekly Report
Recommendations and Reports / Vol. 65 / No. 4

July 29, 2016

U.S. Selected Practice Recommendations for
Contraceptive Use, 2016

Continuing Education Examination available at http://www.cdc.gov/mmwr/cme/conted.html.

U.S. Department of Health and Human Services
Centers for Disease Control and Prevention

Recommendations and Reports

CONTENTS

CONTENTS (Continued)

Introduction ............................................................................................................1

Appendix A: Summary Chart of U.S. Medical Eligibility Criteria for
Contraceptive Use, 2016 .................................................................................. 53

Summary of Changes from the
2013 U.S. SPR ........................................................................................................2
Methods....................................................................................................................2

Appendix B: When To Start Using Specific Contraceptive Methods ....... 62
Appendix C: Examinations and Tests Needed Before Initiation of

Maintaining Updated Guidance ......................................................................3

Contraceptive Methods ................................................................................. 63

How To Use This Document ...............................................................................3

Appendix D: Routine Follow-Up After Contraceptive Initiation ........ 64

Contraceptive Method Choice .........................................................................4

Appendix E: Management of Women with Bleeding Irregularities

How To Be Reasonably Certain that a Woman Is Not Pregnant ............5
Intrauterine Contraception ................................................................................7
Implants ................................................................................................................. 14

While Using Contraception .......................................................................... 65
Appendix F: Management of Intrauterine Devices When Users are
Found To Have Pelvic Inflammatory Disease ......................................... 66

Injectables............................................................................................................. 18
Combined Hormonal Contraceptives ......................................................... 22
Progestin-Only Pills............................................................................................ 31
Standard Days Method..................................................................................... 34
Disclosure of Relationship

Emergency Contraception .............................................................................. 34
Female Sterilization ........................................................................................... 36
Male Sterilization ................................................................................................ 37
When Women Can Stop Using Contraceptives ....................................... 38
Conclusion ............................................................................................................ 39
References............................................................................................................. 41

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Timothy F. Jones, MD, Chairman
Matthew L. Boulton, MD, MPH
Virginia A. Caine, MD
Katherine Lyon Daniel, PhD
Jonathan E. Fielding, MD, MPH, MBA
David W. Fleming, MD

William E. Halperin, MD, DrPH, MPH
King K. Holmes, MD, PhD
Robin Ikeda, MD, MPH
Rima F. Khabbaz, MD
Phyllis Meadows, PhD, MSN, RN
Jewel Mullen, MD, MPH, MPA

Jeff Niederdeppe, PhD
Patricia Quinlisk, MD, MPH
Patrick L. Remington, MD, MPH
Carlos Roig, MS, MA
William L. Roper, MD, MPH
William Schaffner, MD

Recommendations and Reports

U.S. Selected Practice Recommendations for Contraceptive Use, 2016
Kathryn M. Curtis, PhD1
Tara C. Jatlaoui, MD1
Naomi K. Tepper, MD1
Lauren B. Zapata, PhD1
Leah G. Horton, MSPH1
Denise J. Jamieson, MD1
Maura K. Whiteman, PhD1
1Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion

Summary
The 2016 U.S. Selected Practice Recommendations for Contraceptive Use (U.S. SPR) addresses a select group of common, yet
sometimes controversial or complex, issues regarding initiation and use of specific contraceptive methods. These recommendations for health care
providers were updated by CDC after review of the scientific evidence and consultation with national experts who met in Atlanta, Georgia,
during August 26–28, 2015. The information in this report updates the 2013 U.S. SPR (CDC. U.S. selected practice recommendations
for contraceptive use, 2013. MMWR 2013;62[No. RR-5]). Major updates include 1) revised recommendations for starting regular
contraception after the use of emergency contraceptive pills and 2) new recommendations for the use of medications to ease insertion of
intrauterine devices. The recommendations in this report are intended to serve as a source of clinical guidance for health care providers and
provide evidence-based guidance to reduce medical barriers to contraception access and use. Health care providers should always consider the
individual clinical circumstances of each person seeking family planning services. This report is not intended to be a substitute for professional
medical advice for individual patients. Persons should seek advice from their health care providers when considering family planning options.

Introduction
Unintended pregnancy rates remain high in the United
States; approximately 45% of all pregnancies are unintended,
with higher proportions among adolescent and young
women, women who are racial/ethnic minorities, and women
with lower levels of education and income (1). Unintended
pregnancies increase the risk for poor maternal and infant
outcomes (2) and in 2010, resulted in U.S. government health
care expenditures of $21 billion (3). Approximately half of
unintended pregnancies are among women who were not using
contraception at the time they became pregnant; the other
half are among women who became pregnant despite reported
use of contraception (4). Strategies to prevent unintended
pregnancy include assisting women at risk for unintended
pregnancy and their partners with choosing appropriate
contraceptive methods and helping them use methods correctly
and consistently to prevent pregnancy.
In 2013, CDC published the first U.S. Selected Practice
Recommendations for Contraceptive Use (U.S. SPR), adapted
from global guidance developed by the World Health
Organization (WHO SPR), which provided evidence-based
guidance on how to use contraceptive methods safely and
effectively once they are deemed to be medically appropriate.
Corresponding author: Kathryn M. Curtis, PhD, Division of Reproductive
Health, National Center for Chronic Disease Prevention and Health
Promotion, CDC. Telephone: 770-488-5200; E-mail: [email protected].

U.S. SPR is a companion document to U.S. Medical Eligibility
Criteria for Contraceptive Use (U.S. MEC) (http://www.cdc.
gov/reproductivehealth/unintendedpregnancy/usmec.htm),
which provides recommendations on safe use of contraceptive
methods for women with various medical conditions and
other characteristics (5). WHO intended for the global
guidance to be used by local or national policy makers, family
planning program managers, and the scientific community as
a reference when they develop family planning guidance at
the country or program level. During 2012–2013, CDC went
through a formal process to adapt the global guidance for best
implementation in the United States, which included rigorous
identification and critical appraisal of the scientific evidence
through systematic reviews, and input from national experts
on how to translate that evidence into recommendations for
U.S. health care providers (6). At that time, CDC committed
to keeping this guidance up to date and based on the best
available evidence, with full review every few years (6).
This document updates the 2013 U.S. SPR (6) with new
evidence and input from experts. Major updates include
1) revised recommendations for starting regular contraception
after the use of emergency contraceptive pills and 2) new
recommendations for the use of medications to ease insertion
of intrauterine devices (IUDs). Recommendations are provided
for health care providers on the safe and effective use of
contraceptive methods and address provision of contraceptive
methods and management of side effects and other problems

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Recommendations and Reports

with contraceptive method use, within the framework of
removing unnecessary medical barriers to accessing and using
contraception. These recommendations are meant to serve as
a source of clinical guidance for health care providers; health
care providers should always consider the individual clinical
circumstances of each person seeking family planning services.
This report is not intended to be a substitute for professional
medical advice for individual patients, who should seek advice
from their health care providers when considering family
planning options.

Summary of Changes from the
2013 U.S. SPR
Updated Recommendations
Recommendations have been updated regarding when
to start regular contraception after ulipristal acetate (UPA)
emergency contraceptive pills:
• Advise the woman to start or resume hormonal
contraception no sooner than 5 days after use of UPA,
and provide or prescribe the regular contraceptive method
as needed. For methods requiring a visit to a health care
provider, such as depo-medroxyprogesterone acetate
(DMPA), implants, and IUDs, starting the method at the
time of UPA use may be considered; the risk that the
regular contraceptive method might decrease the
effectiveness of UPA must be weighed against the risk of
not starting a regular hormonal contraceptive method.
• The woman needs to abstain from sexual intercourse or
use barrier contraception for the next 7 days after starting
or resuming regular contraception or until her next
menses, whichever comes first.
• Any nonhormonal contraceptive method can be started
immediately after the use of UPA.
• Advise the woman to have a pregnancy test if she does not
have a withdrawal bleed within 3 weeks.

New Recommendations
New recommendations have been made for medications to
ease IUD insertion:
• Misoprostol is not recommended for routine use before
IUD insertion. Misoprostol might be helpful in select
circumstances (e.g., in women with a recent failed insertion).
• Paracervical block with lidocaine might reduce patient
pain during IUD insertion.

MMWR / July 29, 2016 / Vol. 65 / No. 4

Methods
Since publication of the 2013 U.S. SPR, CDC has
monitored the literature for new evidence relevant to the
recommendations through the WHO/CDC continuous
identification of research evidence (CIRE) system (7). This
system identifies new evidence as it is published and allows
WHO and CDC to update systematic reviews and facilitate
updates to recommendations as new evidence warrants.
Automated searches are run in PubMed weekly, and the results
are reviewed. Abstracts that meet specific criteria are added to
the web-based CIRE system, which facilitates coordination and
peer review of systematic reviews for both WHO and CDC.
In 2014, CDC reviewed all of the existing recommendations
in the 2013 U.S. SPR for new evidence identified by CIRE
that had the potential to lead to a changed recommendation.
During August 27–28, 2014, CDC held a meeting in Atlanta,
Georgia, of 11 family planning experts and representatives from
partner organizations to solicit their input on the scope of and
process for updating both the 2010 U.S. MEC and the 2013
U.S. SPR. The participants were experts in family planning
and represented different provider types and organizations that
represent health care providers. A list of participants is provided
at the end of this report. The meeting related to topics to be
addressed in the update of U.S. SPR based on new scientific
evidence published since 2013 (identified though the CIRE
system), topics addressed at a 2014 WHO meeting to update
global guidance, and suggestions CDC received from providers
for the addition of recommendations not included in the
2013 U.S. SPR (e.g., from provider feedback through e-mail,
public inquiry, and questions received at conferences). CDC
identified one topic to consider adding to the guidance: the
use of medications to ease IUD insertion (evidence question:
“Among women of reproductive age, does use of medications
before IUD insertion improve the safety or effectiveness
of the procedure [ease of insertion, need for adjunctive
insertion measures, or insertion success] or affect patient
outcomes [pain or side effects] compared with nonuse of
these medications?”). CDC also identified one topic for
which new evidence warranted a review of an existing
recommendation: initiation of regular contraception after
emergency contraceptive pills (evidence question: “Does
ulipristal acetate for emergency contraception interact with
regular use of hormonal contraception leading to decreased
effectiveness of either contraceptive method?”). CDC
determined that all other recommendations in the 2013
U.S. SPR were up to date and consistent with the current
body of evidence for that recommendation.
In preparation for a subsequent expert meeting
August 26–28, 2015, to review the scientific evidence

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

for potential recommendations, CDC staff conducted
independent systematic reviews for each of the topics
being considered. The purpose of these systematic reviews
was to identify direct evidence related to the common
clinical challenges associated with the recommendations.
Preferred Reporting Items for Systematic Reviews and
Meta-Analyses (PRISMA) guidelines were followed for
reporting systematic reviews (8,9), and strength and
quality of the evidence were assigned using the system of
the U.S. Preventive Services Task Force (10). When direct
evidence was limited or not available, indirect evidence
(e.g., evidence on surrogate outcomes) and theoretical issues
were considered and either added to direct evidence within
a systematic review or separately compiled for presentation
to the meeting participants. Completed systematic reviews
were peer reviewed by two or three experts and then
provided to participants before the expert meeting. Reviews
are referenced throughout this document; the full reviews
have been published and contain the details of each review,
including systematic review question, literature search
protocol, inclusion and exclusion criteria, evidence tables,
and quality assessment. CDC staff continued to monitor
new evidence identified through the CIRE system during
the preparation for the August 2015 meeting.
During August 26–28, 2015, CDC held a meeting in
Atlanta, Georgia, of 29 participants who were invited to
provide their individual perspectives on the scientific evidence
presented and to discuss potential recommendations that
followed. Participants represented a wide range of expertise
in family planning provision and research and included
obstetrician/gynecologists, pediatricians, family physicians,
nurse practitioners, epidemiologists, and others with research
and clinical practice expertise in contraceptive safety,
effectiveness, and management. Lists of participants and any
potential conflicts of interest are provided at the end of this
report. During the meeting, the evidence from the systematic
review for each topic was presented, including direct evidence
and any indirect evidence or theoretical concerns. Participants
provided their perspectives on using the evidence to develop
the recommendations that would meet the needs of U.S.
health care providers. After the meeting, CDC determined the
recommendations in this report, taking into consideration the
perspectives provided by the meeting participants. Feedback
also was received from four external reviewers, composed of
health care providers and researchers who had not participated
in the update meetings. These providers were asked to provide
comments on the accuracy, feasibility, and clarity of the
recommendations. Areas of research that need additional
investigation also were considered during the meeting (11).

Maintaining Updated Guidance
As with any evidence-based guidance document, a key
challenge is keeping the recommendations up to date as new
scientific evidence becomes available. Working with WHO,
CDC uses the CIRE system to ensure that WHO and
CDC guidance is based on the best available evidence and
that a mechanism is in place to update guidance when new
evidence becomes available (7). CDC will continue to work
with WHO to identify and assess all new relevant evidence
and determine whether changes in the recommendations are
warranted. In most cases, U.S. SPR will follow any updates
in the WHO guidance, which typically occurs every 5 years
(or sooner if warranted by new data). In addition, CDC will
review any interim WHO updates for their application in
the United States. CDC also will identify and assess any new
literature for the recommendations that are not included in
the WHO guidance and will completely review U.S. SPR
every 5 years. Updates to the guidance can be found on the
U.S. SPR website (http://www.cdc.gov/reproductivehealth/
UnintendedPregnancy/USSPR.htm).

How To Use This Document
The recommendations in this report are intended to
help health care providers address issues related to use of
contraceptives, such as how to help a woman initiate use of a
contraceptive method, which examinations and tests are needed
before initiating use of a contraceptive method, what regular
follow-up is needed, and how to address problems that often
arise during use, including missed pills and side effects such as
unscheduled bleeding. Each recommendation addresses what
a woman or health care provider can do in specific situations.
For situations in which certain groups of women might be
medically ineligible to follow the recommendations, comments
and reference to U.S. MEC are provided (5). The full U.S.
MEC recommendations and the evidence supporting those
recommendations have been updated in 2016 (5) and are
summarized (Appendix A).
The information in this document is organized by
contraceptive method, and the methods generally are presented
in order of effectiveness, from highest to lowest. However, the
recommendations are not intended to provide guidance on
every aspect of provision and management of contraceptive
method use. Instead, they incorporate the best available
evidence to address specific issues regarding common, yet
sometimes complex, clinical issues. Each contraceptive method
section generally includes information about initiation of the
method, regular follow-up, and management of problems
with use (e.g., usage errors and side effects). Each section first

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Recommendations and Reports

provides the recommendation and then includes comments
and a brief summary of the scientific evidence on which the
recommendation is based. The level of evidence from the
systematic reviews for each evidence summary are provided
based on the U.S. Preventive Services Task Force system, which
includes ratings for study design (I: randomized controlled trials;
II-1: controlled trials without randomization; II-2: observational
studies; and II-3: multiple time series or descriptive studies), ratings
for internal validity (good, fair, or poor), and categorization of the
evidence as direct or indirect for the specific review question (10).
Recommendations in this document are provided for
permanent methods of contraception, such as vasectomy
and female sterilization, as well as for reversible methods of
contraception, including the copper-containing intrauterine
device (Cu-IUD); levonorgestrel-releasing IUDs (LNG-IUDs);
the etonogestrel implant; progestin-only injectables; progestinonly pills (POPs); combined hormonal contraceptive methods
that contain both estrogen and a progestin, including combined
oral contraceptives (COCs), a transdermal contraceptive patch,
and a vaginal contraceptive ring; and the standard days method
(SDM). Recommendations also are provided for emergency use
of the Cu-IUD and emergency contraceptive pills (ECPs).
For each contraceptive method, recommendations are provided
on the timing for initiation of the method and indications for
when and for how long additional contraception, or a back-up
method, is needed. Many of these recommendations include
guidance that a woman can start a contraceptive method at any
time during her menstrual cycle if it is reasonably certain that she
is not pregnant. Guidance for health care providers on how to be
reasonably certain that a woman is not pregnant also is provided.
For each contraceptive method, recommendations include the
examinations and tests needed before initiation of the method.
These recommendations apply to persons who are presumed to
be healthy. Those with known medical problems or other special
conditions might need additional examinations or tests before
being determined to be appropriate candidates for a particular
method of contraception. U.S. MEC might be useful in such
circumstances (5). Most women need no or very few examinations
or tests before initiating a contraceptive method although they
might be needed to address other noncontraceptive health needs
(12). Any additional screening needed for preventive health care
can be performed at the time of contraception initiation, and
initiation should not be delayed for test results. The following
classification system was developed by WHO and adopted by
CDC to categorize the applicability of the various examinations
or tests before initiation of contraceptive methods (13):
Class A: These tests and examinations are essential and
mandatory in all circumstances for safe and effective use of
the contraceptive method.

MMWR / July 29, 2016 / Vol. 65 / No. 4

Class B: These tests and examinations contribute substantially
to safe and effective use, although implementation can be
considered within the public health context, service context, or
both. The risk for not performing an examination or test should
be balanced against the benefits of making the contraceptive
method available.
Class C: These tests and examinations do not contribute
substantially to safe and effective use of the contraceptive method.
These classifications focus on the relation of the examinations
or tests to safe initiation of a contraceptive method. They
are not intended to address the appropriateness of these
examinations or tests in other circumstances. For example,
some of the examinations or tests that are not deemed necessary
for safe and effective contraceptive use might be appropriate
for good preventive health care or for diagnosing or assessing
suspected medical conditions. Systematic reviews were
conducted for several different types of examinations and tests
to assess whether a screening test was associated with safe use
of contraceptive methods. Because no single convention exists
for screening panels for certain diseases, including diabetes,
lipid disorders, and liver diseases, the search strategies included
broad terms for the tests and diseases of interest.
Summary charts and clinical algorithms that summarize
the guidance for the various contraceptive methods have been
developed for many of the recommendations, including when
to start using specific contraceptive methods (Appendix B),
examinations and tests needed before initiating the various
contraceptive methods (Appendix C), routine follow-up
after initiating contraception (Appendix D), management of
bleeding irregularities (Appendix E), and management of IUDs
when users are found to have pelvic inflammatory disease (PID)
(Appendix F). These summaries might be helpful to health care
providers when managing family planning patients. Additional
tools are available on the U.S. SPR website (http://www.cdc.
gov/reproductivehealth/UnintendedPregnancy/USSPR.htm).

Contraceptive Method Choice
Many elements need to be considered individually by a
woman, man, or couple when choosing the most appropriate
contraceptive method. Some of these elements include
safety, effectiveness, availability (including accessibility
and affordability), and acceptability. Although most
contraceptive methods are safe for use by most women,
U.S. MEC provides recommendations on the safety of
specific contraceptive methods for women with certain
characteristics and medical conditions (5); a U.S. MEC
summary (Appendix A) and the categories of medical
eligibility criteria for contraceptive use (Box 1) are provided.

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Recommendations and Reports

Voluntary informed choice of contraceptive methods is an
essential guiding principle, and contraceptive counseling,
where applicable, might be an important contributor to the
successful use of contraceptive methods.
Contraceptive method effectiveness is critically important
in minimizing the risk for unintended pregnancy, particularly
BOX 1. Categories of medical eligibility criteria for contraceptive use

• U.S. MEC 1 = A condition for which there is no
restriction for the use of the contraceptive method.
• U.S. MEC 2 = A condition for which the advantages
of using the method generally outweigh the
theoretical or proven risks.
• U.S. MEC 3 = A condition for which the theoretical
or proven risks usually outweigh the advantages of
using the method.
• U.S. MEC 4 = A condition that represents an
unacceptable health risk if the contraceptive method
is used.
Source: Curtis KM, Jatlaoui TC, Tepper NK, et al. U.S. medical eligibility
criteria for contraceptive use. MMWR 2016;65(No. RR-3).
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria for
Contraceptive Use.

among women for whom an unintended pregnancy would
pose additional health risks. The effectiveness of contraceptive
methods depends both on the inherent effectiveness of the
method itself and on how consistently and correctly it is used
(Figure 1). Both consistent and correct use can vary greatly with
characteristics such as age, income, desire to prevent or delay
pregnancy, and culture. Methods that depend on consistent and
correct use by clients have a wide range of effectiveness between
typical use (actual use, including incorrect or inconsistent
use) and perfect use (correct and consistent use according
to directions) (14). IUDs and implants are considered longacting, reversible contraception (LARC); these methods
are highly effective because they do not depend on regular
compliance from the user. LARC methods are appropriate
for most women, including adolescents and nulliparous
women. All women should be counseled about the full range
and effectiveness of contraceptive options for which they are
medically eligible so that they can identify the optimal method.
In choosing a method of contraception, dual protection
from the simultaneous risk for human immunodeficiency
virus (HIV) and other sexually transmitted diseases (STDs)
also should be considered. Although hormonal contraceptives
and IUDs are highly effective at preventing pregnancy, they
do not protect against STDs, including HIV. Consistent and
correct use of the male latex condom reduces the risk for HIV

infection and other STDs, including chlamydial infection,
gonococcal infection, and trichomoniasis (15). Although
evidence is limited, use of female condoms can provide
protection from acquisition and transmission of STDs (15).
All patients, regardless of contraceptive choice, should be
counseled about the use of condoms and the risk for STDs,
including HIV infection (15). Additional information about
prevention and treatment of STDs is available from the CDC
Sexually Transmitted Diseases Treatment Guidelines (http://www.
cdc.gov/std/treatment) (15).
Women, men, and couples have increasing numbers of safe
and effective choices for contraceptive methods, including
LARC methods such as IUDs and implants, to reduce the
risk for unintended pregnancy. However, with these expanded
options comes the need for evidence-based guidance to help
health care providers offer quality family planning care to their
patients, including assistance in choosing the most appropriate
contraceptive method for individual circumstances and
using that method correctly, consistently, and continuously
to maximize effectiveness. Removing unnecessary barriers
can help patients access and successfully use contraceptive
methods. Several medical barriers to initiating and continuing
contraceptive methods might exist, such as unnecessary screening
examinations and tests before starting the method (e.g., a pelvic
examination before initiation of COCs), inability to receive the
contraceptive on the same day as the visit (e.g., waiting for test
results that might not be needed or waiting until the woman’s
next menstrual cycle to start use), and difficulty obtaining
continued contraceptive supplies (e.g., restrictions on number
of pill packs dispensed at one time). Removing unnecessary
steps, such as providing prophylactic antibiotics at the time of
IUD insertion or requiring unnecessary follow-up procedures,
also can help patients access and successfully use contraception.

How To Be Reasonably Certain that a
Woman Is Not Pregnant
In most cases, a detailed history provides the most accurate
assessment of pregnancy risk in a woman who is about
to start using a contraceptive method. Several criteria for
assessing pregnancy risk are listed in the recommendation
that follows. These criteria are highly accurate (i.e., a negative
predictive value of 99%–100%) in ruling out pregnancy
among women who are not pregnant (16–19). Therefore,
CDC recommends that health care providers use these
criteria to assess pregnancy status in a woman who is about
to start using contraceptives (Box 2). If a woman meets one
of these criteria (and therefore the health care provider can be
reasonably certain that she is not pregnant), a urine pregnancy

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Recommendations and Reports

FIGURE 1. Effectiveness of family planning methods*
Most
Effective

Implant

Reversible
Intrauterine Device
(IUD)

Male Sterilization
(Vasectomy)

Permanent
Female Sterilization
(Abdominal, Laparoscopic, Hysteroscopic)

0.05 %

LNG - 0.2 % Copper T - 0.8 %
Pill

0.15 %
Patch

SUN MON TUES WED THUR FRI

0.5 %
Ring

Diaphragm

SAT

Injectable: Get repeat
injections on time.
Pills: Take a pill each day.

6-12 pregnancies per
100 women in a year

After procedure, little or
nothing to do or remember.
Vasectomy and
hysteroscopic sterilization:
Use another method for
first 3 months.

Less than 1 pregnancy
per 100 women in a year

Injectable

How to make your method
most effective

Patch, Ring: Keep in place,
change on time.

2
3
4

6%
Male Condom

9%
Female Condom

9%
Withdrawal

12 %
Sponge

18 or more pregnancies
per 100 women in a year
18 %
Fertility-Awareness
Based Methods
JANUARY
[1

Least
Effective

2 3 4 5 6 7
10] 11 12 13 14

8 9
15 16
22 [23
29 30

17 18 19 20 21
24 25 26 27 28
31 1 2 3 4

24 %

21 %

22 %

Spermicide

Spe

icid

24 % parous women
12 % nulliparous women

Diaphragm: Use correctly
every time you have sex.
Condoms, sponge,
withdrawal, spermicides:
Use correctly every time
you have sex.
Fertility awareness-based
methods: Abstain or
use condoms on fertile
days. Newest methods
(Standard Days Method
and TwoDay Method)
may be the easiest to use
and consequently more
effective.

28 %

CONDOMS SHOULD ALWAYS BE USED TO REDUCE THE RISK OF SEXUALLY TRANSMITTED INFECTIONS.
Other Methods of Contraception
Lactational Amenorrhea Method: LAM is a highly effective, temporary method of contraception.
Emergency Contraception: Emergency contraceptive pills or a copper IUD after unprotected intercourse substantially reduces risk of pregnancy.
Sources: Adapted from World Health Organization (WHO) Department of Reproductive Health and Research, Johns Hopkins Bloomberg School of Public Health/
Center for Communication Programs (CCP). Knowledge for health project. Family planning: a global handbook for providers (2011 update). Baltimore, MD; Geneva,
Switzerland: CCP and WHO; 2011; and Trussell J. Contraceptive failure in the United States. Contraception 2011;83:397–404.
* The percentages indicate the number out of every 100 women who experienced an unintended pregnancy within the first year of typical use of each contraceptive method.

test might be considered in addition to these criteria (based
on clinical judgment), bearing in mind the limitations of the
accuracy of pregnancy testing. If a woman does not meet
any of these criteria, then the health care provider cannot be
reasonably certain that she is not pregnant, even with a negative
pregnancy test. Routine pregnancy testing for every woman
is not necessary.
On the basis of clinical judgment, health care providers
might consider the addition of a urine pregnancy test; however,
they should be aware of the limitations, including accuracy
of the test relative to the time of last sexual intercourse,
recent delivery, or spontaneous or induced abortion. Routine
pregnancy testing for every woman is not necessary. If a woman
has had recent (i.e., within the last 5 days) unprotected sexual

MMWR / July 29, 2016 / Vol. 65 / No. 4

intercourse, consider offering emergency contraception (either
a Cu-IUD or ECPs) if pregnancy is not desired.
Comments and Evidence Summary. The criteria for
determining whether a woman is pregnant depend on the
assurance that she has not ovulated within a certain amount of
time after her last menses, spontaneous or induced abortion, or
delivery. Among menstruating women, the timing of ovulation
can vary widely. During an average 28-day cycle, ovulation
generally occurs during days 9–20 (20). In addition, the
likelihood of ovulation is low from days 1–7 of the menstrual
cycle (21). After a spontaneous or an induced abortion,
ovulation can occur within 2–3 weeks and has been found
to occur as early as 8–13 days after the end of the pregnancy.
Therefore, the likelihood of ovulation is low ≤7 days after

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

BOX 2. How to be reasonably certain that a woman is not pregnant

A health care provider can be reasonably certain that a
woman is not pregnant if she has no symptoms or signs
of pregnancy and meets any one of the following criteria:
• is ≤7 days after the start of normal menses
• has not had sexual intercourse since the start of last
normal menses.
• has been correctly and consistently using a reliable
method of contraception
• is ≤7 days after spontaneous or induced abortion
• is within 4 weeks postpartum
• is fully or nearly fully breastfeeding (exclusively
breastfeeding or the vast majority [≥85%] of feeds are
breastfeeds), amenorrheic, and <6 months postpartum
an abortion (22–24). A systematic review reported that the
mean day of first ovulation among postpartum nonlactating
women occurred 45–94 days after delivery (25). In one study,
the earliest ovulation was reported at 25 days after delivery.
Among women who are within 6 months postpartum, are
fully or nearly fully breastfeeding (exclusively breastfeeding
or the vast majority [≥85%] of feeds are breastfeeds), and are
amenorrheic, the risk for pregnancy is <2% (26,27).
Although pregnancy tests often are performed before
initiating contraception, the accuracy of qualitative urine
pregnancy tests varies depending on the timing of the test
relative to missed menses, recent sexual intercourse, or recent
pregnancy. The sensitivity of a pregnancy test is defined as
the concentration of human chorionic gonadotropin (hCG)
at which 95% of tests are positive. Most qualitative pregnancy
tests approved by the U.S. Food and Drug Administration
(FDA) report a sensitivity of 20–25 mIU/mL in urine (28–31).
However, pregnancy detection rates can vary widely because of
differences in test sensitivity and the timing of testing relative
to missed menses (30,32). Some studies have shown that an
additional 11 days past the day of expected menses are needed
to detect 100% of pregnancies using qualitative tests (29). In
addition, pregnancy tests cannot detect a pregnancy resulting
from recent sexual intercourse. Qualitative tests also might have
positive results for several weeks after termination of pregnancy
because hCG can be present for several weeks after delivery or
abortion (spontaneous or induced) (33–35).
For contraceptive methods other than IUDs, the benefits
of starting to use a contraceptive method likely exceed any
risk, even in situations in which the health care provider is
uncertain whether the woman is pregnant. Therefore, the
health care provider can consider having patients start using

contraceptive methods other than IUDs at any time, with
a follow-up pregnancy test in 2–4 weeks. The risks of not
starting to use contraception should be weighed against the
risks of initiating contraception use in a woman who might
be already pregnant. Most studies have shown no increased
risk for adverse outcomes, including congenital anomalies
or neonatal or infant death, among infants exposed in utero
to COCs (36–38). Studies also have shown no increased risk
for neonatal or infant death or developmental abnormalities
among infants exposed in utero to DMPA (37,39,40).
In contrast, for women who want to begin using an IUD
(Cu-IUD or LNG-IUD), in situations in which the health
care provider is uncertain whether the woman is pregnant, the
woman should be provided with another contraceptive method
to use until the health care provider is reasonably certain that
she is not pregnant and can insert the IUD. Pregnancies among
women with IUDs are at higher risk for complications such as
spontaneous abortion, septic abortion, preterm delivery, and
chorioamnionitis (41).
A systematic review identified four analyses of data
from three diagnostic accuracy studies that evaluated the
performance of the listed criteria (Box 2) through use of a
pregnancy checklist compared with a urine pregnancy test
conducted concurrently (42). The performance of the checklist
to diagnose or exclude pregnancy varied, with sensitivity
of 55%–100% and specificity of 39%–89%. The negative
predictive value was consistent across studies at 99%–100%;
the pregnancy checklist correctly ruled out women who were
not pregnant. One of the studies assessed the added usefulness
of signs and symptoms of pregnancy and found that these
criteria did not substantially improve the performance of the
pregnancy checklist, although the number of women with signs
and symptoms was small (16) (Level of evidence: Diagnostic
accuracy studies, fair, direct).

Intrauterine Contraception
Four IUDs are available in the United States, the coppercontaining IUD and three levonorgestrel-releasing IUDs
(containing a total of either 13.5 mg or 52 mg levonorgestrel).
Fewer than 1 woman out of 100 becomes pregnant in the
first year of using IUDs (with typical use) (14). IUDs are
long-acting, are reversible, and can be used by women of all
ages, including adolescents, and by parous and nulliparous
women. IUDs do not protect against STDs; consistent and
correct use of male latex condoms reduces the risk for STDs,
including HIV.

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Initiation of Cu-IUDs
Timing
• The Cu-IUD can be inserted at any time if it is reasonably
certain that the woman is not pregnant (Box 2).
• The Cu-IUD also can be inserted within 5 days of the first
act of unprotected sexual intercourse as an emergency
contraceptive. If the day of ovulation can be estimated,
the Cu-IUD also can be inserted >5 days after sexual
intercourse as long as insertion does not occur >5 days
after ovulation.

Need for Back-Up Contraception
• No additional contraceptive protection is needed after
Cu-IUD insertion.

Special Considerations
• Timing: The Cu-IUD can be inserted at any time if it is
reasonably certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: No additional
contraceptive protection is needed.
Postpartum (Including After Cesarean Delivery)
• Timing: The Cu-IUD can be inserted at any time
postpartum, including immediately postpartum (U.S.
MEC 1 or 2) (Box 1), if it is reasonably certain that the
woman is not pregnant (Box 2). The Cu-IUD should not
be inserted in a woman with postpartum sepsis (e.g.,
chorioamnionitis or endometritis) (U.S. MEC 4).
• Need for back-up contraception: No additional
contraceptive protection is needed.
Postabortion (Spontaneous or Induced)
• Timing: The Cu-IUD can be inserted within the first
7 days, including immediately postabortion (U.S. MEC
1 for first-trimester abortion and U.S. MEC 2 for secondtrimester abortion). The Cu-IUD should not be inserted
immediately after a septic abortion (U.S. MEC 4).
• Need for back-up contraception: No additional
contraceptive protection is needed.
Switching from Another Contraceptive Method
• Timing: The Cu-IUD can be inserted immediately if it is
reasonably certain that the woman is not pregnant (Box 2).
Waiting for her next menstrual cycle is unnecessary.
• Need for back-up contraception: No additional
contraceptive protection is needed.

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Initiation of LNG-IUDs
Timing of LNG-IUD Insertion

Amenorrhea (Not Postpartum)

Comments and Evidence Summary. In situations in which
the health care provider is not reasonably certain that the
woman is not pregnant, the woman should be provided with
another contraceptive method to use until the health care
provider can be reasonably certain that she is not pregnant
and can insert the Cu-IUD.
A systematic review identified eight studies that suggested
that timing of Cu-IUD insertion in relation to the menstrual
cycle in non-postpartum women had little effect on longterm outcomes (rates of continuation, removal, expulsion,
or pregnancy) or on short-term outcomes (pain at insertion,
bleeding at insertion, or immediate expulsion) (43) (Level of
evidence: II-2, fair, direct).

• The LNG-IUD can be inserted at any time if it is reasonably
certain that the woman is not pregnant (Box 2).

Need for Back-Up Contraception
• If the LNG-IUD is inserted within the first 7 days since
menstrual bleeding started, no additional contraceptive
protection is needed.
• If the LNG-IUD is inserted >7 days since menstrual
bleeding started, the woman needs to abstain from sexual
intercourse or use additional contraceptive protection for
the next 7 days.

Special Considerations
Amenorrhea (Not Postpartum)
• Timing: The LNG-IUD can be inserted at any time if it is
reasonably certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Including After Cesarean Delivery)
• Timing: The LNG-IUD can be inserted at any time,
including immediately postpartum (U.S. MEC 1 or 2) if
it is reasonably certain that the woman is not pregnant
(Box 2). The LNG-IUD should not be inserted in a
woman with postpartum sepsis (e.g., chorioamnionitis or
endometritis) (U.S. MEC 4).
• Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (27), no

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additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycle needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >7 days since menstrual bleeding
began, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postabortion (Spontaneous or Induced)
• Timing: The LNG-IUD can be inserted within the first
7 days, including immediately postabortion (U.S. MEC
1 for first-trimester abortion and U.S. MEC 2 for secondtrimester abortion). The LNG-IUD should not be inserted
immediately after a septic abortion (U.S. MEC 4).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days unless the
IUD is placed at the time of a surgical abortion.
Switching from Another Contraceptive Method
• Timing: The LNG-IUD can be inserted immediately if
it is reasonably certain that the woman is not pregnant
(Box 2). Waiting for her next menstrual cycle is
unnecessary.
• Need for back-up contraception: If it has been >7 days
since menstrual bleeding began, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
• Switching from a Cu-IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle
and it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A
health care provider may consider providing any type of
ECPs at the time of LNG-IUD insertion.
Comments and Evidence Summary. In situations in which
the health care provider is uncertain whether the woman might
be pregnant, the woman should be provided with another
contraceptive method to use until the health care provider
can be reasonably certain that she is not pregnant and can
insert the LNG-IUD. If a woman needs to use additional
contraceptive protection when switching to an LNG-IUD
from another contraceptive method, consider continuing her
previous method for 7 days after LNG-IUD insertion. No
direct evidence was found regarding the effects of inserting
LNG-IUDs on different days of the cycle on short- or longterm outcomes (43).

Examinations and Tests Needed Before
Initiation of a Cu-IUD or an LNG-IUD
Among healthy women, few examinations or tests are
needed before initiation of an IUD (Table 1). Bimanual
examination and cervical inspection are necessary before
IUD insertion. A baseline weight and BMI measurement
might be useful for monitoring IUD users over time. If a
woman has not been screened for STDs according to STD
screening guidelines, screening can be performed at the time
of insertion. Women with known medical problems or other
special conditions might need additional examinations or
tests before being determined to be appropriate candidates
for a particular method of contraception. U.S. MEC might
be useful in such circumstances (5).
Comments and Evidence Summary. Weight (BMI):
Obese women can use IUDs (U.S. MEC 1) (5); therefore,
screening for obesity is not necessary for the safe initiation
of IUDs. However, measuring weight and calculating
TABLE 1. Classification of examinations and tests needed before
IUD insertion
Class*
Examination or test
Examination
Blood pressure
Weight (BMI) (weight [kg] / height [m]2)
Clinical breast examination
Bimanual examination and cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou smear)
STD screening with laboratory tests
HIV screening with laboratory tests

CopperLevonorgestrelcontaining IUD releasing IUD
C
—†
C
A

C
—†
C
A

C
C
C
C
C
C
—§
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
IUD = intrauterine device; STD = sexually transmitted disease; U.S. MEC = U.S.
Medical Eligibility Criteria for Contraceptive Use.
* Class A: essential and mandatory in all circumstances for safe and effective use of
the contraceptive method. Class B: contributes substantially to safe and effective
use, but implementation may be considered within the public health and/or service
context; the risk of not performing an examination or test should be balanced against
the benefits of making the contraceptive method available. Class C: does not
contribute substantially to safe and effective use of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for any
methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 1). However,
measuring weight and calculating BMI at baseline might be helpful for monitoring
any changes and counseling women who might be concerned about weight
change perceived to be associated with their contraceptive method.
§ Most women do not require additional STD screening at the time of IUD insertion.
If a woman with risk factors for STDs has not been screened for gonorrhea and
chlamydia according to CDC’s STD Treatment Guidelines (http://www.cdc.gov/std/
treatment), screening can be performed at the time of IUD insertion, and insertion
should not be delayed. Women with current purulent cervicitis or chlamydial
infection or gonococcal infection should not undergo IUD insertion (U.S. MEC 4).

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BMI (weight [kg] / height [m2]) at baseline might be helpful
for monitoring any changes and counseling women who
might be concerned about weight change perceived to be
associated with their contraceptive method.
Bimanual examination and cervical inspection: Bimanual
examination and cervical inspection are necessary before IUD
insertion to assess uterine size and position and to detect any
cervical or uterine abnormalities that might indicate infection
or otherwise prevent IUD insertion (44,45).
STDs: Women should be routinely screened for chlamydial
infection and gonorrhea according to national screening
guidelines. The CDC Sexually Transmitted Diseases Treatment
Guidelines provide information on screening eligibility, timing,
and frequency of screening and on screening for persons with
risk factors (15) (http://www.cdc.gov/std/treatment). If STD
screening guidelines have been followed, most women do not
need additional STD screening at the time of IUD insertion,
and insertion should not be delayed. If a woman with risk
factors for STDs has not been screened for gonorrhea and
chlamydia according to CDC STD treatment guidelines,
screening can be performed at the time of IUD insertion,
and insertion should not be delayed. Women with current
purulent cervicitis or chlamydial infection or gonococcal
infection should not undergo IUD insertion (U.S. MEC 4). A
systematic review identified two studies that demonstrated no
differences in PID rates among women who screened positive
for gonorrhea or chlamydia and underwent concurrent IUD
insertion compared with women who screened positive and
initiated other contraceptive methods (46). Indirect evidence
demonstrates women who undergo same-day STD screening
and IUD insertion have similar PID rates compared with
women who have delayed IUD insertion. Women who
undergo same-day STD screening and IUD insertion have low
incidence rates of PID. Algorithms for predicting PID among
women with risk factors for STDs have poor predictive value.
Risk for PID among women with risk factors for STDs is low
(15,47–57). Although women with STDs at the time of IUD
insertion have a higher risk for PID, the overall rate of PID
among all IUD users is low (51,54).
Hemoglobin: Women with iron-deficiency anemia can
use the LNG-IUD (U.S. MEC 1) (5); therefore, screening
for anemia is not necessary for safe initiation of the LNGIUD. Women with iron-deficiency anemia generally can use
Cu-IUDs (U.S. MEC 2) (5). Measurement of hemoglobin
before initiation of Cu-IUDs is not necessary because of
the minimal change in hemoglobin among women with
and without anemia using Cu-IUDs. A systematic review
identified four studies that provided direct evidence for changes
in hemoglobin among women with anemia who received
Cu-IUDs (58). Evidence from one randomized trial (59)

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and one prospective cohort study (60) showed no significant
changes in hemoglobin among Cu-IUD users with anemia,
whereas two prospective cohort studies (61,62) showed a
statistically significant decrease in hemoglobin levels during
12 months of follow-up; however, the magnitude of the
decrease was small and most likely not clinically significant.
The systematic review also identified 21 studies that provided
indirect evidence by examining changes in hemoglobin among
healthy women receiving Cu-IUDs (63–83), which generally
showed no clinically significant changes in hemoglobin levels
with up to 5 years of follow up (Level of evidence: I to II-2,
fair, direct).
Lipids: Screening for dyslipidemias is not necessary for the
safe initiation of Cu-IUD or LNG-IUD because of the low
prevalence of undiagnosed disease in women of reproductive
age and the low likelihood of clinically significant changes
with use of hormonal contraceptives. A systematic review
did not identify any evidence regarding outcomes among
women who were screened versus not screened with lipid
measurement before initiation of hormonal contraceptives
(57). During 2009–2012 among women aged 20–44 years in
the United States, 7.6% had high cholesterol, defined as total
serum cholesterol ≥240 mg/dL (84). During 1999–2008,
the prevalence of undiagnosed hypercholesterolemia among
women aged 20–44 years was approximately 2% (85). Studies
have shown mixed results about the effects of hormonal
methods on lipid levels among both healthy women and
women with baseline lipid abnormalities, and the clinical
significance of these changes is unclear (86–89).
Liver enzymes: Women with liver disease can use the
Cu-IUD (U.S. MEC 1) (5); therefore, screening for liver
disease is not necessary for the safe initiation of the Cu-IUD.
Although women with certain liver diseases generally should
not use the LNG-IUD (U.S. MEC 3) (5), screening for liver
disease before initiation of the LNG-IUD is not necessary
because of the low prevalence of these conditions and the
high likelihood that women with liver disease already would
have had the condition diagnosed. A systematic review did not
identify any evidence regarding outcomes among women who
were screened versus not screened with liver enzyme tests before
initiation of hormonal contraceptive use (57). In 2012, among
U.S. women, the percentage with liver disease (not further
specified) was 1.3% (90). In 2013, the incidence of acute
hepatitis A, B, or C was ≤1 per 100,000 U.S. population (91).
During 2002–2011, the incidence of liver carcinoma among
U.S. women was approximately 3.7 per 100,000 population
(92). Because estrogen and progestins are metabolized in
the liver, the use of hormonal contraceptives among women
with liver disease might, theoretically, be a concern. The use
of hormonal contraceptives, specifically COCs and POPs,

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Recommendations and Reports

does not affect disease progression or severity in women with
hepatitis, cirrhosis, or benign focal nodular hyperplasia (93,94),
although evidence is limited, and no evidence exists for the
LNG-IUD.
Clinical breast examination: Women with breast disease
can use the Cu-IUD (U.S. MEC 1) (5); therefore, screening
for breast disease is not necessary for the safe initiation of
the Cu-IUD. Although women with current breast cancer
should not use the LNG-IUD (U.S. MEC 4) (5), screening
asymptomatic women with a clinical breast examination
before inserting an IUD is not necessary because of the low
prevalence of breast cancer among women of reproductive
age. A systematic review did not identify any evidence
regarding outcomes among women who were screened versus
not screened with a breast examination before initiation of
hormonal contraceptives (95). The incidence of breast cancer
among women of reproductive age in the United States is low.
In 2012, the incidence of breast cancer among women aged
20–49 years was approximately 70.7 per 100,000 women (96).
Cervical cytology: Although women with cervical
cancer should not undergo IUD insertion (U.S. MEC 4)
(5), screening asymptomatic women with cervical cytology
before IUD insertion is not necessary because of the high
rates of cervical screening, low incidence of cervical cancer
in the United States, and high likelihood that a woman
with cervical cancer already would have had the condition
diagnosed. A systematic review did not identify any evidence
regarding outcomes among women who were screened versus
not screened with cervical cytology before initiation of IUDs
(57). Cervical cancer is rare in the United States, with an
incidence rate of 9.8 per 100,000 women during 2012 (96).
The incidence and mortality rates from cervical cancer have
declined dramatically in the United States, largely because of
cervical cytology screening (97). Overall screening rates for
cervical cancer in the United States are high; in 2013 among
women aged 18–44 years, approximately 77% reported having
cervical cytology screening within the last 3 years (98).
HIV screening: Women with HIV infection can use
(U.S. MEC 1) or generally can use (U.S. MEC 2) IUDs
(5). Therefore, HIV screening is not necessary before IUD
insertion. A systematic review did not identify any evidence
regarding outcomes among women who were screened versus
not screened for HIV infection before IUD insertion (57).
Limited evidence suggests that IUDs are not associated with
disease progression, increased infection, or other adverse health
effects among women with HIV infection (99–114).
Other screening: Women with hypertension, diabetes, or
thrombogenic mutations can use (U.S. MEC 1) or generally
can use (U.S. MEC 2) IUDs (5). Therefore, screening for these
conditions is not necessary for the safe initiation of IUDs.

Provision of Medications to Ease
IUD Insertion
• Misoprostol is not recommended for routine use before
IUD insertion. Misoprostol might be helpful in select
circumstances (e.g., in women with a recent failed insertion).
• Paracervical block with lidocaine might reduce patient
pain during IUD insertion.
Comments and Evidence Summary. Potential barriers
to IUD use include anticipated pain with insertion and
provider concerns about difficult insertion. Identifying
effective approaches to ease IUD insertion might increase
IUD initiation.
Evidence for misoprostol from two systematic reviews,
including a total of 10 randomized controlled trials, suggests
that misoprostol does not improve provider ease of insertion,
reduce the need for adjunctive insertion measures, or improve
insertion success (Level of evidence: I, good to fair, direct) and
might increase patient pain and side effects (Level of evidence:
I, high quality) (115,116). However, one randomized controlled
trial examined women with a recent failed IUD insertion and
found significantly higher insertion success with second insertion
attempt among women pretreated with misoprostol versus
placebo (Level of evidence: I, good, direct) (117).
Limited evidence for paracervical block with lidocaine from
one systematic review suggests that it might reduce patient pain
(115). In this review, two randomized controlled trials found
significantly reduced pain at either tenaculum placement or
IUD insertion among women receiving paracervical block with
1% lidocaine 3–5 minutes before IUD insertion (118,119).
Neither trial found differences in side effects among women
receiving paracervical block compared with controls (Level of
evidence: I, moderate to low quality) (118,119).
Limited evidence on nonsteroidal antiinflammatory drugs
(NSAIDs) and nitric oxide donors generally suggested no
positive effect; evidence on lidocaine with administration other
than paracervical block was limited and inconclusive (Level of
evidence for provider ease of insertion: I, good to poor, direct;
Level of evidence for need for adjunctive insertion measures:
I, fair, direct; Level of evidence for patient pain: I, high to
low quality; Level of evidence for side effects: I, high to low
quality) (115,116).

Provision of Prophylactic Antibiotics at the
Time of IUD Insertion
• Prophylactic antibiotics are generally not recommended
for Cu-IUD or LNG-IUD insertion.
Comments and Evidence Summary. Theoretically,
IUD insertion could induce bacterial spread and lead to

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complications such as PID or infective endocarditis. A
metaanalysis was conducted of randomized controlled
trials examining antibiotic prophylaxis versus placebo or
no treatment for IUD insertion (120). Use of prophylaxis
reduced the frequency of unscheduled return visits but did not
significantly reduce the incidence of PID or premature IUD
discontinuation. Although the risk for PID was higher within
the first 20 days after insertion, the incidence of PID was low
among all women who had IUDs inserted (51). In addition,
the American Heart Association recommends that the use of
prophylactic antibiotics solely to prevent infective endocarditis
is not needed for genitourinary procedures (121). Studies have
not demonstrated a conclusive link between genitourinary
procedures and infective endocarditis or a preventive benefit
of prophylactic antibiotics during such procedures (121).

Routine Follow-Up After IUD Insertion
These recommendations address when routine follow-up is
needed for safe and effective continued use of contraception
for healthy women. The recommendations refer to general
situations and might vary for different users and different
situations. Specific populations who might benefit from more
frequent follow-up visits include adolescents, persons with
certain medical conditions or characteristics, and persons with
multiple medical conditions.
• Advise the woman to return at any time to discuss side
effects or other problems, if she wants to change the
method being used, and when it is time to remove or
replace the contraceptive method. No routine follow-up
visit is required.
• At other routine visits, health care providers who see IUD
users should do the following:
– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including
medications, that would change the appropriateness of
the IUD for safe and effective continued use on the
basis of U.S. MEC (e.g., category 3 and 4 conditions
and characteristics).
– Consider performing an examination to check for the
presence of the IUD strings.
– Consider assessing weight changes and counseling women
who are concerned about weight changes perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. Evidence from a
systematic review about the effect of a specific follow-up visit
schedule on IUD continuation is very limited and of poor
quality. The evidence did not suggest that greater frequency of

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visits or earlier timing of the first follow-up visit after insertion
improves continuation of use (122) (Level of evidence: II-2,
poor, direct). Evidence from four studies from a systematic
review on the incidence of PID among IUD initiators, or
IUD removal as a result of PID, suggested that the incidence
of PID did not differ between women using Cu- IUDs and
those using DMPA, COCs, or LNG-IUDs (123) (Level of
evidence: I to II-2, good, indirect). Evidence on the timing of
PID after IUD insertion is mixed. Although the rate of PID
generally was low, the largest study suggested that the rate of
PID was significantly higher in the first 20 days after insertion
(51) (Level of evidence: I to II-3, good to poor, indirect).

Bleeding Irregularities with Cu-IUD Use
• Before Cu-IUD insertion, provide counseling about
potential changes in bleeding patterns during Cu-IUD
use. Unscheduled spotting or light bleeding, as well as
heavy or prolonged bleeding, is common during the first
3–6 months of Cu-IUD use, is generally not harmful, and
decreases with continued Cu-IUD use.
• If clinically indicated, consider an underlying gynecological
problem, such as Cu-IUD displacement, an STD,
pregnancy, or new pathologic uterine conditions (e.g.,
polyps or fibroids), especially in women who have already
been using the Cu-IUD for a few months or longer and
who have developed a new onset of heavy or prolonged
bleeding. If an underlying gynecological problem is found,
treat the condition or refer for care.
• If an underlying gynecological problem is not found and
the woman requests treatment, the following treatment
option can be considered during days of bleeding:
– NSAIDs for short-term treatment (5–7 days)
• If bleeding persists and the woman finds it unacceptable,
counsel her on alternative contraceptive methods, and
offer another method if it is desired.
Comments and Evidence Summary. During contraceptive
counseling and before insertion of the Cu-IUD, information
about common side effects such as unscheduled spotting or
light bleeding or heavy or prolonged menstrual bleeding,
especially during the first 3–6 months of use, should be
discussed (64). These bleeding irregularities are generally
not harmful. Enhanced counseling about expected bleeding
patterns and reassurance that bleeding irregularities are
generally not harmful has been shown to reduce method
discontinuation in clinical trials with other contraceptives (i.e.,
DMPA) (124,125).
Evidence is limited on specific drugs, doses, and durations
of use for effective treatments for bleeding irregularities with
Cu-IUD use. Therefore, although this report includes general

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recommendations for treatments to consider, evidence for
specific regimens is lacking.
A systematic review identified 11 studies that examined
various therapeutic treatments for heavy menstrual bleeding,
prolonged menstrual bleeding, or both among women using
Cu-IUDs (126). Nine studies examined the use of various oral
NSAIDs for the treatment of heavy or prolonged menstrual
bleeding among Cu-IUD users and compared them with
either a placebo or a baseline cycle. Three of these trials
examined the use of indomethacin (127–129), three examined
mefenamic acid (130–132), and three examined flufenamic
acid (127,128,133). Other NSAIDs used in the reported trials
included alclofenac (127,128), suprofen (134), and diclofenac
sodium (135). All but one NSAID study (131) demonstrated
statistically significant or notable reductions in mean total
menstrual blood loss with NSAID use. One study among
19 Cu-IUD users with heavy bleeding suggested that treatment
with oral tranexamic acid can significantly reduce mean blood
loss during treatment compared with placebo (135). Data
regarding the overall safety of tranexamic acid are limited; an
FDA warning states that tranexamic acid is contraindicated
in women with active thromboembolic disease or with a
history or intrinsic risk for thrombosis or thromboembolism
(136,137). Treatment with aspirin demonstrated no statistically
significant change in mean blood loss among women whose
pretreatment menstrual blood loss was >80 ml or 60–80 mL;
treatment resulted in a significant increase among women
whose pretreatment menstrual blood loss was <60 mL (138).
One study examined the use of a synthetic form of vasopressin,
intranasal desmopressin (300 µg/day), for the first 5 days of
menses for three treatment cycles and found a significant
reduction in mean blood loss compared with baseline (130)
(Level of evidence: I to II-3, poor to fair, direct). Only one
small study examined treatment of spotting with three separate
NSAIDs and did not observe improvements in spotting in any
of the groups (127) (Level of evidence: I, poor, direct).

Bleeding Irregularities (Including
Amenorrhea) with LNG-IUD Use
• Before LNG-IUD insertion, provide counseling about
potential changes in bleeding patterns during LNG-IUD
use. Unscheduled spotting or light bleeding is expected
during the first 3–6 months of LNG-IUD use, is generally
not harmful, and decreases with continued LNG-IUD
use. Over time, bleeding generally decreases with LNGIUD use, and many women experience only light
menstrual bleeding or amenorrhea. Heavy or prolonged
bleeding, either unscheduled or menstrual, is uncommon
during LNG-IUD use.

Irregular Bleeding (Spotting, Light Bleeding, or
Heavy or Prolonged Bleeding)
• If clinically indicated, consider an underlying gynecological
problem, such as LNG-IUD displacement, an STD,
pregnancy, or new pathologic uterine conditions (e.g.,
polyps or fibroids). If an underlying gynecological problem
is found, treat the condition or refer for care.
• If bleeding persists and the woman finds it unacceptable,
counsel her on alternative contraceptive methods, and
offer another method if it is desired.

Management of the IUD when a Cu-IUD or
an LNG-IUD User Is Found To Have PID
• Treat the PID according to the CDC Sexually Transmitted
Diseases Treatment Guidelines (15).
• Provide comprehensive management for STDs, including
counseling about condom use.
• The IUD does not need to be removed immediately if the
woman needs ongoing contraception.
• Reassess the woman in 48–72 hours. If no clinical
improvement occurs, continue antibiotics and consider
removal of the IUD.
• If the woman wants to discontinue use, remove the IUD
sometime after antibiotics have been started to avoid the

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potential risk for bacterial spread resulting from the
removal procedure.
• If the IUD is removed, consider ECPs if appropriate.
Counsel the woman on alternative contraceptive methods,
and offer another method if it is desired.
• A summary of IUD management in women with PID is
provided (Appendix F).
Comments and Evidence Summary. Treatment outcomes
do not generally differ between women with PID who retain
the IUD and those who have the IUD removed; however,
appropriate antibiotic treatment and close clinical follow-up
are necessary.
A systematic review identified four studies that included
women using copper or nonhormonal IUDs who developed
PID and compared outcomes between women who had the
IUD removed or did not (140). One randomized trial showed
that women with IUDs removed had longer hospitalizations
than those who did not, although no differences in PID
recurrences or subsequent pregnancies were observed (141).
Another randomized trial showed no differences in laboratory
findings among women who removed the IUD compared
with those who did not (142). One prospective cohort study
showed no differences in clinical or laboratory findings during
hospitalization; however, the IUD removal group had longer
hospitalizations (143). One randomized trial showed that the
rate of recovery for most clinical signs and symptoms was higher
among women who had the IUD removed than among women
who did not (144). No evidence was found regarding women
using LNG-IUDs (Level of evidence: I to II-2, fair, direct.)

Management of the IUD when a Cu-IUD or
an LNG-IUD User is Found To Be Pregnant
• Evaluate for possible ectopic pregnancy.
• Advise the woman that she has an increased risk for
spontaneous abortion (including septic abortion that
might be life threatening) and for preterm delivery if the
IUD is left in place. The removal of the IUD reduces these
risks but might not decrease the risk to the baseline level
of a pregnancy without an IUD.
– If she does not want to continue the pregnancy, counsel
her about options.
– If she wants to continue the pregnancy, advise her to
seek care promptly if she has heavy bleeding, cramping,
pain, abnormal vaginal discharge, or fever.

IUD Strings Are Visible or Can Be Retrieved Safely
from the Cervical Canal
• Advise the woman that the IUD should be removed as
soon as possible.

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– If the IUD is to be removed, remove it by pulling on
the strings gently.
– Advise the woman that she should return promptly if
she has heavy bleeding, cramping, pain, abnormal
vaginal discharge, or fever.
• If she chooses to keep the IUD, advise her to seek care
promptly if she has heavy bleeding, cramping, pain,
abnormal vaginal discharge, or fever.

IUD Strings Are Not Visible and Cannot Be
Safely Retrieved
• If ultrasonography is available, consider performing or
referring for ultrasound examination to determine the
location of the IUD. If the IUD cannot be located, it might
have been expelled or have perforated the uterine wall.
• If ultrasonography is not possible or the IUD is determined
by ultrasound to be inside the uterus, advise the woman
to seek care promptly if she has heavy bleeding, cramping,
pain, abnormal vaginal discharge, or fever.
Comments and Evidence Summary. Removing the IUD
improves the pregnancy outcome if the IUD strings are visible
or the device can be retrieved safely from the cervical canal.
Risks for spontaneous abortion, preterm delivery, and infection
are substantial if the IUD is left in place.
Theoretically, the fetus might be affected by hormonal
exposure from an LNG-IUD. However, whether this exposure
increases the risk for fetal abnormalities is unknown.
A systematic review identified nine studies suggesting that
women who did not remove their IUDs during pregnancy
were at greater risk for adverse pregnancy outcomes (including
spontaneous abortion, septic abortion, preterm delivery, and
chorioamnionitis) compared with women who had their IUDs
removed or who did not have an IUD (41). Cu-IUD removal
decreased risks but not to the baseline risk for pregnancies
without an IUD. One case series examined LNG-IUDs.
When they were not removed, 8 out of 10 pregnancies ended
in spontaneous abortions (Level of evidence: II-2, fair, direct).

Implants
The etonogestrel implant, a single rod with 68 mg of
etonogestrel, is available in the United States. Fewer than
1 woman out of 100 become pregnant in the first year of use
of the etonogestrel implant with typical use (14). The implant
is long acting, is reversible, and can be used by women of all
ages, including adolescents. The implant does not protect
against STDs; consistent and correct use of male latex condoms
reduces the risk for STDs, including HIV.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

contraceptive protection for the next 7 days. If her
menstrual cycles have returned and it has been >5 days
since menstrual bleeding started, she needs to abstain from
sexual intercourse or use additional contraceptive
protection for the next 7 days.

Initiation of Implants
Timing
• The implant can be inserted at any time if it is reasonably
certain that the woman is not pregnant (Box 2).

Need for Back-Up Contraception
• If the implant is inserted within the first 5 days since
menstrual bleeding started, no additional contraceptive
protection is needed.
• If the implant is inserted >5 days since menstrual bleeding
started, the woman needs to abstain from sexual intercourse
or use additional contraceptive protection for the next 7 days.

Special Considerations
Amenorrhea (Not Postpartum)
• Timing: The implant can be inserted at any time if it is
reasonably certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Breastfeeding)
• Timing: The implant can be inserted at any time (U.S.
MEC 2 if <1 month postpartum and U.S. MEC 1 if
≥1 month postpartum) if it is reasonably certain that the
woman is not pregnant (Box 2).
• Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (27), no
additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycle needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >5 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postpartum (Not Breastfeeding)
• Timing: The implant can be inserted at any time, including
immediately postpartum (U.S. MEC 1) if it is reasonably
certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: If a woman is <21 days
postpartum, no additional contraceptive protection is
needed. A woman who is ≥21 days postpartum and has
not experienced return of her menstrual cycle needs to
abstain from sexual intercourse or use additional

Postabortion (Spontaneous or Induced)
• Timing: The implant can be inserted within the first 7 days,
including immediately after the abortion (U.S. MEC 1).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days unless the
implant is placed at the time of a surgical abortion.
Switching from Another Contraceptive Method
• Timing: The implant can be inserted immediately if it is
reasonably certain that the woman is not pregnant
(Box 2). Waiting for her next menstrual cycle is unnecessary.
• Need for back-up contraception: If it has been >5 days
since menstrual bleeding started, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days after insertion.
• Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle
and it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A
health care provider may consider any of the following
options:
– Advise the woman to retain the IUD for at least 7 days
after the implant is inserted and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 7 days before removing
the IUD and switching to the new method.
– If the woman cannot return for IUD removal and has
not abstained from sexual intercourse or used barrier
contraception for 7 days, advise the woman to use ECPs
(with the exception of UPA) at the time of IUD removal.
Comments and Evidence Summary. In situations in which
the health care provider is uncertain whether the woman might
be pregnant, the benefits of starting the implant likely exceed
any risk; therefore, starting the implant should be considered
at any time, with a follow-up pregnancy test in 2–4 weeks.
If a woman needs to use additional contraceptive protection
when switching to an implant from another contraceptive
method, consider continuing her previous method for 7 days
after implant insertion. No direct evidence was found regarding
the effects of starting the etonogestrel implant at different
times of the cycle.

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Recommendations and Reports

Examinations and Tests Needed Before
Implant Insertion
Among healthy women, no examinations or tests are needed
before initiation of an implant, although a baseline weight and
BMI measurement might be useful for monitoring implant
users over time (Table 2). Women with known medical
problems or other special conditions might need additional
examinations or tests before being determined to be appropriate
candidates for a particular method of contraception. U.S. MEC
might be useful in such circumstances (5).
Comments and Evidence Summary. Weight (BMI): Obese
women can use implants (U.S. MEC 1) (5); therefore, screening
for obesity is not necessary for the safe initiation of implants.
However, measuring weight and calculating BMI at baseline
might be helpful for monitoring any changes and counseling
women who might be concerned about weight change perceived
to be associated with their contraceptive method.
Bimanual examination and cervical inspection: A pelvic
examination is not necessary before initiation of implants
because it would not facilitate detection of conditions for which
implant use would be unsafe. Women with current breast cancer
should not use implants (U.S. MEC 4); women with certain
liver diseases generally should not (U.S. MEC 3) use implants
(5). However, none of these conditions are likely to be detected
TABLE 2. Classification of examinations and tests needed before
implant insertion
Examination or test

Class*

Examination
Blood pressure
Weight (BMI) (weight [kg] / height [m]2)
Clinical breast examination
Bimanual examination and cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou smear)
STD screening with laboratory tests
HIV screening with laboratory tests

C
—†
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
STD = sexually transmitted disease; U.S. MEC = U.S. Medical Eligibility Criteria for
Contraceptive Use.
* Class A: essential and mandatory in all circumstances for safe and effective use of
the contraceptive method. Class B: contributes substantially to safe and effective
use, but implementation may be considered within the public health and/or service
context; the risk of not performing an examination or test should be balanced against
the benefits of making the contraceptive method available. Class C: does not
contribute substantially to safe and effective use of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for any
methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 1). However,
measuring weight and calculating BMI at baseline might be helpful for monitoring
any changes and counseling women who might be concerned about weight
change perceived to be associated with their contraceptive method.

MMWR / July 29, 2016 / Vol. 65 / No. 4

by pelvic examination (145). A systematic review identified
two case-control studies that compared delayed and immediate
pelvic examination before initiation of hormonal contraceptives,
specifically oral contraceptives or DMPA (95). No differences in
risk factors for cervical neoplasia, incidence of STDs, incidence
of abnormal Papanicolaou smears, or incidence of abnormal
wet mounts were observed. No evidence was found regarding
implants (Level of evidence: II-2 fair, direct).
Lipids: Screening for dyslipidemias is not necessary for the
safe initiation of implants because of the low prevalence of
undiagnosed disease in women of reproductive age and the
low likelihood of clinically significant changes with use of
hormonal contraceptives. A systematic review did not identify
any evidence regarding outcomes among women who were
screened versus not screened with lipid measurement before
initiation of hormonal contraceptives (57). During 2009–2012
among women aged 20–44 years in the United States, 7.6% had
high cholesterol, defined as total serum cholesterol ≥240 mg/
dL (84). During 1999–2008, the prevalence of undiagnosed
hypercholesterolemia among women aged 20–44 years was
approximately 2% (85). Studies have shown mixed results
regarding the effects of hormonal methods on lipid levels
among both healthy women and women with baseline lipid
abnormalities, and the clinical significance of these changes is
unclear (86–89).
Liver enzymes: Although women with certain liver diseases
generally should not use implants (U.S. MEC 3) (5), screening
for liver disease before initiation of implants is not necessary
because of the low prevalence of these conditions and the
high likelihood that women with liver disease already would
have had the condition diagnosed. A systematic review did
not identify any evidence regarding outcomes among women
who were screened versus not screened with liver enzyme tests
before initiation of hormonal contraceptives (57). In 2012,
the percentage of U.S. women with liver disease (not further
specified) was 1.3% (90). In 2013, the incidence of acute
hepatitis A, B, or C was ≤1 per 100,000 U.S. population (91).
During 2002–2011, the incidence of liver carcinoma among
U.S. women was approximately 3.7 per 100,000 population
(92). Because estrogen and progestins are metabolized in
the liver, the use of hormonal contraceptives among women
with liver disease might, theoretically, be a concern. The use
of hormonal contraceptives, specifically COCs and POPs,
does not affect disease progression or severity in women
with hepatitis, cirrhosis, or benign focal nodular hyperplasia
(93,94), although evidence is limited and no evidence exists
for implants.
Clinical breast examination: Although women with
current breast cancer should not use implants (U.S. MEC 4)
(5), screening asymptomatic women with a clinical breast

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Recommendations and Reports

examination before initiation of implants is not necessary
because of the low prevalence of breast cancer among women
of reproductive age (15–49 years). A systematic review did not
identify any evidence regarding outcomes among women who
were screened versus not screened with a breast examination
before initiation of hormonal contraceptives (95). The
incidence of breast cancer among women of reproductive age
in the United States is low. In 2012, the incidence of breast
cancer among women aged 20–49 years was approximately
70.7 per 100,000 women (96).
Other screening: Women with hypertension, diabetes,
anemia, thrombogenic mutations, cervical intraepithelial
neoplasia, cervical cancer, STDs, or HIV infection can use
(U.S. MEC 1) or generally can use (U.S. MEC 2) implants
(5); therefore, screening for these conditions is not necessary
for the safe initiation of implants.

Routine Follow-Up After Implant Insertion
These recommendations address when routine follow-up is
needed for safe and effective continued use of contraception
for healthy women. The recommendations refer to general
situations and might vary for different users and different
situations. Specific populations who might benefit from more
frequent follow-up visits include adolescents, those with certain
medical conditions or characteristics, and those with multiple
medical conditions.
• Advise the woman to return at any time to discuss side
effects or other problems, if she wants to change the
method being used, and when it is time to remove or
replace the contraceptive method. No routine follow-up
visit is required.
• At other routine visits, health care providers seeing implant
users should do the following:
– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including medications,
that would change the appropriateness of the implant
for safe and effective continued use based on U.S. MEC
(e.g., category 3 and 4 conditions and characteristics).
– Consider assessing weight changes and counseling women
who are concerned about weight change perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. A systematic review
did not identify any evidence regarding whether a routine
follow-up visit after initiating an implant improves correct or
continued use (122).

Bleeding Irregularities (Including
Amenorrhea) During Implant Use
• Before implant insertion, provide counseling about
potential changes in bleeding patterns during implant use.
Unscheduled spotting or light bleeding is common with
implant use, and some women experience amenorrhea.
These bleeding changes are generally not harmful and
might or might not decrease with continued implant use.
Heavy or prolonged bleeding, unscheduled or menstrual,
is uncommon during implant use.

Irregular Bleeding (Spotting, Light Bleeding, or
Heavy or Prolonged Bleeding)
• If clinically indicated, consider an underlying gynecological
problem, such as interactions with other medications, an
STD, pregnancy, or new pathologic uterine conditions
(e.g., polyps or fibroids). If an underlying gynecological
problem is found, treat the condition or refer for care.
• If an underlying gynecologic problem is not found and
the woman wants treatment, the following treatment
options during days of bleeding can be considered:
– NSAIDS for short-term treatment (5–7 days)
– Hormonal treatment (if medically eligible) with lowdose COCs or estrogen for short-term treatment
(10–20 days)
• If irregular bleeding persists and the woman finds it
unacceptable, counsel her on alternative methods, and
offer another method if it is desired.

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Recommendations and Reports

and 18% reported prolonged bleeding (146). Unscheduled
bleeding or amenorrhea is generally not harmful. Enhanced
counseling about expected bleeding patterns and reassurance
that bleeding irregularities are generally not harmful has been
shown to reduce discontinuation in clinical trials with other
hormonal contraceptives (i.e., DMPA) (124,125).
A systematic review and four newly published studies
examined several medications for the treatment of bleeding
irregularities with primarily levonorgestrel contraceptive
implants (147–151). Two small studies found significant
cessation of bleeding within 7 days of start of treatment among
women taking oral celecoxib (200 mg) daily for 5 days or oral
mefenamic acid (500 mg) 3 times daily for 5 days compared
with placebo (149,150). Differences in bleeding cessation
were not found among women with etonogestrel implants
taking mifepristone but were found when women with the
implants combined mifepristone with either ethinyl estradiol
or doxycycline (151,152). Doxycycline alone or in combination
with ethinyl estradiol did not improve bleeding cessation
among etonogestrel implant users (151). Among LNG implant
users, mifepristone reduced the number of bleeding or spotting
days but only after 6 months of treatment (153). Evidence also
suggests that estrogen (154–156), daily COCs (154), LNG pills
(155), tamoxifen (157), or tranexamic acid (158) can reduce
the number of bleeding or spotting days during treatment
among LNG implant users. In one small study, vitamin E was
found to significantly reduce the mean number of bleeding days
after the first treatment cycle; however, another larger study
reported no significant differences in length of bleeding and
spotting episodes with vitamin E treatment (159,160). Use
of aspirin did not result in a significant difference in median
length of bleeding or bleeding and spotting episodes after
treatment (159). One study among implant users reported a
reduction in number of bleeding days after initiating ibuprofen;
however, another trial did not demonstrate any significant
differences in the number of spotting and bleeding episodes
with ibuprofen compared with placebo (148,155).

Injectables
Progestin-only injectable contraceptives (DMPA, 150 mg
intramuscularly or 104 mg subcutaneously) are available in
the United States; the only difference between these two
formulations is the route of administration. Approximately 6
out of 100 women will become pregnant in the first year of use
of DMPA with typical use (14). DMPA is reversible and can
be used by women of all ages, including adolescents. DMPA
does not protect against STDs; consistent and correct use of
male latex condoms reduces the risk for STDs, including HIV.

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Initiation of Injectables
Timing
• The first DMPA injection can be given at any time if it is
reasonably certain that the woman is not pregnant (Box 2).

Need for Back-Up Contraception
• If DMPA is started within the first 7 days since menstrual
bleeding started, no additional contraceptive protection
is needed.
• If DMPA is started >7 days since menstrual bleeding started,
the woman needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.

Special Considerations
Amenorrhea (Not Postpartum)
• Timing: The first DMPA injection can be given at any
time if it is reasonably certain that the woman is not
pregnant (Box 2).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Breastfeeding)
• Timing: The first DMPA injection can be given at any
time, including immediately postpartum (U.S. MEC 2 if
<1 month postpartum; U.S. MEC 1 if ≥1 month
postpartum) if it is reasonably certain that the woman is
not pregnant (Box 2).
• Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (27), no
additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycle needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >7 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postpartum (Not Breastfeeding)
• Timing: The first DMPA injection can be given at any time,
including immediately postpartum (U.S. MEC 1) if it is
reasonably certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: If a woman is <21 days
postpartum, no additional contraceptive protection is
needed. A woman who is ≥21 days postpartum and has

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

not experienced return of her menstrual cycle needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days. If her
menstrual cycles have returned and it has been >7 days
since menstrual bleeding started, she needs to abstain from
sexual intercourse or use additional contraceptive
protection for the next 7 days.
Postabortion (Spontaneous or Induced)
• Timing: The first DMPA injection can be given within
the first 7 days, including immediately after the abortion
(U.S. MEC 1).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days unless the
injection is given at the time of a surgical abortion.
Switching from Another Contraceptive Method
• Timing: The first DMPA injection can be given
immediately if it is reasonably certain that the woman is
not pregnant (Box 2). Waiting for her next menstrual cycle
is unnecessary.
• Need for back-up contraception: If it has been >7 days
since menstrual bleeding started, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
• Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle
and it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A health
care provider may consider any of the following options:
– Advise the women to retain the IUD for at least 7 days
after the injection and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 7 days before removing
the IUD and switching to the new method.
– If the woman cannot return for IUD removal and has
not abstained from sexual intercourse or used barrier
contraception for 7 days, advise the woman to use ECPs
(with the exception of UPA) at the time of IUD removal.
Comments and Evidence Summary. In situations in which
the health care provider is uncertain whether the woman might
be pregnant, the benefits of starting DMPA likely exceed
any risk; therefore, starting DMPA should be considered at
any time, with a follow-up pregnancy test in 2–4 weeks. If a
woman needs to use additional contraceptive protection when
switching to DMPA from another contraceptive method,
consider continuing her previous method for 7 days after
DMPA injection.

A systematic review identified eight articles examining
DMPA initiation on different days of the menstrual cycle (161).
Evidence from two studies with small sample sizes indicated
that DMPA injections given up to day 7 of the menstrual
cycle inhibited ovulation; when DMPA was administered after
day 7, ovulation occurred in some women. Cervical mucus
was of poor quality (i.e., not favorable for sperm penetration)
in 90% of women within 24 hours of the injection (Level
of evidence: II-2, fair) (162–164). Studies found that use of
another contraceptive method until DMPA could be initiated
(bridging option) did not help women initiate DMPA and was
associated with more unintended pregnancies than immediate
receipt of DMPA (165–169) (Level of evidence: I to II-3, fair
to poor, indirect).

Examinations and Tests Needed Before
Initiation of an Injectable
Among healthy women, no examinations or tests are needed
before initiation of DMPA, although a baseline weight and
BMI measurement might be useful to monitor DMPA users
over time (Table 3). Women with known medical problems or
other special conditions might need additional examinations
or tests before being determined to be appropriate candidates
for a particular method of contraception. U.S. MEC might
be useful in such circumstances (5).
Comments and Evidence Summary. Weight (BMI): Obese
women can use (U.S. MEC 1) or generally can use (U.S.
MEC 2) DMPA (5); therefore, screening for obesity is not
necessary for the safe initiation of DMPA. However, measuring
weight and calculating BMI at baseline might be helpful for
monitoring any changes and counseling women who might
be concerned about weight change perceived to be associated
with their contraceptive method. (See guidance on follow-up
for DMPA users for evidence on weight gain with DMPA use).
Bimanual examination and cervical inspection: Pelvic
examination is not necessary before initiation of DMPA
because it does not facilitate detection of conditions for which
DMPA would be unsafe. Although women with current breast
cancer should not use DMPA (U.S. MEC 4), and women with
severe hypertension, heart disease, vascular disease, or certain
liver diseases generally should not use DMPA (U.S. MEC 3)
(5), none of these conditions are likely to be detected by pelvic
examination (145). A systematic review identified two casecontrol studies that compared delayed versus immediate pelvic
examination before initiation of hormonal contraceptives,
specifically oral contraceptives or DMPA (95). No differences
in risk factors for cervical neoplasia, incidence of STDs,
incidence of abnormal Papanicolaou smears, or incidence of

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Recommendations and Reports

TABLE 3. Classification of examinations and tests needed before
depo-medroxyprogesterone acetate initiation
Examination or test

Class*

C
—†
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
STD = sexually transmitted disease; U.S. MEC = U.S. Medical Eligibility Criteria for
Contraceptive Use.
* Class A: essential and mandatory in all circumstances for safe and effective use of
the contraceptive method. Class B: contributes substantially to safe and effective
use, but implementation may be considered within the public health and/or service
context; the risk of not performing an examination or test should be balanced against
the benefits of making the contraceptive method available. Class C: does not
contribute substantially to safe and effective use of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for any
methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 1). However,
measuring weight and calculating BMI at baseline might be helpful for monitoring
any changes and counseling women who might be concerned about weight
change perceived to be associated with their contraceptive method.

abnormal wet mounts were observed (Level of evidence: II-2,
fair, direct).
Blood pressure: Women with hypertension generally can
use DMPA (U.S. MEC 2), with the exception of women with
severe hypertension or vascular disease, who generally should
not use DMPA (U.S. MEC 3) (5). Screening for hypertension
before initiation of DMPA is not necessary because of the
low prevalence of undiagnosed severe hypertension and the
high likelihood that women with these conditions already
would have had them diagnosed. A systematic review did
not identify any evidence regarding outcomes among women
who were screened versus not screened with a blood pressure
measurement before initiation of progestin-only contraceptives
(170). The prevalence of undiagnosed hypertension among
women of reproductive age is low. During 2009–2012 among
women aged 20–44 years in the United States, the prevalence
of hypertension was 8.7% (84). During 1999–2008, the
percentage of women aged 20–44 years with undiagnosed
hypertension was 1.9% (85).
Glucose: Although women with complicated diabetes
generally should not use DMPA (U.S. MEC 3) (5), screening
for diabetes before initiation of DMPA is not necessary because
of the low prevalence of undiagnosed diabetes and the high
likelihood that women with complicated diabetes would

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already have had the condition diagnosed. A systematic review
did not identify any evidence regarding outcomes among
women who were screened versus not screened with glucose
measurement before initiation of hormonal contraceptives
(57). The prevalence of diabetes among women of reproductive
age is low. During 2009–2012 among women aged 20–44 years
in the United States, the prevalence of diabetes was 3.3%
(84). During 1999–2008, the percentage of women aged
20–44 years with undiagnosed diabetes was 0.5% (85).
Although hormonal contraceptives can have some adverse
effects on glucose metabolism in healthy and diabetic women,
the overall clinical effect is minimal (171–177).
Lipids: Screening for dyslipidemias is not necessary for the
safe initiation of injectables because of the low prevalence of
undiagnosed disease in women of reproductive age and the
low likelihood of clinically significant changes with use of
hormonal contraceptives. A systematic review did not identify
any evidence regarding outcomes among women who were
screened versus not screened with lipid measurement before
initiation of hormonal contraceptives (57). During 2009–2012
among women aged 20–44 years in the United States, 7.6%
had high cholesterol, defined as total serum cholesterol
≥240 mg/dL (84). During 1999–2008, the prevalence of
undiagnosed hypercholesterolemia among women aged
20–44 years was approximately 2% (85). Studies have shown
mixed results about the effects of hormonal methods on lipid
levels among both healthy women and women with baseline
lipid abnormalities, and the clinical significance of these
changes is unclear (86–89).
Liver enzymes: Although women with certain liver diseases
generally should not use DMPA (U.S. MEC 3) (5), screening
for liver disease before initiation of DMPA is not necessary
because of the low prevalence of these conditions and the
high likelihood that women with liver disease already would
have had the condition diagnosed. A systematic review did not
identify any evidence regarding outcomes among women who
were screened versus not screened with liver enzyme tests before
initiation of hormonal contraceptives (57). In 2012, among
U.S. women, the percentage with liver disease (not further
specified) was 1.3% (90). In 2013, the incidence of acute
hepatitis A, B, or C was ≤1 per 100,000 U.S. population (91).
During 2002–2011, the incidence of liver carcinoma among
U.S. women was approximately 3.7 per 100,000 population
(92). Because estrogen and progestins are metabolized in
the liver, the use of hormonal contraceptives among women
with liver disease might, theoretically, be a concern. The use
of hormonal contraceptives, specifically COCs and POPs,
does not affect disease progression or severity in women with
hepatitis, cirrhosis, or benign focal nodular hyperplasia (93,94),
although evidence is limited and no evidence exists for DMPA.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Clinical breast examination: Although women with current
breast cancer should not use DMPA (U.S. MEC 4) (5), screening
asymptomatic women with a clinical breast examination before
initiating DMPA is not necessary because of the low prevalence
of breast cancer among women of reproductive age. A systematic
review did not identify any evidence regarding outcomes
among women who were screened versus not screened with
a clinical breast examination before initiation of hormonal
contraceptives (95). The incidence of breast cancer among
women of reproductive age in the United States is low. In 2012,
the incidence of breast cancer among women aged 20–49 years
was approximately 70.7 per 100,000 women (96).
Other screening: Women with anemia, thrombogenic
mutations, cervical intraepithelial neoplasia, cervical cancer,
HIV infection, or other STDs can use (U.S. MEC 1) or
generally can use (U.S. MEC 2) DMPA (5); therefore,
screening for these conditions is not necessary for the safe
initiation of DMPA.

A systematic review identified a limited body of evidence
that examined whether weight gain in the few months after
DMPA initiation predicted future weight gain (123). Two
studies found significant differences in weight gain or BMI
at follow-up periods ranging from 12 to 36 months between
early weight gainers (i.e., those who gained >5% of their
baseline body weight within 6 months after initiation) and
those who were not early weight gainers (178,179). The
differences between groups were more pronounced at 18, 24,
and 36 months than at 12 months. One study found that most
adolescent DMPA users who had gained >5% of their baseline
weight by 3 months gained even more weight by 12 months
(180) (Level of evidence: II-2, fair, to II-3, fair, direct).

Routine Follow-Up After Injectable Initiation

Special Considerations

These recommendations address when routine follow-up
is recommended for safe and effective continued use of
contraception for healthy women. The recommendations refer
to general situations and might vary for different users and
different situations. Specific populations who might benefit
from frequent follow-up visits include adolescents, those with
certain medical conditions or characteristics, and those with
multiple medical conditions.
• Advise the woman to return at any time to discuss side
effects or other problems, if she wants to change the
method being used, and when it is time for reinjection.
No routine follow-up visit is required.
• At other routine visits, health care providers seeing
injectable users should do the following:
– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including medications,
that would change the appropriateness of the injectable
for safe and effective continued use based on U.S. MEC
(e.g., category 3 and 4 conditions and characteristics).
– Consider assessing weight changes and counseling women
who are concerned about weight change perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. Although no evidence
exists regarding whether a routine follow-up visit after initiating
DMPA improves correct or continued use, monitoring weight
or BMI change over time is important for DMPA users.

Early Injection

Timing of Repeat Injections
Reinjection Interval
• Provide repeat DMPA injections every 3 months (13 weeks).

• The repeat DMPA injection can be given early when necessary.
Late Injection
• The repeat DMPA injection can be given up to 2 weeks
late (15 weeks from the last injection) without requiring
additional contraceptive protection.
• If the woman is >2 weeks late (>15 weeks from the last
injection) for a repeat DMPA injection, she can have the
injection if it is reasonably certain that she is not pregnant
(Box 2). She needs to abstain from sexual intercourse or
use additional contraceptive protection for the next 7 days.
She might consider the use of emergency contraception
(with the exception of UPA) if appropriate.
Comments and Evidence Summary. No time limits exist
for early injections; injections can be given when necessary
(e.g., when a woman cannot return at the routine interval).
WHO has extended the time that a woman can have a late
reinjection (i.e., grace period) for DMPA use from 2 weeks
to 4 weeks on the basis of data from one study showing low
pregnancy rates through 4 weeks; however, the CDC expert
group did not consider the data to be generalizable to the
United States because a large proportion of women in the
study were breastfeeding. Therefore, U.S. SPR recommends
a grace period of 2 weeks.
A systematic review identified 12 studies evaluating time to
pregnancy or ovulation after the last injection of DMPA (181).
Although pregnancy rates were low during the 2-week interval
following the reinjection date and for 4 weeks following the

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Recommendations and Reports

reinjection date, data were sparse, and one study included a
large proportion of breastfeeding women (182–184). Studies
also indicated a wide variation in time to ovulation after the
last DMPA injection, with the majority ranging from 15 to
49 weeks from the last injection (185–193) (Level of evidence:
level II-2, fair, direct).

Bleeding Irregularities (Including
Amenorrhea) During Injectable Use
• Before DMPA initiation, provide counseling about
potential changes in bleeding patterns during DMPA use.
Amenorrhea and unscheduled spotting or light bleeding
is common with DMPA use, and heavy or prolonged
bleeding can occur with DMPA use. These bleeding
irregularities are generally not harmful and might decrease
with continued DMPA use.

Unscheduled Spotting or Light Bleeding
• If clinically indicated, consider an underlying gynecological
problem, such as interactions with other medications, an
STD, pregnancy, or new pathologic uterine conditions
(e.g., polyps or fibroids). If an underlying gynecological
problem is found, treat the condition or refer for care.
• If an underlying gynecologic problem is not found and
the woman wants treatment, the following treatment
option during days of bleeding can be considered:
– NSAIDs for short-term treatment (5–7 days)
• If unscheduled spotting or light bleeding persists and the
woman finds it unacceptable, counsel her on alternative
contraceptive methods, and offer another method if it is desired.

Heavy or Prolonged Bleeding
• If clinically indicated, consider an underlying gynecological
problem, such as interactions with other medications, an
STD, pregnancy, or new pathologic uterine conditions
(such as fibroids or polyps). If an underlying gynecologic
problem is identified, treat the condition or refer for care.
• If an underlying gynecologic problem is not found and
the woman wants treatment, the following treatment
options during days of bleeding can be considered:
– NSAIDS for short-term treatment (5–7 days)
– Hormonal treatment (if medically eligible) with lowdose COCs or estrogen for short-term treatment
(10–20 days)
• If heavy or prolonged bleeding persists and the woman finds
it unacceptable, counsel her on alternative contraceptive
methods, and offer another method if it is desired.

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Amenorrhea
• Amenorrhea does not require any medical treatment.
Provide reassurance.
– If a woman’s regular bleeding pattern changes abruptly
to amenorrhea, consider ruling out pregnancy if
clinically indicated.
• If amenorrhea persists and the woman finds it unacceptable,
counsel her on alternative contraceptive methods, and
offer another method if it is desired.
Comments and Evidence Summary. During contraceptive
counseling and before initiation of DMPA, information
about common side effects such as irregular bleeding should
be discussed. Unscheduled bleeding or spotting is common
with DMPA use (194). In addition, amenorrhea is common
after ≥1 years of continuous use (194,195). These bleeding
irregularities are generally not harmful. Enhanced counseling
among DMPA users detailing expected bleeding patterns and
reassurance that these irregularities generally are not harmful
has been shown to reduce DMPA discontinuation in clinical
trials (124,125).
A systematic review, as well as two additional studies,
examined the treatment of bleeding irregularities during
DMPA use (195–197). Two small studies found significant
cessation of bleeding within 7 days of starting treatment among
women taking valdecoxib for 5 days or mefenamic acid for
5 days compared with placebo (198,199). Treatment with
ethinyl estradiol was found to stop bleeding better than placebo
during the treatment period, although rates of discontinuation
were high and safety outcomes were not examined (200). In one
small study among DMPA users who had been experiencing
amenorrhea for 2 months, treatment with COCs was found
to alleviate amenorrhea better than placebo (201). No studies
examined the effects of aspirin on bleeding irregularities among
DMPA users.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

21–24 consecutive days, followed by 4–7 hormone-free days
(either no use or placebo pills). These methods are sometimes
used for an extended period with infrequent or no hormonefree days. Combined hormonal contraceptives do not protect
against STDs; consistent and correct use of male latex condoms
reduces the risk for STDs, including HIV.

Initiation of Combined Hormonal
Contraceptives
Timing
• Combined hormonal contraceptives can be initiated at
any time if it is reasonably certain that the woman is not
pregnant (Box 2).

Need for Back-Up Contraception
• If combined hormonal contraceptives are started within
the first 5 days since menstrual bleeding started, no
additional contraceptive protection is needed.
• If combined hormonal contraceptives are started >5 days
since menstrual bleeding started, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.

Special Considerations
Amenorrhea (Not Postpartum)
• Timing: Combined hormonal contraceptives can be
started at any time if it is reasonably certain that the
woman is not pregnant (Box 2).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days.
Postpartum (Breastfeeding)
• Timing: Combined hormonal contraceptives can be
started when the woman is medically eligible to use the
method (5) and if it is reasonably certain that she is not
pregnant. (Box 2).
• Postpartum women who are breastfeeding should not use
combined hormonal contraceptives during the first
3 weeks after delivery (U.S. MEC 4) because of concerns
about increased risk for venous thromboembolism and
generally should not use combined hormonal contraceptives
during the fourth week postpartum (U.S. MEC 3) because
of concerns about potential effects on breastfeeding
performance. Postpartum breastfeeding women with other
risk factors for venous thromboembolism generally should
not use combined hormonal contraceptives 4–6 weeks
after delivery (U.S. MEC 3).

• Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (27), no
additional contraceptive protection is needed. Otherwise,
a woman who is ≥21 days postpartum and has not
experienced return of her menstrual cycle needs to abstain
from sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >5 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postpartum (Not Breastfeeding)
• Timing: Combined hormonal contraceptives can be
started when the woman is medically eligible to use the
method (5) and if it is reasonably certain that the she is
not pregnant (Box 2).
• Postpartum women should not use combined hormonal
contraceptives during the first 3 weeks after delivery
(U.S. MEC 4) because of concerns about increased risk
for venous thromboembolism. Postpartum women with
other risk factors for venous thromboembolism generally
should not use combined hormonal contraceptives
3–6 weeks after delivery (U.S. MEC 3).
• Need for back-up contraception: If a woman is <21 days
postpartum, no additional contraceptive protection is
needed. A woman who is ≥21 days postpartum and whose
menstrual cycles have not returned needs to abstain from
sexual intercourse or use additional contraceptive
protection for the next 7 days. If her menstrual cycles have
returned and it has been >5 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 7 days.
Postabortion (Spontaneous or Induced)
• Timing: Combined hormonal contraceptives can be
started within the first 7 days following first-trimester or
second-trimester abortion, including immediately
postabortion (U.S. MEC 1).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 7 days unless
combined hormonal contraceptives are started at the time
of a surgical abortion.
Switching from Another Contraceptive Method
• Timing: Combined hormonal contraceptives can be
started immediately if it is reasonably certain that the

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Recommendations and Reports

woman is not pregnant (Box 2). Waiting for her next
menstrual cycle is unnecessary.
• Need for back-up contraception: If it has been >5 days
since menstrual bleeding started, she needs to abstain from
sexual intercourse or use additional contraceptive
protection for the next 7 days.
• Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle
and it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A health
care provider may consider any of the following options:
– Advise the women to retain the IUD for at least 7 days
after combined hormonal contraceptives are initiated
and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 7 days before removing
the IUD and switching to the new method.
– If the woman cannot return for IUD removal and has
not abstained from sexual intercourse or used barrier
contraception for 7 days, advise the woman to use ECPs
at the time of IUD removal. Combined hormonal
contraceptives can be started immediately after use of
ECPs (with the exception of UPA). Combined
hormonal contraceptives can be started no sooner than
5 days after use of UPA.
Comments and Evidence Summary. In situations in which
the health care provider is uncertain whether the woman might
be pregnant, the benefits of starting combined hormonal
contraceptives likely exceed any risk; therefore, starting
combined hormonal contraceptives should be considered at
any time, with a follow-up pregnancy test in 2–4 weeks. If a
woman needs to use additional contraceptive protection when
switching to combined hormonal contraceptives from another
contraceptive method, consider continuing her previous method
for 7 days after starting combined hormonal contraceptives.
A systematic review of 18 studies examined the effects of
starting combined hormonal contraceptives on different days
of the menstrual cycle (202). Overall, the evidence suggested
that pregnancy rates did not differ by the timing of combined
hormonal contraceptive initiation (169,203–205) (Level
of evidence: I to II-3, fair, indirect). The more follicular
activity that occurred before starting COCs, the more likely
ovulation was to occur; however, no ovulations occurred
when COCs were started at a follicle diameter of 10 mm
(mean cycle day 7.6) or when the ring was started at 13 mm
(median cycle day 11) (206–215) (Level of evidence: I to II-3,
fair, indirect). Bleeding patterns and other side effects did not
vary with the timing of combined hormonal contraceptive
initiation (204,205,216–220) (Level of evidence: I to II-2,

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good to poor, direct). Although continuation rates of combined
hormonal contraceptives were initially improved by the “quick
start” approach (i.e., starting on the day of the visit), the
advantage disappeared over time (203,204,216–221) (Level
of evidence: I to II-2, good to poor, direct).

Examinations and Test Needed Before
Initiation of Combined Hormonal
Contraceptives
Among healthy women, few examinations or tests are
needed before initiation of combined hormonal contraceptives
(Table 4). Blood pressure should be measured before initiation
of combined hormonal contraceptives. Baseline weight
and BMI measurements might be useful for monitoring
combined hormonal contraceptive users over time. Women
with known medical problems or other special conditions
might need additional examinations or tests before being
determined to be appropriate candidates for a particular
method of contraception. U.S. MEC might be useful in such
circumstances (5).
Comments and Evidence Summary. Blood pressure:
Women who have more severe hypertension (systolic pressure of
≥160 mmHg or diastolic pressure of ≥100 mm Hg) or vascular
disease should not use combined hormonal contraceptives
(U.S. MEC 4), and women who have less severe hypertension
(systolic pressure of 140–159 mm Hg or diastolic pressure
of 90–99 mm Hg) or adequately controlled hypertension
generally should not use combined hormonal contraceptives
(U.S. MEC 3) (5). Therefore, blood pressure should be
evaluated before initiating combined hormonal contraceptives.
In instances in which blood pressure cannot be measured by
a provider, blood pressure measured in other settings can be
reported by the woman to her provider. Evidence suggests
that cardiovascular outcomes are worse among women who
did not have their blood pressure measured before initiating
COCs. A systematic review identified six articles from three
studies that reported cardiovascular outcomes among women
who had blood pressure measurements and women who did
not have blood pressure measurements before initiating COCs
(170). Three case-control studies showed that women who did
not have blood pressure measurements before initiating COCs
had a higher risk for acute myocardial infarction than women
who did have blood pressure measurements (222–224). Two
case-control studies showed that women who did not have
blood pressure measurements before initiating COCs had
a higher risk for ischemic stroke than women who did have
blood pressure measurements (225,226). One case-control
study showed no difference in the risk for hemorrhagic stroke
among women who initiated COCs regardless of whether their

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE 4. Classification of examinations and tests needed before
combined hormonal contraceptive initiation
Examination or test
Examination
Blood pressure
Weight (BMI) (weight [kg]/height [m]2)
Clinical breast examination
Bimanual examination and cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou smear)
STD screening with laboratory tests
HIV screening with laboratory tests

Class*
A†
—§
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
STD = sexually transmitted disease; U.S. MEC = U.S. Medical Eligibility Criteria for
Contraceptive Use.
* Class A: essential and mandatory in all circumstances for safe and effective use of
the contraceptive method. Class B: contributes substantially to safe and effective
use, but implementation may be considered within the public health and/or service
context; the risk of not performing an examination or test should be balanced against
the benefits of making the contraceptive method available. Class C: does not
contribute substantially to safe and effective use of the contraceptive method.
† In instances in which blood pressure cannot be measured by a provider, blood
pressure measured in other settings can be reported by the woman to her provider.
§ Weight (BMI) measurement is not needed to determine medical eligibility for any
methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 1). However,
measuring weight and calculating BMI at baseline might be helpful for monitoring
any changes and counseling women who might be concerned about weight
change perceived to be associated with their contraceptive method.

blood pressure was measured (227). Studies that examined
hormonal contraceptive methods other than COCs were not
identified (Level of evidence: II-2, fair, direct).
Weight (BMI): Obese women generally can use combined
hormonal contraceptives (U.S. MEC 2) (5); therefore,
screening for obesity is not necessary for the safe initiation
of combined hormonal contraceptives. However, measuring
weight and calculating BMI at baseline might be helpful for
monitoring any changes and counseling women who might
be concerned about weight change perceived to be associated
with their contraceptive method.
Bimanual examination and cervical inspection: Pelvic
examination is not necessary before initiation of combined
hormonal contraceptives because it does not facilitate detection
of conditions for which hormonal contraceptives would be
unsafe. Women with certain conditions such as current breast
cancer, severe hypertension or vascular disease, heart disease,
migraine headaches with aura, and certain liver diseases, as
well as women aged ≥35 years and who smoke ≥15 cigarettes
per day, should not use (U.S. MEC 4) or generally should
not use (U.S. MEC 3) combined hormonal contraceptives
(5); however, none of these conditions are likely to be
detected by pelvic examination (145). A systematic review

identified two case-control studies that compared delayed and
immediate pelvic examination before initiation of hormonal
contraceptives, specifically oral contraceptives or DMPA (95).
No differences in risk factors for cervical neoplasia, incidence
of STDs, incidence of abnormal Papanicolaou smears, or
incidence of abnormal wet mounts were found (Level of
evidence: Level II-2 fair, direct).
Glucose: Although women with complicated diabetes
should not use (U.S. MEC 4) or generally should not use
(U.S. MEC 3) combined hormonal contraceptives, depending
on the severity of the condition (5), screening for diabetes
before initiation of hormonal contraceptives is not necessary
because of the low prevalence of undiagnosed diabetes and the
high likelihood that women with complicated diabetes already
would have had the condition diagnosed. A systematic review
did not identify any evidence regarding outcomes among
women who were screened versus not screened with glucose
measurement before initiation of hormonal contraceptives
(57). The prevalence of diabetes among women of reproductive
age is low. During 2009–2012 among women aged 20–44 years
in the United States, the prevalence of diabetes was 3.3%
(84). During 1999–2008, the percentage of women aged
20–44 years with undiagnosed diabetes was 0.5% (85).
Although hormonal contraceptives can have some adverse
effects on glucose metabolism in healthy and diabetic women,
the overall clinical effect is minimal (171–177).
Lipids: Screening for dyslipidemias is not necessary for the
safe initiation of combined hormonal contraceptives because
of the low prevalence of undiagnosed disease in women of
reproductive age and the low likelihood of clinically significant
changes with use of hormonal contraceptives. A systematic
review did not identify any evidence regarding outcomes
among women who were screened versus not screened with
lipid measurement before initiation of hormonal contraceptives
(57). During 2009–2012 among women aged 20–44 years in
the United States, 7.6% had high cholesterol, defined as total
serum cholesterol ≥240 mg/dL (84). During 1999–2008,
the prevalence of undiagnosed hypercholesterolemia among
women aged 20–44 years was approximately 2% (85). A
systematic review identified few studies, all of poor quality,
that suggest that women with known dyslipidemias using
combined hormonal contraceptives might be at increased
risk for myocardial infarction, cerebrovascular accident, or
venous thromboembolism compared with women without
dyslipidemias; no studies were identified that examined risk for
pancreatitis among women with known dyslipidemias using
combined hormonal contraceptives (89). Studies have shown
mixed results regarding the effects of hormonal contraceptives
on lipid levels among both healthy women and women with

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Recommendations and Reports

baseline lipid abnormalities, and the clinical significance of
these changes is unclear (86–89).
Liver enzymes: Although women with certain liver
diseases should not use (U.S. MEC 4) or generally should
not use (U.S. MEC 3) combined hormonal contraceptives
(5), screening for liver disease before initiation of combined
hormonal contraceptives is not necessary because of the
low prevalence of these conditions and the high likelihood
that women with liver disease already would have had the
condition diagnosed. A systematic review did not identify
any evidence regarding outcomes among women who were
screened versus not screened with liver enzyme tests before
initiation of hormonal contraceptives (57). In 2012, among
U.S. women, the percentage with liver disease (not further
specified) was 1.3% (90). In 2013, the incidence of acute
hepatitis A, B, or C was ≤1 per 100,000 U.S. population (91).
During 2002–2011, the incidence of liver carcinoma among
U.S. women was approximately 3.7 per 100,000 population
(92). Because estrogen and progestins are metabolized in
the liver, the use of hormonal contraceptives among women
with liver disease might, theoretically, be a concern. The use
of hormonal contraceptives, specifically COCs and POPs,
does not affect disease progression or severity in women with
hepatitis, cirrhosis, or benign focal nodular hyperplasia (93,94),
although evidence is limited; no evidence exists for other types
of combined hormonal contraceptives.
Thrombogenic mutations: Women with thrombogenic
mutations should not use combined hormonal contraceptives
(U.S. MEC 4) (5) because of the increased risk for venous
thromboembolism (228). However, studies have shown
that universal screening for thrombogenic mutations before
initiating COCs is not cost-effective because of the rarity of
the conditions and the high cost of screening (229–231).
Clinical breast examination: Although women with current
breast cancer should not use combined hormonal contraceptives
(U.S. MEC 4) (5), screening asymptomatic women with a
clinical breast examination before initiating combined hormonal
contraceptives is not necessary because of the low prevalence of
breast cancer among women of reproductive age. A systematic
review did not identify any evidence regarding outcomes among
women who were screened versus not screened with a breast
examination before initiation of hormonal contraceptives (95).
The incidence of breast cancer among women of reproductive
age in the United States is low. In 2012, the incidence of breast
cancer among women aged 20–49 years was approximately 70.7
per 100,000 women (96).
Other screening: Women with anemia, cervical intraepithelial
neoplasia, cervical cancer, HIV infection, or other STDs can
use (U.S. MEC 1) or generally can use (U.S. MEC 2) combined

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hormonal contraceptives (5); therefore, screening for these
conditions is not necessary for the safe initiation of combined
hormonal contraceptives.

Number of Pill Packs that Should Be
Provided at Initial and Return Visits
• At the initial and return visits, provide or prescribe up to a
1-year supply of COCs (e.g., 13 28-day pill packs),
depending on the woman’s preferences and anticipated use.
• A woman should be able to obtain COCs easily in the
amount and at the time she needs them.
Comments and Evidence Summary. The more pill packs
given up to 13 cycles, the higher the continuation rates.
Restricting the number of pill packs distributed or prescribed
can result in unwanted discontinuation of the method and
increased risk for pregnancy.
A systematic review of the evidence suggested that providing
a greater number of pill packs was associated with increased
continuation (232). Studies that compared provision of one
versus 12 packs, one versus 12 or 13 packs, or three versus
seven packs found increased continuation of pill use among
women provided with more pill packs (233–235). However,
one study found no difference in continuation when patients
were provided one and then three packs versus four packs all
at once (236). In addition to continuation, a greater number
of pills packs provided was associated with fewer pregnancy
tests, fewer pregnancies, and lower cost per client. However, a
greater number of pill packs (i.e., 13 packs versus three packs)
also was associated with increased pill wastage in one study
(234) (Level of evidence: I to II-2, fair, direct).

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Recommendations and Reports

– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including
medications, that would change the appropriateness of
combined hormonal contraceptives for safe and
effective continued use based on U.S. MEC (e.g.,
category 3 and 4 conditions and characteristics).
– Assess blood pressure.
– Consider assessing weight changes and counseling women
who are concerned about weight change perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. No evidence exists
regarding whether a routine follow-up visit after initiating
combined hormonal contraceptives improves correct or
continued use. Monitoring blood pressure is important for
combined hormonal contraceptive users. Health care providers
might consider recommending women obtain blood pressure
measurements in other settings.
A systematic review identified five studies that examined the
incidence of hypertension among women who began using
a COC versus those who started a nonhormonal method
of contraception or a placebo (123). Few women developed
hypertension after initiating COCs, and studies examining
increases in blood pressure after COC initiation found mixed
results. No studies were identified that examined changes in
blood pressure among patch or vaginal ring users (Level of
evidence: I, fair, to II-2, fair, indirect).

Late or Missed Doses and Side Effects from
Combined Hormonal Contraceptive Use
For the following recommendations, a dose is considered
late when <24 hours have elapsed since the dose should have
been taken. A dose is considered missed if ≥24 hours have
elapsed since the dose should have been taken. For example,
if a COC pill was supposed to have been taken on Monday at
9:00 a.m. and is taken at 11:00 a.m., the pill is late; however,
by Tuesday morning at 11:00 a.m., Monday’s 9:00 a.m. pill
has been missed and Tuesday’s 9:00 a.m. pill is late. For COCs,
the recommendations only apply to late or missed hormonally
active pills and not to placebo pills. Recommendations are
provided for late or missed pills (Figure 2), the patch (Figure 3),
and the ring (Figure 4).
Comments and Evidence Summary. Inconsistent or
incorrect use of combined hormonal contraceptives is a major
cause of combined hormonal contraceptive failure. Extending
the hormone-free interval is considered to be a particularly risky
time to miss combined hormonal contraceptives. Seven days of
continuous combined hormonal contraceptive use is deemed

necessary to reliably prevent ovulation. The recommendations
reflect a balance between simplicity and precision of science.
Women who frequently miss COCs or experience other usage
errors with combined hormonal patch or combined vaginal
ring should consider an alternative contraceptive method
that is less dependent on the user to be effective (e.g., IUD,
implant, or injectable).
A systematic review identified 36 studies that examined
measures of contraceptive effectiveness of combined hormonal
contraceptives during cycles with extended hormone-free
intervals, shortened hormone-free intervals, or deliberate
nonadherence on days not adjacent to the hormone-free
interval (237). Most of the studies examined COCs (215,238–
265), two examined the combined hormonal patch (259,266),
and six examined the combined vaginal ring (211,267–271).
No direct evidence on the effect of missed pills on the risk
for pregnancy was found. Studies of women deliberately
extending the hormone-free interval up to 14 days found
wide variability in the amount of follicular development and
occurrence of ovulation (241,244,246,247,249,250,252–255);
in general, the risk for ovulation was low, and among women
who did ovulate, cycles were usually abnormal. In studies of
women who deliberately missed pills on various days during
the cycle not adjacent to the hormone-free interval, ovulation
occurred infrequently (239,245–247,255,256,258,259).
Studies comparing 7-day hormone-free intervals with shorter
hormone-free intervals found lower rates of pregnancy
(238,242,251,257) and significantly greater suppression of
ovulation (240,250,261–263,265) among women with shorter
intervals in all but one study (260), which found no difference.
Two studies that compared 30-µg ethinyl estradiol pills with
20-µg ethinyl estradiol pills showed more follicular activity
when 20-µg ethinyl estradiol pills were missed (241,244). In
studies examining the combined vaginal ring, three studies
found that nondeliberate extension of the hormone-free
interval for 24 to <48 hours from the scheduled period
did not increase the risk for pregnancy (267,268,270); one
study found that ring insertion after a deliberately extended
hormone-free interval that allowed a 13-mm follicle to develop
interrupted ovarian function and further follicular growth
(211); and one study found that inhibition of ovulation was
maintained after deliberately forgetting to remove the ring
for up to 2 weeks after normal ring use (271). In studies
examining the combined hormonal patch, one study found
that missing 1–3 consecutive days before patch replacement
(either wearing one patch 3 days longer before replacement
or going 3 days without a patch before replacing the next
patch) on days not adjacent to the patch-free interval resulted
in little follicular activity and low risk for ovulation (259),
and one pharmacokinetic study found that serum levels of

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Recommendations and Reports

FIGURE 2. Recommended actions after late or missed combined oral contraceptives
If one hormonal pill is late:
(<24 hours since a pill
should have been taken)

If one hormonal pill has been missed:
(24 to <48 hours since a pill should
have been taken)

• Take the late or missed pill as soon as possible.
• Continue taking the remaining pills at the usual time (even if it
means taking two pills on the same day).
• No additional contraceptive protection is needed.
• Emergency contraception is not usually needed but can be
considered (with the exception of UPA) if hormonal pills were
missed earlier in the cycle or in the last week of the previous cycle.

If two or more consecutive hormonal pills have been missed:
(≥48 hours since a pill should have been taken)

• Take the most recent missed pill as soon as possible. (Any other
missed pills should be discarded.)
• Continue taking the remaining pills at the usual time (even if it
means taking two pills on the same day).
• Use back-up contraception (e.g., condoms) or avoid sexual intercourse
until hormonal pills have been taken for 7 consecutive days.
• If pills were missed in the last week of hormonal pills (e.g., days
15–21 for 28-day pill packs):
o Omit the hormone-free interval by finishing the hormonal pills
in the current pack and starting a new pack the next day.
o If unable to start a new pack immediately, use back-up contraception
(e.g., condoms) or avoid sexual intercourse until hormonal pills from
a new pack have been taken for 7 consecutive days.
• Emergency contraception should be considered (with the exception
of UPA) if hormonal pills were missed during the first week and
unprotected sexual intercourse occurred in the previous 5 days.
• Emergency contraception may also be considered (with the
exception of UPA) at other times as appropriate.

Abbreviation: UPA = ulipristal acetate.

FIGURE 3. Recommended actions after delayed application or detachment* with combined hormonal patch
Delayed application or detachment for <48 hours since a patch
should have been applied or reattached

Delayed application or detachment for ≥48 hours since a patch
should have been applied or reattached

• Apply a new patch as soon as possible. (If detachment occurred
<24 hours since the patch was applied, try to reapply the patch or
replace with a new patch.)
• Keep the same patch change day.
• No additional contraceptive protection is needed.
• Emergency contraception is not usually needed but can be
considered (with the exception of UPA) if delayed application or
detachment occurred earlier in the cycle or in the last week of the
previous cycle.

• Apply a new patch as soon as possible.
• Keep the same patch change day.
• Use back-up contraception (e.g., condoms) or avoid sexual
intercourse until a patch has been worn for 7 consecutive days.
• If the delayed application or detachment occurred in the third
patch week:
o Omit the hormone-free week by finishing the third week of
patch use (keeping the same patch change day) and starting a
new patch immediately;
o If unable to start a new patch immediately, use back-up
contraception (e.g., condoms) or avoid sexual intercourse until a
new patch has been worn for 7 consecutive days.
• Emergency contraception should be considered (with the exception
of UPA) if the delayed application or detachment occurred within
the first week of patch use and unprotected sexual intercourse
occurred in the previous 5 days.
• Emergency contraception may also be considered (with the
exception of UPA) at other times as appropriate.

Abbreviation: UPA = ulipristal acetate.
* If detachment takes place but the woman is unsure when the detachment occurred, consider the patch to have been detached for ≥48 hours since a patch should
have been applied or reattached.

MMWR / July 29, 2016 / Vol. 65 / No. 4

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Recommendations and Reports

FIGURE 4. Recommended actions after delayed insertion or reinsertion* with combined vaginal ring
Delayed insertion of a new ring or delayed reinsertion of a current
ring for <48 hours since a ring should have been inserted

Delayed insertion of a new ring or delayed reinsertion for ≥48 hours
since a ring should have been inserted

• Insert ring as soon as possible.
• Keep the ring in until the scheduled ring removal day.
• No additional contraceptive protection is needed.
• Emergency contraception is not usually needed but can be
considered (with the exception of UPA) if delayed insertion or
reinsertion occurred earlier in the cycle or in the last week of the
previous cycle.

• Insert ring as soon as possible.
• Keep the ring in until the scheduled ring removal day.
• Use back-up contraception (e.g., condoms) or avoid sexual
intercourse until a ring has been worn for 7 consecutive days.
• If the ring removal occurred in the third week of ring use:
o Omit the hormone-free week by finishing the third week of ring
use and starting a new ring immediately.
o If unable to start a new ring immediately, use back-up
contraception (e.g., condoms) or avoid sexual intercourse until a
new ring has been worn for 7 consecutive days.
• Emergency contraception should be considered (with the exception
of UPA) if the delayed insertion or reinsertion occurred within the
first week of ring use and unprotected sexual intercourse occurred
in the previous 5 days.
• Emergency contraception may also be considered (with the
exception of UPA) at other times as appropriate.

Abbreviation: UPA = ulipristal acetate.
* If removal takes place but the woman is unsure of how long the ring has been removed, consider the ring to have been removed for ≥48 hours since a ring should
have been inserted or reinserted.

ethinyl estradiol and progestin norelgestromin remained within
reference ranges after extending patch wear for 3 days (266).
No studies were found on extending the patch-free interval. In
studies that provide indirect evidence on the effects of missed
combined hormonal contraception on surrogate measures of
pregnancy, how differences in surrogate measures correspond
to pregnancy risk is unclear (Level of evidence: I, good, indirect
to II-3, poor, direct).

Vomiting or Severe Diarrhea
While Using COCs
Certain steps should be taken by women who experience
vomiting or severe diarrhea while using COCs (Figure 5).
Comments and Evidence Summary. Theoretically, the
contraceptive effectiveness of COCs might be decreased because
of vomiting or severe diarrhea. Because of the lack of evidence
that addresses vomiting or severe diarrhea while using COCs,
these recommendations are based on the recommendations
for missed COCs. No evidence was found on the effects of
vomiting or diarrhea on measures of contraceptive effectiveness
including pregnancy, follicular development, hormone levels,
or cervical mucus quality.

Unscheduled Bleeding with Extended or
Continuous Use of Combined Hormonal
Contraceptives
• Before initiation of combined hormonal contraceptives,
provide counseling about potential changes in bleeding
patterns during extended or continuous combined
hormonal contraceptive use. (Extended contraceptive use
is defined as a planned hormone-free interval after at least
two contiguous cycles. Continuous contraceptive use is
defined as uninterrupted use of hormonal contraception
without a hormone-free interval) (272).
• Unscheduled spotting or bleeding is common during the
first 3–6 months of extended or continuous combined
hormonal contraceptive use. It is generally not harmful
and decreases with continued combined hormonal
contraceptive use.
• If clinically indicated, consider an underlying gynecological
problem, such as inconsistent use, interactions with other
medications, cigarette smoking, an STD, pregnancy, or
new pathologic uterine conditions (e.g., polyps or
fibroids). If an underlying gynecological problem is found,
treat the condition or refer for care.
• If an underlying gynecological problem is not found and
the woman wants treatment, the following treatment
option can be considered:

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Recommendations and Reports

FIGURE 5. Recommended actions after vomiting or diarrhea while using combined oral contraceptives
Vomiting or diarrhea (for
any reason, for any
duration), that occurs
within 24 hours after taking
a hormonal pill

Vomiting or diarrhea, for any reason,
continuing for 24 to <48 hours after
taking any hormonal pill

• Taking another hormonal pill (redose) is unnecessary.
• Continue taking pills daily at the usual time (if possible,
despite discomfort).
• No additional contraceptive protection is needed.
• Emergency contraception is not usually needed but can be
considered (with the exception of UPA) as appropriate.

Vomiting or diarrhea, for any reason, continuing for ≥48 hours after
taking any hormonal pill

• Continue taking pills daily at the usual time (if possible,
despite discomfort).
• Use back-up contraception (e.g., condoms) or avoid sexual
intercourse until hormonal pills have been taken for 7 consecutive
days after vomiting or diarrhea has resolved.
• If vomiting or diarrhea occurred in the last week of hormonal pills
(e.g., days 15–21 for 28-day pill packs):
o Omit the hormone-free interval by finishing the hormonal pills in
the current pack and starting a new pack the next day.
o If unable to start a new pack immediately, use back-up
contraception (e.g., condoms) or avoid sexual intercourse until
hormonal pills from a new pack have been taken for
7 consecutive days.
• Emergency contraception should be considered (with the exception
of UPA) if vomiting or diarrhea occurred within the first week of a
new pill pack and unprotected sexual intercourse occurred in the
previous 5 days.
• Emergency contraception may also be considered (with the
exception of UPA) at other times as appropriate.

Abbreviation: UPA = ulipristal acetate.

– Advise the woman to discontinue combined hormonal
contraceptive use (i.e., a hormone-free interval) for 3–4
consecutive days; a hormone-free interval is not
recommended during the first 21 days of using the
continuous or extended combined hormonal
contraceptive method. A hormone-free interval also is
not recommended more than once per month because
contraceptive effectiveness might be reduced.
• If unscheduled spotting or bleeding persists and the woman
finds it unacceptable, counsel her on alternative contraceptive
methods, and offer another method if it is desired.
Comments and Evidence Summary. During contraceptive
counseling and before initiating extended or continuous
combined hormonal contraceptives, information about
common side effects such as unscheduled spotting or bleeding,
especially during the first 3–6 months of use, should be
discussed (273). These bleeding irregularities are generally
not harmful and usually improve with persistent use of the
hormonal method. To avoid unscheduled spotting or bleeding,
counseling should emphasize the importance of correct use and
timing; for users of contraceptive pills, emphasize consistent
pill use. Enhanced counseling about expected bleeding patterns

MMWR / July 29, 2016 / Vol. 65 / No. 4

and reassurance that bleeding irregularities are generally not
harmful has been shown to reduce method discontinuation in
clinical trials with DMPA (124,125,274).
A systematic review identified three studies with small
study populations that addressed treatments for unscheduled
bleeding among women using extended or continuous
combined hormonal contraceptives (275). In two separate
randomized clinical trials in which women were taking either
contraceptive pills or using the contraceptive ring continuously
for 168 days, women assigned to a hormone-free interval
of 3 or 4 days reported improved bleeding. Although they
noted an initial increase in flow, this was followed by an
abrupt decrease 7–8 days later with eventual cessation of flow
11–12 days later. These findings were compared with women
who continued to use their method without a hormonefree interval, in which a greater proportion reported either
treatment failure or fewer days of amenorrhea (276,277).
In another randomized trial of 66 women with unscheduled
bleeding among women using 84 days of hormonally active
contraceptive pills, oral doxycycline (100 mg twice daily)
initiated the first day of bleeding and taken for 5 days did not
result in any improvement in bleeding compared with placebo
(278) (Level of evidence: I, fair, direct).

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Recommendations and Reports

Progestin-Only Pills
POPs contain only a progestin and no estrogen and are
available in the United States. Approximately 9 out of
100 women become pregnant in the first year of use with
POPs with typical use (14). POPs are reversible and can be
used by women of all ages. POPs do not protect against STDs;
consistent and correct use of male latex condoms reduces the
risk for STDs, including HIV.

Initiation of POPs
Timing
• POPs can be started at any time if it is reasonably certain
that the woman is not pregnant (Box 2).

Need for Back-Up Contraception
• If POPs are started within the first 5 days since menstrual
bleeding started, no additional contraceptive protection
is needed.
• If POPs are started >5 days since menstrual bleeding started,
the woman needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 2 days.

Special Considerations
Amenorrhea (Not Postpartum)
• Timing: POPs can be started at any time if it is reasonably
certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 2 days.
Postpartum (Breastfeeding)
• Timing: POPs can be started at any time, including
immediately postpartum (U.S. MEC 2 if <1 month
postpartum; U.S. MEC 1 if ≥1 month postpartum) if it is
reasonably certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: If the woman is
<6 months postpartum, amenorrheic, and fully or nearly
fully breastfeeding (exclusively breastfeeding or the vast
majority [≥85%] of feeds are breastfeeds) (27), no additional
contraceptive protection is needed. Otherwise, a woman
who is ≥21 days postpartum and has not experienced return
of her menstrual cycles, she needs to abstain from sexual
intercourse or use additional contraceptive protection for
the next 2 days. If her menstrual cycles have returned and
it has been >5 days since menstrual bleeding started, she
needs to abstain from sexual intercourse or use additional
contraceptive protection for the next 2 days.

Postpartum (Not Breastfeeding)
• Timing: POPs can be started at any time, including
immediately postpartum (U.S. MEC 1), if it is reasonably
certain that the woman is not pregnant (Box 2).
• Need for back-up contraception: If a woman is <21 days
postpartum, no additional contraceptive protection is
needed. Women who are ≥21 days postpartum and whose
menstrual cycles have not returned need to abstain from
sexual intercourse or use additional contraceptive
protection for the next 2 days. If her menstrual cycles have
returned and it has been >5 days since menstrual bleeding
started, she needs to abstain from sexual intercourse or use
additional contraceptive protection for the next 2 days.
Postabortion (Spontaneous or Induced)
• Timing: POPs can be started within the first 7 days,
including immediately postabortion (U.S. MEC 1).
• Need for back-up contraception: The woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 2 days unless POPs
are started at the time of a surgical abortion.
Switching from Another Contraceptive Method
• Timing: POPs can be started immediately if it is reasonably
certain that the woman is not pregnant (Box 2). Waiting
for her next menstrual cycle is unnecessary.
• Need for back-up contraception: If it has been >5 days
since menstrual bleeding started, the woman needs to
abstain from sexual intercourse or use additional
contraceptive protection for the next 2 days.
• Switching from an IUD: If the woman has had sexual
intercourse since the start of her current menstrual cycle
and it has been >5 days since menstrual bleeding started,
theoretically, residual sperm might be in the genital tract,
which could lead to fertilization if ovulation occurs. A health
care provider may consider any of the following options:
– Advise the women to retain the IUD for at least 2 days
after POPs are initiated and return for IUD removal.
– Advise the woman to abstain from sexual intercourse
or use barrier contraception for 7 days before removing
the IUD and switching to the new method.
– If the woman cannot return for IUD removal and has
not abstained from sexual intercourse or used barrier
contraception for 7 days, advise the woman to use ECPs
at the time of IUD removal. POPs can be started
immediately after use of ECPs (with the exception of
UPA). POPs can be started no sooner than 5 days after
use of UPA.
Comments and Evidence Summary. In situations in which
the health care provider is uncertain whether the woman might

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Recommendations and Reports

be pregnant, the benefits of starting POPs likely exceed any
risk; therefore, starting POPs should be considered at any time,
with a follow-up pregnancy test in 2–4 weeks.
Unlike COCs, POPs inhibit ovulation in about half of cycles,
although the rates vary widely by individual (279). Peak serum
steroid levels are reached about 2 hours after administration,
followed by rapid distribution and elimination, such that by
24 hours after administration, serum steroid levels are near
baseline (279). Therefore, taking POPs at approximately
the same time each day is important. An estimated 48 hours
of POP use has been deemed necessary to achieve the
contraceptive effects on cervical mucus (279). If a woman needs
to use additional contraceptive protection when switching to
POPs from another contraceptive method, consider continuing
her previous method for 2 days after starting POPs. No direct
evidence was found regarding the effects of starting POPs at
different times of the cycle.

Examinations and Tests Needed Before
Initiation of POPs
Among healthy women, no examinations or tests are needed
before initiation of POPs, although a baseline weight and BMI
measurement might be useful for monitoring POP users over
time (Table 5). Women with known medical problems or other
special conditions might need additional examinations or tests
before being determined to be appropriate candidates for a
particular method of contraception. The U.S. MEC might be
useful in such circumstances (5).
Comments and Evidence Summary. Weight (BMI): Obese
women can use POPs (U.S. MEC 1) (5); therefore, screening
for obesity is not necessary for the safe initiation of POPs.
However, measuring weight and calculating BMI at baseline
might be helpful for monitoring any changes and counseling
women who might be concerned about weight change
perceived to be associated with their contraceptive method.
Bimanual examination and cervical inspection: Pelvic
examination is not necessary before initiation of POPs because
it does not facilitate detection of conditions for which POPs
would be unsafe. Women with current breast cancer should not
use POPs (U.S. MEC 4), and women with certain liver diseases
generally should not use POPs (U.S. MEC 3) (5); however,
neither of these conditions are likely to be detected by pelvic
examination (145). A systematic review identified two casecontrol studies that compared delayed versus immediate pelvic
examination before initiation of hormonal contraceptives,
specifically oral contraceptives or DMPA (95). No differences
in risk factors for cervical neoplasia, incidence of STDs,
incidence of abnormal Papanicolaou smears, or incidence of

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TABLE 5. Classification of examinations and tests needed before
progestin-only pill initiation
Examination or test
Examination
Blood pressure
Weight (BMI) (weight [kg]/height [m]2)
Clinical breast examination
Bimanual examination and cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou smear)
STD screening with laboratory tests
HIV screening with laboratory tests

Class*
C
—†
C
C
C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus;
STD = sexually transmitted disease; U.S. MEC = U.S. Medical Eligibility Criteria for
Contraceptive Use.
* Class A: essential and mandatory in all circumstances for safe and effective use of
the contraceptive method. Class B: contributes substantially to safe and effective
use, but implementation may be considered within the public health and/or service
context; the risk of not performing an examination or test should be balanced against
the benefits of making the contraceptive method available. Class C: does not
contribute substantially to safe and effective use of the contraceptive method.
† Weight (BMI) measurement is not needed to determine medical eligibility for any
methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 1). However,
measuring weight and calculating BMI at baseline might be helpful for monitoring
any changes and counseling women who might be concerned about weight
change perceived to be associated with their contraceptive method.

abnormal findings from wet mounts were observed (Level of
evidence: II-2 fair, direct).
Lipids: Screening for dyslipidemias is not necessary for
the safe initiation of POPs because of the low prevalence of
undiagnosed disease in women of reproductive age and the
low likelihood of clinically significant changes with use of
hormonal contraceptives. A systematic review did not identify
any evidence regarding outcomes among women who were
screened versus not screened with lipid measurement before
initiation of hormonal contraceptives (57). During 2009–2012
among women aged 20–44 years in the United States, 7.6%
had high cholesterol, defined as total serum cholesterol
≥240 mg/dL (84). During 1999–2008, the prevalence of
undiagnosed hypercholesterolemia among women aged
20–44 years was approximately 2% (85). Studies have shown
mixed results about the effects of hormonal methods on lipid
levels among both healthy women and women with baseline
lipid abnormalities, and the clinical significance of these
changes is unclear (86–89).
Liver enzymes: Although women with certain liver diseases
generally should not use POPs (U.S. MEC 3) (5), screening
for liver disease before initiation of POPs is not necessary
because of the low prevalence of these conditions and the
high likelihood that women with liver disease already would

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Recommendations and Reports

have had the condition diagnosed. A systematic review did not
identify any evidence regarding outcomes among women who
were screened versus not screened with liver enzyme tests before
initiation of hormonal contraceptives (57). In 2012, among
U.S. women, the percentage with liver disease (not further
specified) was 1.3% (90). In 2013, the incidence of acute
hepatitis A, B, or C was ≤1 per 100,000 U.S. population (91).
During 2002–2011, the incidence of liver carcinoma among
U.S. women was approximately 3.7 per 100,000 population
(92). Because estrogen and progestins are metabolized in
the liver, the use of hormonal contraceptives among women
with liver disease might, theoretically, be a concern. The use
of hormonal contraceptives, specifically COCs and POPs,
does not affect disease progression or severity in women with
hepatitis, cirrhosis, or benign focal nodular hyperplasia (93,94).
Clinical breast examination: Although women with current
breast cancer should not use POPs (U.S. MEC 4) (5), screening
asymptomatic women with a clinical breast examination
before initiating POPs is not necessary because of the low
prevalence of breast cancer among women of reproductive age.
A systematic review did not identify any evidence regarding
outcomes among women who were screened versus not
screened with a clinical breast examination before initiation of
hormonal contraceptives (95). The incidence of breast cancer
among women of reproductive age in the United States is low.
In 2012, the incidence of breast cancer among women aged
20–49 years was approximately 70.7 per 100,000 women (96).
Other screening: Women with hypertension, diabetes,
anemia, thrombogenic mutations, cervical intraepithelial
neoplasia, cervical cancer, STDs, or HIV infection can use
(U.S. MEC 1) or generally can use (U.S. MEC 2) POPs (5);
therefore, screening for these conditions is not necessary for
the safe initiation of POPs.

Number of Pill Packs that Should Be
Provided at Initial and Return Visits
• At the initial and return visit, provide or prescribe up to a
1-year supply of POPs (e.g., 13 28-day pill packs),
depending on the woman’s preferences and anticipated use.
• A woman should be able to obtain POPs easily in the
amount and at the time she needs them.
Comments and Evidence Summary. The more pill packs
given up to 13 cycles, the higher the continuation rates.
Restricting the number of pill packs distributed or prescribed
can result in unwanted discontinuation of the method and
increased risk for pregnancy.
A systematic review of the evidence suggested that providing
a greater number of pill packs was associated with increased
continuation (232). Studies that compared provision of one

versus 12 packs, one versus 12 or 13 packs, or three versus
seven packs found increased continuation of pill use among
women provided with more pill packs (233–235). However,
one study found no difference in continuation when patients
were provided one and then three packs versus four packs all
at once (236). In addition to continuation, a greater number
of pill packs provided was associated with fewer pregnancy
tests, fewer pregnancies, and lower cost per client. However, a
greater number of pill packs (13 packs versus three packs) also
was associated with increased pill wastage in one study (234)
(Level of evidence: I to II-2, fair, direct).

Routine Follow-Up After POP Initiation
These recommendations address when routine follow-up
is recommended for safe and effective continued use of
contraception for healthy women. The recommendations refer
to general situations and might vary for different users and
different situations. Specific populations who might benefit
from more frequent follow-up visits include adolescents, those
with certain medical conditions or characteristics, and those
with multiple medical conditions.
• Advise the woman to return at any time to discuss side
effects or other problems or if she wants to change the
method being used. No routine follow-up visit is required.
• At other routine visits, health care providers seeing POP
users should do the following:
– Assess the woman’s satisfaction with her contraceptive
method and whether she has any concerns about
method use.
– Assess any changes in health status, including medications,
that would change the appropriateness of POPs for safe
and effective continued use based on U.S. MEC (e.g.,
category 3 and 4 conditions and characteristics).
– Consider assessing weight changes and counseling women
who are concerned about weight change perceived to be
associated with their contraceptive method.
Comments and Evidence Summary. No evidence was
found regarding whether a routine follow-up visit after
initiating POPs improves correct and continued use.

Missed POPs
For the following recommendations, a dose is considered
missed if it has been >3 hours since it should have been taken.
• Take one pill as soon as possible.
• Continue taking pills daily, one each day, at the same time
each day, even if it means taking two pills on the same day.
• Use back-up contraception (e.g., condoms) or avoid sexual
intercourse until pills have been taken correctly, on time,
for 2 consecutive days.

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Recommendations and Reports

• Emergency contraception should be considered (with the
exception of UPA) if the woman has had unprotected
sexual intercourse.
Comments and Evidence Summary. Inconsistent or
incorrect use of oral contraceptive pills is a major reason for oral
contraceptive failure. Unlike COCs, POPs inhibit ovulation
in about half of cycles, although this rate varies widely by
individual (279). Peak serum steroid levels are reached about
2 hours after administration, followed by rapid distribution
and elimination, such that by 24 hours after administration,
serum steroid levels are near baseline (279). Therefore, taking
POPs at approximately the same time each day is important.
An estimated 48 hours of POP use was deemed necessary to
achieve the contraceptive effects on cervical mucus (279).
Women who frequently miss POPs should consider an
alternative contraceptive method that is less dependent on
the user to be effective (e.g., IUD, implant, or injectable).
No evidence was found regarding the effects of missed POPs
available in the United States on measures of contraceptive
effectiveness including pregnancy, follicular development,
hormone levels, or cervical mucus quality.

Vomiting or Diarrhea (for any Reason or
Duration) that Occurs Within 3 Hours After
Taking a Pill
• Take another pill as soon as possible (if possible,
despite discomfort).
• Continue taking pills daily, one each day, at the same time
each day.
• Use back-up contraception (e.g., condoms) or avoid sexual
intercourse until 2 days after vomiting or diarrhea has resolved.
• Emergency contraception should be considered (with the
exception of UPA) if the woman has had unprotected
sexual intercourse.
Comments and Evidence Summary. Theoretically, the
contraceptive effectiveness of POPs might be decreased because
of vomiting or severe diarrhea. Because of the lack of evidence
to address this question, these recommendations are based on
the recommendations for missed POPs. No evidence was found
regarding the effects of vomiting or diarrhea on measures of
contraceptive effectiveness, including pregnancy, follicular
development, hormone levels, or cervical mucus quality.

Standard Days Method

become pregnant in the first year of use with perfect (i.e.,
correct and consistent) use of SDM (280); effectiveness based
on typical use is not available for this method but is expected
to be lower than that for perfect use. SDM is reversible and can
be used by women of all ages. SDM does not protect against
STDs; consistent and correct use of male latex condoms reduces
the risk for STDs, including HIV.

Use of SDM Among Women with Various
Durations of the Menstrual Cycle
Menstrual Cycles of 26–32 Days
• The woman may use the method.
• Provide a barrier method of contraception for protection
on days 8–19 if she wants one.
• If she has unprotected sexual intercourse during days 8–19,
consider the use of emergency contraception if appropriate.

Two or More Cycles of <26 or >32 Days Within Any
1 Year of SDM Use
• Advise the woman that the method might not be
appropriate for her because of a higher risk for pregnancy.
Help her consider another method.
Comments and Evidence Summary. The probability of
pregnancy is increased when the menstrual cycle is outside the
range of 26–32 days, even if unprotected sexual intercourse
is avoided on days 8–19. A study of 7,600 menstrual cycles,
including information on cycle length and signs of ovulation,
concluded that the theoretical effectiveness of SDM is greatest
for women with cycles of 26–32 days, that the method is still
effective for women who occasionally have a cycle outside this
range, and that it is less effective for women who consistently
have cycles outside this range. Information from daily
hormonal measurements shows that the timing of the 6-day
fertile window varies greatly, even among women with regular
cycles (21,281,282).

SDM is a method based on fertility awareness; users must
avoid unprotected sexual intercourse on days 8–19 of the
menstrual cycle (280). Approximately 5 out of 100 women

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Recommendations and Reports

Types of Emergency Contraception
Intrauterine Device
• Cu-IUD

when ECPs were taken after 3 days (288–292). A meta-analysis
of levonorgestrel ECPs found that pregnancy rates were low
when administered within 4 days after unprotected sexual
intercourse but increased at 4–5 days (293) (Level of evidence:
I to II-2, good to poor, direct).

ECPs
• UPA in a single dose (30 mg)
• Levonorgestrel in a single dose (1.5 mg) or as a split dose
(1 dose of 0.75 mg of levonorgestrel followed by a second
dose of 0.75 mg of levonorgestrel 12 hours later)
• Combined estrogen and progestin in 2 doses (Yuzpe
regimen: 1 dose of 100 µg of ethinyl estradiol plus
0.50 mg of levonorgestrel followed by a second dose of
100 µg of ethinyl estradiol plus 0.50 mg of levonorgestrel
12 hours later)

Initiation of Emergency Contraception
Timing
Cu-IUD
• The Cu-IUD can be inserted within 5 days of the first act of
unprotected sexual intercourse as an emergency contraceptive.
• In addition, when the day of ovulation can be estimated,
the Cu-IUD can be inserted beyond 5 days after sexual
intercourse, as long as insertion does not occur >5 days
after ovulation.
ECPs
• ECPs should be taken as soon as possible within 5 days of
unprotected sexual intercourse.
Comments and Evidence Summary. Cu-IUDs are highly
effective as emergency contraception (283) and can be
continued as regular contraception. UPA and levonorgestrel
ECPs have similar effectiveness when taken within 3 days
after unprotected sexual intercourse; however, UPA has been
shown to be more effective than the levonorgestrel formulation
3–5 days after unprotected sexual intercourse (284). The
combined estrogen and progestin regimen is less effective than
UPA or levonorgestrel and also is associated with more frequent
occurrence of side effects (nausea and vomiting) (285). The
levonorgestrel formulation might be less effective than UPA
among obese women (286).
Two studies of UPA use found consistent decreases in
pregnancy rates when administered within 120 hours of
unprotected sexual intercourse (284,287). Five studies found
that the levonorgestrel and combined regimens decreased risk
for pregnancy through the fifth day after unprotected sexual
intercourse; however, rates of pregnancy were slightly higher

Advance Provision of ECPs
• An advance supply of ECPs may be provided so that ECPs
will be available when needed and can be taken as soon as
possible after unprotected sexual intercourse.
Comments and Evidence Summary. A systematic review
identified 17 studies that reported on safety or effectiveness
of advance ECPs in adult or adolescent women (294). Any
use of ECPs was two to seven times greater among women
who received an advance supply of ECPs. However, a
summary estimate (relative risk = 0.97; 95% confidence
interval = 0.77–1.22) of five randomized controlled trials did
not indicate a significant reduction in unintended pregnancies
at 12 months with advance provision of ECPs. In the majority
of studies among adults or adolescents, patterns of regular
contraceptive use, pregnancy rates, and incidence of STDs did
not vary between those who received advance ECPs and those
who did not. Although available evidence supports the safety of
advance provision of ECPs, effectiveness of advance provision
of ECPs in reducing pregnancy rates at the population level
has not been demonstrated (Level of evidence: I to II-3, good
to poor, direct).

Initiation of Regular Contraception After ECPs
UPA
• Advise the woman to start or resume hormonal contraception
no sooner than 5 days after use of UPA, and provide or
prescribe the regular contraceptive method as needed. For
methods requiring a visit to a health care provider, such as
DMPA, implants, and IUDs, starting the method at the
time of UPA use may be considered; the risk that the regular
contraceptive method might decrease the effectiveness of
UPA must be weighed against the risk of not starting a
regular hormonal contraceptive method.
• The woman needs to abstain from sexual intercourse or
use barrier contraception for the next 7 days after starting
or resuming regular contraception or until her next
menses, whichever comes first.
• Any nonhormonal contraceptive method can be started
immediately after the use of UPA.
• Advise the woman to have a pregnancy test if she does not
have a withdrawal bleed within 3 weeks.

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Recommendations and Reports

Levonorgestrel and Combined Estrogen and
Progestin ECPs

Prevention and Management of Nausea
and Vomiting with ECP Use

• Any regular contraceptive method can be started
immediately after the use of levonorgestrel or combined
estrogen and progestin ECPs.
• The woman needs to abstain from sexual intercourse or
use barrier contraception for 7 days.
• Advise the woman to have a pregnancy test if she does not
have a withdrawal bleed within 3 weeks.
Comments and Evidence Summary. The resumption or
initiation of regular hormonal contraception after ECP use
involves consideration of the risk for pregnancy if ECPs fail and
the risks for unintended pregnancy if contraception initiation
is delayed until the subsequent menstrual cycle. A health care
provider may provide or prescribe pills, the patch, or the ring
for a woman to start no sooner than 5 days after use of UPA.
For methods requiring a visit to a health care provider, such
as DMPA, implants, and IUDs, starting the method at the
time of UPA use may be considered; the risk that the regular
contraceptive method might decrease the effectiveness of UPA
must be weighed against the risk of not starting a regular
hormonal contraceptive method.
Data on when a woman can start regular contraception
after ECPs are limited to pharmacodynamic data and expert
opinion (295–297). In one pharmacodynamic study of women
who were randomly assigned to either UPA or placebo groups
mid-cycle followed by a 21-day course of combined hormonal
contraception found no difference between UPA and placebo
groups in the time for women’s ovaries to reach quiescence by
ultrasound and serum estradiol (296); this finding suggests
that UPA did not have an effect on the combined hormonal
contraception. In another pharmacodynamic study with a
crossover design, women were randomly assigned to one of
three groups: 1) UPA followed by desogestrel for 20 days
started 1 day later; 2) UPA plus placebo; or 3) placebo plus
desogestrel for 20 days (295). Among women taking UPA
followed by desogestrel, a higher incidence of ovulation in the
first 5 days was found compared with UPA alone (45% versus
3%, respectively), suggesting desogestrel might decrease the
effectiveness of UPA. No concern exists that administering
combined estrogen and progestin or levonorgestrel formulations
of ECPs concurrently with systemic hormonal contraception
decreases the effectiveness of either emergency or regular
contraceptive methods because these formulations do not have
antiprogestin properties like UPA. If a woman is planning to
initiate contraception after the next menstrual bleeding after
ECP use, the cycle in which ECPs are used might be shortened,
prolonged, or involve unscheduled bleeding.

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Nausea and Vomiting
• Levonorgestrel and UPA ECPs cause less nausea and
vomiting than combined estrogen and progestin ECPs.
• Routine use of antiemetics before taking ECPs is not
recommended. Pretreatment with antiemetics may be
considered depending on availability and clinical judgment.

Vomiting Within 3 Hours of Taking ECPs
• Another dose of ECP should be taken as soon as possible.
Use of an antiemetic should be considered.
Comments and Evidence Summary. Many women do
not experience nausea or vomiting when taking ECPs, and
predicting which women will experience nausea or vomiting
is difficult. Although routine use of antiemetics before taking
ECPs is not recommended, antiemetics are effective in some
women and can be offered when appropriate. Health care
providers who are deciding whether to offer antiemetics to
women taking ECPs should consider the following: 1) women
taking combined estrogen and progestin ECPs are more
likely to experience nausea and vomiting than those who
take levonorgestrel or UPA ECPs; 2) evidence indicates that
antiemetics reduce the occurrence of nausea and vomiting in
women taking combined estrogen and progestin ECPs; and
3) women who take antiemetics might experience other side
effects from the antiemetics.
A systematic review examined incidence of nausea and
vomiting with different ECP regimens and effectiveness of
antinausea drugs in reducing nausea and vomiting with ECP
use (298). The levonorgestrel regimen was associated with
significantly less nausea than a nonstandard dose of UPA
(50 mg) and the standard combined estrogen and progestin
regimen (299–301). Use of the split-dose levonorgestrel
showed no differences in nausea and vomiting compared
with the single-dose levonorgestrel (288,290,292,302) (Level
of evidence: I, good-fair, indirect). Two trials of antinausea
drugs, meclizine and metoclopramide, taken before combined
estrogen and progestin ECPs, reduced the severity of nausea
(303,304). Significantly less vomiting occurred with meclizine
but not metoclopramide (Level of evidence: I, good-fair,
direct). No direct evidence was found regarding the effects of
vomiting after taking ECPs.

Female Sterilization
Laparoscopic, abdominal, and hysteroscopic methods of
female sterilization are available in the United States, and

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

some of these procedures can be performed in an outpatient
procedure or office setting. Fewer than 1 out of 100 women
become pregnant in the first year after female sterilization
(14). Because these methods are intended to be irreversible,
all women should be appropriately counseled about the
permanency of sterilization and the availability of highly
effective, long-acting, reversible methods of contraception.
Female sterilization does not protect against STDs; consistent
and correct use of male latex condoms reduces the risk for
STDs, including HIV.

When Hysteroscopic Sterilization is
Reliable for Contraception
• Before a woman can rely on hysteroscopic sterilization for
contraception, a hysterosalpingogram (HSG) must be
performed 3 months after the sterilization procedure to
confirm bilateral tubal occlusion.
• The woman should be advised that she needs to abstain
from sexual intercourse or use additional contraceptive
protection until she has confirmed bilateral tubal occlusion.

When Laparoscopic and Abdominal
Approaches are Reliable for Contraception
• A woman can rely on sterilization for contraception
immediately after laparoscopic and abdominal approaches.
No additional contraceptive protection is needed.
Comments and Evidence Summary. HSG confirmation
is necessary to confirm bilateral tubal occlusion after
hysteroscopic sterilization. The inserts for the hysteroscopic
sterilization system available in the United States are placed
bilaterally into the fallopian tubes and require 3 months
for adequate fibrosis and scarring leading to bilateral tubal
occlusion. After hysteroscopic sterilization, advise the woman
to correctly and consistently use an effective method of
contraception while awaiting confirmation. If compliance
with another method might be a problem, a woman and her
health care provider may consider DMPA injection at the time
of sterilization to ensure adequate contraception for 3 months.
Unlike laparoscopic and abdominal sterilizations, pregnancy
risk beyond 7 years of follow-up has not been studied among
women who received hysteroscopic sterilization.
Pregnancy risk with at least 10 years of follow-up has
been studied among women who received laparoscopic and
abdominal sterilizations (305,306). Although these methods
are highly effective, pregnancies can occur many years after
the procedure, and the risk for pregnancy is higher among
younger women (306,307).

A systematic review was conducted to identify studies that
reported whether pregnancies occurred after hysteroscopic
sterilization (308). Twenty-four studies were identified that
reported whether pregnancies occurred after hysteroscopic
sterilization and found that very few pregnancies occurred
among women with confirmed bilateral tubal occlusion;
however, few studies include long-term follow-up, and
none with follow up for >7 years. Among women who had
successful bilateral placement, most pregnancies that occurred
after hysteroscopic sterilization were in women who did not
have confirmed bilateral tubal occlusion at 3 months, either
because of lack of follow up or misinterpretation of HSG
results (309–311). Some pregnancies occurred within 3 months
of placement, including among women who were already
pregnant at the time of the procedure, women who did not
use alternative contraception, or women who had failures of
alternative contraception (310–315). Although these studies
generally demonstrated high rates of bilateral placement, some
pregnancies occurred as a result of lack of bilateral placement
identified on later imaging (310,311,313–316). Most
pregnancies occurred after deviations from FDA directions,
which include placement in the early follicular phase of the
menstrual cycle, imaging at 3 months to document proper
placement, and use of effective alternative contraception until
documented occlusion (Level of evidence: II-3, fair, direct).

Male Sterilization
Male sterilization, or vasectomy, is one of the few
contraceptive methods available to men and can be performed
in an outpatient procedure or office setting. Fewer than
1 woman out of 100 becomes pregnant in the first year after
her male partner undergoes sterilization (14). Because male
sterilization is intended to be irreversible, all men should be
appropriately counseled about the permanency of sterilization
and the availability of highly effective, long-acting, reversible
methods of contraception for women. Male sterilization does
not protect against STDs; consistent and correct use of male
latex condoms reduces the risk for STDs, including HIV.

When Vasectomy is Reliable for
Contraception
• A semen analysis should be performed 8–16 weeks after
a vasectomy to ensure the procedure was successful.
• The man should be advised that he should use additional
contraceptive protection or abstain from sexual intercourse
until he has confirmation of vasectomy success by
postvasectomy semen analysis.

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Recommendations and Reports

Other Postprocedure Recommendations
• The man should refrain from ejaculation for approximately
1 week after the vasectomy to allow for healing of surgical
sites and, after certain methods of vasectomy, occlusion
of the vas.
Comments and Evidence Summary. The Vasectomy
Guideline Panel of the American Urological Association
performed a systematic review of key issues concerning the
practice of vasectomy (317). All English-language publications
on vasectomy published during 1949–2011 were reviewed. For
more information, see the American Urological Association
Vasectomy Guidelines (https://www.auanet.org/common/pdf/
education/clinical-guidance/Vasectomy.pdf ).
Motile sperm disappear within a few weeks after vasectomy
(318–321). The time to azoospermia varies widely in different
studies; however, by 12 weeks after the vasectomy, 80% of men
have azoospermia, and almost all others have rare nonmotile
sperm (defined as ≤100,000 nonmotile sperm per milliliter)
(317). The number of ejaculations after vasectomy is not a
reliable indicator of when azoospermia or rare nonmotile sperm
will be achieved (317). Once azoospermia or rare nonmotile
sperm has been achieved, patients can rely on the vasectomy for
contraception, although not with 100% certainty. The risk for
pregnancy after a man has achieved postvasectomy azoospermia
is approximately one in 2,000 (322–326).
A median of 78% (range 33%–100%) of men return for
a single postvasectomy semen analysis (317). In the largest
cohorts that appear typical of North American vasectomy
practice, approximately two thirds of men (55%–71%) return
for at least one postvasectomy semen analysis (322,327–331).
Assigning men an appointment after their vasectomy might
improve compliance with follow-up (332).

When Women Can Stop Using
Contraceptives
• Contraceptive protection is still needed for women aged
>44 years if the woman wants to avoid pregnancy.
Comments and Evidence Summary. The age at which a
woman is no longer at risk for pregnancy is not known. Although
uncommon, spontaneous pregnancies occur among women
aged >44 years. Both the American College of Obstetricians
and Gynecologists and the North American Menopause Society
recommend that women continue contraceptive use until
menopause or age 50–55 years (333,334). The median age of
menopause is approximately 51 years in North America (333)

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but can vary from ages 40–60 years (335). The median age
of definitive loss of natural fertility is 41 years but can range
up to age 51 years (336,337). No reliable laboratory tests are
available to confirm definitive loss of fertility in a woman. The
assessment of follicle-stimulating hormone levels to determine
when a woman is no longer fertile might not be accurate (333).
Health care providers should consider the risks for becoming
pregnant in a woman of advanced reproductive age, as well as any
risks of continuing contraception until menopause. Pregnancies
among women of advanced reproductive age are at higher
risk for maternal complications, such as hemorrhage, venous
thromboembolism, and death, and fetal complications, such
as spontaneous abortion, stillbirth, and congenital anomalies
(338–340). Risks associated with continuing contraception,
in particular risks for acute cardiovascular events (venous
thromboembolism, myocardial infarction, or stroke) or breast
cancer, also are important to consider. U.S. MEC states that
on the basis of age alone, women aged >45 years can use POPs,
implants, the LNG-IUD, or the Cu- IUD (U.S. MEC 1) (5).
Women aged >45 years generally can use combined hormonal
contraceptives and DMPA (U.S. MEC 2) (5). However, women
in this age group might have chronic conditions or other risk
factors that might render use of hormonal contraceptive methods
unsafe; U.S. MEC might be helpful in guiding the safe use of
contraceptives in these women.
In two studies, the incidence of venous thromboembolism
was higher among oral contraceptive users aged ≥45 years
compared with younger oral contraceptive users (341–343);
however, an interaction between hormonal contraception
and increased age compared with baseline risk was not
demonstrated (341,342) or was not examined (343). The
relative risk for myocardial infarction was higher among all
oral contraceptive users than in nonusers, although a trend of
increased relative risk with increasing age was not demonstrated
(344,345). No studies were found regarding the risk for stroke
in COC users aged ≥45 years (Level of evidence: II-2, good
to poor, direct).
A pooled analysis by the Collaborative Group on Hormonal
Factors and Breast Cancer in 1996 (346) found small increased
relative risks for breast cancer among women aged ≥45 years
whose last use of combined hormonal contraceptives was
<5 years previously and for those whose last use was 5–9 years
previously. Seven more recent studies suggested small but
nonsignificant increased relative risks for breast carcinoma
in situ or breast cancer among women who had used oral
contraceptives or DMPA when they were aged ≥40 years
compared with those who had never used either method
(347–353) (Level of evidence: II-2, fair, direct).

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Conclusion
Most women can start most contraceptive methods at
any time, and few examinations or tests, if any, are needed
before starting a contraceptive method. Routine follow-up
for most women includes assessment of her satisfaction with
the contraceptive method, concerns about method use, and
changes in health status or medications that could affect
medical eligibility for continued use of the method. Because
changes in bleeding patterns are one of the major reasons
for discontinuation of contraception, recommendations are
provided for the management of bleeding irregularities with
various contraceptive methods. In addition, because women
and health care providers can be confused about the procedures
for missed pills and dosing errors with the contraceptive patch
and ring, the instructions are streamlined for easier use. ECPs
and emergency use of the Cu-IUD are important options for
women, and recommendations on using these methods, as
well as starting regular contraception after use of emergency
contraception, are provided. Male and female sterilization are
highly effective methods of contraception for men, women, and
couples who have completed childbearing; for men undergoing
vasectomy and women undergoing a hysteroscopic sterilization
procedure, additional contraceptive protection is needed until
the success of the procedure can be confirmed.
CDC is committed to working with partners at the federal,
national, and local levels to disseminate, implement, and
evaluate U.S. SPR recommendations so that the information
reaches health care providers. Strategies for dissemination
and implementation include collaborating with other federal
agencies and professional and service organizations to widely
distribute the recommendations through presentations,
electronic distribution, newsletters, and other publications;
development of provider tools and job aids to assist providers
in implementing the new recommendations; and training
activities for students, as well as for continuing education.
CDC conducts surveys of family planning health care providers
to assess attitudes and practices related to contraceptive use.
Results from these surveys will assist CDC in evaluating
the impact of these recommendations on the provision
of contraceptives in the United States. Finally, CDC will
continually monitor new scientific evidence and will update

these recommendations as warranted by new evidence. Updates
to the recommendations, as well as provider tools and other
resources, are available on the CDC U.S. SPR website: http://
www.cdc.gov/reproductivehealth/UnintendedPregnancy/
USSPR.htm.
Acknowledgments
This report is based, in part, on the work of the Promoting Family
Planning Team, Department of Reproductive Health and Research,
World Health Organization, and its development of the Selected
Practice Recommendations for Contraceptive Use, 3rd edition.
U.S. Selected Practice Recommendations for
Contraceptive Use Participants
CDC Guideline Development Group for U.S. Medical Eligibility
Criteria for Contraceptive Use and U.S. Selected Practice
Recommendations for Contraceptive Use
Kathryn M. Curtis, PhD (Chair), Erin Berry-Bibee, MD, Suzanne
G. Folger, PhD, Leah G. Horton, MSPH, Denise J. Jamieson, MD,
Tara C. Jatlaoui, MD, Polly A. Marchbanks, PhD, H. Pamela Pagano,
MPH, Halley E.M. Riley, MPH, Mirelys Rodriguez, Katharine B.
Simmons, MD, Naomi K. Tepper, MD, Maura K. Whiteman, PhD,
Lauren B. Zapata, PhD, CDC, Atlanta, Georgia.
Invited Meeting Participants
August 27–28, 2014, Atlanta, Georgia
Herbert Peterson, MD, University of North Carolina, Chapel
Hill, North Carolina (Chair); Gale Burstein, MD, Erie County
Department of Health, Buffalo, New York; Alison Edelman, MD,
Oregon Health and Science University, Portland, Oregon; Eve Espey,
MD, University of New Mexico, Albuquerque, New Mexico; Emily
Godfrey, MD, University of Washington, Seattle, WA; Andrew
Kaunitz, MD, University of Florida, Jacksonville, Florida; Susan
Moskosky, MS, U.S. Department of Health and Human Services,
Rockville, Maryland; Kavita Nanda, MD, FHI360 and American
College of Obstetricians and Gynecologists, Durham, NC; Deborah
Nucatola, MD, Planned Parenthood Federation of America, New
York, New York; Michael Policar, MD, University of California, San
Francisco, California; Carolyn Westhoff, MD, Columbia University,
New York, New York.
Systematic Review Presenters and Authors
Meeting, August 26–28, 2015, Atlanta, Georgia
Kathryn M. Curtis, PhD, Tara C. Jatlaoui, MD, Polly A.
Marchbanks, PhD, Lauren B. Zapata, PhD, CDC, Atlanta, Georgia;
Nathalie Kapp, MD, HRA Pharma, Paris, France.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

Invited Meeting Participants
August 26–28, 2015, Atlanta, Georgia
Herbert Peterson, MD, University of North Carolina, Chapel
Hill, North Carolina (Chair); Rebecca Allen, MD, American Society
for Reproductive Medicine and Women and Infants Hospital,
Providence, Rhode Island; Abbey Berenson, MD, University of Texas
Medical Branch, Galveston, Texas; Amanda Black, MD, University
of Ottawa, Ontario, Canada; Cora Collette Breuner, MD, American
Academy of Pediatrics and Seattle Children’s Hospital, Seattle,
Washington; Gale Burstein, MD, Erie County Department of
Health, Buffalo, New York; Alicia Christy, MD, National Institutes
of Health, Rockville, Maryland; Mitchell D. Creinin, MD, University
of California, Davis, California; Linda Dominguez, Southwest
Women’s Health, Albuquerque, New Mexico; Alison Edelman,
MD, Oregon Health and Science University, Portland, Oregon; Eve
Espey, MD, University of New Mexico, Albuquerque, New Mexico;
Emily Godfrey, MD, University of Washington, Seattle, WA; Marji
Gold, MD, Albert Einstein College of Medicine, Bronx, New York;
Robert Hatcher, MD, Emory University, Atlanta, Georgia; Mark
Hathaway, MD, JHPIEGO and Unity Healthcare, Washington,
DC; Stephen Heartwell, MD, Susan Thompson Buffett Foundation,
Omaha, Nebraska; Paula Hillard, MD, Stanford University, Palo
Alto, California; Andrew Kaunitz, MD, University of Florida,
Jacksonville, Florida; Reagan McDonald-Mosley, MD, Planned
Parenthood Federation of America, New York, New York; Susan
Moskosky, MS, U.S. Department of Health and Human Services,
Rockville, Maryland; Kavita Nanda, MD, FHI360, Durham,
North Carolina; Jeffrey Peipert, MD, Washington University, St.
Louis, Missouri; Michael Policar, MD, University of California, San
Francisco, California; Sarah Prager, MD, University of Washington,
Seattle Washington; David Soper, MD, Medical University of South
Carolina, Charleston, South Carolina; Lisa Soule, MD, Food and
Drug Administration, Rockville, Maryland; James Trussell, PhD,
Princeton University, Princeton, New Jersey; Carolyn Westhoff,
MD, Columbia University, New York, New York; Christopher
Zahn, MD, American College of Obstetricians and Gynecologists,
Washington, DC.
CDC Attendees
Wanda D. Barfield, MD, Peter Briss, MD, W. Craig Hooper, PhD,
Jill Huppert, MD, Caroline King, PhD, Michele Mandel, Titilope
Oduyebo, MD, Cria Perrine, MD, Sam Posner, PhD.
External Reviewers
Claude Burnett, MD, Northeast Health District, Georgia
Department of Public Health, Athens, Georgia; Carrie Cwiak, MD,
Emory University, Atlanta, Georgia; David Klein, MD, Uniformed
Services University, Bethesda, Maryland; Seema Menon, MD,
Medical College of Wisconsin, Milwaukee, Wisconsin.

MMWR / July 29, 2016 / Vol. 65 / No. 4

Conflicts of Interest for Invited Meeting Participants
August 26–28, 2015, Atlanta, Georgia
Rebecca Allen, Nexplanon trainer for Merck and Liletta trainer for
Actavis, consultant, advisory board, and education grant from Bayer;
Mitchell D. Creinin, Nexplanon trainer for Merck, litigation consultant
for Bayer, advisory board for Merck and Teva Pharmaceutical Industries
Ltd., consultant for Lemonaid — PolkaDoc app, research support
to University of California, Davis from Medicines360, Contramed,
Merck, Eunice Kennedy Shriver National Institute of Child Health
and Human Development, and Society of Family Planning; Linda
Dominguez, speaker for Bayer, Merck, and Actavis; Alison Edelman,
royalties from Up to Date, Inc., consultant for Genzyme, grant support
from National Institutes of Health and Gates Foundation, travel funds
from World Health Organization, grant support and honorarium
from Society of Family Planning, honorarium and travel funds from
Contemporary Forum, trainer for Merck, consultant for Gynuity Health
Projects, honorarium from CDC, Projects In Knowledge, and American
Congress of Obstetricians and Gynecologists, advisory board for Agile
Therapeutics; Eve Espey, travel funds from the American Congress
of Obstetricians and Gynecologists, Society for Family Planning, and
U.S. Food and Drug Administration, Reproductive and Drug Advisory
Committee for U.S. Food and Drug Administration, travel funds
and honoraria from Wayne State University, Telluride Conference,
New Mexico Department of Health Clinician Conference, Planned
Parenthood National Medical Conference and Society of Family
Planning, British Columbia Contraception Access Research Team
Conference, and American Congress of Obstetricians and Gynecologists
annual meeting; Emily Godfrey, research funding from Bayer Women’s
Health, Prima-Temp, and Teva Pharmaceutical Industries Ltd., trainer
for Merck and Upstream USA, grant reviewer for Fellowship of Family
Planning and Society of Family Planning Research Fund; Mark
Hathaway, Liletta trainer and speaker for Actavis and Medicines360,
Nexplanon trainer for Merck, advisory board for Contramed LLC
and Afaxys Pharmaceuticals; Paula Hillard consultant for American
Civil Liberties Union, Advanced Health Media, CMEology, National
Sleep Foundation, and Planned Parenthood Federation of America,
honoraria from National Sleep Foundation, Dignity Health, CMEology,
Advance Health Media, and Medscape, editorial board for Advanstar
— Contemporary OB/GYN, board examiner for the American Board
of Obstetrics and Gynecology, contract reviewer for the Department of
Health and Human Services, editorial board for EBSCO — PEMSoft,
Nexplanon trainer for Merck, scientific advisor to Proctor and Gamble,
publication royalties from Wiley Blackwell Publishing; Nathalie Kapp,
employee of HRA Pharma; Andrew Kaunitz, advisory board participant
of Allergan, Bayer, Merck, and Pfizer, clinical trial funding to University
of Florida from Agile Therapeutics, Bayer, Merck; Jeffrey Peipert, research
funding from Bayer and Teva Pharmaceutical Industries Ltd., advisory
board for Perrigo; Michael Policar, litigation consultant for Bayer; James
Trussell, advisory board for Merck and Teva Pharmaceutical Industries
Ltd., consultant for Bayer; Carolyn Westhoff, data and safety monitoring
board for Merck and Bayer, advisory board for Agile Therapeutics,
MicroChips Biotech, and Actavis, research support to Columbia
University from Medicines360, León Farma, and ContraMed.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Handling Conflict of Interest
To promote transparency, all participants were asked to disclose any
potential conflicts of interest to CDC prior to the expert meeting and
to report any potential conflicts of interest during the introductory
portion of the expert meeting. All potential conflicts of interest are
listed above. No participants were excluded from discussion based
on potential conflicts of interest. One presenter was an employee of a
pharmaceutical company and participated by teleconference; after the
presentation and questions related to the presentation, the presenter
was excused from the discussion. CDC staff who ultimately decided
and developed these recommendations have no financial interests or
other relationships with the manufacturers of commercial products,
suppliers of commercial services, or commercial supporters relevant
to these recommendations.
References
1. Finer LB, Zolna MR. Declines in unintended pregnancy in the United
States, 2008–2011. N Engl J Med 2016;374:843–52. http://dx.doi.
org/10.1056/NEJMsa1506575
2. Gipson JD, Koenig MA, Hindin MJ. The effects of unintended pregnancy on
infant, child, and parental health: a review of the literature. Stud Fam Plann
2008;39:18–38. http://dx.doi.org/10.1111/j.1728-4465.2008.00148.x
3. Sonfield A, Kost K. Public costs from unintended pregnancies and the
role of public insurance programs in paying for pregnancy-related care:
national and state estimates for 2010. New York, NY: The Guttmacher
Institute; 2015.
4. Finer LB, Henshaw SK. Disparities in rates of unintended pregnancy in
the United States, 1994 and 2001. Perspect Sex Reprod Health
2006;38:90–6. http://dx.doi.org/10.1363/3809006
5. CDC. U.S. medical eligibility criteria for contraceptive use, 2016.
MMWR Recomm Rep (No. RR-3);2016.
6. CDC. U.S. selected practice recommendations for contraceptive use,
2013: adapted from the World Health Organization selected practice
recommendations for contraceptive use, 2nd edition. MMWR Recomm
Rep 2013;62(No. RR-5).
7. Mohllajee AP, Curtis KM, Flanagan RG, Rinehart W, Gaffield ML,
Peterson HB. Keeping up with evidence: a new system for WHO’s
evidence-based family planning guidance. Am J Prev Med 2005;28:483–
90. http://dx.doi.org/10.1016/j.amepre.2005.02.008
8. Liberati A, Altman DG, Tetzlaff J, et al. The PRISMA statement for
reporting systematic reviews and meta-analyses of studies that evaluate
health care interventions: explanation and elaboration. J Clin Epidemiol
2009;62:e1–34. http://dx.doi.org/10.1016/j.jclinepi.2009.06.006
9. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred
reporting items for systematic reviews and meta-analyses: the PRISMA
statement. BMJ 2009;339:b2535.
10. Harris RP, Helfand M, Woolf SH, et al; Methods Work Group, Third US
Preventive Services Task Force. Current methods of the U.S. Preventive Services
Task Force: a review of the process. Am J Prev Med 2001;20(Suppl):21–35.
http://dx.doi.org/10.1016/S0749-3797(01)00261-6
11. Horton LG, Folger SG, Berry-Bibee E, Jatlaoui TC, Tepper NK, Curtis
KM. Research gaps from evidence-based contraceptives guidance: the
U.S. Medical Eligibility Criteria for Contraceptive Use, 2016, and the
U.S. Selected Practice Recommendations for Contraceptive Use, 2016.
Contraception. In press 2016.
12. Gavin L, Moskosky S, Carter M, et al. Providing quality family planning
services: Recommendations of CDC and the U.S. Office of Population
Affairs. MMWR Recomm Rep 2014;63(No. RR-4).
13. World Health Organization. Selected practice recommendations for
contraceptive use. 2nd ed. Geneva, Switzerland: WHO Press; 2004.

14. Trussell J. Contraceptive failure in the United States. Contraception
2011;83:397–404. http://dx.doi.org/10.1016/j.contraception.2011.01.021
15. Workowski KA, Bolan GA. Sexually transmitted diseases treatment
guidelines, 2015. MMWR Recomm Rep 2015;64(No. RR-3).
16. Stanback J, Nakintu N, Qureshi Z, Nasution M. Does assessment of
signs and symptoms add to the predictive value of an algorithm to rule
out pregnancy? J Fam Plann Reprod Health Care 2006;32:27–9. http://
dx.doi.org/10.1783/147118906775275370
17. Stanback J, Nanda K, Ramirez Y, Rountree W, Cameron SB. Validation
of a job aid to rule out pregnancy among family planning clients in
Nicaragua. Rev Panam Salud Publica 2008;23:116–8. http://dx.doi.
org/10.1590/S1020-49892008000200007
18. Stanback J, Qureshi Z, Sekadde-Kigondu C, Gonzalez B, Nutley T.
Checklist for ruling out pregnancy among family-planning clients in
primary care. Lancet 1999;354:566. http://dx.doi.org/10.1016/
S0140-6736(99)01578-0
19. Torpey K, Mwenda L, Kabaso M, et al. Excluding pregnancy among women
initiating antiretroviral therapy: efficacy of a family planning job aid. BMC
Public Health 2010;10:249. http://dx.doi.org/10.1186/1471-2458-10-249
20. Cole LA, Ladner DG, Byrn FW. The normal variabilities of the menstrual
cycle. Fertil Steril 2009;91:522–7. http://dx.doi.org/10.1016/j.
fertnstert.2007.11.073
21. Wilcox AJ, Dunson D, Baird DD. The timing of the “fertile window”
in the menstrual cycle: day specific estimates from a prospective study.
BMJ 2000;321:1259–62. http://dx.doi.org/10.1136/bmj.321.7271.1259
22. Donnet ML, Howie PW, Marnie M, Cooper W, Lewis M. Return of
ovarian function following spontaneous abortion. Clin Endocrinol (Oxf )
1990;33:13–20. http://dx.doi.org/10.1111/j.1365-2265.1990.
tb00460.x
23. Lähteenmäki P. Postabortal contraception. Ann Med 1993;25:185–9.
http://dx.doi.org/10.3109/07853899309164166
24. Stoddard A, Eisenberg DL. Controversies in family planning: timing of
ovulation after abortion and the conundrum of postabortion intrauterine
device insertion. Contraception 2011;84:119–21. http://dx.doi.
org/10.1016/j.contraception.2010.12.010
25. Jackson E, Glasier A. Return of ovulation and menses in postpartum
nonlactating women: a systematic review. Obstet Gynecol 2011;117:657–
62. http://dx.doi.org/10.1097/AOG.0b013e31820ce18c
26. Kennedy KI, Rivera R, McNeilly AS. Consensus statement on the use
of breastfeeding as a family planning method. Contraception
1989;39:477–96. http://dx.doi.org/10.1016/0010-7824(89)90103-0
27. Labbok MH, Perez A, Valdes V, et al. The lactational amenorrhea method
(LAM): a postpartum introductory family planning method with policy
and program implications. Adv Contracept 1994;10:93–109. http://
dx.doi.org/10.1007/BF01978103
28. US Food and Drug Administration. 510(k) premarket notification.
Silver Spring, MD; 2015. https://www.accessdata.fda.gov/scripts/cdrh/
cfdocs/cfpmn/pmn.cfm
29. Cervinski MA, Gronowski AM. Reproductive-endocrine point-of-care
testing: current status and limitations. Clin Chem Lab Med
2010;48:935–42. http://dx.doi.org/10.1515/CCLM.2010.183
30. Cole LA. Human chorionic gonadotropin tests. Expert Rev Mol Diagn
2009;9:721–47. http://dx.doi.org/10.1586/erm.09.51
31. Eichner SF, Timpe EM. Urinary-based ovulation and pregnancy: pointof-care testing. Ann Pharmacother 2004;38:325–31. http://dx.doi.
org/10.1345/aph.1D210
32. Wilcox AJ, Baird DD, Dunson D, McChesney R, Weinberg CR. Natural
limits of pregnancy testing in relation to the expected menstrual period.
JAMA 2001;286:1759–61. http://dx.doi.org/10.1001/jama.286.14.1759
33. Korhonen J, Alfthan H, Ylöstalo P, Veldhuis J, Stenman UH.
Disappearance of human chorionic gonadotropin and its alpha- and
beta-subunits after term pregnancy. Clin Chem 1997;43:2155–63.

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Recommendations and Reports

34. Reyes FI, Winter JS, Faiman C. Postpartum disappearance of
chorionic gonadotropin from the maternal and neonatal
circulations. Am J Obstet Gynecol 1985;153:486–9. http://dx.doi.
org/10.1016/0002-9378(85)90458-2
35. Steier JA, Bergsjø P, Myking OL. Human chorionic gonadotropin in
maternal plasma after induced abortion, spontaneous abortion, and
removed ectopic pregnancy. Obstet Gynecol 1984;64:391–4.
36. Bracken MB. Oral contraception and congenital malformations in
offspring: a review and meta-analysis of the prospective studies. Obstet
Gynecol 1990;76:552–7.
37. Gray RH, Pardthaisong T. In utero exposure to steroid contraceptives
and survival during infancy. Am J Epidemiol 1991;134:804–11.
38. Pardthaisong T, Gray RH. In utero exposure to steroid contraceptives
and outcome of pregnancy. Am J Epidemiol 1991;134:795–803.
39. Jaffe B, Harlap S, Baras M, et al. Long-term effects of MPA on human
progeny: intellectual development. Contraception 1988;37:607–19.
http://dx.doi.org/10.1016/0010-7824(88)90007-8
40. Pardthaisong T, Yenchit C, Gray R. The long-term growth and
development of children exposed to Depo-Provera during pregnancy
or lactation. Contraception 1992;45:313–24. http://dx.doi.
org/10.1016/0010-7824(92)90053-V
41. Brahmi D, Steenland MW, Renner RM, Gaffield ME, Curtis
KM. Pregnancy outcomes with an IUD in situ: a systematic
review. Contraception 2012;85:131–9. http://dx.doi.org/10.1016/j.
contraception.2011.06.010
42. Tepper NK, Marchbanks PA, Curtis KM. Use of a checklist to rule out
pregnancy: a systematic review. Contraception 2013;87:661–5. http://
dx.doi.org/10.1016/j.contraception.2012.08.007
43. Whiteman MK, Tyler CP, Folger SG, Gaffield ME, Curtis KM. When
can a woman have an intrauterine device inserted? A systematic review.
Contraception 2013;87:666–73. http://dx.doi.org/10.1016/j.
contraception.2012.08.015
44. Teva Women’s Health Inc. ParaGard T 380a intrauterine copper
contraceptive [Prescribing information]. Sellersville, PA; 2013. http://
paragard.com/Pdf/ParaGard-PI.pdf
45. Bayer HealthCare Pharmaceuticals Inc. Mirena (levonorgestrel-releasing
intrauterine system) [Prescribing information]. Whippany, NJ; 2014.
http://labeling.bayerhealthcare.com/html/products/pi/Mirena_PI. pdf
46. Jatlaoui TC, Simmons KB, Curtis KM. The safety of intrauterine
contraception initiation among women with current asymptomatic
cervical infections or at increased risk of sexually transmitted infections.
Contraception 2016. Epub June 1, 2016. http://dx.doi.org/10.1016/j.
contraception.2016.05.013
47. Avonts D, Sercu M, Heyerick P, Vandermeeren I, Meheus A, Piot P.
Incidence of uncomplicated genital infections in women using oral
contraception or an intrauterine device: a prospective study. Sex Transm Dis
1990;17:23–9. http://dx.doi.org/10.1097/00007435-199017010-00006
48. Birgisson NE, Zhao Q, Secura GM, Madden T, Peipert JF. Positive
testing for Neisseria gonorrhoeae and Chlamydia trachomatis and the
risk of pelvic inflammatory disease in IUD users. J Womens Health
(Larchmt) 2015;24:354–9. http://dx.doi.org/10.1089/jwh.2015.5190
49. Campbell SJ, Cropsey KL, Matthews CA. Intrauterine device use in a
high-risk population: experience from an urban university clinic. Am J
Obstet Gynecol 2007;197: 193.e1–6; discussion 193.e6–7.
50. Cropsey KL, Matthews C, Campbel S, Ivey S, Adawadkar S. Long-term,
reversible contraception use among high-risk women treated in a
university-based gynecology clinic: comparison between IUD and DepoProvera. J Womens Health (Larchmt) 2010;19:349–53. http://dx.doi.
org/10.1089/jwh.2009.1518
51. Farley TMM, Rosenberg MJ, Rowe PJ, Chen JH, Meirik O. Intrauterine
devices and pelvic inflammatory disease: an international perspective. Lancet
1992;339:785–8. http://dx.doi.org/10.1016/0140-6736(92)91904-M
52. Grimes DA, Schulz KF. Antibiotic prophylaxis for intrauterine
contraceptive device insertion. Cochrane Database Syst Rev
2001;(2):CD001327.

MMWR / July 29, 2016 / Vol. 65 / No. 4

53. LeFevre ML; US Preventive Services Task Force. Screening for chlamydia
and gonorrhea: U.S. Preventive Services Task Force recommendation
statement. Ann Intern Med 2014;161:902–10. http://dx.doi.
org/10.7326/M14-1981
54. Mohllajee AP, Curtis KM, Peterson HB. Does insertion and use of an
intrauterine device increase the risk of pelvic inflammatory disease among
women with sexually transmitted infection? A systematic review.
Contraception 2006;73:145–53. http://dx.doi.org/10.1016/j.
contraception.2005.08.007
55. Morrison CS, Turner AN, Jones LB. Highly effective contraception and
acquisition of HIV and other sexually transmitted infections. Best Pract
Res Clin Obstet Gynaecol 2009;23:263–84. http://dx.doi.org/10.1016/j.
bpobgyn.2008.11.004
56. Sufrin CB, Postlethwaite D, Armstrong MA, Merchant M, Wendt JM,
Steinauer JE. Neisseria gonorrhea and Chlamydia trachomatis screening
at intrauterine device insertion and pelvic inflammatory disease. Obstet
Gynecol 2012;120:1314–21.
57. Tepper NK, Steenland MW, Marchbanks PA, Curtis KM. Laboratory
screening prior to initiating contraception: a systematic review.
Contraception 2013;87:645–9. http://dx.doi.org/10.1016/j.
contraception.2012.08.009
58. Tepper NK, Steenland MW, Marchbanks PA, Curtis KM. Hemoglobin
measurement prior to initiating copper intrauterine devices: a systematic
review. Contraception 2013;87:639–44. http://dx.doi.org/10.1016/j.
contraception.2012.08.008
59. Rivera R, Almonte H, Arreola M, et al. The effects of three different
regimens of oral contraceptives and three different intrauterine devices
on the levels of hemoglobin, serum iron and iron binding capacity in
anemic women. Contraception 1983;27:311–27. http://dx.doi.
org/10.1016/0010-7824(83)90009-4
60. Ursin G, Ross RK, Sullivan-Halley J, Hanisch R, Henderson B, Bernstein
L. Use of oral contraceptives and risk of breast cancer in young women.
Breast Cancer Res Treat 1998;50:175–84. http://dx.doi.
org/10.1023/A:1006037823178
61. Hassan EO, el-Husseini M, el-Nahal N. The effect of 1-year use of the
CuT 380A and oral contraceptive pills on hemoglobin and ferritin levels.
Contraception 1999;60:101–5. http://dx.doi.org/10.1016/
S0010-7824(99)00065-7
62. Calzolari E, Guglielmo R, Viola F, Migliore L. Hematological parameters
and iron therapy in women with IUDs. Experimental study [Italian].
Minerva Ginecol 1981;33:355–62.
63. Andersson K, Odlind V, Rybo G. Levonorgestrel-releasing and copperreleasing (Nova T) IUDs during five years of use: a randomized
comparative trial. Contraception 1994;49:56–72. http://dx.doi.
org/10.1016/0010-7824(94)90109-0
64. Andrade AT, Pizarro E, Shaw STJ Jr, Souza JP, Belsey EM, Rowe
PJ; World Health Organization. Consequences of uterine blood
loss caused by various intrauterine contraceptive devices in South
American women. Contraception 1988;38:1–18. http://dx.doi.
org/10.1016/0010-7824(88)90091-1
65. Blum M, Ariel J, Zacharowitch D. Ferritin, a faithful reflection of iron
deficiency in IUD wearers with mild vaginal spotting. Adv Contracept
1991;7:39–42. http://dx.doi.org/10.1007/BF01850717
66. El-sheikha Z, Hamza A, Mahmoud M. Menstrual blood loss of TCu-380
A and TCu-200 B IUDs. Popul Sci 1990;July:55–62.
67. Gallegost AJ, Aznar R, Merino G, Guizer E. Intrauterine devices and
menstrual blood loss. A comparative study of eight devices during the
first six months of use. Contraception 1978;17:153–61. http://dx.doi.
org/10.1016/0010-7824(78)90071-9
68. Gao J, Zeng S, Sun BL, et al. Menstrual blood loss, haemoglobin and
ferritin concentration of Beijing women wearing steel ring, VCu 200,
and TCu 220c IUDs. Contraception 1986;34:559–71. http://dx.doi.
org/10.1016/S0010-7824(86)80012-9

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

69. Goh TH, Hariharan M. Effect of laparoscopic sterilization and
insertion of Multiload Cu 250 and Progestasert IUDs on serum
ferritin levels. Contraception 1983;28:329–36. http://dx.doi.
org/10.1016/0010-7824(83)90034-3
70. Goh TH, Hariharan M, Tan CH. A longitudinal study of serum
iron indices and haemoglobin concentration following copperIUD insertion. Contraception 1980;22:389–95. http://dx.doi.
org/10.1016/0010-7824(80)90024-4
71. Guillebaud J, Bonnar J, Morehead J, Matthews A. Menstrual blood-loss
with intrauterine devices. Lancet 1976;1:387–90. http://dx.doi.
org/10.1016/S0140-6736(76)90216-6
72. Haugan T, Skjeldestad FE, Halvorsen LE, Kahn H. A randomized trial
on the clinical performance of Nova T380 and Gyne T380 Slimline
copper IUDs. Contraception 2007;75:171–6. http://dx.doi.
org/10.1016/j.contraception.2006.09.005
73. Kivijärvi A, Timonen H, Rajamäki A, Grönroos M. Iron deficiency in
women using modern copper intrauterine devices. Obstet Gynecol
1986;67:95–8.
74. Larsson B, Hamberger L, Rybo G. Influence of copper intrauterine
contraceptive devices (Cu-7-IUD) on the menstrual blood-loss. Acta
Obstet Gynecol Scand 1975;54:315–8. http://dx.doi.
org/10.3109/00016347509156760
75. Larsson G, Milsom I, Jonasson K, Lindstedt G, Rybo G. The long-term
effects of copper surface area on menstrual blood loss and iron status in
women fitted with an IUD. Contraception 1993;48:471–80. http://
dx.doi.org/10.1016/0010-7824(93)90136-U
76. Malmqvist R, Petersohn L, Bengtsson LP. Menstrual bleeding with
copper-covered intrauterine contraceptive devices. Contraception
1974;9:627–33. http://dx.doi.org/10.1016/0010-7824(74)90048-1
77. Milsom I, Rybo G, Lindstedt G. The influence of copper surface
area on menstrual blood loss and iron status in women fitted
with an IUD. Contraception 1990;41:271–81. http://dx.doi.
org/10.1016/0010-7824(90)90068-7
78. Piedras J, Córdova MS, Pérez-Toral MC, Lince E, Garza-Flores J.
Predictive value of serum ferritin in anemia development after insertion
of T Cu 220 intrauterine device. Contraception 1983;27:289–97. http://
dx.doi.org/10.1016/0010-7824(83)90007-0
79. Sivin I, Alvarez F, Diaz J, et al. Intrauterine contraception with copper
and with levonorgestrel: a randomized study of the TCu 380Ag and
levonorgestrel 20 mcg/day devices. Contraception 1984;30:443–56.
http://dx.doi.org/10.1016/0010-7824(84)90036-2
80. Sivin I, Stern J, Diaz J, et al. Two years of intrauterine contraception
with levonorgestrel and with copper: a randomized comparison of the
TCu 380Ag and levonorgestrel 20 mcg/day devices. Contraception
1987;35:245–55. http://dx.doi.org/10.1016/0010-7824(87)90026-6
81. Tchai BS, Kim SW, Han JH, Im MW. Menstrual blood loss, iron
nutriture, and the effects of Alza-T IPCS 52, T-Cu 220C and Lippes
Loop D in Korean women. Seoul J Med 1987;28:51–9.
82. Wright EA, Kapu MM, Isichei UP. Zinc depletion and menorrhagia in
Nigerians using copper T-200 intrauterine device. Trace Elem Med
1989;6:147–9.
83. Milsom I, Andersson K, Jonasson K, Lindstedt G, Rybo G. The
influence of the Gyne-T 380S IUD on menstrual blood loss
and iron status. Contraception 1995;52:175–9. http://dx.doi.
org/10.1016/0010-7824(95)00163-5
84. CDC. Safe motherhood at a glance: Hyattsville, MD: CDC; 2015.
http://www.cdc.gov/chronicdisease/resources/publications/aag/
pdf/2015/safe-motherhood-aag-2015.pdf
85. Cox S, Dietz P, Bowman B, Posner S. Prevalence of chronic conditions
among women of reproductive age. Third National Summit on
Preconception Health and Health Care: Tampa, FL; 2011.
86. Berenson AB, Rahman M, Wilkinson G. Effect of injectable and oral
contraceptives on serum lipids. Obstet Gynecol 2009;114:786–94.
http://dx.doi.org/10.1097/AOG.0b013e3181b76bea

87. Dilbaz B, Ozdegirmenci O, Caliskan E, Dilbaz S, Haberal A. Effect
of etonogestrel implant on serum lipids, liver function tests and
hemoglobin levels. Contraception 2010;81:510–4. http://dx.doi.
org/10.1016/j.contraception.2010.01.014
88. Nelson AL, Cwiak C. Combined oral contraceptives. In: Hatcher RA,
Trussel J, Nelson A, Cates W Jr, Kowal D, Policar M, editors.
Contraceptive technology. 20th ed. New York, NY: Ardent Media;
2011:249–342.
89. Dragoman M, Curtis KM, Gaffield ME. Combined hormonal
contraceptive use among women with known dyslipidemias: a
systematic review of critical safety outcomes. Contraception
2015;S0010-7824(15)00509-0.
90. US Department of Health and Human Services. Summary health
statistics for U.S. adults: National Health Interview Survey, 2012.
Report No. 0083–1972. Hyattsville, MD: US Department of Health
and Human Services; 2014.
91. CDC. Surveillance for viral hepatitis—United States, 2013. Atlanta, GA:
CDC; 2013. http://www.cdc.gov/hepatitis/statistics/2013surveillance/
index.htm
92. Kohler BA, Sherman RL, Howlader N, et al. Annual report to the
nation on the status of cancer, 1975-2011, featuring incidence of breast
cancer subtypes by race/ethnicity, poverty, and state. J Natl Cancer Inst
2015;107:djv048. http://dx.doi.org/10.1093/jnci/djv048
93. Kapp N, Tilley IB, Curtis KM. The effects of hormonal contraceptive
use among women with viral hepatitis or cirrhosis of the liver: a
systematic review. Contraception 2009;80:381–6. http://dx.doi.
org/10.1016/j.contraception.2009.04.007
94. Kapp N, Curtis KM. Hormonal contraceptive use among women with
liver tumors: a systematic review. Contraception 2009;80:387–90.
http://dx.doi.org/10.1016/j.contraception.2009.01.021
95. Tepper NK, Curtis KM, Steenland MW, Marchbanks PA. Physical
examination prior to initiating hormonal contraception: a systematic
review. Contraception 2013;87:650–4. http://dx.doi.org/10.1016/j.
contraception.2012.08.010
96. National Cancer Institute. SEER Fast Stats. Washington DC:
Surveillance Research Program, National Cancer Institute; 2015. http://
seer.cancer.gov/faststats
97. Watson M, Saraiya M, Benard V, et al. Burden of cervical cancer in the
United States, 1998–2003. Cancer 2008;113(Suppl):2855–64. http://
dx.doi.org/10.1002/cncr.23756
98. National Center for Health Statistics, CDC. Health, United States,
2014: with special feature on adults. Hyattsville, MD: CDC; 2015.
99. European Study Group on Heterosexual Transmission of HIV.
Comparison of female to male and male to female transmission of HIV
in 563 stable couples. BMJ 1992;304:809–13. http://dx.doi.
org/10.1136/bmj.304.6830.809
100. Coleman JS, Mwachari C, Balkus J, et al. Effect of the levonorgestrel
intrauterine device on genital HIV-1 RNA shedding among HIV-1infected women not taking antiretroviral therapy in Nairobi, Kenya. J
Acquir Immune Defic Syndr 2013;63:245–8. http://dx.doi.
org/10.1097/QAI.0b013e31828decf8
101. Haddad LB, Cwiak C, Jamieson DJ, et al. Contraceptive adherence
among HIV-infected women in Malawi: a randomized controlled trial
of the copper intrauterine device and depot medroxyprogesterone
acetate. Contraception 2013;88:737–43. http://dx.doi.org/10.1016/j.
contraception.2013.08.006

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102. Heikinheimo O, Lehtovirta P, Aho I, Ristola M, Paavonen J. The
levonorgestrel-releasing intrauterine system in human immunodeficiency
virus-infected women: a 5-year follow-up study. Am J Obstet Gynecol
2011;204:126 e1–4.
103. Heikinheimo O, Lehtovirta P, Suni J, Paavonen J. The levonorgestrelreleasing intrauterine system (LNG-IUS) in HIV-infected women—
effects on bleeding patterns, ovarian function and genital shedding of
HIV. Hum Reprod 2006;21:2857–61. http://dx.doi.org/10.1093/
humrep/del264
104. Kakaire O, Byamugisha JK, Tumwesigye NM, Gemzell-Danielsson K.
Clinical versus laboratory screening for sexually transmitted infections
prior to insertion of intrauterine contraception among women living
with HIV/AIDS: a randomized controlled trial. Hum Reprod
2015;30:1573–9. http://dx.doi.org/10.1093/humrep/dev109
105. Kovacs A, Wasserman SS, Burns D, et al; DATRI Study Group; WIHS
Study Group. Determinants of HIV-1 shedding in the genital tract of
women. Lancet 2001;358:1593–601. http://dx.doi.org/10.1016/
S0140-6736(01)06653-3
106. Landolt NK, Phanuphak N, Teeratakulpisarn N, et al. Uptake and
continuous use of copper intrauterine device in a cohort of HIV-positive
women. AIDS Care 2013;25:710–4. http://dx.doi.org/10.1080/0954
0121.2012.752786
107. Lehtovirta P, Paavonen J, Heikinheimo O. Experience with the
levonorgestrel-releasing intrauterine system among HIV-infected
women. Contraception 2007;75:37–9. http://dx.doi.org/10.1016/j.
contraception.2006.09.006
108. Morrison CS, Sekadde-Kigondu C, Sinei SK, Weiner DH, Kwok C,
Kokonya D. Is the intrauterine device appropriate contraception for
HIV-1-infected women? BJOG 2001;108:784–90. http://dx.doi.
org/10.1111/j.1471-0528.2001.00204.x
109. Mostad SB, Overbaugh J, DeVange DM, et al. Hormonal contraception,
vitamin A deficiency, and other risk factors for shedding of HIV-1
infected cells from the cervix and vagina. Lancet 1997;350:922–7.
http://dx.doi.org/10.1016/S0140-6736(97)04240-2
110. Richardson BA, Morrison CS, Sekadde-Kigondu C, et al. Effect of intrauterine
device use on cervical shedding of HIV-1 DNA. AIDS 1999;13:2091–7.
http://dx.doi.org/10.1097/00002030-199910220-00012
111. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D.
Complications of use of intrauterine devices among HIV-1-infected
women. Lancet 1998;351:1238–41. http://dx.doi.org/10.1016/
S0140-6736(97)10319-1
112. Stringer EM, Kaseba C, Levy J, Sinkala M, Goldenberg RL, Chi BH,
et al. A randomized trial of the intrauterine contraceptive device vs
hormonal contraception in women who are infected with the human
immunodeficiency virus. Am J Obstet Gynecol 2007;197:144 e1–8.
113. Stringer EM, Levy J, Sinkala M, et al. HIV disease progression by
hormonal contraceptive method: secondary analysis of a randomized
trial. AIDS 2009;23:1377–82. http://dx.doi.org/10.1097/
QAD.0b013e32832cbca8
114. Tepper NK, Curtis KM, Nanda K, Jamieson DJ. Safety of intrauterine devices
among women with HIV: a systematic review. Contraception 2016. Epub
June 22, 2016. http://dx.doi.org/10.1016/j.contraception.2016.06.011
115. Lopez LM, Bernholc A, Zeng Y, et al. Interventions for pain with
intrauterine device insertion. Cochrane Database Syst Rev
2015;7:CD007373.
116. Zapata LB, Jatlaoui TC, Marchbanks PA, Curtis KM. Medications to ease
intrauterine device insertion: a systematic review. Contraception 2016. Epub
June 29, 2016. http://dx.doi.org/10.1016/j.contraception.2016.06.014

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117. Bahamondes MV, Espejo-Arce X, Bahamondes L. Effect of vaginal
administration of misoprostol before intrauterine contraceptive
insertion following previous insertion failure: a double blind RCT.
Hum Reprod 2015;30:1861–6. http://dx.doi.org/10.1093/humrep/
dev137
118. Cirik D, Taskin E, Tuglu A, Ortac A, Dai O. Paracervical block with
1% lidocaine for pain control during intrauterine device insertion: a
prospective, single-blinded, controlled study. Int J Reprod Contracept
Obstet Gynecol 2013;2:263–7.
119. Mody SK, Kiley J, Rademaker A, Gawron L, Stika C, Hammond C.
Pain control for intrauterine device insertion: a randomized trial of 1%
lidocaine paracervical block. Contraception 2012;86:704–9. http://
dx.doi.org/10.1016/j.contraception.2012.06.004
120. Grimes DA, Schulz KF. Prophylactic antibiotics for intrauterine device
insertion: a metaanalysis of the randomized controlled trials.
Contraception 1999;60:57–63. http://dx.doi.org/10.1016/
S0010-7824(99)00071-2
121. Wilson W, Taubert KA, Gewitz M, et al; American Heart Association
Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee;
American Heart Association Council on Cardiovascular Disease in the
Young; American Heart Association Council on Clinical Cardiology;
American Heart Association Council on Cardiovascular Surgery and
Anesthesia; Quality of Care and Outcomes Research Interdisciplinary
Working Group. Prevention of infective endocarditis: guidelines from
the American Heart Association: a guideline from the American Heart
Association Rheumatic Fever, Endocarditis, and Kawasaki Disease
Committee, Council on Cardiovascular Disease in the Young, and the
Council on Clinical Cardiology, Council on Cardiovascular Surgery
and Anesthesia, and the Quality of Care and Outcomes Research
Interdisciplinary Working Group. Circulation 2007;116:1736–54.
http://dx.doi.org/10.1161/CIRCULATIONAHA.106.183095
122. Steenland MW, Zapata LB, Brahmi D, Marchbanks PA, Curtis KM.
The effect of follow-up visits or contacts after contraceptive initiation
on method continuation and correct use. Contraception 2013;87:625–
30. http://dx.doi.org/10.1016/j.contraception.2012.09.018
123. Steenland MW, Zapata LB, Brahmi D, Marchbanks PA, Curtis
KM. Appropriate follow up to detect potential adverse events after
initiation of select contraceptive methods: a systematic review.
Contraception 2013;87:611–24. http://dx.doi.org/10.1016/j.
contraception.2012.09.017
124. Canto De Cetina TE, Canto P, Ordoñez Luna M. Effect of counseling
to improve compliance in Mexican women receiving depotmedroxyprogesterone acetate. Contraception 2001;63:143–6. http://
dx.doi.org/10.1016/S0010-7824(01)00181-0
125. Lei ZW, Wu SC, Garceau RJ, et al. Effect of pretreatment
counseling on discontinuation rates in Chinese women given depomedroxyprogesterone acetate for contraception. Contraception
1996;53:357–61. http://dx.doi.org/10.1016/0010-7824(96)00085-6
126. Godfrey EM, Folger SG, Jeng G, Jamieson DJ, Curtis KM. Treatment
of bleeding irregularities in women with copper-containing IUDs: a
systematic review. Contraception 2013;87:549–66. http://dx.doi.
org/10.1016/j.contraception.2012.09.006
127. Toppozada M, Anwar M, Abdel Rahman H, Gaweesh S. Control of
IUD-induced bleeding by three non-steroidal anti-inflammatory drugs.
Contracept Deliv Syst 1982;3:117–25.
128. Toppozada M, El-Attar A, El-Ayyat MA, Khamis Y. Management of
uterine bleeding by PGs or their synthesis inhibitors. Adv Prostaglandin
Thromboxane Res 1980;8:1459–63.

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Recommendations and Reports

129. Wu S, Wang C, Cheng W, et al. Randomized multi-center study of
baofuxin for treatment of bleeding side-effect induced by IUD. Reprod
Contracept 2000;11:152–7.
130. Mercorio F, De Simone R, Di Carlo C, et al. Effectiveness and
mechanism of action of desmopressin in the treatment of copper
intrauterine device-related menorrhagia: a pilot study. Hum Reprod
2003;18:2319–22. http://dx.doi.org/10.1093/humrep/deg449
131. Pedron N, Lozano M, Aznar R. Treatment of hypermenorrhea with
mefenamic acid in women using IUDs. Contracept Deliv Syst
1982;3:135–9.
132. Pizarro E, Mehech G, Hidalgo M, Muñoz G, Romero C. Effect of
meclofenamic acid on menstruation in hypermenorrheic women using
intrauterine devices [Spanish]. Rev Chil Obstet Ginecol
1988;53:43–56.
133. Chinese National IUD Research Working Group. Prevention and
treatment of IUD-induced menorrhagia with antifibrinolytic and
antiprostaglandin drugs [Chinese]. Zhonghua Fu Chan Ke Za Zhi
1987;22:291–4, 312.
134. Di Lieto A, Catalano D, Miranda L, Paladini A. Action of a
prostaglandin synthetase inhibitor on IUD associated uterine bleeding.
Clin Exp Obstet Gynecol 1987;14:41–4.
135. Ylikorkala O, Viinikka L. Comparison between antifibrinolytic
and antiprostaglandin treatment in the reduction of increased
menstrual blood loss in women with intrauterine contraceptive
devices. Br J Obstet Gynaecol 1983;90:78–83. http://dx.doi.
org/10.1111/j.1471-0528.1983.tb06751.x
136. US Food and Drug Administration. Cyklokapron: tranexamic acid
injection [Prescribing information]. New York, NY; 2011.
137. US Food and Drug Administration. Lysteda: tranexamic acid tablets
[Prescribing information]. Parsippany; NJ. 2011.
138. Pedrón N, Lozano M, Gallegos AJ. The effect of acetylsalicylic
acid on menstrual blood loss in women with IUDs. Contraception
1987;36:295–303. http://dx.doi.org/10.1016/0010-7824(87)90099-0
139. Hidalgo M, Bahamondes L, Perrotti M, Diaz J, Dantas-Monteiro C,
Petta C. Bleeding patterns and clinical performance of the
levonorgestrel-releasing intrauterine system (Mirena) up to two years.
Contraception 2002;65:129–32. http://dx.doi.org/10.1016/
S0010-7824(01)00302-X
140. Tepper NK, Steenland MW, Gaffield ME, Marchbanks PA, Curtis
KM. Retention of intrauterine devices in women who acquire pelvic
inflammatory disease: a systematic review. Contraception 2013;87:655–
60. http://dx.doi.org/10.1016/j.contraception.2012.08.011
141. Larsson B, Wennergren M. Investigation of a copper-intrauterine device
(Cu-IUD) for possible effect on frequency and healing of pelvic
inflammatory disease. Contraception 1977;15:143–9. http://dx.doi.
org/10.1016/0010-7824(77)90012-9
142. Söderberg G, Lindgren S. Influence of an intrauterine device on the
course of an acute salpingitis. Contraception 1981;24:137–43. http://
dx.doi.org/10.1016/0010-7824(81)90086-X
143. Teisala K. Removal of an intrauterine device and the treatment of acute
pelvic inflammatory disease. Ann Med 1989;21:63–5. http://dx.doi.
org/10.3109/07853898909149184
144. Altunyurt S, Demir N, Posaci C. A randomized controlled trial of coil
removal prior to treatment of pelvic inflammatory disease. Eur J Obstet
Gynecol Reprod Biol 2003;107:81–4. http://dx.doi.org/10.1016/
S0301-2115(02)00342-1

145. Stewart FH, Harper CC, Ellertson CE, Grimes DA, Sawaya GF, Trussell
J. Clinical breast and pelvic examination requirements for hormonal
contraception: current practice vs evidence. JAMA 2001;285:2232–9.
http://dx.doi.org/10.1001/jama.285.17.2232
146. Mansour D, Korver T, Marintcheva-Petrova M, Fraser IS. The effects
of Implanon on menstrual bleeding patterns. Eur J Contracept
Reprod Health Care 2008;13(Suppl 1):13–28. http://dx.doi.
org/10.1080/13625180801959931
147. Abdel-Aleem H, d’Arcangues C, Vogelsong K, Gülmezoglu AM.
Treatment of vaginal bleeding irregularities induced by progestin only
contraceptives. Cochrane Database Syst Rev 2007;(2):CD003449.
148. Archer DF, Philput CB, Levine AS, et al. Effects of ethinyl estradiol
and ibuprofen compared to placebo on endometrial bleeding, cervical
mucus and the postcoital test in levonorgestrel subcutaneous implant
users. Contraception 2008;78:106–12. http://dx.doi.org/10.1016/j.
contraception.2008.04.003
149. Buasang K, Taneepanichskul S. Efficacy of celecoxib on controlling
irregular uterine bleeding secondary to Jadelle use. J Med Assoc Thai
2009;92:301–7.
150. Phaliwong P, Taneepanichskul S. The effect of mefenamic acid on
controlling irregular uterine bleeding second to Implanon use. J Med
Assoc Thai 2004;87(Suppl 3):S64–8.
151. Weisberg E, Hickey M, Palmer D, et al. A randomized controlled trial
of treatment options for troublesome uterine bleeding in Implanon
users. Hum Reprod 2009;24:1852–61. http://dx.doi.org/10.1093/
humrep/dep081
152. Weisberg E, Hickey M, Palmer D, et al. A pilot study to assess the
effect of three short-term treatments on frequent and/or prolonged
bleeding compared to placebo in women using Implanon. Hum Reprod
2006;21:295–302. http://dx.doi.org/10.1093/humrep/dei273
153. Cheng L, Zhu H, Wang A, Ren F, Chen J, Glasier A. Once a month
administration of mifepristone improves bleeding patterns in women using
subdermal contraceptive implants releasing levonorgestrel. Hum Reprod
2000;15:1969–72. http://dx.doi.org/10.1093/humrep/15.9.1969
154. Alvarez-Sanchez F, Brache V, Thevenin F, Cochon L, Faundes A.
Hormonal treatment for bleeding irregularities in Norplant implant
users. Am J Obstet Gynecol 1996;174:919–22. http://dx.doi.
org/10.1016/S0002-9378(96)70326-5
155. Díaz S, Croxatto HB, Pavez M, Belhadj H, Stern J, Sivin I. Clinical
assessment of treatments for prolonged bleeding in users of Norplant
implants. Contraception 1990;42:97–109. http://dx.doi.
org/10.1016/0010-7824(90)90094-C
156. Witjaksono J, Lau TM, Affandi B, Rogers PA. Oestrogen treatment
for increased bleeding in Norplant users: preliminary results. Hum
Reprod 1996;11(Suppl 2):109–14. http://dx.doi.org/10.1093/
humrep/11.suppl_2.109
157. Abdel-Aleem H, Shaaban OM, Amin AF, Abdel-Aleem AM. Tamoxifen
treatment of bleeding irregularities associated with Norplant use.
Contraception 2005;72:432–7. http://dx.doi.org/10.1016/j.
contraception.2005.05.015
158. Phupong V, Sophonsritsuk A, Taneepanichskul S. The effect of
tranexamic acid for treatment of irregular uterine bleeding secondary
to Norplant use. Contraception 2006;73:253–6. http://dx.doi.
org/10.1016/j.contraception.2005.09.012
159. d’Arcangues C, Piaggio G, Brache V, et al; Study Group on Progestogeninduced Vaginal Bleeding Disturbances. Effectiveness and acceptability
of vitamin E and low-dose aspirin, alone or in combination, on
Norplant-induced prolonged bleeding. Contraception 2004;70:451–
62. http://dx.doi.org/10.1016/j.contraception.2004.05.012

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160. Subakir SB, Setiadi E, Affandi B, Pringgoutomo S, Freisleben HJ.
Benefits of vitamin E supplementation to Norplant users—in vitro and
in vivo studies. Toxicology 2000;148:173–8. http://dx.doi.org/10.1016/
S0300-483X(00)00208-0
161. Kapp N, Gaffield ME. Initiation of progestogen-only injectables on
different days of the menstrual cycle and its effect on contraceptive
effectiveness and compliance: a systematic review. Contraception
2013;87:576–82. http://dx.doi.org/10.1016/j.contraception.2012.08.017
162. Petta CA, Faúndes A, Dunson TR, et al. Timing of onset of
contraceptive effectiveness in Depo-Provera users. II. Effects on ovarian
function. Fertil Steril 1998;70:817–20. http://dx.doi.org/10.1016/
S0015-0282(98)00309-4
163. Petta CA, Faundes A, Dunson TR, et al. Timing of onset of
contraceptive effectiveness in Depo-Provera users: Part I. Changes in
cervical mucus. Fertil Steril 1998;69:252–7. http://dx.doi.org/10.1016/
S0015-0282(97)00477-9
164. Siriwongse T, Snidvongs W, Tantayaporn P, Leepipatpaiboon S. Effect
of depo-medroxyprogesterone acetate on serum progesterone levels
when administered on various cycle days. Contraception 1982;26:487–
93. http://dx.doi.org/10.1016/0010-7824(82)90147-0
165. Balkus J, Miller L. Same-day administration of depot-medroxyprogesterone
acetate injection: a retrospective chart review. Contraception
2005;71:395–8. http://dx.doi.org/10.1016/j.contraception.2004.10.014
166. Morroni C, Grams M, Tiezzi L, Westhoff C. Immediate monthly
combination contraception to facilitate initiation of the depot
medroxyprogesterone acetate contraceptive injection. Contraception
2004;70:19–23. http://dx.doi.org/10.1016/j.contraception.2004.02.007
167. Nelson AL, Katz T. Initiation and continuation rates seen in 2-year
experience with Same Day injections of DMPA. Contraception
2007;75:84–7. http://dx.doi.org/10.1016/j.contraception.2006.09.007
168. Rickert VI, Tiezzi L, Lipshutz J, León J, Vaughan RD, Westhoff C.
Depo Now: preventing unintended pregnancies among adolescents
and young adults. J Adolesc Health 2007;40:22–8. http://dx.doi.
org/10.1016/j.jadohealth.2006.10.018
169. Sneed R, Westhoff C, Morroni C, Tiezzi L. A prospective study of
immediate initiation of depo medroxyprogesterone acetate contraceptive
injection. Contraception 2005;71:99–103. http://dx.doi.org/10.1016/j.
contraception.2004.08.014
170. Tepper NK, Curtis KM, Steenland MW, Marchbanks PA. Blood
pressure measurement prior to initiating hormonal contraception: a
systematic review. Contraception 2013;87:631–8. http://dx.doi.
org/10.1016/j.contraception.2012.08.025
171. Diab KM, Zaki MM. Contraception in diabetic women: comparative
metabolic study of Norplant, depot medroxyprogesterone acetate, low dose
oral contraceptive pill and CuT380A. J Obstet Gynaecol Res 2000;26:17–
26. http://dx.doi.org/10.1111/j.1447-0756.2000.tb01195.x
172. Garg SK, Chase HP, Marshall G, Hoops SL, Holmes DL, Jackson WE.
Oral contraceptives and renal and retinal complications in young women
with insulin-dependent diabetes mellitus. JAMA 1994;271:1099–102.
http://dx.doi.org/10.1001/jama.1994.03510380055037
173. Grigoryan OR, Grodnitskaya EE, Andreeva EN, Chebotnikova TV,
Melnichenko GA. Use of the NuvaRing hormone-releasing system in late
reproductive-age women with type 1 diabetes mellitus. Gynecol Endocrinol
2008;24:99–104. http://dx.doi.org/10.1080/09513590701708795
174. Kahn HS, Curtis KM, Marchbanks PA. Effects of injectable or
implantable progestin-only contraceptives on insulin-glucose
metabolism and diabetes risk. Diabetes Care 2003;26:216–25. http://
dx.doi.org/10.2337/diacare.26.1.216

MMWR / July 29, 2016 / Vol. 65 / No. 4

175. Lopez LM, Grimes DA, Schulz KF. Steroidal contraceptives: effect on
carbohydrate metabolism in women without diabetes mellitus.
Cochrane Database Syst Rev 2009; (4):CD006133.
176. Rogovskaya S, Rivera R, Grimes DA, et al. Effect of a levonorgestrel
intrauterine system on women with type 1 diabetes: a randomized trial.
Obstet Gynecol 2005;105:811–5. http://dx.doi.org/10.1097/01.
AOG.0000156301.11939.56
177. Troisi RJ, Cowie CC, Harris MI. Oral contraceptive use and glucose
metabolism in a national sample of women in the United States. Am J Obstet
Gynecol 2000;183:389–95. http://dx.doi.org/10.1067/mob.2000.105909
178. Bonny AE, Secic M, Cromer B. Early weight gain related to later weight
gain in adolescents on depot medroxyprogesterone acetate. Obstet Gynecol
2011;117:793–7. http://dx.doi.org/10.1097/AOG.0b013e31820f387c
179. Le YC, Rahman M, Berenson AB. Early weight gain predicting later weight
gain among depot medroxyprogesterone acetate users. Obstet Gynecol
2009;114:279–84. http://dx.doi.org/10.1097/AOG.0b013e3181af68b2
180. Risser WL, Gefter LR, Barratt MS, Risser JM. Weight change in
adolescents who used hormonal contraception. J Adolesc Health
1999;24:433–6. http://dx.doi.org/10.1016/S1054-139X(98)00151-7
181. Paulen ME, Curtis KM. When can a woman have repeat progestogenonly injectables—depot medroxyprogesterone acetate or norethisterone
enantate? Contraception 2009;80:391–408. http://dx.doi.
org/10.1016/j.contraception.2009.03.023
182. Pardthaisong T. Return of fertility after use of the injectable
contraceptive Depo Provera: up-dated data analysis. J Biosoc Sci
1984;16:23–34. http://dx.doi.org/10.1017/S0021932000014760
183. Schwallie PC, Assenzo JR. The effect of depo-medroxyprogesterone
acetate on pituitary and ovarian function, and the return of fertility
following its discontinuation: a review. Contraception 1974;10:181–
202. http://dx.doi.org/10.1016/0010-7824(74)90073-0
184. Steiner MJ, Kwok C, Stanback J, et al. Injectable contraception:
what should the longest interval be for reinjections? Contraception
2008;77:410–4. http://dx.doi.org/10.1016/j.contraception.2008.01.017
185. Bassol S, Garza-Flores J, Cravioto MC, et al. Ovarian function following
a single administration of depo-medroxyprogesterone acetate (DMPA)
at different doses. Fertil Steril 1984;42:216–22.
186. Fotherby K, Koetsawang S, Mathrubutham M. Pharmacokinetic study
of different doses of Depo Provera. Contraception 1980;22:527–36.
http://dx.doi.org/10.1016/0010-7824(80)90105-5
187. Fotherby K, Saxena BN, Shrimanker K, et al. A preliminary
pharmacokinetic and pharmacodynamic evaluation of depotmedroxyprogesterone acetate and norethisterone oenanthate. Fertil
Steril 1980;34:131–9.
188. Garza-Flores J, Cardenas S, Rodríguez V, Cravioto MC, Diaz-Sanchez
V, Perez-Palacios G. Return to ovulation following the use of long-acting
injectable contraceptives: a comparative study. Contraception
1985;31:361–6. http://dx.doi.org/10.1016/0010-7824(85)90004-6
189. Jain J, Dutton C, Nicosia A, Wajszczuk C, Bode FR, Mishell DR Jr.
Pharmacokinetics, ovulation suppression and return to ovulation
following a lower dose subcutaneous formulation of Depo-Provera.
Contraception 2004;70:11–8. http://dx.doi.org/10.1016/j.
contraception.2004.01.011
190. Lan PT, Aedo AR, Landgren BM, Johannisson E, Diczfalusy E. Return
of ovulation following a single injection of depo-medroxyprogesterone
acetate: a pharmacokinetic and pharmacodynamic study. Contraception
1984;29:1–18. http://dx.doi.org/10.1016/0010-7824(84)90054-4

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

191. Ortiz A, Hirol M, Stanczyk FZ, Goebelsmann U, Mishell DR Jr. Serum
medroxyprogesterone acetate (MPA) concentrations and ovarian function
following intramuscular injection of depo-MPA. J Clin Endocrinol Metab
1977;44:32–8. http://dx.doi.org/10.1210/jcem-44-1-32
192. Saxena BN, Dusitsin N, Tankeyoon M, Chaudhury RR. Return of
ovulation after the cessation of depot-medroxy progesterone acetate
treatment in Thai women. J Med Assoc Thai 1980;63:66–9.
193. Toh YC, Jain J, Rahnny MH, Bode FR, Ross D. Suppression of
ovulation by a new subcutaneous depot medroxyprogesterone
acetate (104 mg/0. 65 mL) contraceptive formulation in Asian
women. Clin Ther 2004;26:1845–54. http://dx.doi.org/10.1016/j.
clinthera.2004.11.013
194. Arias RD, Jain JK, Brucker C, Ross D, Ray A. Changes in bleeding
patterns with depot medroxyprogesterone acetate subcutaneous
injection 104 mg. Contraception 2006;74:234–8. http://dx.doi.
org/10.1016/j.contraception.2006.03.008
195. Dempsey A, Roca C, Westhoff C. Vaginal estrogen supplementation during
Depo-Provera initiation: a randomized controlled trial. Contraception
2010;82:250–5. http://dx.doi.org/10.1016/j.contraception.2010.04.003
196. Abdel-Aleem H, d’Arcangues C, Vogelsong KM, Gülmezoglu AM.
Treatment of vaginal bleeding irregularities induced by progestin only
contraceptives. Cochrane Database Syst Rev 2007; (4):CD003449.
197. Harel Z, Biro F, Kollar L, Riggs S, Flanagan P, Vaz R. Supplementation
with vitamin C and/or vitamin B(6) in the prevention of Depo-Provera
side effects in adolescents. J Pediatr Adolesc Gynecol 2002;15:153–8.
http://dx.doi.org/10.1016/S1083-3188(02)00148-1
198. Nathirojanakun P, Taneepanichskul S, Sappakitkumjorn N. Efficacy
of a selective COX-2 inhibitor for controlling irregular uterine bleeding
in DMPA users. Contraception 2006;73:584–7. http://dx.doi.
org/10.1016/j.contraception.2005.09.013
199. Tantiwattanakul P, Taneepanichskul S. Effect of mefenamic acid on
controlling irregular uterine bleeding in DMPA users. Contraception
2004;70:277–9. http://dx.doi.org/10.1016/j.contraception.2004.04.003
200. Said S, Sadek W, Rocca M, et al. Clinical evaluation of the therapeutic
effectiveness of ethinyl oestradiol and oestrone sulphate on prolonged
bleeding in women using depot medroxyprogesterone acetate for
contraception. World Health Organization, Special Programme of Research,
Development and Research Training in Human Reproduction, Task Force
on Long-acting Systemic Agents for Fertility Regulation. Hum Reprod
1996;11(Suppl 2):1–13. http://dx.doi.org/10.1093/humrep/11.suppl_2.1
201. Sadeghi-Bazargani H, Ehdaeivand F, Arshi S, Eftekhar H, Sezavar H,
Amanati L. Low-dose oral contraceptive to re-induce menstrual
bleeding in amenorrheic women on DMPA treatment: a randomized
clinical trial. Med Sci Monit 2006;12:CR420–5.
202. Brahmi D, Curtis KM. When can a woman start combined hormonal
contraceptives (CHCs)? A systematic review. Contraception 2013;87:524–
38. http://dx.doi.org/10.1016/j.contraception.2012.09.010
203. Edwards SM, Zieman M, Jones K, Diaz A, Robilotto C, Westhoff C.
Initiation of oral contraceptives—start now! J Adolesc Health
2008;43:432–6. http://dx.doi.org/10.1016/j.jadohealth.2008.06.008
204. Westhoff C, Heartwell S, Edwards S, et al. Initiation of oral
contraceptives using a quick start compared with a conventional start:
a randomized controlled trial. Obstet Gynecol 2007;109:1270–6.
http://dx.doi.org/10.1097/01.AOG.0000264550.41242.f2
205. Westhoff C, Morroni C, Kerns J, Murphy PA. Bleeding patterns after
immediate vs. conventional oral contraceptive initiation: a randomized,
controlled trial. Fertil Steril 2003;79:322–9. http://dx.doi.org/10.1016/
S0015-0282(02)04680-0

206. Baerwald AR, Olatunbosun OA, Pierson RA. Ovarian follicular
development is initiated during the hormone-free interval of oral
contraceptive use. Contraception 2004;70:371–7. http://dx.doi.
org/10.1016/j.contraception.2004.05.006
207. Baerwald AR, Pierson RA. Ovarian follicular development during the
use of oral contraception: a review. J Obstet Gynaecol Can 2004;26:19–
24. http://dx.doi.org/10.1016/S1701-2163(16)30692-2
208. Duijkers IJM, Klipping C, Verhoeven CHJ, Dieben TOM. Ovarian
function with the contraceptive vaginal ring or an oral contraceptive:
a randomized study. Hum Reprod 2004;19:2668–73. http://dx.doi.
org/10.1093/humrep/deh493
209. Killick S, Eyong E, Elstein M. Ovarian follicular development in oral
contraceptive cycles. Fertil Steril 1987;48:409–13.
210. Molloy BG, Coulson KA, Lee JM, Watters JK. “Missed pill” conception:
fact or fiction? Br Med J (Clin Res Ed) 1985;290:1474–5. http://dx.doi.
org/10.1136/bmj.290.6480.1474-a
211. Mulders TM, Dieben TO, Bennink HJ. Ovarian function with a novel
combined contraceptive vaginal ring. Hum Reprod 2002;17:2594–9.
http://dx.doi.org/10.1093/humrep/17.10.2594
212. Schwartz JL, Creinin MD, Pymar HC, Reid L. Predicting risk of
ovulation in new start oral contraceptive users. Obstet Gynecol
2002;99:177–82.
213. Sitavarin S, Jaisamrarn U, Taneepanichskul S. A randomized trial on
the impact of starting day on ovarian follicular activity in very low dose
oral contraceptive pills users. J Med Assoc Thai 2003;86:442–8.
214. Taylor DR, Anthony FW, Dennis KJ. Suppression of ovarian function
by Microgynon 30 in day 1 and day 5 “starters.” Contraception
1986;33:463–71. http://dx.doi.org/10.1016/S0010-7824(86)80005-1
215. Smith SK, Kirkman RJ, Arce BB, McNeilly AS, Loudon NB, Baird
DT. The effect of deliberate omission of Trinordiol or Microgynon on
the hypothalamo-pituitary-ovarian axis. Contraception 1986;34:513–
22. http://dx.doi.org/10.1016/0010-7824(86)90060-0
216. Lara-Torre E, Schroeder B. Adolescent compliance and side effects with
Quick Start initiation of oral contraceptive pills. Contraception
2002;66:81–5. http://dx.doi.org/10.1016/S0010-7824(02)00326-8
217. Murthy AS, Creinin MD, Harwood B, Schreiber CA. Same-day initiation
of the transdermal hormonal delivery system (contraceptive patch)
versus traditional initiation methods. Contraception 2005;72:333–6.
http://dx.doi.org/10.1016/j.contraception.2005.05.009
218. Westhoff C, Osborne LM, Schafer JE, Morroni C. Bleeding patterns
after immediate initiation of an oral compared with a vaginal hormonal
contraceptive. Obstet Gynecol 2005;106:89–96. http://dx.doi.
org/10.1097/01.AOG.0000164483.13326.59
219. Yeshaya A, Orvieto R, Kaplan B, et al. Flexible starting schedule for
oral contraception: effect on the incidence of breakthrough bleeding
and compliance. Eur J Contracept Reprod Health Care 1998;3:121–3.
http://dx.doi.org/10.3109/13625189809051414
220. Yeshaya A, Orvieto R, Kauschansky A, et al. A delayed starting schedule
of oral contraception: the effect on the incidence of breakthrough
bleeding and compliance in women. Eur J Contracept Reprod Health
Care 1996;1:263–5. http://dx.doi.org/10.3109/13625189609150668
221. Westhoff C, Kerns J, Morroni C, Cushman LF, Tiezzi L, Murphy PA.
Quick start: novel oral contraceptive initiation method. Contraception
2002;66:141–5. http://dx.doi.org/10.1016/S0010-7824(02)00351-7
222. WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Acute myocardial infarction and combined
oral contraceptives: results of an international multicentre case-control
study. Lancet 1997;349:1202–9. http://dx.doi.org/10.1016/
S0140-6736(97)02358-1

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223. Dunn N, Thorogood M, Faragher B, et al. Oral contraceptives and
myocardial infarction: results of the MICA case-control study. BMJ
1999;318:1579–83. http://dx.doi.org/10.1136/bmj.318.7198.1579
224. Lewis MA, Heinemann LA, Spitzer WO, MacRae KD, Bruppacher R.
The use of oral contraceptives and the occurrence of acute myocardial
infarction in young women. Results from the Transnational Study on
Oral Contraceptives and the Health of Young Women. Contraception
1997;56:129–40. http://dx.doi.org/10.1016/S0010-7824(97)00118-2
225. WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Ischaemic stroke and combined oral
contraceptives: results of an international, multicentre, case-control
study. Lancet 1996;348:498–505. http://dx.doi.org/10.1016/
S0140-6736(95)12393-8
226. Heinemann LA, Lewis MA, Spitzer WO, Thorogood M, GuggenmoosHolzmann I, Bruppacher R; Transnational Research Group on Oral
Contraceptives and the Health of Young Women. Thromboembolic
stroke in young women. A European case-control study on oral
contraceptives. Contraception 1998;57:29–37. http://dx.doi.
org/10.1016/S0010-7824(97)00204-7
227. WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Haemorrhagic stroke, overall stroke risk,
and combined oral contraceptives: results of an international,
multicentre, case-control study. Lancet 1996;348:505–10. http://
dx.doi.org/10.1016/S0140-6736(95)12394-6
228. Mohllajee AP, Curtis KM, Martins SL, Peterson HB. Does use of
hormonal contraceptives among women with thrombogenic mutations
increase their risk of venous thromboembolism? A systematic review.
Contraception 2006;73:166–78. http://dx.doi.org/10.1016/j.
contraception.2005.08.011
229. Wu O, Robertson L, Twaddle S, et al. Screening for thrombophilia in
high-risk situations: systematic review and cost-effectiveness analysis.
The Thrombosis: Risk and Economic Assessment of Thrombophilia
Screening (TREATS) study. Health Technol Assess 2006;10:1–110.
http://dx.doi.org/10.3310/hta10110
230. Wu O, Greer IA. Is screening for thrombophilia cost-effective? Curr
Opin Hematol 2007;14:500–3. http://dx.doi.org/10.1097/
MOH.0b013e32825f5318
231. Blickstein D, Blickstein I. Oral contraception and thrombophilia. Curr
Opin Obstet Gynecol 2007;19:370–6. http://dx.doi.org/10.1097/
GCO.0b013e32821642e6
232. Steenland MW, Rodriguez MI, Marchbanks PA, Curtis KM. How does
the number of oral contraceptive pill packs dispensed or prescribed
affect continuation and other measures of consistent and correct use?
A systematic review. Contraception 2013;87:605–10. http://dx.doi.
org/10.1016/j.contraception.2012.08.004
233. White KO, Westhoff C. The effect of pack supply on oral
contraceptive pill continuation: a randomized controlled trial.
Obstet Gynecol 2011;118:615–22. http://dx.doi.org/10.1097/
AOG.0b013e3182289eab
234. Foster DG, Parvataneni R, de Bocanegra HT, Lewis C, Bradsberry M,
Darney P. Number of oral contraceptive pill packages dispensed,
method continuation, and costs. Obstet Gynecol 2006;108:1107–14.
http://dx.doi.org/10.1097/01.AOG.0000239122.98508.39
235. Foster DG, Hulett D, Bradsberry M, Darney P, Policar M. Number
of oral contraceptive pill packages dispensed and subsequent unintended
pregnancies. Obstet Gynecol 2011;117:566–72. http://dx.doi.
org/10.1097/AOG.0b013e3182056309

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236. Chin-Quee DS, Cuthbertson C, Janowitz B. Over-the-counter pill
provision: evidence from Jamaica. Stud Fam Plann 2006;37:99–110.
http://dx.doi.org/10.1111/j.1728-4465.2006.00089.x
237. Zapata LB, Steenland MW, Brahmi D, Marchbanks PA, Curtis KM.
Effect of missed combined hormonal contraceptives on contraceptive
effectiveness: a systematic review. Contraception 2013;87:685–700.
http://dx.doi.org/10.1016/j.contraception.2012.08.035
238. Anttila L, Kunz M, Marr J. Bleeding pattern with drospirenone
3 mg+ethinyl estradiol 20 mcg 24/4 combined oral contraceptive
compared with desogestrel 150 mcg+ethinyl estradiol 20 mcg 21/7
combined oral contraceptive. Contraception 2009;80:445–51. http://
dx.doi.org/10.1016/j.contraception.2009.03.013
239. Chowdhury V, Joshi UM, Gopalkrishna K, Betrabet S, Mehta S, Saxena
BN. ‘Escape’ ovulation in women due to the missing of low dose
combination oral contraceptive pills. Contraception 1980;22:241–7.
http://dx.doi.org/10.1016/S0010-7824(80)80003-5
240. Christin-Maitre S, Serfaty D, Chabbert-Buffet N, Ochsenbein E,
Chassard D, Thomas JL. Comparison of a 24-day and a 21-day pill
regimen for the novel combined oral contraceptive, nomegestrol acetate
and 17b-estradiol (NOMAC/E2): a double-blind, randomized study.
Hum Reprod 2011;26:1338–47. http://dx.doi.org/10.1093/humrep/der058
241. Creinin MD, Lippman JS, Eder SE, Godwin AJ, Olson W. The
effect of extending the pill-free interval on follicular activity:
triphasic norgestimate/35 µg ethinyl estradiol versus monophasic
levonorgestrel/20 µg ethinyl estradiol. Contraception 2002;66:147–52.
http://dx.doi.org/10.1016/S0010-7824(02)00344-X
242. Dinger J, Minh TD, Buttmann N, Bardenheuer K. Effectiveness of
oral contraceptive pills in a large U.S. cohort comparing progestogen
and regimen. Obstet Gynecol 2011;117:33–40. http://dx.doi.
org/10.1097/AOG.0b013e31820095a2
243. Elomaa K, Lähteenmäki P. Ovulatory potential of preovulatory
sized follicles during oral contraceptive treatment. Contraception
1999;60:275–9. http://dx.doi.org/10.1016/S0010-7824(99)00094-3
244. Elomaa K, Rolland R, Brosens I, et al. Omitting the first oral
contraceptive pills of the cycle does not automatically lead to ovulation.
Am J Obstet Gynecol 1998;179:41–6. http://dx.doi.org/10.1016/
S0002-9378(98)70249-2
245. Endrikat J, Wessel J, Rosenbaum P, Düsterberg B. Plasma concentrations
of endogenous hormones during one regular treatment cycle with a
low-dose oral contraceptive and during two cycles with deliberate
omission of two tablets. Gynecol Endocrinol 2004;18:318–26. http://
dx.doi.org/10.1080/0951359042000199869
246. Hamilton CJ, Hoogland HJ. Longitudinal ultrasonographic study of
the ovarian suppressive activity of a low-dose triphasic oral contraceptive
during correct and incorrect pill intake. Am J Obstet Gynecol
1989;161:1159–62. http://dx.doi.org/10.1016/0002-9378(89)90655-8
247. Hedon B, Cristol P, Plauchut A, et al. Ovarian consequences of the
transient interruption of combined oral contraceptives. Int J Fertil
1992;37:270–6.
248. Killick SR. Ovarian follicles during oral contraceptive cycles: their
potential for ovulation. Fertil Steril 1989;52:580–2.
249. Killick SR, Bancroft K, Oelbaum S, Morris J, Elstein M. Extending the
duration of the pill-free interval during combined oral contraception.
Adv Contracept 1990;6:33–40. http://dx.doi.org/10.1007/BF01849485
250. Klipping C, Duijkers I, Trummer D, Marr J. Suppression of ovarian
activity with a drospirenone-containing oral contraceptive in a 24/4
regimen. Contraception 2008;78:16–25. http://dx.doi.org/10.1016/j.
contraception.2008.02.019

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Recommendations and Reports

251. Klipping C, Marr J. Effects of two combined oral contraceptives
containing ethinyl estradiol 20 microg combined with either
drospirenone or desogestrel on lipids, hemostatic parameters and
carbohydrate metabolism. Contraception 2005;71:409–16. http://
dx.doi.org/10.1016/j.contraception.2004.12.005
252. Landgren BM, Csemiczky G. The effect of follicular growth and luteal
function of “missing the pill.” A comparison between a monophasic and
a triphasic combined oral contraceptive. Contraception 1991;43:149–
59. http://dx.doi.org/10.1016/0010-7824(91)90042-E
253. Landgren BM, Diczfalusy E. Hormonal consequences of missing the pill
during the first two days of three consecutive artificial cycles. Contraception
1984;29:437–46. http://dx.doi.org/10.1016/0010-7824(84)90017-9
254. Letterie GS. A regimen of oral contraceptives restricted to the
periovulatory period may permit folliculogenesis but inhibit ovulation.
Contraception 1998;57:39–44. http://dx.doi.org/10.1016/
S0010-7824(97)00205-9
255. Letterie GS, Chow GE. Effect of “missed” pills on oral contraceptive
effectiveness. Obstet Gynecol 1992;79:979–82.
256. Morris SE, Groom GV, Cameron ED, Buckingham MS, Everitt
JM, Elstein M. Studies on low dose oral contraceptives: plasma
hormone changes in relation to deliberate pill (‘Microgynon
30’) omission. Contraception 1979;20:61–9. http://dx.doi.
org/10.1016/0010-7824(79)90045-3
257. Nakajima ST, Archer DF, Ellman H. Efficacy and safety of a new 24-day
oral contraceptive regimen of norethindrone acetate 1 mg/ethinyl
estradiol 20 µg (Loestrin 24 Fe). Contraception 2007;75:16–22. http://
dx.doi.org/10.1016/j.contraception.2006.08.004
258. Nuttall ID, Elstein M, McCafferty E, Seth J, Cameron ED. The
effect of ethinyl estradiol 20 mcg and levonorgestrel 250 mcg on the
pituitary-ovarian function during normal tablet-taking and when
tablets are missed. Contraception 1982;26:121–35. http://dx.doi.
org/10.1016/0010-7824(82)90081-6
259. Pierson RA, Archer DF, Moreau M, Shangold GA, Fisher AC, Creasy
GW. Ortho Evra/Evra versus oral contraceptives: follicular development
and ovulation in normal cycles and after an intentional dosing error.
Fertil Steril 2003;80:34–42. http://dx.doi.org/10.1016/
S0015-0282(03)00556-9
260. Rible RD, Taylor D, Wilson ML, Stanczyk FZ, Mishell DR Jr. Follicular
development in a 7-day versus 4-day hormone-free interval with an
oral contraceptive containing 20 mcg ethinyl estradiol and 1 mg
norethindrone acetate. Contraception 2009;79:182–8. http://dx.doi.
org/10.1016/j.contraception.2008.10.005
261. Schlaff WD, Lynch AM, Hughes HD, Cedars MI, Smith DL.
Manipulation of the pill-free interval in oral contraceptive pill users:
the effect on follicular suppression. Am J Obstet Gynecol 2004;190:943–
51. http://dx.doi.org/10.1016/j.ajog.2004.02.012
262. Spona J, Elstein M, Feichtinger W, et al. Shorter pill-free
interval in combined oral contraceptives decreases follicular
development. Contraception 1996;54:71–7. http://dx.doi.
org/10.1016/0010-7824(96)00137-0
263. Sullivan H, Furniss H, Spona J, Elstein M. Effect of 21-day and 24-day
oral contraceptive regimens containing gestodene (60 µg) and ethinyl
estradiol (15 µg) on ovarian activity. Fertil Steril 1999;72:115–20.
http://dx.doi.org/10.1016/S0015-0282(99)00205-8
264. Wang E, Shi S, Cekan SZ, Landgren BM, Diczfalusy E. Hormonal
consequences of “missing the pill.” Contraception 1982;26:545–66.
http://dx.doi.org/10.1016/0010-7824(82)90131-7

265. Willis SA, Kuehl TJ, Spiekerman AM, Sulak PJ. Greater inhibition of
the pituitary—ovarian axis in oral contraceptive regimens with a
shortened hormone-free interval. Contraception 2006;74:100–3.
http://dx.doi.org/10.1016/j.contraception.2006.02.006
266. Abrams LS, Skee DM, Natarajan J, et al. Pharmacokinetics of
norelgestromin and ethinyl estradiol delivered by a contraceptive
patch (Ortho Evra/Evra) under conditions of heat, humidity,
and exercise. J Clin Pharmacol 2001;41:1301–9. http://dx.doi.
org/10.1177/00912700122012887
267. Ahrendt HJ, Nisand I, Bastianelli C, et al. Efficacy, acceptability and
tolerability of the combined contraceptive ring, NuvaRing, compared
with an oral contraceptive containing 30 microg of ethinyl estradiol
and 3 mg of drospirenone. Contraception 2006;74:451–7. http://
dx.doi.org/10.1016/j.contraception.2006.07.004
268. Bjarnadóttir RI, Tuppurainen M, Killick SR. Comparison of cycle
control with a combined contraceptive vaginal ring and oral
levonorgestrel/ethinyl estradiol. Am J Obstet Gynecol 2002;186:389–
95. http://dx.doi.org/10.1067/mob.2002.121103
269. Brucker C, Karck U, Merkle E. Cycle control, tolerability, efficacy and
acceptability of the vaginal contraceptive ring, NuvaRing: results of
clinical experience in Germany. Eur J Contracept Reprod Health Care
2008;13:31–8. http://dx.doi.org/10.1080/13625180701577122
270. Dieben TO, Roumen FJ, Apter D. Efficacy, cycle control, and user
acceptability of a novel combined contraceptive vaginal ring. Obstet
Gynecol 2002;100:585–93.
271. Mulders TM, Dieben TO. Use of the novel combined contraceptive
vaginal ring NuvaRing for ovulation inhibition. Fertil Steril
2001;75:865–70. http://dx.doi.org/10.1016/S0015-0282(01)01689-2
272. Guilbert E, Boroditsky R, Black A, et al; Society of Obstetricians and
Gynaecologists of Canada. Canadian Consensus Guideline on
Continuous and Extended Hormonal Contraception, 2007. J Obstet
Gynaecol Can 2007;29(Suppl 2):S1–32. http://dx.doi.org/10.1016/
S1701-2163(16)32526-9
273. Wiegratz I, Stahlberg S, Manthey T, et al. Effect of extended-cycle
regimen with an oral contraceptive containing 30 mcg ethinylestradiol
and 2 mg dienogest on bleeding patterns, safety, acceptance and
contraceptive efficacy. Contraception 2011;84:133–43. http://dx.doi.
org/10.1016/j.contraception.2011.01.002
274. Hubacher D, Fortney J. Follow-up visits after IUD insertion. Are more
better? J Reprod Med 1999;44:801–6.
275. Godfrey EM, Whiteman MK, Curtis KM. Treatment of
unscheduled bleeding in women using extended- or continuoususe combined hormonal contraception: a systematic review.
Contraception 2013;87:567–75. http://dx.doi.org/10.1016/j.
contraception.2012.08.005
276. Sulak PJ, Kuehl TJ, Coffee A, Willis S. Prospective analysis of
occurrence and management of breakthrough bleeding during an
extended oral contraceptive regimen. Am J Obstet Gynecol
2006;195:935–41. http://dx.doi.org/10.1016/j.ajog.2006.02.048
277. Sulak PJ, Smith V, Coffee A, Witt I, Kuehl AL, Kuehl TJ. Frequency
and management of breakthrough bleeding with continuous use of
the transvaginal contraceptive ring: a randomized controlled trial.
Obstet Gynecol 2008;112:563–71. http://dx.doi.org/10.1097/
AOG.0b013e3181842071
278. Kaneshiro B, Edelman A, Carlson N, Morgan K, Nichols M,
Jensen J. Treatment of unscheduled bleeding in continuous oral
contraceptive users with doxycycline: a randomized controlled trial.
Obstet Gynecol 2010;115:1141–9. http://dx.doi.org/10.1097/
AOG.0b013e3181e0119c

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Recommendations and Reports

279. McCann MF, Potter LS. Progestin-only oral contraception: a
comprehensive review. Contraception 1994;50(Suppl 1):S1–195.
http://dx.doi.org/10.1016/0010-7824(94)90124-4
280. Arévalo M, Jennings V, Sinai I. Efficacy of a new method of family
planning: the Standard Days Method. Contraception 2002;65:333–8.
http://dx.doi.org/10.1016/S0010-7824(02)00288-3
281. Arévalo M, Sinai I, Jennings V. A fixed formula to define the fertile
window of the menstrual cycle as the basis of a simple method of natural
family planning. Contraception 1999;60:357–60. http://dx.doi.
org/10.1016/S0010-7824(99)00106-7
282. Wilcox AJ, Dunson DB, Weinberg CR, Trussell J, Baird DD. Likelihood
of conception with a single act of intercourse: providing benchmark
rates for assessment of post-coital contraceptives. Contraception
2001;63:211–5. http://dx.doi.org/10.1016/S0010-7824(01)00191-3
283. Cleland K, Zhu H, Goldstuck N, Cheng L, Trussell J. The efficacy of
intrauterine devices for emergency contraception: a systematic review
of 35 years of experience. Hum Reprod 2012;27:1994–2000. http://
dx.doi.org/10.1093/humrep/des140
284. Glasier AF, Cameron ST, Fine PM, et al. Ulipristal acetate versus
levonorgestrel for emergency contraception: a randomised noninferiority trial and meta-analysis. Lancet 2010;375:555–62. http://
dx.doi.org/10.1016/S0140-6736(10)60101-8
285. Raymond E, Taylor D, Trussell J, Steiner MJ. Minimum effectiveness
of the levonorgestrel regimen of emergency contraception.
Contraception 2004;69:79–81. http://dx.doi.org/10.1016/j.
contraception.2003.09.013
286. Jatlaoui TC, Curtis KM. Safety and effectiveness data for emergency
contraceptive pills among women with obesity: a systematic review.
Contraception 2016. Epub May 24, 2016. http://dx.doi.org/10.1016/j.
contraception.2016.05.002
287. Fine P, Mathé H, Ginde S, Cullins V, Morfesis J, Gainer E. Ulipristal
acetate taken 48-120 hours after intercourse for emergency
contraception. Obstet Gynecol 2010;115:257–63. http://dx.doi.
org/10.1097/AOG.0b013e3181c8e2aa
288. Dada OA, Godfrey EM, Piaggio G, von Hertzen H; Nigerian Network
for Reproductive Health Research and Training. A randomized, doubleblind, noninferiority study to compare two regimens of levonorgestrel
for emergency contraception in Nigeria. Contraception 2010;82:373–
8. http://dx.doi.org/10.1016/j.contraception.2010.06.004
289. Ellertson C, Evans M, Ferden S, et al. Extending the time limit for
starting the Yuzpe regimen of emergency contraception to 120 hours.
Obstet Gynecol 2003;101:1168–71.
290. Ngai SW, Fan S, Li S, et al. A randomized trial to compare 24 h versus 12
h double dose regimen of levonorgestrel for emergency contraception. Hum
Reprod 2005;20:307–11. http://dx.doi.org/10.1093/humrep/deh583
291. Rodrigues I, Grou F, Joly J. Effectiveness of emergency contraceptive pills
between 72 and 120 hours after unprotected sexual intercourse. Am J Obstet
Gynecol 2001;184:531–7. http://dx.doi.org/10.1067/mob.2001.111102
292. von Hertzen H, Piaggio G, Ding J, et al; WHO Research Group on
Post-ovulatory Methods of Fertility Regulation. Low dose mifepristone
and two regimens of levonorgestrel for emergency contraception: a
WHO multicentre randomised trial. Lancet 2002;360:1803–10. http://
dx.doi.org/10.1016/S0140-6736(02)11767-3
293. Piaggio G, Kapp N, von Hertzen H. Effect on pregnancy rates of the
delay in the administration of levonorgestrel for emergency
contraception: a combined analysis of four WHO trials. Contraception
2011;84:35–9. http://dx.doi.org/10.1016/j.contraception.2010.11.010

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294. Rodriguez MI, Curtis KM, Gaffield ML, Jackson E, Kapp N.
Advance supply of emergency contraception: a systematic review.
Contraception 2013;87:590–601. http://dx.doi.org/10.1016/j.
contraception.2012.09.011
295. Brache V, Cochon L, Duijkers IJ, et al. A prospective, randomized,
pharmacodynamic study of quick-starting a desogestrel progestin-only
pill following ulipristal acetate for emergency contraception. Hum
Reprod 2015;30:2785–93.
296. Cameron ST, Berger C, Michie L, Klipping C, Gemzell-Danielsson K.
The effects on ovarian activity of ulipristal acetate when ‘quickstarting’
a combined oral contraceptive pill: a prospective, randomized, doubleblind parallel-arm, placebo-controlled study. Hum Reprod
2015;30:1566–72. http://dx.doi.org/10.1093/humrep/dev115
297. Salcedo J, Rodriguez MI, Curtis KM, Kapp N. When can a woman
resume or initiate contraception after taking emergency contraceptive
pills? A systematic review. Contraception 2013;87:602–4. http://dx.doi.
org/10.1016/j.contraception.2012.08.013
298. Rodriguez MI, Godfrey EM, Warden M, Curtis KM. Prevention and
management of nausea and vomiting with emergency contraception:
a systematic review. Contraception 2013;87:583–9. http://dx.doi.
org/10.1016/j.contraception.2012.09.031
299. Creinin MD, Schlaff W, Archer DF, et al. Progesterone receptor
modulator for emergency contraception: a randomized controlled trial.
Obstet Gynecol 2006;108:1089–97. http://dx.doi.org/10.1097/01.
AOG.0000239440.02284.45
300. Farajkhoda T, Khoshbin A, Enjezab B, Bokaei M, Karimi Zarchi M.
Assessment of two emergency contraceptive regimens in Iran:
levonorgestrel versus the Yuzpe. Niger J Clin Pract 2009;12:450–2.
301. Ho PC, Kwan MSW. A prospective randomized comparison of
levonorgestrel with the Yuzpe regimen in post-coital contraception.
Hum Reprod 1993;8:389–92.
302. Arowojolu AO, Okewole IA, Adekunle AO. Comparative evaluation
of the effectiveness and safety of two regimens of levonorgestrel for
emergency contraception in Nigerians. Contraception 2002;66:269–
73. http://dx.doi.org/10.1016/S0010-7824(02)00337-2
303. Ragan RE, Rock RW, Buck HW. Metoclopramide pretreatment
attenuates emergency contraceptive-associated nausea. Am J Obstet
Gynecol 2003;188:330–3. http://dx.doi.org/10.1067/mob.2003.90
304. Raymond EG, Creinin MD, Barnhart KT, Lovvorn AE, Rountree RW,
Trussell J. Meclizine for prevention of nausea associated with use of emergency
contraceptive pills: a randomized trial. Obstet Gynecol 2000;95:271–7.
305. Peterson HB. Sterilization. Obstet Gynecol 2008;111:189–203. http://
dx.doi.org/10.1097/01.AOG.0000298621.98372.62
306. Peterson HB, Xia Z, Hughes JM, Wilcox LS, Tylor LR, Trussell J. The risk
of pregnancy after tubal sterilization: findings from the U.S. Collaborative
Review of Sterilization. Am J Obstet Gynecol 1996;174:1161–8, discussion
1168–70. http://dx.doi.org/10.1016/S0002-9378(96)70658-0
307. Lawrie TA, Nardin JM, Kulier R, Boulvain M. Techniques for the
interruption of tubal patency for female sterilisation. Cochrane
Database Syst Rev 2011; (2):CD003034.
308. Cleary TP, Tepper NK, Cwiak C, et al. Pregnancies after hysteroscopic
sterilization: a systematic review. Contraception 2013;87:539–48.
http://dx.doi.org/10.1016/j.contraception.2012.08.006
309. Legendre G, Levaillant JM, Faivre E, Deffieux X, Gervaise A, Fernandez H.
3D ultrasound to assess the position of tubal sterilization microinserts. Hum
Reprod 2011;26:2683–9. http://dx.doi.org/10.1093/humrep/der242
310. Levy B, Levie MD, Childers ME. A summary of reported pregnancies
after hysteroscopic sterilization. J Minim Invasive Gynecol
2007;14:271–4. http://dx.doi.org/10.1016/j.jmig.2006.11.007

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

311. Veersema S, Vleugels MP, Moolenaar LM, Janssen CA, Brölmann HA.
Unintended pregnancies after Essure sterilization in the Netherlands. Fertil
Steril 2010;93:35–8. http://dx.doi.org/10.1016/j.fertnstert.2008.10.005
312. Arjona JE, Miño M, Cordón J, Povedano B, Pelegrin B, Castelo-Branco C.
Satisfaction and tolerance with office hysteroscopic tubal sterilization. Fertil
Steril 2008;90:1182–6. http://dx.doi.org/10.1016/j.fertnstert.2007.08.007
313. Duffy S, Marsh F, Rogerson L, et al. Female sterilisation: a cohort controlled
comparative study of ESSURE versus laparoscopic sterilisation. BJOG
2005;112:1522–8. http://dx.doi.org/10.1111/j.1471-0528.2005.00726.x
314. Grosdemouge I, Engrand JB, Dhainault C, et al. Essure implants for
tubal sterilisation in France [French]. Gynecol Obstet Fertil
2009;37:389–95. http://dx.doi.org/10.1016/j.gyobfe.2009.03.024
315. Levie MD, Chudnoff SG. Prospective analysis of office-based
hysteroscopic sterilization. J Minim Invasive Gynecol 2006;13:98–101.
http://dx.doi.org/10.1016/j.jmig.2005.11.010
316. Shavell VI, Abdallah ME, Diamond MP, Berman JM. Placement of a
permanent birth control device at a university medical center. J Reprod
Med 2009;54:218–22.
317. Teisala K. Removal of an intrauterine device and the treatment of acute
pelvic inflammatory disease. Ann Med 1989;21:63–5. http://dx.doi.
org/10.3109/07853898909149184
318. Bedford JM, Zelikovsky G. Viability of spermatozoa in the human
ejaculate after vasectomy. Fertil Steril 1979;32:460–3.
319. Edwards IS. Earlier testing after vasectomy, based on the absence of
motile sperm. Fertil Steril 1993;59:431–6.
320. Jouannet P, David G. Evolution of the properties of semen immediately
following vasectomy. Fertil Steril 1978;29:435–41.
321. Labrecque M, Hays M, Chen-Mok M, Barone MA, Sokal D. Frequency
and patterns of early recanalization after vasectomy. BMC Urol
2006;6:25. http://dx.doi.org/10.1186/1471-2490-6-25
322. Alderman PM. The lurking sperm. A review of failures in 8879
vasectomies performed by one physician. JAMA 1988;259:3142–4.
http://dx.doi.org/10.1001/jama.1988.03720210032024
323. Black T, Francome C. The evolution of the Marie Stopes electrocautery
no-scalpel vasectomy procedure. J Fam Plann Reprod Health Care
2002;28:137–8. http://dx.doi.org/10.1783/147118902101196270
324. Davies AH, Sharp RJ, Cranston D, Mitchell RG. The long-term outcome
following “special clearance” after vasectomy. Br J Urol 1990;66:211–2.
http://dx.doi.org/10.1111/j.1464-410X.1990.tb14907.x
325. Philp T, Guillebaud J, Budd D. Late failure of vasectomy after two
documented analyses showing azoospermic semen. Br Med J (Clin Res
Ed) 1984;289:77–9. http://dx.doi.org/10.1136/bmj.289.6437.77
326. Philp T, Guillebaud J, Budd D. Complications of vasectomy: review
of 16,000 patients. Br J Urol 1984;56:745–8. http://dx.doi.
org/10.1111/j.1464-410X.1984.tb06161.x
327. Belker AM, Sexter MS, Sweitzer SJ, Raff MJ. The high rate of
noncompliance for post-vasectomy semen examination: medical and
legal considerations. J Urol 1990;144:284–6.
328. Chawla A, Bowles B, Zini A. Vasectomy follow-up: clinical significance
of rare nonmotile sperm in postoperative semen analysis. Urology
2004;64:1212–5. http://dx.doi.org/10.1016/j.urology.2004.07.007
329. Labrecque M, Bédard L, Laperrière L. Efficacy and complications
associated with vasectomies in two clinics in the Quebec region
[French]. Can Fam Physician 1998;44:1860–6.
330. Labrecque M, Nazerali H, Mondor M, Fortin V, Nasution M.
Effectiveness and complications associated with 2 vasectomy occlusion
techniques. J Urol 2002;168:2495–8, discussion 2498. http://dx.doi.
org/10.1016/S0022-5347(05)64176-6

331. Maatman TJ, Aldrin L, Carothers GG. Patient noncompliance after
vasectomy. Fertil Steril 1997;68:552–5. http://dx.doi.org/10.1016/
S0015-0282(97)00251-3
332. Dhar NB, Jones JS, Bhatt A, Babineau D. A prospective evaluation
of the impact of scheduled follow-up appointments with compliance
rates after vasectomy. BJU Int 2007;99:1094–7. http://dx.doi.
org/10.1111/j.1464-410X.2006.06725.x
333. Hillard PJ, Berek JS, Barss VA, et al. Guidelines for women’s health
care: A resource manual. 3rd ed. Washington, DC: American College
of Obstetricians and Gynecologists; 2007.
334. Shifren J, Gass M; NAMS Recommendations for Clinical Care of
Midlife Women Working Group. The North American Menopause
Society recommendation for clinical care of midlife women. Menopause
2014;21;1038–62.
335. te Velde ER, Pearson PL. The variability of female reproductive ageing. Hum
Reprod Update 2002;8:141–54. http://dx.doi.org/10.1093/humupd/8.2.141
336. Broekmans FJ, Soules MR, Fauser BC. Ovarian aging: mechanisms
and clinical consequences. Endocr Rev 2009;30:465–93. http://dx.doi.
org/10.1210/er.2009-0006
337. Wood JW. Fecundity and natural fertility in humans. Oxf Rev Reprod
Biol 1989;11:61–109.
338. Balasch J, Gratacós E. Delayed childbearing: effects on fertility and the
outcome of pregnancy. Curr Opin Obstet Gynecol 2012;24:187–93.
http://dx.doi.org/10.1097/GCO.0b013e3283517908
339. Bateman BT, Simpson LL. Higher rate of stillbirth at the extremes of
reproductive age: a large nationwide sample of deliveries in the United
States. Am J Obstet Gynecol 2006;194:840–5. http://dx.doi.
org/10.1016/j.ajog.2005.08.038
340. Berg CJ, Callaghan WM, Syverson C, Henderson Z. Pregnancyrelated mortality in the United States, 1998 to 2005. Obstet Gynecol
2010;116:1302–9. http://dx.doi.org/10.1097/AOG.0b013e3181fdfb11
341. Lidegaard Ø, Løkkegaard E, Svendsen AL, Agger C. Hormonal
contraception and risk of venous thromboembolism: national follow-up
study. BMJ 2009;339:b2890.
342. Lidegaard Ø, Nielsen LH, Skovlund CW, Skjeldestad FE, Løkkegaard
E. Risk of venous thromboembolism from use of oral contraceptives
containing different progestogens and oestrogen doses: Danish cohort
study, 2001–9. BMJ 2011;343:d6423.
343. Nightingale AL, Lawrenson RA, Simpson EL, Williams TJ, MacRae
KD, Farmer RD. The effects of age, body mass index, smoking and
general health on the risk of venous thromboembolism in users of
combined oral contraceptives. Eur J Contracept Reprod Health Care
2000;5:265–74. http://dx.doi.org/10.1080/13625180008500402
344. Slone D, Shapiro S, Kaufman DW, Rosenberg L, Miettinen OS, Stolley
PD. Risk of myocardial infarction in relation to current and
discontinued use of oral contraceptives. N Engl J Med 1981;305:420–4.
http://dx.doi.org/10.1056/NEJM198108203050802
345. Tanis BC, van den Bosch MA, Kemmeren JM, et al. Oral contraceptives
and the risk of myocardial infarction. N Engl J Med 2001;345:1787–
93. http://dx.doi.org/10.1056/NEJMoa003216
346. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer
and hormonal contraceptives: collaborative reanalysis of individual data
on 53 297 women with breast cancer and 100 239 women without breast
cancer from 54 epidemiological studies. Lancet 1996;347:1713–27.
http://dx.doi.org/10.1016/S0140-6736(96)90806-5
347. Gill JK, Press MF, Patel AV, Bernstein L. Oral contraceptive use and
risk of breast carcinoma in situ (United States). Cancer Causes Control
2006;17:1155–62. http://dx.doi.org/10.1007/s10552-006-0056-0

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Recommendations and Reports

348. Kumle M, Weiderpass E, Braaten T, Persson I, Adami HO, Lund E.
Use of oral contraceptives and breast cancer risk: The NorwegianSwedish Women’s Lifestyle and Health Cohort Study. Cancer Epidemiol
Biomarkers Prev 2002;11:1375–81.
349. Marchbanks PA, McDonald JA, Wilson HG, et al. Oral contraceptives
and the risk of breast cancer. N Engl J Med 2002;346:2025–32. http://
dx.doi.org/10.1056/NEJMoa013202
350. Newcomb PA, Longnecker MP, Storer BE, et al. Recent oral contraceptive
use and risk of breast cancer (United States). Cancer Causes Control
1996;7:525–32. http://dx.doi.org/10.1007/BF00051885

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351. Rosenberg L, Palmer JR, Rao RS, et al. Case-control study of oral
contraceptive use and risk of breast cancer. Am J Epidemiol 1996;143:25–
37. http://dx.doi.org/10.1093/oxfordjournals.aje.a008654
352. Rosenberg L, Zhang Y, Coogan PF, Strom BL, Palmer JR. A case-control
study of oral contraceptive use and incident breast cancer. Am J
Epidemiol 2009;169:473–9. http://dx.doi.org/10.1093/aje/kwn360
353. Shapiro S, Rosenberg L, Hoffman M, et al. Risk of breast cancer in
relation to the use of injectable progestogen contraceptives and combined
estrogen/progestogen contraceptives. Am J Epidemiol 2000;151:396–
403. http://dx.doi.org/10.1093/oxfordjournals.aje.a010219

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix A
Summary Chart of U.S. Medical Eligibility Criteria for Contraceptive Use, 2016
complete guidance, see the 2016 U.S. Medical Eligibility
Criteria for Contraceptive Use (U.S. MEC) (Curtis
KM, Tepper NK, Jatlaoui TC, et al. U.S. medical
eligibility criteria for contraceptive use, 2016. MMWR
Recomm Rep 2016;65[No. RR-3]) for clarifications
to the numeric categories, as well as for summaries
of the evidence and additional comments. Hormonal
contraceptives and intrauterine devices do not protect
against sexually transmitted diseases (STDs), including
human immunodeficiency virus (HIV), and women using
these methods should be counseled that consistent and
correct use of the male latex condom reduces the risk
for transmission of HIV and other STDs. Use of female
condoms can provide protection from transmission of
STDs, although data are limited.

Health-care providers can use the summary table as a quick
reference guide to the classifications for hormonal contraceptive
methods and intrauterine contraception to compare
classifications across these methods (Box A1) (Table A1). For
BOX A1. Categories for classifying hormonal contraceptives and
intrauterine devices

TABLE A1. Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

LNG-IUD

Implants

DMPA

POP

CHCs

4*
Menarche to
<20 years: 2
≥20 years: 1

NA*
Menarche to
<18 years: 1
18–45 years: 1
>45 years: 1

NA*
Menarche to
<18 years: 2
18–45 years: 1
>45 years: 2

NA*
Menarche to
<18 years: 1
18–45 years: 1
>45 years: 1

NA*
Menarche to
<40 years: 1
≥40 years: 2

2
1

1
1

—

Personal Characteristics and Reproductive History
Pregnancy
Age

Parity
a. Nulliparous
b. Parous
Breastfeeding
a. <21 days postpartum
b. 21 to <30 days postpartum
i. With other risk factors for
VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility,
transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
ii. Without other risk factors
for VTE
c. 30–42 days postpartum
i. With other risk factors for
VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility,
transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
See table footnotes on page 61.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 4

Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
ii. Without other risk factors
for VTE
d. >42 days postpartum
Postpartum
(nonbreastfeeding women)
a. <21 days postpartum
b. 21–42 days postpartum
i. With other risk factors for
VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility,
transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
ii. Without other risk factors
for VTE
c. >42 days postpartum
Postpartum (including
cesarean delivery)
a. <10 minutes after delivery
of the placenta
i. Breastfeeding
ii. Nonbreastfeeding
b. 10 minutes after delivery
of the placenta to <4 weeks
(breastfeeding or
nonbreastfeeding)
c. ≥4 weeks (breastfeeding or
nonbreastfeeding)
d. Postpartum sepsis
Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic
abortion
Past ectopic pregnancy
History of pelvic surgery (see
Postpartum [Including
Cesarean Delivery] section)
Smoking
a. Age <35 years
b. Age ≥35 years
i. <15 cigarettes/day
ii. ≥15 cigarettes/day
Obesity
a. BMI ≥30 kg/m2
b. Menarche to <18 years
and BMI ≥30 kg/m2
History of bariatric surgery
This condition is associated
with increased risk for adverse
health events as a result of
pregnancy.
a. Restrictive procedures:
decrease storage capacity of
the stomach (vertical banded
gastroplasty, laparoscopic
adjustable gastric band, or
laparoscopic sleeve
gastrectomy)
b. Malabsorptive procedures:
decrease absorption of
nutrients and calories by
shortening the functional
length of the small intestine
(Roux-en-Y gastric bypass or
biliopancreatic diversion)

Cu-IUD

LNG-IUD

Implants

—

DMPA

POP

CHCs

—

1*
1*
2*

2*
1*
2*

—
—
—

—

1*
2*
4

1*
1*
1*

1
1

2
1

1
1

3
4

1
1

1
2

1
1

2
2

COCs: 3
Patch and ring: 1

See table footnotes on page 61.

MMWR / July 29, 2016 / Vol. 65 / No. 4

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

LNG-IUD

Implants

DMPA

POP

CHCs

3/4*

1*
1

2*
1

3*
1

2*
1

4*
2

Cardiovascular Disease
Multiple risk factors for
atherosclerotic cardiovascular disease (e.g., older age,
smoking, diabetes,
hypertension, low HDL, high
LDL, or high triglyceride levels)
Hypertension
Systolic blood pressure ≥160
mm Hg or diastolic blood
pressure ≥100 mm Hg are
associated with increased risk
for adverse health events as a
result of pregnancy.
a. Adequately controlled
hypertension
b. Elevated blood pressure
levels (properly taken
measurements)
i. Systolic 140–159 mm Hg
or diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or
diastolic ≥100 mm Hg
c. Vascular disease
History of high blood
pressure during pregnancy
(when current blood pressure
is measurable and normal)
Deep venous thrombosis/
Pulmonary embolism
a. History of DVT/PE, not
receiving anticoagulant
therapy
i. Higher risk for recurrent
DVT/PE (one or more risk
factors)
• History of estrogenassociated DVT/PE
• Pregnancy-associated
DVT/PE
• Idiopathic DVT/PE
• Known thrombophilia,
including antiphospholipid syndrome
• Active cancer (metastatic,
receiving therapy, or
within 6 months after
clinical remission),
excluding nonmelanoma
skin cancer
• History of recurrent
DVT/PE
ii. Lower risk for recurrent
DVT/PE (no risk factors)
b. Acute DVT/PE
c. DVT/PE and established
receiving anticoagulant
therapy for at least 3 months
i. Higher risk for recurrent
2
DVT/PE (one or more risk
factors)
• Known thrombophilia,
including antiphospholipid syndrome
• Active cancer (metastatic,
receiving therapy, or within
6 months after clinical
remission), excluding
nonmelanoma skin cancer
• History of recurrent DVT/
PE
ii. Lower risk for recurrent
DVT/PE (no risk factors)

See table footnotes on page 61.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 4

Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
d. Family history (first-degree
relatives)
e. Major surgery
i. With prolonged
immobilization
ii. Without prolonged
immobilization
f. Minor surgery without
immobilization
Known thrombogenic
mutations (e.g., factor V
Leiden; prothrombin
mutation; and protein S,
protein C, and antithrombin
deficiencies)
This condition is associated
with increased risk for adverse
health events as a result of
pregnancy.
Superficial venous disorders
a. Varicose veins
b. Superficial venous
thrombosis (acute or history)
Current and history of ischemic
heart disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
Stroke (history of cerebrovascular accident)
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
Valvular heart disease
Complicated valvular heart
disease is associated with
increased risk for adverse health
events as a result of pregnancy.
a. Uncomplicated
b. Complicated (pulmonary
hypertension, risk for atrial
fibrillation, or history of
subacute bacterial
endocarditis)
Peripartum cardiomyopathy
This condition is associated
with increased risk for adverse
health events as a result of
pregnancy.
a. Normal or mildly impaired
cardiac function (New York
Heart Association Functional
Class I or II: patients with no
limitation of activities or
patients with slight, mild
limitation of activity) (2)
i. <6 months
ii. ≥6 months
b. Moderately or severely
impaired cardiac function
(New York Heart Association
Functional Class III or IV:
patients with marked
limitation of activity or
patients who should be at
complete rest) (2).

Cu-IUD

LNG-IUD

Implants

DMPA

POP

CHCs

1
1

1
3*

Initiation Continuation Initiation Continuation
2
3
2
3

Initiation Continuation
2
3

1
1

2
4

2
2
2

1
1
2

4
3
4

Rheumatic Diseases
Systemic lupus
Initiation Continuation
erythematosus
This condition is associated
with increased risk for
adverse health events as a
result of pregnancy.
a. Positive (or unknown)
1*
1*
antiphospholipid antibodies

Initiation Continuation

See table footnotes on page 61.

MMWR / July 29, 2016 / Vol. 65 / No. 4

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

LNG-IUD

b. Severe thrombocytopenia
3*
2*
2*
c. Immunosuppressive therapy
2*
1*
2*
d. None of the above
1*
1*
2*
Rheumatoid arthritis
Initiation Continuation Initiation Continuation
a. Receiving immunosup2
1
2
1
pressive therapy
b. Not receiving immunosup1
1
pressive therapy

Implants
2*
2*
2*

DMPA
3*
2*
2*

2*
2*
2*

POP

CHCs

2*
2*
2*

2/3*

Neurologic Conditions
Headaches
a. Nonmigraine (mild or
severe)
b. Migraine
i. Without aura (This
category of migraine
includes menstrual
migraine.)
ii. With aura
Epilepsy
This condition is associated
with increased risk for adverse
health events as a result of
pregnancy.
Multiple sclerosis
a. With prolonged
immobility
b. Without prolonged
immobility

1
1

1
1*

4*
1*

1
1

1*
1*

Depressive Disorders
Depressive disorders

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
Initiation Continuation
1
1
a. Irregular pattern without
1
heavy bleeding
2*
1*
2*
b. Heavy or prolonged
bleeding (includes regular
and irregular patterns)
Unexplained vaginal bleeding Initiation Continuation Initiation Continuation
(suspicious for serious condition)
4*
2*
4*
2*
before evaluation
Endometriosis
2
1
Benign ovarian tumors
1
1
(including cysts)
Severe dysmenorrhea
2
1
Gestational trophoblastic
disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
a. Suspected gestational
trophoblastic disease
(immediate postevacuation)
i. Uterine size first trimester
1*
1*
ii. Uterine size second
2*
2*
trimester
b. Confirmed gestational
Initiation Continuation Initiation Continuation
trophoblastic disease (after
initial evacuation and during
monitoring)
i. Undetectable/
1*
1*
1*
1*
nonpregnant β-hCG levels
ii. Decreasing β-hCG levels
2*
1*
2*
1*
iii. Persistently elevated
2*
1*
2*
1*
β-hCG levels or malignant
disease, with no evidence
or suspicion of intrauterine
disease
See table footnotes on page 61.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

iv. Persistently elevated
4*
β-hCG levels or malignant
disease, with evidence or
suspicion of intrauterine
disease
Cervical ectropion
Cervical intraepithelial
neoplasia
Cervical cancer (awaiting
Initiation
treatment)
4
Breast disease
Breast cancer is associated
with increased risk of adverse
health events as a result of
pregnancy.
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer
d. Breast cancer
i. Current
ii. Past and no evidence of
current disease for 5 years
Endometrial hyperplasia
Endometrial cancer
Initiation
This condition is associated with
4
increased risk for adverse health
events as a result of pregnancy.
Ovarian cancer
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
Uterine fibroids
Anatomical abnormalities
a. Distorted uterine cavity (any
congenital or acquired uterine
abnormality distorting the
uterine cavity in a manner that
is incompatible with
IUD insertion)
b. Other abnormalities
(including cervical stenosis or
cervical lacerations) not
distorting the uterine cavity or
interfering with IUD insertion
Pelvic inflammatory disease
a. Past PID (assuming no
Initiation
current risk factors for STDs)
i. With subsequent
1
pregnancy
ii. Without subsequent
2
pregnancy
b. Current PID
4
Sexually transmitted diseases Initiation
a. Current purulent cervicitis
4
or chlamydial infection or
gonococcal infection
b. Vaginitis (including
2
Trichomonas vaginalis and
bacterial vaginosis)
c. Other factors related to STDs 2*

LNG-IUD
2*

1
1

Implants

1
2

Continuation Initiation Continuation
2
4
2

POP

CHCs

DMPA
1*

1
2

1
1

1
2

1
1
1

2
1
1

2*
1
1

1
1

4
3

1
1
Continuation Initiation Continuation
2
4
2
1

—

Continuation Initiation Continuation
1

2*
4
2*
Continuation Initiation Continuation
2*
4
2*

1
1*

1*
1*

1
1*

HIV
High risk for HIV
HIV infection
For women with HIV infection
who are not clinically well or not
receiving ARV therapy, this
condition is associated with
increased risk for adverse health
events as a result of pregnancy.
a. Clinically well receiving
ARV therapy

Initiation Continuation Initiation Continuation
2
2
2
2
—
—
—
—

—

See table footnotes on page 61.

MMWR / July 29, 2016 / Vol. 65 / No. 4

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
b. Not clinically well or not
receiving ARV therapy

Cu-IUD
2

LNG-IUD
1

Implants

DMPA

POP

CHCs

—

1
1

1*
1*
1

Other Infections
Schistosomiasis
Schistosomiasis with fibrosis of
the liver is associated with
increased risk for adverse health
events as a result of pregnancy.
a. Uncomplicated
1
1
b. Fibrosis of the liver (if
1
1
severe, see Cirrhosis)
Tuberculosis
Initiation Continuation Initiation Continuation
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
a. Nonpelvic
1
1
1
1
b. Pelvic
4
3
4
3
Malaria
1
1

Endocrine Conditions
Diabetes
Insulin-dependent diabetes;
diabetes with nephropathy,
retinopathy, neuropathy, or
diabetes with other vascular
disease; or diabetes of >20 years’
duration are associated with
increased risk of adverse health
events as a result of pregnancy.
a. History of gestational disease
b. Nonvascular disease
i. Non-insulin dependent
ii. Insulin dependent
c. Nephropathy, retinopathy,
or neuropathy
d. Other vascular disease or
diabetes of >20 years’ duration
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

1
1
1

2
2
2

2
2
3

2
2
2

2
2
3/4*

3/4*

1
1
1

Inflammatory bowel disease
(ulcerative colitis or Crohn’s
disease)
Gallbladder disease
a. Symptomatic
i. Treated by
cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic
History of cholestasis
a. Pregnancy related
b. Past COC related
Viral hepatitis

2/3*

1
1
1

2
2
2

3
3
2

1
1

1
2

2
3

a. Acute or flare
b. Carrier
c. Chronic
Cirrhosis
Severe cirrhosis is associated
with increased risk for adverse
health events as a result of
pregnancy.
a. Mild (compensated)
b. Severe (decompensated)
Liver tumors
Hepatocellular adenoma and
malignant liver tumors are
associated with increased risk
for adverse health events as a
result of pregnancy.
a. Benign

1
1
1

Initiation Continuation
3/4*
2
1
1
1
1

1
1

1
3

1
4

Gastrointestinal Conditions

See table footnotes on page 61.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma
b. Malignant (hepatoma)

Cu-IUD

LNG-IUD

Implants

DMPA

POP

CHCs

1
1
1

2
3
3

2
4
4

2
2

1
1

1
2

1
1
1
1
1
1
1

2*
1
1
1

1*
1
1
1

2*
1
1
1

1
2*
1
2*

1
2*
1
1*

1
2*
1
2*

2*
3*
1
2*

1
1
1

Respiratory Conditions
Cystic fibrosis
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
Anemias
Thalassemia
Sickle cell disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
Iron-deficiency anemia

Solid Organ Transplantation
Solid organ transplantation
Initiation Continuation Initiation Continuation
This condition is associated with
increased risk for adverse health
events as a result of pregnancy.
a. Complicated: graft failure
3
2
3
2
(acute or chronic), rejection,
or cardiac allograft
vasculopathy
b. Uncomplicated
2
2

Drug Interactions
Antiretroviral therapy
Initiation Continuation Initiation Continuation
a. Nucleoside reverse
transcriptase inhibitors (NRTIs)
i. Abacavir (ABC)
1/2*
1*
1/2*
1*
ii. Tenofovir (TDF)
1/2*
1*
1/2*
1*
iii. Zidovudine (AZT)
1/2*
1*
1/2*
1*
1/2*
1*
1/2*
1*
iv. Lamivudine (3TC)
v. Didanosine (DDI)
1/2*
1*
1/2*
1*
vi. Emtricitabine (FTC)
1/2*
1*
1/2*
1*
vii. Stavudine (D4T)
1/2*
1*
1/2*
1*
b. Nonnucleoside reverse
transcriptase inhibitors
(NNRTIs)
i. Efavirenz (EFV)
1/2*
1*
1/2*
1*
ii. Etravirine (ETR)
1/2*
1*
1/2*
1*
iii. Nevirapine (NVP)
1/2*
1*
1/2*
1*
iv. Rilpivirine (RPV)
1/2*
1*
1/2*
1*
c. Ritonavir-boosted
protease inhibitors
i. Ritonavir-boosted
1/2*
1*
1/2*
1*
atazanavir (ATV/r)
ii. Ritonavir-boosted
1/2*
1*
1/2*
1*
darunavir (DRV/r)
iii. Ritonavir-boosted
1/2*
1*
1/2*
1*
fosemprenavir (FPV/r)
iv. Ritonavir-boosted
1/2*
1*
1/2*
1*
lopinavir (LPV/r)
v. Ritonavir-boosted
1/2*
1*
1/2*
1*
saquinavir (SQV/r)
vi. Ritonavir-boosted
1/2*
1*
1/2*
1*
tipranavir (TPV/r)
d. Protease inhibitors
without ritonavir
i. Atazanavir (ATV)
1/2*
1*
1/2*
1*
ii. Fosamprenavir (FPV)
1/2*
1*
1/2*
1*
iii. Indinavir (IDV)
1/2*
1*
1/2*
1*
iv. Nelfinavir (NFV)
1/2*
1*
1/2*
1*
e. CCR5 co-receptor
antagonists
i. Maraviroc (MVC)
1/2*
1*
1/2*
1*
f. HIV integrase strand
transfer inhibitors
i. Raltegravir (RAL)
1/2*
1*
1/2*
1*
ii. Dolutegravir (DTG)
1/2*
1*
1/2*
1*
iii. Elvitegravir (EVG)
1/2*
1*
1/2*
1*
See table footnotes on next page.

MMWR / July 29, 2016 / Vol. 65 / No. 4

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
g. Fusion inhibitors
i. Enfuvirtide
Anticonvulsant therapy
a. Certain anticonvulsants
(phenytoin, carbamazepine,
barbiturates, primidone,
topiramate, and
oxcarbazepine)
b. Lamotrigine
Antimicrobial therapy
a. Broad-spectrum
antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampin or rifabutin
therapy
Psychotropic medications
a. SSRIs
St. John’s wort

Cu-IUD
1/2*

LNG-IUD
1*

1/2*

Implants

DMPA

POP

CHCs

1
1
1

1
1
2*

1
1
1*

1
1
3*

1
1

1
2

1
1

1
2

Abbreviations: BMI = body mass index; COC = combined oral contraceptive; Cu-IUD = copper-containing IUD; DMPA = depot medroxyprogesterone acetate; DVT = deep venous thrombosis;
hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; HIV = human immunodeficiency virus.; IUD = intrauterine device; LDL = low-density lipoprotein; LNG-IUD =
levonorgestrel-releasing IUD; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease; POP = progestin-only pill; SSRI = selective serotonin reuptake inhibitor;
STD = sexually transmitted disease.
* Consult the respective appendix for each contraceptive method in the 2016 U.S. Medical Eligibility Criteria for Contraceptive Use (1) for clarifications to the numeric categories.

References
1. Curtis KM, Tepper NK, Jatlaoui TC, et al. U.S. medical eligibility criteria
for contraceptive use, 2016. MMWR Recomm Rep 2016;65(No. RR-3).

2. The Criteria Committee of the New York Heart Association. Nomenclature
and criteria for diagnosis of diseases of the heart and great vessels. 9th ed.
Boston, MA: Little, Brown & Co; 1994.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 4

Recommendations and Reports

Appendix B
When To Start Using Specific Contraceptive Methods
When to start (if the provider is
reasonably certain that the woman
is not pregnant)

Contraceptive method

Additional contraception
(i.e., back-up) needed

Copper-containing IUD

Anytime

Not needed

Levonorgestrel-releasing IUD

Anytime

Implant

Anytime

Injectable

Anytime

Combined hormonal contraceptive

Anytime

Progestin-only pill

Anytime

If >7 days after menses started, use back-up
method or abstain for 7 days.
If >5 days after menses started, use back-up
method or abstain for 7 days.
If >7 days after menses started, use back-up
method or abstain for 7 days.
If >5 days after menses started, use back-up
method or abstain for 7 days.
If >5 days after menses started, use back-up
method or abstain for 2 days.

Examinations or tests needed
before initiation*
Bimanual examination and cervical
inspection†
Bimanual examination and cervical
inspection†
None
None
Blood pressure measurement
None

Abbreviations: BMI = body mass index; HIV = human immunodeficiency virus; IUD = intrauterine device; STD = sexually transmitted disease; U.S. MEC = U.S. Medical
Eligibility Criteria for Contraceptive Use.
* Weight (BMI) measurement is not needed to determine medical eligibility for any methods of contraception because all methods can be used (U.S. MEC 1) or generally
can be used (U.S. MEC 2) among obese women (Box 1). However, measuring weight and calculating BMI (weight [kg] / height [m]2) at baseline might be helpful for
monitoring any changes and counseling women who might be concerned about weight change perceived to be associated with their contraceptive method.
† Most women do not require additional STD screening at the time of IUD insertion. If a woman with risk factors for STDs has not been screened for gonorrhea and
chlamydia according to CDC’s STD Treatment Guidelines (http://www.cdc.gov/std/treatment), screening can be performed at the time of IUD insertion, and insertion
should not be delayed. Women with current purulent cervicitis or chlamydial infection or gonococcal infection should not undergo IUD insertion (U.S. MEC 4).

MMWR / July 29, 2016 / Vol. 65 / No. 4

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix C
Examinations and Tests Needed Before Initiation of Contraceptive Methods

The examinations or tests noted apply to women who are
presumed to be healthy (Table C1). Those with known medical
problems or other special conditions might need additional
examinations or tests before being determined to be appropriate
candidates for a particular method of contraception. The
2016 U.S. Medical Eligibility Criteria for Contraceptive Use
(U.S. MEC) might be useful in such circumstances (1). The
following classification was considered useful in differentiating
the applicability of the various examinations or tests:
• Class A: essential and mandatory in all circumstances for
safe and effective use of the contraceptive method.
• Class B: contributes substantially to safe and effective use,
but implementation may be considered within the public
health and/or service context; risk of not performing an
examination or test should be balanced against the benefits
of making the contraceptive method available.
• Class C: does not contribute substantially to safe and
effective use of the contraceptive method.

These classifications focus on the relationship of the
examinations or tests to safe initiation of a contraceptive
method. They are not intended to address the appropriateness
of these examinations or tests in other circumstances. For
example, some of the examinations or tests that are not deemed
necessary for safe and effective contraceptive use might be
appropriate for good preventive health care or for diagnosing
or assessing suspected medical conditions. Any additional
screening needed for preventive health care can be performed
at the time of contraception initiation and initiation should
not be delayed for test results.
No examinations or tests are needed before initiating
condoms or spermicides. A bimanual examination is necessary
for diaphragm fitting. A bimanual examination and cervical
inspection are needed for cervical cap fitting.
References
1. Curtis KM, Tepper NK, Jatlaoui TC, et al. U.S. medical eligibility criteria
for contraceptive use, 2016. MMWR Recomm Rep 2016;65(No. RR-3).

TABLE C1. Examinations and tests needed before initiation of contraceptive methods
Contraceptive method and class

Examination or test
Examination
Blood pressure
Weight (BMI) (weight [kg] / height [m]2)
Clinical breast examination
Bimanual examination and cervical inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou test)
STD screening with laboratory tests
HIV screening with laboratory tests

Diaphragm
or
cervical cap Spermicide

Cu-IUD and
LNG-IUD

Implant

Injectable

CHC

POP

Condom

C
—†
C
A

C
—†
C
C

A*
—†
C
C

C
—†
C
C

C
C
C
C

C
C
C
A§

C
C
C
C

C
C
C
C
C
C
—¶
C

C
C
C
C
C
C
C
C

Abbreviations: BMI = body mass index; CHC = combined hormonal contraceptive; Cu-IUD = copper-containing intrauterine device; HIV = human immunodeficiency
virus; LNG-IUD = levonorgestrel-releasing intrauterine device; POP = progestin-only pill; STD = sexually transmitted disease; U.S. MEC = U.S. Medical Eligibility Criteria
for Contraceptive Use.
* In instances in which blood pressure cannot be measured by a provider, blood pressure measured in other settings can be reported by the woman to her provider.
† Weight (BMI) measurement is not needed to determine medical eligibility for any methods of contraception because all methods can be used (U.S. MEC 1) or
generally can be used (U.S. MEC 2) among obese women (Box 1). However, measuring weight and calculating BMI at baseline might be helpful for monitoring any
changes and counseling women who might be concerned about weight change perceived to be associated with their contraceptive method.
§ A bimanual examination (not cervical inspection) is needed for diaphragm fitting.
¶ Most women do not require additional STD screening at the time of IUD insertion. If a woman with risk factors for STDs has not been screened for gonorrhea and chlamydia
according to CDC’s STD Treatment Guidelines (http://www.cdc.gov/std/treatment), screening can be performed at the time of IUD insertion, and insertion should not be
delayed. Women with current purulent cervicitis or chlamydial infection or gonococcal infection should not undergo IUD insertion (U.S. MEC 4).

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 4

Recommendations and Reports

Appendix D
Routine Follow-Up After Contraceptive Initiation
These recommendations address when routine follow-up
is recommended for safe and effective continued use
of contraception for healthy women (Table D1). The
recommendations refer to general situations and might

vary for different users and different situations. Specific
populations who might benefit from frequent follow-up visits
include adolescents, those with certain medical conditions or
characteristics, and those with multiple medical conditions.

TABLE D1. Routine follow-up after contraceptive initiation
Contraceptive method
Cu-IUD or LNG-IUD

Action
General follow-up
Advise women to return at any time to discuss side effects or
other problems or if they want to change the method. Advise
women using IUDs, implants, or injectables when the IUD or
implant needs to be removed or when a reinjection is needed.
No routine follow-up visit is required.
Other routine visits
Assess the woman’s satisfaction with her current method and
whether she has any concerns about method use.
Assess any changes in health status, including medications, that
would change the method’s appropriateness for safe and
effective continued use based on U.S. MEC (i.e., category 3 and 4
conditions and characteristics) (Box 1).
Consider performing an examination to check for the presence
of IUD strings.
Consider assessing weight changes and counseling women
who are concerned about weight change perceived to be
associated with their contraceptive method.
Measure blood pressure.

Implant

Injectable

CHC

POP

—

Abbreviations: CHC = combined hormonal contraceptives; Cu-IUD = copper-containing intrauterine device; HIV = human immunodeficiency virus; IUD = intrauterine
device; LNG-IUD = levonorgestrel-releasing intrauterine device; POP = progestin-only pills; U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use.

MMWR / July 29, 2016 / Vol. 65 / No. 4

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix E
Management of Women with Bleeding Irregularities While Using Contraception*
Management of women with bleeding irregularities while using contraception

If bleeding persists, or if the woman requests it, medical treatment can be considered.

Cu-IUD
users

LNG-IUD
users

For unscheduled
spotting or light
bleeding or for heavy
or prolonged bleeding:
• NSAIDs (5–7 days
of treatment)

Implant
users

Injectable
(DMPA) users

For unscheduled
spotting or light
bleeding or heavy/
prolonged bleeding:
• NSAIDs (5–7 days
of treatment)
• Hormonal treatment
(if medically eligible)
with COCs or
estrogen (10–20 days
of treatment)

For unscheduled
spotting or light
bleeding:
• NSAIDs (5–7 days
of treatment)

For heavy or
prolonged bleeding:
• NSAIDs (5–7 days of
treatment)
• Hormonal treatment
(if medically eligible)
with COCs or estrogen
(10–20 days of
treatment)

CHC users (extended or
continuous regimen)

Hormone-free interval
for 3–4 consecutive days

Not recommended during
the first 21 days of
extended or continuous
CHC use

Not recommended more
than once per month
because contraceptive
effectiveness might be
reduced

If bleeding disorder persists or woman finds it unacceptable

Counsel on alternative methods and offer another method, if desired.

Abbreviations: CHC = combined hormonal contraceptive; COC = combined oral contraceptive; Cu-IUD = copper-containing intrauterine device; DMPA = depot
medroxyprogesterone acetate; LNG-IUD = levonorgestrel-releasing intrauterine device; NSAIDs = nonsteroidal antiinflammatory drugs.
* If clinically warranted, evaluate for underlying condition. Treat the condition or refer for care. Heavy or prolonged bleeding, either unscheduled or menstrual, is
uncommon among LNG-IUD users and implant users.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 4

Recommendations and Reports

Appendix F
Management of Intrauterine Devices When Users are Found To Have
Pelvic Inflammatory Disease*
Management of intrauterine devices when users of copper-containing intrauterine devices or levonorgestrel-releasing intrauterine devices
are found to have pelvic inflammatory disease
• Treat PID.
• Counsel about condom use.
• IUD does not need to be removed.

Woman wants to continue IUD.

Woman wants to discontinue IUD.

Reassess in 24–48 hours.

Remove IUD after beginning antibiotics.

Clinical improvement

No clinical improvement

Continue IUD.

• Continue antibiotics.
• Consider removal of IUD.

• Offer another contraceptive method.
• Offer emergency contraception.

Abbreviations: IUD = intrauterine device; PID = pelvic inflammatory disease.
* Treat according to the CDC Sexually Transmitted Diseases Treatment Guidelines (http://www.cdc.gov/std/treatment).

MMWR / July 29, 2016 / Vol. 65 / No. 4

US Department of Health and Human Services/Centers for Disease Control and Prevention

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ISSN: 1057-5987 (Print)

Morbidity and Mortality Weekly Report
Recommendations and Reports / Vol. 65 / No. 3

U.S. Medical Eligibility Criteria
for Contraceptive Use, 2016

U.S. Department of Health and Human Services
Centers for Disease Control and Prevention

July 29, 2016

Recommendations and Reports

Disclosure of Relationship

Appendix I: Female and Male Sterilization ................................................ 92

Appendix J: Classifications for Emergency Contraception.................. 93
Appendix K: Summary of Classifications for Hormonal Contraceptive
Methods and Intrauterine Devices ............................................................ 96

MMWR Editorial Board
Timothy F. Jones, MD, Chairman
Matthew L. Boulton, MD, MPH
Virginia A. Caine, MD
Katherine Lyon Daniel, PhD
Jonathan E. Fielding, MD, MPH, MBA
David W. Fleming, MD

William E. Halperin, MD, DrPH, MPH
King K. Holmes, MD, PhD
Robin Ikeda, MD, MPH
Rima F. Khabbaz, MD
Phyllis Meadows, PhD, MSN, RN
Jewel Mullen, MD, MPH, MPA

Jeff Niederdeppe, PhD
Patricia Quinlisk, MD, MPH
Patrick L. Remington, MD, MPH
Carlos Roig, MS, MA
William L. Roper, MD, MPH
William Schaffner, MD

Recommendations and Reports

U.S. Medical Eligibility Criteria for Contraceptive Use, 2016
Kathryn M. Curtis, PhD1
Naomi K. Tepper, MD1
Tara C. Jatlaoui, MD1
Erin Berry-Bibee, MD1,2
Leah G. Horton, MSPH1
Lauren B. Zapata, PhD1
Katharine B. Simmons, MD1,2
H. Pamela Pagano, MPH1
Denise J. Jamieson, MD1
Maura K. Whiteman, PhD1
1Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, CDC, Atlanta, Georgia
2Department of Obstetrics and Gynecology, University of North Carolina School of Medicine, Chapel Hill, North Carolina

Summary
The 2016 U.S. Medical Eligibility Criteria for Contraceptive Use (U.S. MEC) comprises recommendations for the use of
specific contraceptive methods by women and men who have certain characteristics or medical conditions. These recommendations
for health care providers were updated by CDC after review of the scientific evidence and consultation with national experts who
met in Atlanta, Georgia, during August 26–28, 2015. The information in this report updates the 2010 U.S. MEC (CDC. U.S.
medical eligibility criteria for contraceptive use, 2010. MMWR 2010:59 [No. RR-4]). Notable updates include the addition
of recommendations for women with cystic fibrosis, women with multiple sclerosis, and women receiving certain psychotropic drugs
or St. John’s wort; revisions to the recommendations for emergency contraception, including the addition of ulipristal acetate; and
revisions to the recommendations for postpartum women; women who are breastfeeding; women with known dyslipidemias, migraine
headaches, superficial venous disease, gestational trophoblastic disease, sexually transmitted diseases, and human immunodeficiency
virus; and women who are receiving antiretroviral therapy. The recommendations in this report are intended to assist health care
providers when they counsel women, men, and couples about contraceptive method choice. Although these recommendations are
meant to serve as a source of clinical guidance, health care providers should always consider the individual clinical circumstances
of each person seeking family planning services. This report is not intended to be a substitute for professional medical advice for
individual patients. Persons should seek advice from their health care providers when considering family planning options.

Introduction
Approximately 45% of all pregnancies that occur in the
United States are unintended (1), with associated increased
risks for adverse maternal and infant health outcomes (2) and
increased health care costs (3). Women, men, and couples
have increasing numbers of safe and effective choices for
contraceptive methods, including long-acting reversible
contraception methods such as intrauterine devices (IUDs)
and implants, to reduce the risk for an unintended pregnancy.
However, with these expanded options comes the need for
evidence-based guidance to help health care providers offer
quality family planning care to their patients, including
choosing the most appropriate contraceptive method for
Corresponding author: Kathryn M. Curtis, PhD, Division of
Reproductive Health, National Center for Chronic Disease Prevention
and Health Promotion, CDC. Telephone: 770-488-5200; E-mail:
[email protected].

individual circumstances and using that method correctly,
consistently, and continuously to maximize effectiveness.
In 2010, CDC published the first U.S. Medical Eligibility
Criteria for Contraceptive Use (U.S. MEC), which provided
recommendations on safe use of contraceptive methods
for women with various medical conditions and other
characteristics (and was adapted from global guidance
developed by the World Health Organization [WHO MEC])
(4,5). U.S. MEC is a companion document to the U.S. Selected
Practice Recommendations for Contraceptive Use (U.S. SPR),
which provides guidance on how to use contraceptive methods
safely and effectively once they are deemed to be medically
appropriate (6). WHO intended for the global guidance to
be used by local or national policy makers, family planning
program managers, and the scientific community as a reference
when they develop family planning guidance at the country
or program level. During 2008–2010, CDC participated in a
formal process to adapt the global guidance for appropriateness

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

for use in the United States, which included rigorous
identification and critical appraisal of the scientific evidence
through systematic reviews, and input from national experts
on how to translate that evidence into recommendations for
U.S. health care providers (5). At that time, CDC committed
to keeping this guidance up to date and based on the best
available evidence, with full review every few years (5).
This document updates CDC’s U.S. MEC 2010 (5), based
on new evidence and input from experts. A summary of
changes from U.S. MEC 2010 is provided (Appendix A).
Notable updates include the following:
• addition of recommendations for women with cystic
fibrosis, women with multiple sclerosis, and women
receiving certain psychotropic drugs or St. John’s wort
• revisions to the recommendations for emergency
contraception, including the addition of ulipristal acetate
• revisions to the recommendations for postpartum women;
women who are breastfeeding; women with known
dyslipidemias, migraine headaches, superficial venous
disease, gestational trophoblastic disease, sexually transmitted
diseases (STDs), and human immunodeficiency virus
(HIV); and women who are receiving antiretroviral therapy
The goal of these recommendations is to remove unnecessary
medical barriers to accessing and using contraception, thereby
decreasing the number of unintended pregnancies. These
recommendations are meant to serve as a source of clinical
guidance for health care providers; health care providers should
always consider the individual clinical circumstances of each
person seeking family planning services. This report is not
intended to be a substitute for professional medical advice for
individual patients, who should seek advice from their health
care providers when considering family planning options.

Methods
Since publication of U.S. MEC 2010, CDC has monitored
the literature for new evidence relevant to the recommendations
through the WHO/CDC continuous identification of research
evidence (CIRE) system. This system identifies new evidence
as it is published and allows WHO and CDC to update
systematic reviews and facilitate updates to recommendations
as new evidence warrants. Automated searches are run in
PubMed weekly, and the results are reviewed. Abstracts that
meet specific criteria are added to the web-based CIRE system,
which facilitates coordination and peer review of systematic
reviews for both WHO and CDC (7). In 2014, CDC reviewed
all of the existing recommendations in U.S. MEC 2010 for
new evidence identified by CIRE that had the potential to
lead to a changed recommendation. During August 27–28,

MMWR / July 29, 2016 / Vol. 65 / No. 3

2014, CDC held a meeting in Atlanta, Georgia, of 11
family planning experts and representatives from partner
organizations to solicit their input on the scope of and process
for updating both U.S. MEC 2010 and U.S. SPR 2013. The
participants were experts in family planning and represented
various types of health care providers, as well as health care
provider organizations. A list of participants is provided
at the end of this report. Meeting participants discussed
topics to be addressed in the update of U.S. MEC based on
new evidence published since 2010 (identified through the
CIRE system), topics addressed at a 2014 WHO meeting to
update global guidance, and suggestions CDC received from
health care providers for the addition of recommendations
for women with medical conditions not yet included in
U.S. MEC (e.g., from provider feedback through e-mail,
public inquiry, and questions received at conferences). CDC
identified several topics to consider when updating the
guidance, including revision of existing recommendations for
certain medical conditions or characteristics (breastfeeding,
postpartum, HIV, receiving antiretroviral therapy, obesity,
dyslipidemia, increased risk for STDs, superficial venous
thrombosis, gestational trophoblastic disease, and migraine
headaches), addition of recommendations for new medical
conditions (cystic fibrosis, multiple sclerosis, use of certain
psychotropic drugs, and St. John’s wort), and addition of
recommendations for new contraceptive methods (ulipristal
acetate for emergency contraception). CDC determined that
all other recommendations in U.S. MEC 2010 were up to
date and consistent with the existing body of evidence for
that recommendation.
In preparation for a subsequent expert meeting held during
August 26–28, 2015, to review the scientific evidence for
potential recommendations, CDC staff members and other
invited authors listed at the end of this report conducted
independent systematic reviews for each of the topics being
considered. The purpose of these systematic reviews was to
identify direct evidence about the safety of contraceptive
method use by women with selected conditions (e.g., risk for
disease progression or other adverse health effects in women with
multiple sclerosis who use combined hormonal contraceptives
[CHCs]). Preferred Reporting Items for Systematic Reviews
and Meta-Analyses (PRISMA) guidelines were followed for
reporting systematic reviews (8,9), and strength and quality
of the evidence were assigned using the system of the U.S.
Preventive Services Task Force (10). When direct evidence
was limited or not available, indirect evidence (e.g., evidence
on surrogate outcomes or among healthy women) and
theoretical issues were considered and either added to direct
evidence within a systematic review or separately compiled for
presentation to the meeting participants. Completed systematic

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

reviews were peer reviewed by two or three experts and then
provided to participants before the expert meeting. Reviews
are referenced and cited throughout this document; the full
reviews appear in the published literature and contain the
details of each review, including the systematic review question,
literature search protocol, inclusion and exclusion criteria,
evidence tables, and quality assessments. CDC staff continued
to monitor new evidence identified through the CIRE system
during the preparation for the August 2015 meeting.
During August 26–28, 2015, in Atlanta, Georgia, CDC
held a meeting with 44 participants who were invited to
provide their individual perspectives on the scientific evidence
presented and potential recommendations. Twenty-nine of the
participants represented a wide range of expertise in family
planning provision and research, and included obstetricians/
gynecologists, pediatricians, family physicians, nurse
practitioners, epidemiologists, and others with research and
clinical practice expertise in contraceptive safety, effectiveness,
and management; these individuals participated in the entire
meeting. Fifteen participants with expertise relevant to
specific topics on the meeting agenda provided information
and participated in the discussion (e.g., an expert in cystic
fibrosis was asked to provide general information about the
condition and to assist in interpreting the evidence and any
theoretical concerns on the use of contraceptive methods in
women with the condition); these participants provided input
only during the session for which their topics were discussed.
Lists of participants and any potential conflicts of interest
are provided at the end of this report. During the meeting,
the evidence from the systematic review for each topic was
presented, including direct evidence and any indirect evidence
or theoretical concerns. Participants provided their perspectives
on using the evidence to develop recommendations that would
meet the needs of U.S. health care providers. After the meeting,
CDC determined the recommendations in this report, taking
into consideration the perspectives provided by the meeting
participants. Feedback also was received from three external
reviewers, composed of health care providers and researchers
who had not participated in the update meetings. These
reviewers were asked to provide comments on the accuracy,
feasibility, and clarity of the recommendations. Areas of
research that need additional investigation also were considered
during the meeting (11).

How to Use This Document
These recommendations are intended to help health care
providers determine the safe use of contraceptive methods
among women and men with various characteristics and

medical conditions. Providers also can use the information in
these recommendations when consulting with women, men,
and couples about their selection of contraceptive methods. The
tables in this document include recommendations for the use
of contraceptive methods by women and men with particular
characteristics or medical conditions. Each condition is defined
as representing either an individual’s characteristics (e.g., age
or history of pregnancy) or a known preexisting medical or
pathologic condition (e.g., diabetes or hypertension). The
recommendations refer to contraceptive methods being used
for contraceptive purposes; the recommendations do not
consider the use of contraceptive methods for treatment of
medical conditions because the eligibility criteria in these
situations might differ. The conditions affecting eligibility for
the use of each contraceptive method are classified into one of
four categories (Box 1).

Using the Categories in Practice
Health care providers can use the eligibility categories when
assessing the safety of contraceptive method use for women
and men with specific medical conditions or characteristics.
Category 1 comprises conditions for which no restrictions
exist for use of the contraceptive method. Classification
of a method/condition as category 2 indicates the method
generally can be used, although careful follow-up might be
required. For a method/condition classified as category 3,
use of that method usually is not recommended unless other
more appropriate methods are not available or acceptable. The
severity of the condition and the availability, practicality, and
acceptability of alternative methods should be considered,
and careful follow-up is required. Hence, provision of a
contraceptive method to a woman with a condition classified
as category 3 requires careful clinical judgement and access to
clinical services. Category 4 comprises conditions that represent
an unacceptable health risk if the method is used. For example,
a smoker aged <35 years generally can use combined oral
contraceptives (COCs) (category 2). However, for a woman
BOX 1. Categories of medical eligibility criteria for contraceptive use

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

aged ≥35 years who smokes <15 cigarettes per day, the use
of COCs usually is not recommended unless other methods
are not available or acceptable to her (category 3). A woman
aged ≥35 years who smokes ≥15 cigarettes per day should not
use COCs because of unacceptable health risks, primarily the
risk for myocardial infarction and stroke (category 4). The
programmatic implications of these categories might depend
on the circumstances of particular professional or service
organizations. For example, in some settings, a category 3
might mean that a special consultation is warranted.
The recommendations address medical eligibility criteria for
the initiation and continued use of all methods evaluated. The
issue of continuation criteria is clinically relevant whenever
a medical condition develops or worsens during use of a
contraceptive method. When the categories differ for initiation
and continuation, these differences are noted in the Initiation
and Continuation columns. When initiation and continuation
are not indicated, the category is the same for initiation and
continuation of use.
On the basis of this classification system, the eligibility criteria
for initiating and continuing use of a specific contraceptive
method are presented in tables (Appendices A–K). In these
tables, the first column indicates the condition. Several
conditions are divided into subconditions to differentiate
between varying types or severity of the condition. The second
column classifies the condition for initiation or continuation
(or both) into category 1, 2, 3, or 4. For certain conditions,
the numeric classification does not adequately capture the
recommendation; in these cases, the third column clarifies the
numeric category. These clarifications were determined during
the discussions of the scientific evidence and are considered a
necessary element of the recommendation. The third column
also summarizes the evidence for the recommendation if
evidence exists. The recommendations for which no evidence
is cited are based on expert opinion from either the WHO or
U.S. expert meeting in which these recommendations were
developed, and might be based on evidence from sources
other than systematic reviews. For certain recommendations,
additional comments appear in the third column and generally
come from the WHO meeting or the U.S. meeting.

Recommendations for Use of
Contraceptive Methods
The classifications for whether women with certain medical
conditions or characteristics can use specific contraceptive
methods are provided for intrauterine contraception, including
the copper-containing IUD and levonorgestrel-releasing IUDs

MMWR / July 29, 2016 / Vol. 65 / No. 3

(Appendix B); progestin-only contraceptives (POCs), including
etonogestrel implants, depot medroxyprogesterone acetate
injections, and progestin-only pills (Appendix C); CHCs,
including low-dose (containing ≤35 µg ethinyl estradiol)
COCs, combined hormonal patch, and combined vaginal
ring (Appendix D); barrier contraceptive methods, including
male and female condoms, spermicides, diaphragm with
spermicide, and cervical cap (Appendix E); fertility awareness–
based methods (Appendix F); lactational amenorrhea method
(Appendix G); coitus interruptus (Appendix H); female and
male sterilization (Appendix I); and emergency contraception,
including emergency use of the copper-containing IUD and
emergency contraceptive pills (Appendix J). A table at the end
of this report summarizes the classifications for the hormonal
and intrauterine methods (Appendix K).

Contraceptive Method Choice
Many elements need to be considered by women, men, or
couples at any given point in their lifetimes when choosing
the most appropriate contraceptive method. These elements
include safety, effectiveness, availability (including accessibility
and affordability), and acceptability. The guidance in this
report focuses primarily on the safety of a given contraceptive
method for a person with a particular characteristic or medical
condition. Therefore, the classification of category 1 means
that the method can be used in that circumstance with no
restrictions with regard to safety but does not necessarily imply
that the method is the best choice for that person; other factors,
such as effectiveness, availability, and acceptability, might
play an important role in determining the most appropriate
choice. Voluntary informed choice of contraceptive methods
is an essential guiding principle, and contraceptive counseling,
when applicable, might be an important contributor to the
successful use of contraceptive methods.
In choosing a method of contraception, dual protection from
the simultaneous risk for HIV and other STDs also should be
considered. Although hormonal contraceptives and IUDs are
highly effective at preventing pregnancy, they do not protect
against STDs, including HIV. Consistent and correct use of the
male latex condom reduces the risk for HIV infection and other
STDs, including chlamydial infection, gonococcal infection,
and trichomoniasis (12). Although evidence is limited, use
of female condoms can provide protection from acquisition
and transmission of STDs (12). All patients, regardless of
contraceptive choice, should be counseled about the use of
condoms and the risk for STDs, including HIV infection (12).
Additional information about prevention and treatment of
STDs is available from the CDC Sexually Transmitted Diseases
Treatment Guidelines (http://www.cdc.gov/std/treatment) (12).

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Contraceptive Method Effectiveness
Contraceptive method effectiveness is critical for minimizing
the risk for an unintended pregnancy, particularly among women
for whom an unintended pregnancy would pose additional
health risks. The effectiveness of contraceptive methods depends
both on the inherent effectiveness of the method itself and on
how consistently and correctly it is used (Figure). Methods
that depend on consistent and correct use have a wide range of
effectiveness. IUDs and implants are considered long-acting,
reversible contraception (LARC); these methods are highly
effective because they do not depend on regular compliance
from the user. LARC methods are appropriate for most women,
including adolescents and nulliparous women. All women
should be counseled about the full range and effectiveness of
contraceptive options for which they are medically eligible so
that they can identify the optimal method.

Unintended Pregnancy and Increased
Health Risk
For women with conditions that might make pregnancy
an unacceptable health risk, long-acting, highly effective
contraceptive methods might be the best choice to avoid
unintended pregnancy (Figure). Women with these conditions
should be advised that sole use of barrier methods for
contraception and behavior-based methods of contraception
might not be the most appropriate choice because of their
relatively higher typical-use rates of failure (Figure). Conditions
included in U.S. MEC that are associated with increased
risk for adverse health events as a result of pregnancy are
identified throughout the document (Box 2). Some of the
medical conditions included in U.S. MEC recommendations
are treated with teratogenic drugs. While the woman’s
medical condition may not affect her eligibility to use certain
contraceptive methods, women using teratogenic drugs are
at increased risk for poor pregnancy outcomes; long-acting,
highly effective contraceptive methods might be the best
option to avoid unintended pregnancy or delay pregnancy
until teratogenic drugs are no longer needed.

Keeping Guidance Up to Date
Updating the evidence-based recommendations as new
scientific evidence becomes available is a challenge. CDC
will continue to work with WHO to identify and assess new
relevant evidence as it becomes available and to determine
whether changes in the recommendations are warranted (7).
In most cases, U.S. MEC follows the WHO guidance updates,

BOX 2. Conditions associated with increased risk for adverse health
events as a result of pregnancy*

Breast cancer
Complicated valvular heart disease
Cystic fibrosis
Diabetes: insulin dependent; with nephropathy,
retinopathy, or neuropathy or other vascular disease;
or of >20 years’ duration
Endometrial or ovarian cancer
Epilepsy
Hypertension (systolic ≥160 mm Hg or diastolic
≥100 mm Hg)
History of bariatric surgery within the past 2 years
HIV: not clinically well or not receiving antiretroviral therapy
Ischemic heart disease
Gestational trophoblastic disease
Hepatocellular adenoma and malignant liver
tumors (hepatoma)
Peripartum cardiomyopathy
Schistosomiasis with fibrosis of the liver
Severe (decompensated) cirrhosis
Sickle cell disease
Solid organ transplantation within the past 2 years
Stroke
Systemic lupus erythematosus
Thrombogenic mutations
Tuberculosis
* Long-acting, highly effective contraceptive methods might be the best
choice for women with conditions that are associated with increased risk
for adverse health events as a result of pregnancy. These women should
be advised that sole use of barrier methods for contraception and behaviorbased methods of contraception might not be the most appropriate choice
because of their relatively higher typical-use rates of failure.

which typically occur every 5 years (or sooner if warranted
by new data). However, CDC will review all WHO updates
for their application in the United States. CDC also will
identify and assess any new literature for the recommendations
and medical conditions that are not included in the WHO
guidance. CDC will completely review U.S. MEC every 5 years
as well. Updates to the guidance will appear on the CDC
U.S. MEC website (http://www.cdc.gov/reproductivehealth/
UnintendedPregnancy/USMEC.htm).
Acknowledgments
This report is based, in part, on the work of the Promoting Family
Planning Team, Department of Reproductive Health and Research,
World Health Organization, and its development of Medical
Eligibility Criteria for Contraceptive Use, 5th edition.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

FIGURE. Effectiveness of family planning methods*
Most
Effective

Implant

Reversible
Intrauterine Device
(IUD)

Male Sterilization
(Vasectomy)

Permanent
Female Sterilization
(Abdominal, Laparoscopic, Hysteroscopic)

0.05 %

LNG - 0.2 % Copper T - 0.8 %
Pill

0.15 %
Patch

SUN MON TUES WED THUR FRI

0.5 %
Ring

Diaphragm

SAT

Injectable: Get repeat
injections on time.
Pills: Take a pill each day.

6-12 pregnancies per
100 women in a year

After procedure, little or
nothing to do or remember.
Vasectomy and
hysteroscopic sterilization:
Use another method for
first 3 months.

Less than 1 pregnancy
per 100 women in a year

Injectable

How to make your method
most effective

Patch, Ring: Keep in place,
change on time.

2
3
4

6%
Male Condom

9%
Female Condom

9%
Withdrawal

12 %
Sponge

18 or more pregnancies
per 100 women in a year
18 %
Fertility-Awareness
Based Methods
JANUARY
[1

Least
Effective

2 3 4 5 6 7
10] 11 12 13 14

8 9
15 16
22 [23
29 30

17 18 19 20 21
24 25 26 27 28
31 1 2 3 4

24 %

21 %

22 %

Spermicide

Spe

icid

24 % parous women
12 % nulliparous women

28 %

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

U.S. Medical Eligibility Criteria for
Contraceptive Use Participants
CDC Guideline Development Group for U.S. Medical Eligibility
Criteria for Contraceptive Use and U.S. Selected Practice
Recommendations for Contraceptive Use
Kathryn M. Curtis, PhD (Chair), Erin Berry-Bibee, MD,
Suzanne G. Folger, PhD, Leah G. Horton, MSPH, Denise J.
Jamieson, MD, Tara C. Jatlaoui, MD, Polly A. Marchbanks, PhD, H.
Pamela Pagano, MPH, Halley E.M. Riley, MPH, Mirelys Rodriguez,
Katharine B. Simmons, MD, Naomi K. Tepper, MD, Maura K.
Whiteman, PhD, Lauren B. Zapata, PhD, CDC, Atlanta, Georgia.
Invited Meeting Participants, August 27–28, 2014, Atlanta, Georgia
Herbert Peterson, MD, University of North Carolina, Chapel
Hill, North Carolina (Chair); Gale Burstein, MD, Erie County
Department of Health, Buffalo, New York; Alison Edelman, MD,
Oregon Health and Science University, Portland, Oregon; Eve Espey,
MD, University of New Mexico, Albuquerque, New Mexico; Emily
Godfrey, MD, University of Washington, Seattle, Washington;
Andrew Kaunitz, MD, University of Florida, Jacksonville, Florida;
Susan Moskosky, MS, U.S. Department of Health and Human
Services, Rockville, Maryland; Kavita Nanda, MD, FHI360 and
American College of Obstetricians and Gynecologists, Durham,
North Carolina; Deborah Nucatola, MD, Planned Parenthood
Federation of America, New York, New York; Michael Policar, MD,
University of California, San Francisco, California; Carolyn Westhoff,
MD, Columbia University, New York, New York.
Systematic Review Presenters and Authors, Meeting, August 26–28,
2015, Atlanta, Georgia
Erin Berry-Bibee, MD, Kathryn M. Curtis, PhD, Leah G. Horton,
MSPH, Denise J. Jamieson, MD, Tara C. Jatlaoui, MD, Polly A.
Marchbanks PhD, Titilope Oduyebo, MD, Pamela Pagano, MPH,
Halley E.M. Riley, MPH, Katharine B. Simmons, MD, Naomi K.
Tepper, MD, Maura K. Whiteman, PhD, Lauren B. Zapata, PhD,
CDC, Atlanta, Georgia; Monica Dragoman, MD, Mary E. Gaffield,
PhD, Sharon J. Phillips, MD, Marleen Temmerman, MD, World Health
Organization, Geneva, Switzerland; Andra James, MD, Duke University
Medical Center, Durham, North Carolina; Nathalie Kapp, MD, HRA
Pharma, Paris, France; Kavita Nanda, MD, FHI360, Durham, North
Carolina; Seth Walker, MD, Emory University, Atlanta, Georgia.
Invited Meeting Participants, August 26–28, 2015, Atlanta, Georgia
Herbert Peterson, MD, University of North Carolina, Chapel
Hill, North Carolina (Chair); Rebecca Allen, MD, American Society
for Reproductive Medicine and Women and Infants Hospital,
Providence, Rhode Island; Jean Anderson, MD, Johns Hopkins
University, Baltimore, Maryland; Abbey Berenson, MD, University
of Texas Medical Branch, Galveston, Texas; Amanda Black, MD,
University of Ottawa, Ontario, Canada; Cora Collette Breuner, MD,
American Academy of Pediatrics and Seattle Children’s Hospital,
Seattle, Washington; Gale Burstein MD, Erie County Department
of Health, Buffalo, New York; Anne Calhoun, MD, University of
North Carolina, Chapel Hill, North Carolina; Nahida Chakhtoura,

MD, National Institutes of Health, Rockville, Maryland; Alicia
Christy, MD, National Institutes of Health, Rockville, Maryland;
Mitchell D. Creinin, MD, University of California, Davis, California;
Linda Dominguez, Southwest Women’s Health, Albuquerque,
New Mexico; Alison Edelman, MD, Oregon Health and Science
University, Portland, Oregon; Eve Espey, MD, University of
New Mexico, Albuquerque, New Mexico; Emily Godfrey, MD,
University of Washington, Seattle, Washington; Marji Gold, MD,
Albert Einstein College of Medicine, Bronx, New York; Donald
Goldstein, MD, Harvard Medical School, Boston, Massachusetts;
Robert Hatcher, MD, Emory University, Atlanta, Georgia; Mark
Hathaway, MD, JHPIEGO and Unity Healthcare, Washington,
DC; Stephen Heartwell, MD, Susan Thompson Buffett Foundation,
Omaha, Nebraska; Paula Hillard, MD, Stanford University, Palo
Alto, California; Maria Houtchens, MD, Harvard Medical School,
Boston, Massachusetts; Andra James, MD, Duke University Medical
Center, Durham, North Carolina; Andrew Kaunitz, MD, University
of Florida, Jacksonville, Florida; Myong-Jin Kim, Pharm-D, Food
and Drug Administration, Rockville, Maryland; Barbara Konkle,
MD, Bloodworks Northwest, Seattle, Washington; Tobias Kurth,
MD, INSERM, Bordeaux, France; Miriam Labbok, MD, Academy
of Breastfeeding Medicine and University of North Carolina, Chapel
Hill, North Carolina; Reagan McDonald-Mosley, MD, Planned
Parenthood Federation of America, New York, New York; Joan
Meek, MD, American Academy of Pediatrics and Florida State
University College of Medicine, Orlando, Florida; Mark Mirochnick,
MD, Boston University, Boston, Massachusetts; Susan Moskosky,
MS, U.S. Department of Health and Human Services, Rockville,
Maryland; Kavita Nanda, MD, FHI360, Durham, North Carolina;
Jeffrey Peipert, MD, Washington University, St. Louis, Missouri;
Michael Policar, MD, University of California, San Francisco,
California; Sarah Prager, MD, University of Washington, Seattle
Washington; David Soper, MD, Medical University of South
Carolina, Charleston, South Carolina; Lisa Soule, MD, Food and
Drug Administration, Rockville, Maryland; Alison Stuebe, MD,
American College of Obstetricians and Gynecologist and University
of North Carolina, Chapel Hill, North Carolina; James Trussell,
PhD, Princeton University, Princeton, New Jersey; Seth Walker, MD,
Emory University, Atlanta, Georgia; Nanette Wenger, MD, Emory
University, Atlanta, Georgia; Carolyn Westhoff, MD, Columbia
University, New York, New York; Christopher Zahn, MD, American
College of Obstetricians and Gynecologists, Washington, DC.
CDC Attendees
Wanda D. Barfield, MD, Peter Briss, MD, W. Craig Hooper, PhD,
Jill Huppert, MD, Caroline King, PhD, Michele Mandel, Titilope
Oduyebo, MD, Cria Perrine, MD, Sam Posner, PhD.
External Reviewers
Abigail R.A. Aiken, PhD, Princeton University, Princeton, New
Jersey; Linda Burdette, PA-C, Premier Women’s Health of Yakima,
Yakima, Washington; Mimi Zieman, MD, Planned Parenthood
Southeast, Atlanta, Georgia.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Conflicts of Interest for Invited Meeting Participants,
August 26–28, 2015, Atlanta, Georgia
Rebecca Allen, Nexplanon trainer for Merck and Liletta trainer for
Actavis, consultant, advisory board and education grant from Bayer;
Mitchell D. Creinin, Nexplanon trainer for Merck, litigation consultant
for Bayer, advisory board for Merck and Teva Pharmaceutical Industries,
Ltd., consultant for Lemonaid – PolkaDoc app, research support
to University of California, Davis from Medicines360, Contramed,
Merck, Eunice Kennedy Shriver National Institute of Child Health
and Human Development, and Society of Family Planning; Linda
Dominguez, speaker for Bayer, Merck, and Actavis; Alison Edelman,
royalties from Up to Date, Inc., consultant for Genzyme, grant support
from the National Institutes of Health and the Gates Foundation,
travel funds from the World Health Organization, grant support and
honorarium from Society of Family Planning, honorarium and travel
funds from Contemporary Forum, trainer for Merck, consultant
for Gynuity Health Projects, honorarium from CDC, Projects In
Knowledge, and American Congress of Obstetricians and Gynecologists,
advisory board for Agile Therapeutics; Eve Espey, travel funds from
the American Congress of Obstetricians and Gynecologists, Society
for Family Planning, and U.S. Food and Drug Administration,
Reproductive and Drug Advisory Committee for U.S. Food and Drug
Administration, travel funds and honoraria from Wayne State University,
Telluride Conference, New Mexico Department of Health Clinician
Conference, Planned Parenthood National Medical Conference and
Society of Family Planning, British Columbia Contraception Access
Research Team Conference, and American Congress of Obstetricians
and Gynecologists annual meeting; Emily Godfrey, research funding
from Bayer Women’s Health, Prima-Temp, and Teva Pharmaceutical
Industries, Ltd., trainer for Merck and Upstream USA, grant reviewer
for Fellowship of Family Planning and Society of Family Planning
Research Fund; Mark Hathaway, Liletta trainer and speaker for Actavis
and Medicines360, Nexplanon trainer for Merck, advisory board for
Contramed and Afaxys Pharmaceuticals; Paula Hillard, consultant for
American Civil Liberties Union, Advanced Health Media, CMEology,
National Sleep Foundation, and Planned Parenthood Federation of
America, honoraria from National Sleep Foundation, Dignity Health,
CMEology, Advance Health Media, and Medscape, editorial board for
Advanstar–Contemporary OB/GYN, board examiner for the American
Board of Obstetrics and Gynecology, contract reviewer for the U.S.
Department of Health and Human Services, editorial board for EBSCO–
PEMSoft, Nexplanon trainer for Merck, scientific advisor to Proctor and
Gamble, publication royalties from Wiley Blackwell Publishing; Andrew
Kaunitz, advisory board participant of Allergan, Bayer, Merck, and Pfizer,
clinical trial funding to University of Florida from Agile Therapeutics,
Bayer, Merck; Mark Mirochnick, data and safety monitoring board for
Merck and ViiV Healthcare, advisory board for Merck; Jeffrey Peipert,
research funding from Bayer and Teva Pharmaceutical Industries, Ltd.,
advisory board for Perrigo; Michael Policar, litigation consultant for
Bayer; James Trussell, advisory board for Merck and Teva Pharmaceutical
Industries, Ltd., consultant for Bayer; Nanette Wenger, research grants

MMWR / July 29, 2016 / Vol. 65 / No. 3

from Alnylam Pharmaceuticals, Gilead Sciences, National Heart, Lung,
and Blood Institute, Pfizer, and Society for Women’s Health Research,
consultant for Amgen, AstraZeneca, Gilead Sciences and Merck;
Carolyn Westhoff, data and safety monitoring board for Merck and
Bayer, advisory board for Agile Therapeutics, MicroChips Biotech, and
Actavis, research support to Columbia University from Medicines360,
León Farma, and ContraMed.
Handling Conflicts of Interest
To promote transparency, all participants were asked to disclose any
potential conflicts of interest to CDC prior to the expert meeting and
to report any potential conflicts of interest during the introductory
portion of the expert meeting. All potential conflicts of interest are
listed above. No participants were excluded from discussion based
on potential conflicts of interest. CDC staff who ultimately decided
and developed these recommendations have no financial interests or
other relationships with the manufacturers of commercial products,
suppliers of commercial services, or commercial supporters relevant
to these recommendations.
References
1. Finer LB, Zolna MR. Declines in unintended pregnancy in the United
States, 2008–2011. N Engl J Med 2016;374:843–52.http://dx.doi.
org/10.1056/NEJMsa1506575
2. Gipson JD, Koenig MA, Hindin MJ. The effects of unintended pregnancy
on infant, child, and parental health: a review of the literature. Stud Fam Plann
2008;39:18–38. http://dx.doi.org/10.1111/j.1728-4465.2008.00148.x
3. Sonfield A, Kost K. Public costs from unintended pregnancies and the role
of public insurance programs in paying for pregnancy-related care: national
and state estimates for 2010. New York: Guttmacher Institute; 2015.
4. World Health Organization. Medical eligibility criteria for contraceptive
use. 4th ed. Geneva, Switzerland: World Health Organization; 2009.
5. CDC. U.S. medical eligibility criteria for contraceptive use, 2010.
MMWR Recomm Rep 2010;59(No. RR-4).
6. Curtis KM, Jatlaoui TC, Tepper NK, et al. U.S. selected practice
recommendations for contraceptive use, 2016. MMWR Recomm Rep
2016;65(No. RR-4).
7. Mohllajee AP, Curtis KM, Flanagan RG, Rinehart W, Gaffield ML,
Peterson HB. Keeping up with evidence a new system for WHO’s
evidence-based family planning guidance. Am J Prev Med 2005;28:483–
90.http://dx.doi.org/10.1016/j.amepre.2005.02.008
8. Liberati A, Altman DG, Tetzlaff J, et al. The PRISMA statement for
reporting systematic reviews and meta-analyses of studies that evaluate
health care interventions: explanation and elaboration. J Clin Epidemiol
2009;62:e1–34. http://dx.doi.org/10.1016/j.jclinepi.2009.06.006
9. Moher D, Liberati A, Tetzlaff J, Altman DG; PRISMA Group. Preferred
reporting items for systematic reviews and meta-analyses: the PRISMA
statement. Int J Surg 2010;8:336–41. http://dx.doi.org/10.1016/j.
ijsu.2010.02.007
10. Harris RP, Helfand M, Woolf SH, et al; Methods Work Group, Third US
Preventive Services Task Force. Current methods of the US Preventive Services
Task Force: a review of the process. Am J Prev Med 2001;20(Suppl):21–35.
http://dx.doi.org/10.1016/S0749-3797(01)00261-6
11. Horton L, Folger SG, Berry-Bibee E, Jatlaoui TC, Tepper NK, Curtis KM.
Research gaps from evidence-based contraception guidance: the U.S. Medical
Eligibility Criteria for Contraceptive Use, 2016, and the U.S. Selected Practice
Recommendations for Contraceptive Use, 2016. Contraception. In press 2016.
12. Workowski KA, Bolan GA. Sexually transmitted diseases treatment
guidelines, 2015. MMWR Recomm Rep 2015;64(No. RR-3).

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Abbreviations and Acronyms
ARV = antiretroviral [therapy]
BMD = bone mineral density
BMI = body mass index
CHC = combined hormonal contraceptive
COC = combined oral contraceptive
Cu-IUD = copper-containing intrauterine device
DMPA = depot medroxyprogesterone acetate
DVT = deep venous thrombosis
ECP = emergency contraceptive pills
FAB = fertility awareness–based [methods]
hCG = human chorionic gonadotropin
HDL = high-density lipoprotein
HIV = human immunodeficiency virus
IBD = inflammatory bowel disease
IUD = intrauterine device
LARC = long-acting reversible contraception

LDL = low-density lipoprotein
LNG = levonorgestrel
LNG-IUD = levonorgestrel-releasing intrauterine device
NET-EN = norethisterone enantate
NNRTI = nonnucleoside reverse transcriptase inhibitor
NRTI = nucleoside reverse transcriptase inhibitor
PE = pulmonary embolism
PID = pelvic inflammatory disease
POC = progestin-only contraceptive
POP = progestin-only pill
SLE = systemic lupus erythematosus
SSRI = selective serotonin reuptake inhibitors
STD = sexually transmitted disease
UPA = ulipristal acetate
U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use
U.S. SPR = U.S. Selected Practice Recommendations for Contraceptive Use
VTE = venous thromboembolism

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Appendix A
Summary of Changes from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010
The classification additions, deletions, and modifications
from the 2010 U.S. Medical Eligibility Criteria for Contraceptive
Use (U.S. MEC) are summarized in the following tables
(Box A1) (Tables A1 and A2). For conditions for which
classifications changed for one or more contraceptive methods
or the condition description underwent a major modification,
the changes or modifications are in bold italics (Tables A1
and A2). Conditions that do not appear in this table remain
unchanged from the 2010 U.S. MEC.

BOX A1. Categories for classifying intrauterine devices and
hormonal contraceptives

TABLE A1. Summary of changes in classifications from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Condition

Cu-IUD

LNG-IUD

Implants DMPA POP

CHCs

Clarification

Breastfeeding
a. <21 days postpartum

—

Breastfeeding provides important health benefits for
mother and infant. The U.S. Department of Health and
Human Services recommends increasing the proportion
of infants initially breastfed, exclusively breastfed through
6 months of life, and continuing breastfeeding through at
least 1 year of life as key public health goals (1).

i. With other risk factors for
VTE (e.g., age ≥35 years,
previous VTE, thrombophilia,
immobility, transfusion at
delivery, peripartum
cardiomyopathy, BMI ≥30 kg/
m2, postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)

—

ii. Without other risk factors
for VTE

—

b. 21 to <30 days postpartum

CHCs: For women with other risk factors for VTE, these risk
factors might increase the classification to a category 4.

c. 30–42 days postpartum
i. With other risk factors for
VTE (e.g., age ≥35 years,
previous VTE, thrombophilia,
immobility, transfusion at
delivery, peripartum
cardiomyopathy, BMI ≥30 kg/
m2, postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
ii. Without other risk factors
for VTE

d. >42 days postpartum

CHCs: For women with other risk factors for VTE, these risk
factors might increase the classification to a category 4.
—

—

See table footnotes on page 16.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A1. (Continued) Summary of changes in classifications from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Condition
Postpartum (nonbreastfeeding
women)
a. <21 days postpartum

Cu-IUD

LNG-IUD

Implants DMPA POP

CHCs

Clarification

—

CHCs: For women with other risk factors for VTE, these risk
factors might increase the classification to a category 4.

—

b. 21–42 days postpartum
i. With other risk factors for
VTE (e.g., age ≥35 years,
previous VTE, thrombophilia,
immobility, transfusion at
delivery, peripartum
cardiomyopathy, BMI ≥30 kg/
m2, postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
ii. Without other risk factors
for VTE
c. >42 days postpartum
Postpartum (including cesarean
delivery)
a. <10 minutes after delivery of
the placenta
i. Breastfeeding
ii. Nonbreastfeeding

b. 10 minutes after delivery of
the placenta to <4 weeks
(breastfeeding or
nonbreastfeeding)

1
1

2
1

—
—

—

IUDs: Insertion of IUDs among postpartum women is safe
and does not appear to increase health risks associated
with IUD use such as infection. Higher rates of expulsion
during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower.
Breastfeeding: Breastfeeding provides important health
benefits for mother and infant. The U.S. Department of
Health and Human Services recommends increasing the
proportion of infants initially breastfed, exclusively
breastfed through 6 months of life, and continuing
breastfeeding through at least 1 year of life as key public
health goals (1).
IUDs: Insertion of IUDs among postpartum women is safe
and does not appear to increase health risks associated
with IUD use such as infection. Higher rates of expulsion
during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower.
Breastfeeding: Breastfeeding provides important health
benefits for mother and infant. The U.S. Department of
Health and Human Services recommends increasing the
proportion of infants initially breastfed, exclusively
breastfed through 6 months of life, and continuing
breastfeeding through at least 1 year of life as key public
health goals (1).

c. ≥4 weeks (breastfeeding or
nonbreastfeeding)

—

d. Postpartum sepsis

—

See table footnotes on page 16.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE A1. (Continued) Summary of changes in classifications from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Condition
Multiple risk factors for
atherosclerotic cardiovascular
disease (e.g., older age,
smoking, diabetes, hypertension, low HDL, high LDL, or
high triglyceride levels)

Cu-IUD

LNG-IUD

Implants DMPA POP
2

CHCs

Clarification

3/4

Implants, DMPA, POP: When multiple major risk factors
exist, risk for cardiovascular disease might increase
substantially. Certain POCs might increase the risk for
thrombosis, although this increase is substantially less
than with COCs. The effects of DMPA might persist for
some time after discontinuation.
CHCs: When a woman has multiple major risk factors, any
of which alone would substantially increase her risk for
cardiovascular disease, use of CHCs might increase her risk
to an unacceptable level. However, a simple addition of
categories for multiple risk factors is not intended; for
example, a combination of two category 2 risk factors
might not necessarily warrant a higher category.
Implants, DMPA, POP, CHCs: The recommendations
apply to known preexisting medical conditions or
characteristics. Few if any screening tests are needed
before initiation of contraception. See the U.S. Selected
Practice Recommendations for Contraceptive Use (http://
www.cdc.gov/reproductivehealth/unintendedpregnancy/usspr.htm)

Superficial venous disorders
a. Varicose veins

—

b. Superficial venous
thrombosis (acute or history)

CHCs: Superficial venous thrombosis might be associated
with an increased risk for VTE. If a woman has risk factors
for concurrent DVT (e.g., known thrombophilia or cancer)
or has current or history of DVT, see recommendations
for DVT/PE. Superficial venous thrombosis associated
with a peripheral intravenous catheter is less likely to be
associated with additional thrombosis and use of CHCs
may be considered.

CHCs: Classification depends on accurate diagnosis of
those severe headaches that are migraines and those
headaches that are not, as well as diagnosis of ever
experiencing aura. Aura is a specific focal neurologic
symptom. For more information about headache
classification see The International Headache Classification,
3rd edition (http://www.ihs-classification.org/_downloads/
mixed/International-Headache-Classification-III-ICHD-III2013-Beta.pdf). Any new headaches or marked changes in
headaches should be evaluated.

Headaches
a. Nonmigraine (mild or severe)

b. Migraine
i. Without aura (This category
of migraine includes
menstrual migraine.)
ii. With aura

CHCs: Classification depends on accurate diagnosis of those
severe headaches that are migraines and those headaches
that are not, as well as diagnosis of ever experiencing aura.
Aura is a specific focal neurologic symptom. For more
information about headache classification see The
International Headache Society Classification, 3rd edition
(http://www.ihs-classification.org/_downloads/mixed/
International-Headache-Classification-III-ICHD-III-2013-Beta.
pdf). Any new headaches or marked changes in headaches
should be evaluated.
CHCs: Classification is for women without any other risk
factors for stroke (e.g., age, hypertension, and smoking).

Multiple sclerosis
a. With prolonged immobility

—

b. Without prolonged
immobility
Gestational trophoblastic
disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy
(Box 2).
a. Suspected gestational
trophoblastic disease
(immediate postevacuation)
i. Uterine size first trimester
ii. Uterine size second
trimester

—
For all subconditions of gestational trophoblastic
disease, classifications are based on the assumption that
women are under close medical supervision because of
the need for monitoring of β-hCG levels for appropriate
disease surveillance.

1
2

1
1

See table footnotes on page 16.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A1. (Continued) Summary of changes in classifications from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Condition

Cu-IUD

b. Confirmed gestational
Initiation
trophoblastic disease (after
initial evacuation and during
monitoring)
i. Undetectable/nonpregnant
1
β-hCG levels

ii. Decreasing β-hCG levels

LNG-IUD

Implants DMPA POP

Continuation

Initiation

Continuation

CHCs

Clarification

For all subconditions of gestational trophoblastic
disease, classifications are based on the assumption that
women are under close medical supervision because of
the need for monitoring of β-hCG levels for appropriate
disease surveillance.
IUD: For women at higher risk for disease progression, the
benefits of effective contraception must be weighed against
the potential need for early IUD removal.

iii. Persistently elevated
β-hCG levels or malignant
disease, with no evidence or
suspicion of intrauterine
disease

iv. Persistently elevated
β-hCG levels or malignant
disease, with evidence or
suspicion of intrauterine
disease

Sexually transmitted diseases

IUD continuation: Treat the STD using appropriate
antibiotics. The IUD usually does not need to be removed
if the woman wants to continue using it. Continued use of
an IUD depends on the woman’s informed choice and her
current risk factors for STDs and PID.
—

Initiation

Continuation

Initiation

Continuation

a. Current purulent cervicitis or
chlamydial infection or
gonococcal infection

b. Vaginitis (including
Trichomonas vaginalis and
bacterial vaginosis)
c. Other factors related to STDs

Initiation
2

Continuation
2

Initiation
2

Continuation
2

High risk for HIV

HIV infection
For women with HIV infection
who are not clinically well or not
receiving ARV therapy, this
condition is associated with
increased risk for adverse health
events as a result of pregnancy
(Box 2).
a. Clinically well receiving ARV
therapy
b. Not clinically well or not
receiving ARV therapy

IUD initiation: Most women do not require additional STD
screening at the time of IUD insertion. If a woman with risk
factors for STDs has not been screened for gonorrhea and
chlamydia according to CDC STD treatment guidelines (2),
screening may be performed at the time of IUD insertion
and insertion should not be delayed.
DMPA: Some studies suggest that women using
progestin-only injectable contraception might be at
increased risk for HIV acquisition; other studies do not
show this association. CDC reviewed all available
evidence and agreed that the data were not sufficiently
conclusive to change current guidance. However,
because of the inconclusive nature of the body of
evidence on possible increased risk for HIV acquisition,
women using progestin-only injectable contraception
should be strongly advised to also always use condoms
(male or female) and take other HIV preventive
measures. Expansion of contraceptive method mix and
further research on the relationship between hormonal
contraception and HIV infection are essential. These
recommendations will be continually reviewed in light of
new evidence.

—

Implants, DMPA, POP, CHCs: Drug interactions might
exist between hormonal contraceptives and ARV drugs;
see Drug Interactions section.

—

See table footnotes on page 16.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE A1. (Continued) Summary of changes in classifications from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Condition

Cu-IUD

LNG-IUD

Cystic fibrosis
This condition is associated with
increased risk for adverse health
events as a result of pregnancy
(Box 2).

Implants DMPA POP
1

CHCs

Clarification

Persons with cystic fibrosis are at increased risk for
diabetes, liver disease, gallbladder disease, and VTE
(particularly related to use of central venous catheters)
and are frequently prescribed antibiotics. Categories
assigned to such conditions in U.S. MEC should be the
same for women with cystic fibrosis who have these
conditions. For cystic fibrosis, classifications are based on
the assumption that no other conditions are present;
these classifications must be modified in the presence of
such conditions.
Implants, DMPA, POP, CHCs: Certain drugs to treat cystic
fibrosis (e.g., lumacaftor) might reduce effectiveness of
hormonal contraceptives, including oral, injectable,
transdermal, and implantable contraceptives.

Antiretroviral therapy

Initiation

a. Nucleoside reverse
transcriptase inhibitors (NRTIs)
i. Abacavir (ABC)
ii. Tenofovir (TDF)

Continuation

Initiation

Continuation

IUD: No known interaction exists between ARV therapy
and IUD use. However, IUD insertion is classified as
category 2 if the woman is not clinically well or not
receiving ARV therapy. Otherwise, both insertion and
continuation are classified as category 1 (see HIV
Infection section).

1/2

—

1/2

—

iii. Zidovudine (AZT)

1/2

—

iv. Lamivudine (3TC)

1/2

—

v. Didanosine (DDI)

1/2

—

vi. Emtricitabine (FTC)

1/2

—

vii. Stavudine (D4T)

1/2

—

1/2

b. Nonnucleoside reverse
transcriptase inhibitors
(NNRTIs)
i. Efavirenz (EFV)

Implants, DMPA, POP, CHCs: Evidence suggests drug
interactions between efavirenz and certain hormonal
contraceptives. These interactions might reduce the
effectiveness of the hormonal contraceptive.

ii. Etravirine (ETR)

1/2

—

iii. Nevirapine (NVP)

1/2

—

iv. Rilpivirine (RPV)

1/2

—

1/2

c. Ritonavir-boosted protease
inhibitors
i. Ritonavir-boosted
atazanavir (ATV/r)

CHCs: Theoretically, drug interactions might occur
between certain ritonavir-boosted protease inhibitors
and certain hormonal contraceptives that might reduce
the effectiveness of the hormonal contraceptive.
ii. Ritonavir-boosted
darunavir (DRV/r)

1/2

Implants, DMPA, POP: Theoretically, drug interactions
might occur between certain ritonavir-boosted protease
inhibitors and certain hormonal contraceptives that
might reduce the effectiveness of the hormonal
contraceptive. Any potential effect on contraceptive
effectiveness is likely to be lower with DMPA than with
other POCs because of the higher dose of DMPA.
CHCs: Theoretically, drug interactions might occur
between certain ritonavir-boosted protease inhibitors
and certain hormonal contraceptives that might reduce
the effectiveness of the hormonal contraceptive.

See table footnotes on page 16.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A1. (Continued) Summary of changes in classifications from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Condition
iii. Ritonavir-boosted
fosamprenavir (FPV/r)

Cu-IUD
1/2

LNG-IUD
1

1/2

Implants DMPA POP
2

CHCs

Clarification

iv. Ritonavir-boosted
lopinavir (LPV/r)
v. Ritonavir-boosted
saquinavir (SQV/r)

1/2

—

1/2

vi. Ritonavir-boosted
tipranavir (TPV/r)

1/2

d. Protease inhibitors without
ritonavir
i. Atazanavir (ATV)

ii. Fosamprenavir (FPV)

1/2

CHCs: Theoretical concern exists that increased levels of
ethinyl estradiol because of interactions with ATV might
increase the risk for adverse events.

1/2

Implants, DMPA, POP: Theoretical concern exists that
interactions between FPV and hormonal contraceptives
leading to decreased levels of FPV might diminish
effectiveness of the antiretroviral drug. The drug
interaction likely involves CYP3A4 pathways; POCs have
less effect on CYP3A4 enzymes than CHCs.
CHCs: Concern exists that interactions between FPV and
hormonal contraceptives leading to decreased levels of FPV
might diminish effectiveness of the antiretroviral drug.

iii. Indinavir (IDV)

1/2

iv. Nelfinavir (NFV)

1/2

1
2

1
1

1
2

—
Implants, DMPA, POP: Theoretically, drug interactions
might occur between certain protease inhibitors and
certain hormonal contraceptives that might reduce the
effectiveness of the hormonal contraceptive. Any
potential effect on contraceptive effectiveness is likely to
be lower with DMPA than with other POCs because of the
higher dose of DMPA. Concern exists that interactions
between NFV and POCs might decrease NFV levels.
CHCs: Evidence suggests drug interactions between
certain protease inhibitors and certain hormonal
contraceptives. These interactions might reduce the
effectiveness of the hormonal contraceptive.

See table footnotes on page 16.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE A1. (Continued) Summary of changes in classifications from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Condition

Cu-IUD

e. CCR5 co-receptor
antagonists
i. Maraviroc (MVC)

1/2

f. HIV integrase strand transfer
inhibitors
i. Raltegravir (RAL)

LNG-IUD

1/2

Implants DMPA POP

CHCs

Clarification

—

1/2

—

ii. Dolutegravir (DTG)

1/2

—

iii. Elvitegravir (EVG)

1/2

—

1/2

—

g. Fusion inhibitors
i. Enfuvirtide
Psychotropic medications
a. SSRIs
St. John’s wort

—

Abbreviations: ARV = antiretroviral; BMI = body mass index; CHC = combined hormonal contraceptive; COC = combined oral contraceptive; Cu-IUD = copper-containing intrauterine device;
DMPA = depot medroxyprogesterone acetate; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; HIV = human immunodeficiency
virus; LDL = low-density lipoprotein; LNG-IUD = levonorgestrel-releasing intrauterine device; PE = pulmonary embolism; PID = pelvic inflammatory disease; POC = progestin-only contraceptive;
POP = progestin-only pill; SSRI = selective serotonin uptake inhibitor; STD = sexually transmitted disease; VTE = venous thromboembolism.
* For conditions for which classification changed for one or more contraceptive methods or the condition description underwent a major modification, the changes or modifications are in
bold italics.

TABLE A2. Summary of changes for emergency contraception from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Category
Condition

Cu-IUD

UPA

LNG

COC

Pregnancy

Clarification
IUD: The IUD is not indicated during pregnancy and should not be used
because of the risk for serious pelvic infection and septic spontaneous
abortion.
ECPs: Although this method is not indicated for a woman with a known or
suspected pregnancy, no harm to the woman, the course of her pregnancy, or
the fetus if ECPs are inadvertently used is known to exist.

Breastfeeding

UPA: Breastfeeding is not recommended for 24 hours after taking UPA
because it is excreted in breast milk with highest concentrations in the first
24 hours, and maximum maternal serum levels are reached 1-3 hours after
administration. Mean UPA concentrations in breast milk decrease markedly
from 0 to 24–48 hours and then slowly decrease over 5 days (3). Breast milk
should be expressed and discarded for 24 hours after taking UPA.

Past ectopic pregnancy

—

a. Restrictive procedures: decrease storage capacity of
the stomach (vertical banded gastroplasty, laparoscopic
adjustable gastric band, or laparoscopic sleeve gastrectomy)

—

b. Malabsorptive procedures: decrease absorption of nutrients
and calories by shortening the functional length of the
small intestine (Roux-en-Y gastric bypass or biliopancreatic
diversion)

—

a. Receiving immunosuppressive therapy

—

b. Not receiving immunosuppressive therapy

—

Migraine

—

Inflammatory bowel disease (ulcerative colitis or Crohn’s disease)

—

Severe liver disease (including jaundice)
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).

—

History of bariatric surgery
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).

History of severe cardiovascular disease (ischemic heart disease,
cerebrovascular attack, or other thromboembolic conditions)
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Rheumatoid arthritis

See table footnotes on page 17.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE A2. (Continued) Summary of changes for emergency contraception from U.S. Medical Eligibility Criteria for Contraceptive Use, 2010*
Category
Condition

Cu-IUD

UPA

LNG

COC

Clarification

a. Complicated: graft failure (acute or chronic), rejection, or
cardiac allograft vasculopathy

—

Solid organ transplantation
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).

b. Uncomplicated

—

Repeated ECP use

ECPs: Recurrent ECP use is an indication that the woman requires further
counseling about other contraceptive options. Frequently repeated ECP use
might be harmful for women with conditions classified as 2, 3, or 4 for CHC or
POC use.

Sexual assault

IUD: Women who have experienced sexual assault are at increased risk
for STDs. According to CDC STD treatment guidelines, routine presumptive
treatment of chlamydia, gonorrhea, and trichomonas is recommended after
sexual assault (2). Women with current purulent cervicitis or chlamydial
infection or gonococcal infection should not undergo IUD insertion (category 4).

Obesity (BMI ≥30 kg/m2)

ECPs: ECPs might be less effective among women with BMI ≥30 kg/m2 than
among women with BMI <25 kg/m2. Despite this, no safety concerns exist.

CYP3A4 inducers (e.g., bosentan, carbamazepine, felbamate,
griseofulvin, oxcarbazepine, phenytoin, rifampin, St. John’s
wort, topiramate, efavirenz, and lumacaftor)

ECPs: Strong CYP3A4 inducers might reduce the effectiveness of ECPs.

Abbreviations: BMI = body mass index; CHC = combined hormonal contraceptive; COC = combined oral contraceptive; Cu-IUD = copper-containing intrauterine device; ECP = emergency
contraceptive pill; IUD = intrauterine device; LNG = levonorgestrel; NA = not applicable; POC = progestin-only contraceptive; STD = sexually transmitted disease; UPA = ulipristal acetate.
* For conditions for which classification changed for one or more contraceptive methods or the condition description underwent a major modification, the changes or modifications are in bold italics.

References
1. US Department of Health and Human Services. Healthy people 2020:
maternal, infant, and child health objectives. Washington, DC: US
Department of Health and Human Services; 2015. http://www.
healthypeople.gov/2020/topics-objectives/topic/maternal-infant-andchild-health/objectives

2. Workowski KA, Bolan GA. Sexually transmitted diseases treatment
guidelines, 2015. MMWR Recomm Rep 2015;64(No. RR-03).
3. Watson Pharmaceuticals. Ella [Prescribing information]. Morristown, NJ; 2010.
https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/022474s000lbl.pdf

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Appendix B
Classifications for Intrauterine Devices
Classifications for intrauterine devices (IUDs) are for
the copper-containing IUD and levonorgestrel-releasing
IUD (containing a total of either 13.5 mg or 52 mg
levonorgestrel) (Box B1) (Table B1). IUDs do not protect
against sexually transmitted diseases (STDs), including human
immunodeficiency virus (HIV), and women using these
methods should be counseled that consistent and correct use of
the male latex condom reduces the risk for transmission of HIV
and other STDs. Use of female condoms can provide protection
from transmission of STDs, although data are limited.

MMWR / July 29, 2016 / Vol. 65 / No. 3

BOX B1. Categories for classifying intrauterine devices

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE B1. Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrel-releasing
intrauterine device
Category
Condition

Cu-IUD

LNG-IUD

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy

Clarification: The IUD is not indicated during pregnancy and should not be
used because of the risk for serious pelvic infection and septic spontaneous
abortion.

Age
a. Menarche to <20 years

b. ≥20 years
Parity
a. Nulliparous

Comment: Concern exists both about the risk for expulsion from nulliparity
and for STDs from sexual behavior in younger age groups.
—

b. Parous
Postpartum (including cesarean
delivery)
a. <10 minutes after delivery of the
placenta

i. Breastfeeding

Evidence: Data conflict about whether IUD use is associated with infertility
among nulliparous women, although well-conducted studies suggest no
increased risk (1–9).
—

ii. Nonbreastfeeding

Evidence: Studies suggest that immediate postplacental (<10 minutes) and
early postpartum (10 minutes up until 72 hours) placement of Cu-IUDs and
LNG-IUDs is associated with increased risk for expulsion compared with
interval placement (i.e., not related to pregnancy). Early postpartum placement
has similar or increased risk for expulsion compared with immediate
postplacental placement. Although immediate postplacental placement at the
time of cesarean delivery might have increased risk for expulsion compared
with interval placement, risk appears lower than that for placement at the time
of vaginal delivery. Evidence for infection, perforation, and removals for pain or
bleeding are limited; however, these events are rare (11–62).
Evidence (breastfeeding): Two randomized controlled trials found
conflicting results on breastfeeding outcomes when LNG-IUDs were initiated
immediately postpartum compared with 6–8 weeks postpartum. Initiation
of LNG-IUDs immediately postpartum had no other harmful effect on infant
health, growth, or development (63,64). Breastfeeding women using IUDs do
not have an increased risk for certain IUD-related adverse events including
expulsion, infection, pain, or bleeding compared with nonbreastfeeding
women. The risk for perforation is increased independently among
breastfeeding women and among women ≤36 weeks postpartum,
compared with non-postpartum women; however, the absolute risk for
perforation remains low (11–62,65).
Comment (breastfeeding): Certain women might be at risk for breastfeeding
difficulties, such as women with previous breastfeeding difficulties, certain
medical conditions, or certain perinatal complications and those who
deliver preterm. For these women, as for all women, discussions about
contraception for breastfeeding women should include information about
risks, benefits, and alternatives.

See table footnotes on page 30.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Cu-IUD

LNG-IUD

Clarifications/Evidence/Comments

Clarification: Insertion of IUDs among postpartum women is safe and does
not appear to increase health risks associated with IUD use such as infection.
Higher rates of expulsion during the postpartum period should be considered
as they relate to effectiveness, along with patient access to interval placement
(i.e., not related to pregnancy) when expulsion rates are lower.
Clarification (breastfeeding): Breastfeeding provides important health
benefits for mother and infant. The U.S. Department of Health and Human
Services recommends increasing the proportion of infants initially breastfed,
exclusively breastfed through 6 months of life, and continuing breastfeeding
through at least 1 year of life as key public health goals (10).
Evidence: Studies suggest that immediate postplacental (<10 minutes) and
early postpartum (10 minutes up until 72 hours) placement of Cu-IUDs and
LNG-IUDs is associated with increased risk for expulsion compared with
interval placement (i.e., not related to pregnancy). Early postpartum placement
has similar or increased risk for expulsion compared with immediate
postplacental placement. Although immediate postplacental placement at the
time of cesarean delivery might have increased risk for expulsion compared
with interval placement, risk appears lower than that for placement at the time
of vaginal delivery. Evidence for infection, perforation, and removals for pain or
bleeding are limited; however, these events are rare (11–62).
Evidence (breastfeeding): Two randomized controlled trials found
conflicting results on breastfeeding outcomes when LNG-IUDs were initiated
immediately postpartum compared with 6–8 weeks postpartum. Initiation
of LNG-IUDs immediately postpartum had no other harmful effect on infant
health, growth, or development (63,64). Breastfeeding women using IUDs do
not have an increased risk for certain IUD-related adverse events including
expulsion, infection, pain, or bleeding compared with nonbreastfeeding
women. The risk for perforation is increased independently among
breastfeeding women and among women ≤36 weeks postpartum,
compared with non-postpartum women; however, the absolute risk for
perforation remains low (11–62,65).
Comment (breastfeeding): Certain women might be at risk for breastfeeding
difficulties, such as women with previous breastfeeding difficulties, certain
medical conditions, or certain perinatal complications and those who
deliver preterm. For these women, as for all women, discussions about
contraception for breastfeeding women should include information about
risks, benefits, and alternatives.

c. ≥4 weeks (breastfeeding or
nonbreastfeeding)

d. Postpartum sepsis

Comment: Theoretical concern exists that postpartum insertion of an IUD
in a women with recent chorioamnionitis or current endometritis might be
associated with increased complications.

See table footnotes on page 30.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Cu-IUD

LNG-IUD

Clarifications/Evidence/Comments
Clarification: IUDs can be inserted immediately after spontaneous or
induced abortion.
Evidence: Risk for complications from immediate versus delayed insertion of
an IUD after abortion did not differ. Expulsion was greater when an IUD was
inserted after a second trimester abortion than when inserted after a first
trimester abortion. Safety or expulsion for postabortion insertion of an LNGIUD did not differ from that of a Cu-IUD (66).

b. Second trimester
c. Immediate postseptic abortion

2
4

Past ectopic pregnancy

History of pelvic surgery
(see Postpartum [Including Cesarean
Delivery] section)
Smoking
a. Age <35 years
b. Age ≥35 years
i. <15 cigarettes per day
ii. ≥15 cigarettes per day
Obesity
a. BMI ≥30 kg/m2
b. Menarche to <18 years and BMI
≥30 kg/m2
History of bariatric surgery
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Restrictive procedures: decrease
storage capacity of the stomach
(vertical banded gastroplasty,
laparoscopic adjustable gastric
band, or laparoscopic sleeve
gastrectomy)
b. Malabsorptive procedures:
decrease absorption of nutrients
and calories by shortening the
functional length of the small
intestine (Roux-en-Y gastric bypass
or biliopancreatic diversion)

Comment: The absolute risk for ectopic pregnancy is extremely low because
of the high effectiveness of IUDs. However, when a woman becomes
pregnant during IUD use, the relative likelihood of ectopic pregnancy
increases substantially.
—

—

1
1

—
—

1
1

—
—

—

Comment: Insertion of an IUD might substantially worsen the condition.

b. Elevated blood pressure levels
(properly taken measurements)
i. Systolic 140–159 mm Hg or
diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic
≥100 mm Hg

Clarification: For all categories of hypertension, classifications are based
on the assumption that no other risk factors for cardiovascular disease
exist. When multiple risk factors do exist, risk for cardiovascular disease
might increase substantially. A single reading of blood pressure level is not
sufficient to classify a woman as hypertensive.
Clarification: For all categories of hypertension, classifications are based
on the assumption that no other risk factors for cardiovascular disease
exist. When multiple risk factors do exist, risk for cardiovascular disease
might increase substantially. A single reading of blood pressure level is not
sufficient to classify a woman as hypertensive.
Comment: Theoretical concern exists about the effect of LNG on lipids. Use
of Cu-IUDs has no restrictions.

See table footnotes on page 30.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

History of high blood pressure during
pregnancy (when current blood
pressure is measurable and normal)
Deep venous thrombosis/
Pulmonary embolism
a. History of DVT/PE, not receiving
anticoagulant therapy
i. Higher risk for recurrent DVT/PE
(one or more risk factors)
• History of estrogen-associated
DVT/PE
• Pregnancy-associated DVT/PE
• Idiopathic DVT/PE
• Known thrombophilia,
including antiphospholipid
syndrome
• Active cancer (metastatic, receiving
therapy, or within 6 months after
clinical remission), excluding
nonmelanoma skin cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE
(no risk factors)
b. Acute DVT/PE

Cu-IUD

LNG-IUD

Clarifications/Evidence/Comments
Clarification: For all categories of hypertension, classifications are based
on the assumption that no other risk factors for cardiovascular disease
exist. When multiple risk factors do exist, risk for cardiovascular disease
might increase substantially. A single reading of blood pressure level is not
sufficient to classify a woman as hypertensive.
Comment: Theoretical concern exists about the effect of LNG on lipids. Use
of Cu-IUDs has no restrictions
—

—

c. DVT/PE and established
anticoagulant therapy for at least
3 months

Evidence: No direct evidence exists on the use of POCs among women with
acute DVT/PE. Although findings on the risk for venous thrombosis with
the use of POCs in otherwise healthy women are inconsistent, any small
increased risk is substantially less than that with COCs (67–69).
Evidence: No direct evidence exists on the use of POCs among women with
acute DVT/PE. Although findings on the risk for venous thrombosis with
the use of POCs in otherwise healthy women are inconsistent, any small
increased risk is substantially less than that with COCs (67–69).
Evidence: Limited evidence indicates that insertion of the LNG-IUD does not
pose major bleeding risks in women receiving chronic anticoagulant therapy
(70–73).

i. Higher risk for recurrent DVT/PE
(one or more risk factors)
• Known thrombophilia,
including antiphospholipid
syndrome
• Active cancer (metastatic, receiving
therapy, or within 6 months after
clinical remission), excluding
nonmelanoma skin cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE
(no risk factors)
d. Family history (first-degree
relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged
immobilization
f. Minor surgery without
immobilization

Comment: The LNG-IUD might be a useful treatment for menorrhagia in
women receiving long-term anticoagulation therapy.
—

—

1
1

2
1

—
—

See table footnotes on page 30.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition
Known thrombogenic mutations
(e.g., factor V Leiden; prothrombin
mutation; and protein S, protein C, and
antithrombin deficiencies)
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Superficial venous disorders
a. Varicose veins
b. Superficial venous thrombosis
(acute or history)
Current and history of ischemic
heart disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Stroke (history of cerebrovascular
accident)
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Valvular heart disease
Complicated valvular heart disease is
a condition associated with increased
risk for adverse health events as a
result of pregnancy (Box 2).
a. Uncomplicated
b. Complicated (pulmonary
hypertension, risk for atrial
fibrillation, or history of subacute
bacterial endocarditis)
Peripartum cardiomyopathy
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Normal or mildly impaired
cardiac function (New York Heart
Association Functional Class I or
II: patients with no limitation of
activities or patients with slight,
mild limitation of activity) (76)
i. <6 months
ii. ≥6 months
b. Moderately or severely impaired
cardiac function (New York Heart
Association Functional Class III or IV:
patients with marked limitation of
activity or patients who should be at
complete rest) (76)

Cu-IUD

LNG-IUD

1
1

Initiation
2

Clarifications/Evidence/Comments
Clarification: Routine screening is not appropriate because of the rarity of
the conditions and the high cost of screening.

—
—
Continuation
3

Comment: Theoretical concern exists about the effect of LNG on lipids. Use
of Cu-IUDs has no restrictions.

1
1

Evidence: No direct evidence exists on the safety of IUDs among women
with peripartum cardiomyopathy. Limited indirect evidence from
noncomparative studies did not demonstrate any cases of arrhythmia or
infective endocarditis in women with cardiac disease who used IUDs (75).
Comment: IUD insertion might induce cardiac arrhythmias in healthy
women; women with peripartum cardiomyopathy have a high incidence of
cardiac arrhythmias.

2
2
2

Initiation

Continuation

Clarification: Persons with SLE are at increased risk for ischemic heart
disease, stroke, and VTE. Categories assigned to such conditions in U.S. MEC
should be the same for women with SLE who have these conditions. For all
subconditions of SLE, classifications are based on the assumption that no
other risk factors for cardiovascular disease are present; these classifications
must be modified in the presence of such risk factors. Many women with
SLE can be considered good candidates for most contraceptive methods,
including hormonal contraceptives (73,77–94).
Evidence: Antiphospholipid antibodies are associated with a higher risk for
both arterial and venous thrombosis (95,96)

See table footnotes on page 30.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition

Cu-IUD

b. Severe thrombocytopenia

LNG-IUD
2

Clarifications/Evidence/Comments
Clarification: Persons with SLE are at increased risk for ischemic heart
disease, stroke, and VTE. Categories assigned to such conditions in U.S. MEC
should be the same for women with SLE who have these conditions. For all
subconditions of SLE, classifications are based on the assumption that no
other risk factors for cardiovascular disease are present; these classifications
must be modified in the presence of such risk factors. Many women with
SLE can be considered good candidates for most contraceptive methods,
including hormonal contraceptives (73,77–94).
Clarification: Severe thrombocytopenia increases the risk for bleeding. The
category should be assessed according to the severity of thrombocytopenia
and its clinical manifestations. In women with very severe thrombocytopenia
who are at risk for spontaneous bleeding, consultation with a specialist and
certain pretreatments might be warranted.
Evidence: The LNG-IUD might be a useful treatment for menorrhagia in
women with severe thrombocytopenia (73).

c. Immunosuppressive therapy

d. None of the above

Rheumatoid arthritis
a. Receiving immunosuppressive
therapy
b. Not receiving immunosuppressive
therapy

Initiation
2

Continuation
1

Initiation
2

Continuation
1

—

Evidence: No studies directly examined the risk for stroke among women
with migraine using LNG-IUDs (97). Limited evidence demonstrated that
women using LNG-IUDs do not have an increased risk for ischemic stroke
compared with women not using hormonal contraceptives (98).

Comment: Menstrual migraine is a subtype of migraine without aura. For
more information see The International Headache Society Classification, 3rd
edition (http://www.ihs-classification.org/_downloads/mixed/InternationalHeadache-Classification-III-ICHD-III-2013-Beta.pdf ).
—

1
1

Neurologic Conditions
Headaches
a. Nonmigraine (mild or severe)
b. Migraine
i. Without aura (This category
of migraine includes menstrual
migraine.)
ii. With aura

Epilepsy
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Multiple sclerosis
a. With prolonged immobility
b. Without prolonged immobility

—
—

Depressive Disorders
Depressive disorders

Clarification: If a woman is receiving psychotropic medications or St. John’s
wort, see Drug Interactions section.
Evidence: The frequency of psychiatric hospitalizations for women with
bipolar disorder or depression did not significantly differ among women
using DMPA, LNG-IUD, Cu-IUD, or sterilization (99).

See table footnotes on page 30.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition

Cu-IUD

LNG-IUD

Clarifications/Evidence/Comments

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without heavy
bleeding
b. Heavy or prolonged bleeding
(includes regular and irregular
patterns)

Unexplained vaginal bleeding
(suspicious for serious condition)
before evaluation

Initiation
1

1
2

Continuation
1

—
Clarification: Unusually heavy bleeding should raise suspicion of a serious
underlying condition.
Evidence: Evidence from studies examining the treatment effects of the
LNG-IUD among women with heavy or prolonged bleeding reported no
increase in adverse effects and found the LNG-IUD to be beneficial in treating
menorrhagia (100–107).

Initiation
4

Continuation
2

Initiation
4

Continuation
2

Endometriosis

Benign ovarian tumors (including cysts)
Severe dysmenorrhea

1
2

1
1

1
2

Clarification: If pregnancy or an underlying pathological condition (e.g., pelvic
malignancy) is suspected, it must be evaluated and the category adjusted after
evaluation. The IUD does not need to be removed before evaluation.
Evidence: LNG-IUD use among women with endometriosis decreased
dysmenorrhea, pelvic pain, and dyspareunia (108–112).
—
Comment: Dysmenorrhea might intensify with Cu-IUD use. LNG-IUD use has
been associated with reduction of dysmenorrhea.

1
2

Evidence: Limited evidence suggests that women using an IUD after uterine
evacuation for a molar pregnancy are not at greater risk for postmolar
trophoblastic disease than are women using other methods of contraception (113).
Comment: The risk for expulsion immediately postevacuation for gestational
trophoblastic disease is unknown. Expulsion is greater after IUD insertion
immediately postevacuation for a spontaneous or induced abortion in the
second trimester compared with IUD insertion after a first trimester abortion.

b. Confirmed gestational
trophoblastic disease (after initial
evacuation and during monitoring)
i. Undetectable/nonpregnant
β-hCG levels

Initiation

Continuation

Initiation

Continuation

Clarification: For all subconditions of gestational trophoblastic disease,
classifications are based on the assumption that women are under close
medical supervision because of the need for monitoring of β-hCG levels for
appropriate disease surveillance.
Evidence: Limited evidence suggests that women using an IUD after uterine
evacuation for a molar pregnancy are not at greater risk for postmolar
trophoblastic disease than are women using other methods of contraception (113).
Comment: Once β-hCG levels have decreased to nonpregnant levels, the risk
for disease progression is likely to be very low.

ii. Decreasing β-hCG levels

Clarification: For all subconditions of gestational trophoblastic disease,
classifications are based on the assumption that women are under close
medical supervision because of the need for monitoring of β-hCG levels for
appropriate disease surveillance.
Clarification: For women at higher risk for disease progression, the benefits
of effective contraception must be weighed against the potential need for
early IUD removal.
Evidence: Limited evidence suggests that women using an IUD after uterine
evacuation for a molar pregnancy are not at greater risk for postmolar
trophoblastic disease than are women using other methods of contraception (113).

See table footnotes on page 30.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition

Cu-IUD

iii. Persistently elevated β-hCG
levels or malignant disease,
with no evidence or suspicion of
intrauterine disease

LNG-IUD
1

Clarifications/Evidence/Comments
1

iv. Persistently elevated β-hCG
levels or malignant disease,
with evidence or suspicion of
intrauterine disease

Cervical ectropion
Cervical intraepithelial neoplasia
Cervical cancer (awaiting treatment)

1
1
Initiation
4

Endometrial cancer
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Ovarian cancer
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Uterine fibroids

1
2
Continuation
2

Initiation
4

Continuation
2

1
1
1

2
1
1

1
1

4
3

Continuation
2

Initiation
4

Comment: For women with suspected or confirmed intrauterine disease,
an IUD should not be inserted because of theoretical risk for perforation,
infection, and hemorrhage. For women who already have an IUD in place,
individual circumstance along with the benefits of effective contraception
must be weighed against theoretical risks of either removal or continuation
of the IUD.
—
Comment: Theoretical concern exists that LNG-IUDs might enhance
progression of cervical intraepithelial neoplasia.

Initiation
4

Comment: Concern exists about the increased risk for infection and bleeding
at insertion. The IUD most likely will need to be removed at the time of
treatment but until then, the woman is at risk for pregnancy.

—
—
—
Comment: Breast cancer is a hormonally sensitive tumor. Concerns about
progression of the disease might be less with LNG-IUDs than with COCs or
higher-dose POCs.
Evidence: Among women with endometrial hyperplasia, no adverse health
events occurred with LNG-IUD use; most women experienced disease
regression (114).
Continuation
2

Comment: Concern exists about the increased risk for infection, perforation,
and bleeding at insertion. The IUD most likely will need to be removed at the
time of treatment, but until then, the woman is at risk for pregnancy.

Comment: Women with ovarian cancer who undergo fertility-sparing
treatment and need contraception may use an IUD.

Evidence: Among women with uterine fibroids using an LNG-IUD, most
experienced improvements in serum levels of hemoglobin, hematocrit,
and ferritin and in menstrual blood loss (115). Rates of LNG-IUD expulsion
were higher in women with uterine fibroids (11%) than in women without
fibroids (0%–3%); these findings were either not statistically significant or
significance testing was not conducted (115). Rates of expulsion found in
noncomparative studies ranged from 0%–20% (115).
Comment: Women with heavy or prolonged bleeding should be assigned
the category for that condition.

See table footnotes on page 30.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition
Anatomical abnormalities
a. Distorted uterine cavity (any
congenital or acquired uterine
abnormality distorting the
uterine cavity in a manner that is
incompatible with IUD insertion)
b. Other abnormalities (including
cervical stenosis or cervical
lacerations) not distorting the
uterine cavity or interfering with
IUD insertion
Pelvic inflammatory disease
a. Past PID
i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID

Initiation
1
2
4

Cu-IUD

LNG-IUD

Clarifications/Evidence/Comments

Comment: An anatomical abnormality that distorts the uterine cavity might
preclude proper IUD placement.

—

Continuation
1
2
2

Initiation
1
2
4

Continuation
1
2
2

Comment: IUDs do not protect against STDs, including HIV, or PID. In women
at low risk for STDs, IUD insertion poses little risk for PID.
Clarification (continuation): Treat the PID using appropriate antibiotics. The
IUD usually does not need to be removed if the woman wants to continue
using it. Continued use of an IUD depends on the woman’s informed choice
and her current risk factors for STDs and PID.
Evidence: Among IUD users treated for PID, clinical course did not differ
regardless of whether the IUD was removed or left in place (116).

Sexually transmitted diseases
a. Current purulent cervicitis or
chlamydial infection or gonococcal
infection

b. Vaginitis (including Trichomonas
vaginalis and bacterial vaginosis)
c. Other factors related to STDs

Initiation
4

Continuation
2

Initiation
4

Continuation
2

Clarification (continuation): Treat the STD using appropriate antibiotics. The
IUD usually does not need to be removed if the woman wants to continue
using it. Continued use of an IUD depends on the woman’s informed choice
and her current risk factors for STDs and PID.
Evidence: Among women who had an IUD inserted, the absolute risk for
subsequent PID was low among women with STD at the time of insertion but
greater than among women with no STD at the time of IUD insertion (117–123).
—
Clarification (initiation): Most women do not require additional STD
screening at the time of IUD insertion. If a woman with risk factors for STDs
has not been screened for gonorrhea and chlamydia according to CDC STD
treatment guidelines (124), screening may be performed at the time of IUD
insertion and insertion should not be delayed.
Evidence: Women who undergo same-day STD screening and IUD insertion
have low incidence rates of PID. Algorithms for predicting PID among
women with risk factors for STDs have poor predictive value. Risk for PID
among women with risk factors for STDs is low (125).

HIV
High risk for HIV

Initiation
2

HIV infection
For women with HIV infection
who are not clinically well or not
receiving ARV therapy, this condition
is associated with increased risk for
adverse health events as a result of
pregnancy (Box 2).
a. Clinically well receiving ARV
therapy
b. Not clinically well or not receiving
ARV therapy

Continuation
2

Initiation
2

Continuation
2

Evidence: Among women at risk for HIV, Cu-IUD use did not increase risk for
HIV acquisition (126–136).
Evidence: Among IUD users, limited evidence shows a low risk for PID among
HIV-infected women using IUDs and no higher risk for pelvic infectious
complications in HIV-infected than in HIV-noninfected women or among
women with varying degrees of HIV severity. IUD use did not adversely affect
progression of HIV during 6–45 months of follow-up or when compared with
hormonal contraceptive use among HIV-infected women. Furthermore, IUD
use among HIV-infected women was not associated with increased risk for
transmission to sex partners or with increased genital viral shedding (137).

See table footnotes on page 30.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition

Cu-IUD

LNG-IUD

Clarifications/Evidence/Comments

1
1

—
—

Other Infections
Schistosomiasis
Schistosomiasis with fibrosis of the
liver is associated with increased risk
for adverse health events as a result
of pregnancy (Box 2).
a. Uncomplicated
b. Fibrosis of the liver (if severe, see
Cirrhosis section)
Tuberculosis
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Nonpelvic
b. Pelvic
Malaria

Initiation

Continuation

1
4

1
3

Initiation

Continuation

1
4

1
3

—
Comment: Insertion of an IUD might substantially worsen the condition.
—

1
1

2
2

—
Evidence: Limited evidence on the use of the LNG-IUD among women with
insulin-dependent or non–insulin-dependent diabetes suggests that these
methods have little effect on short-term or long-term diabetes control (e.g.,
glycosylated hemoglobin levels), hemostatic markers, or lipid profile (138,139).
—

—

1
1
1

—
—
—

1
1
1
1

2
2
2
2

—
—
—
—

1
1

1
2

—
Comment: Concern exists that history of COC related cholestasis might
predict subsequent cholestasis with LNG use. Whether risk exists with use of
LNG-IUD is unclear.

1
1
1

—
—
—

1
1

1
3

—
—

Endocrine Conditions
Diabetes
Insulin-dependent diabetes; diabetes
with nephropathy, retinopathy, or
neuropathy; diabetes with other
vascular disease; or diabetes of
>20 years’ duration are associated
with increased risk for adverse health
events as a result of pregnancy (Box 2).
a. History of gestational disease
b. Nonvascular disease
i. Non-insulin dependent
ii. Insulin dependent
c. Nephropathy, retinopathy, or
neuropathy
d. Other vascular disease or diabetes
of >20 years’ duration
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Gastrointestinal Conditions
Inflammatory bowel disease
(ulcerative colitis or Crohn’s disease)

Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic
History of cholestasis
a. Pregnancy related
b. Past COC related

Evidence: Although two case reports described three women with IBD
who experienced exacerbation of disease 5 days–25 months after LNG-IUD
insertion, no comparative studies have examined the safety of IUD use
among women with IBD (140).

See table footnotes on page 30.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition

Cu-IUD

LNG-IUD

1
1

2
3

Thalassemia

Comment: Concern exists about an increased risk for blood loss with Cu-IUDs.

Sickle cell disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Iron deficiency anemia

Comment: Concern exists about an increased risk for blood loss with Cu-IUDs.

Liver tumors
Hepatocellular adenoma and
malignant liver tumors are associated
with increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma

b. Malignant (hepatoma)

Clarifications/Evidence/Comments

—
Comment: No evidence is available about hormonal contraceptive use
in women with hepatocellular adenoma. COC use in healthy women is
associated with development and growth of hepatocellular adenoma;
whether other hormonal contraceptives have similar effects is not known.
—

Respiratory Conditions
Cystic fibrosis
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).

Anemias

Solid Organ Transplantation
Solid organ transplantation
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Complicated: graft failure (acute
or chronic), rejection, or cardiac
allograft vasculopathy
b. Uncomplicated

Initiation

Continuation

Initiation

Continuation

Initiation

Continuation

Initiation

Continuation

Evidence: No comparative studies have examined IUD use among transplant
patients. Four case reports of transplant patients using IUDs provided
inconsistent results, including beneficial effects and contraceptive failures (141).

Drug Interactions
Antiretroviral therapy

a. Nucleoside reverse transcriptase
inhibitors (NRTIs)
i. Abacavir (ABC)
ii. Tenofovir (TDF)
iii. Zidovudine (AZT)
iv. Lamivudine (3TC)
v. Didanosine (DDI)
vi. Emtricitabine (FTC)
vii. Stavudine (D4T)
b. Nonnucleoside reverse
transcriptase inhibitors (NNRTIs)
i. Efavirenz (EFV)
ii. Etravirine (ETR)
iii. Nevirapine (NVP)
iv. Rilpivirine (RPV)
c. Ritonavir-boosted protease
inhibitors
i. Ritonavir-boosted atazanavir (ATV/r)
ii. Ritonavir-boosted darunavir (DRV/r)

Clarification: No known interaction exists between ARV therapy and IUD
use. However, IUD insertion is classified as category 2 if the woman is not
clinically well or not receiving ARV therapy. Otherwise, both insertion and
continuation are classified as category 1 (see HIV Infection section).

1/2
1/2
1/2
1/2
1/2
1/2
1/2

1
1
1
1
1
1
1

1/2
1/2
1/2
1/2
1/2
1/2
1/2

1
1
1
1
1
1
1

—
—
—
—
—
—
—

1/2
1/2
1/2
1/2

1
1
1
1

1/2
1/2
1/2
1/2

1
1
1
1

—
—
—
—

1/2
1/2

1
1

1/2
1/2

1
1

—
—

See table footnotes on page 30.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE B1. (Continued) Classifications for intrauterine devices, including the copper-containing intrauterine device and levonorgestrelreleasing intrauterine device
Category
Condition

Cu-IUD

iii. Ritonavir-boosted
fosamprenavir (FPV/r)
iv. Ritonavir-boosted lopinavir (LPV/r)
v. Ritonavir-boosted saquinavir (SQV/r)
vi. Ritonavir-boosted tipranavir (TPV/r)
d. Protease inhibitors without
ritonavir
i. Atazanavir (ATV)
ii. Fosamprenavir (FPV)
iii. Indinavir (IDV)
iv. Nelfinavir (NFV)
e. CCR5 co-receptor antagonists
i. Maraviroc (MVC)
f. HIV integrase strand transfer
inhibitors
i. Raltegravir (RAL)
ii. Dolutegravir (DTG)
iii. Elvitegravir (EVG)
g. Fusion inhibitors
i. Enfuvirtide
Anticonvulsant therapy
a. Certain anticonvulsants
(phenytoin, carbamazepine,
barbiturates, primidone, topiramate,
and oxcarbazepine)
b. Lamotrigine

LNG-IUD

Clarifications/Evidence/Comments

1/2

—

1/2
1/2
1/2

1
1
1

1/2
1/2
1/2

1
1
1

—
—
—

1/2
1/2
1/2
1/2

1
1
1
1

1/2
1/2
1/2
1/2

1
1
1
1

—
—
—
—

1/2

—

1/2
1/2
1/2

1
1
1

1/2
1/2
1/2

1
1
1

—
—
—

1/2

—

Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampin or rifabutin therapy

Evidence: Limited evidence suggests use of certain anticonvulsants does not
interfere with the contraceptive effectiveness of the LNG-IUD (142).

Evidence: No drug interactions have been reported among women with epilepsy
who are receiving lamotrigine and using the LNG-IUD (143).

1
1
1
1

—
—
—
Evidence: One cross-sectional survey found that rifabutin had no impact on
the effectiveness of the LNG-IUD (142).

Psychotropic medications

a. SSRIs
St. John’s wort

1
1

Abbreviations: ARV = antiretroviral; BMI = body mass index; COC = combined oral contraceptive; Cu-IUD = copper-containing IUD; DVT = deep venous thrombosis; hCG = human chorionic
gonadotropin; HDL = high-density lipoprotein; HIV = human immunodeficiency virus; IBD = inflammatory bowel disease; IUD = intrauterine device; LDL = low-density lipoprotein;
LNG = levonorgestrel; LNG-IUD = levonorgestrel-releasing IUD; PE = pulmonary embolism; PID = pelvic inflammatory disease; POC = progestin-only contraceptive; SLE = systemic lupus
erythematosus; SSRI = selective serotonin reuptake inhibitor; STD = sexually transmitted disease; VTE = venous thromboembolism.

References
1. Cramer DW, Schiff I, Schoenbaum SC, et al. Tubal infertility and the
intrauterine device. N Engl J Med 1985;312:941–7. http://dx.doi.
org/10.1056/NEJM198504113121502
2. Daling JR, Weiss NS, Metch BJ, et al. Primary tubal infertility in relation
to the use of an intrauterine device. N Engl J Med 1985;312:937–41.
http://dx.doi.org/10.1056/NEJM198504113121501
3. Daling JR, Weiss NS, Voigt LF, McKnight B, Moore DE. The intrauterine
device and primary tubal infertility. N Engl J Med 1992;326:203–4.
http://dx.doi.org/10.1056/NEJM199201163260314
4. Delbarge W, Bátár I, Bafort M, et al. Return to fertility in nulliparous
and parous women after removal of the GyneFix intrauterine contraceptive
system. Eur J Contracept Reprod Health Care 2002;7:24–30. http://
dx.doi.org/10.1080/ejc.7.1.24.30
5. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women
after discontinuation of the intrauterine device: comparison with women
discontinuing other methods of contraception. BJOG 2001;108:304–14.
http://dx.doi.org/10.1111/j.1471-0528.2001.00075.x

MMWR / July 29, 2016 / Vol. 65 / No. 3

6. Hubacher D, Lara-Ricalde R, Taylor DJ, Guerra-Infante F, GuzmánRodríguez R. Use of copper intrauterine devices and the risk of tubal
infertility among nulligravid women. N Engl J Med 2001;345:561–7.
http://dx.doi.org/10.1056/NEJMoa010438
7. Skjeldestad FE, Bratt H. Return of fertility after use of IUDs (Nova-T,
MLCu250 and MLCu375). Adv Contracept 1987;3:139–45. http://
dx.doi.org/10.1007/BF01890702
8. Urbach DR, Marrett LD, Kung R, Cohen MM. Association of
perforation of the appendix with female tubal infertility. Am J Epidemiol
2001;153:566–71. http://dx.doi.org/10.1093/aje/153.6.566
9. Wilson JC. A prospective New Zealand study of fertility after removal
of copper intrauterine contraceptive devices for conception and because
of complications: a four-year study. Am J Obstet Gynecol 1989;160:391–
6. http://dx.doi.org/10.1016/0002-9378(89)90455-9
10. US Department of Health and Human Services. Healthy people 2020:
Maternal, infant, and child health objectives. Washington, DC: US
Department of Health and Human Services; 2015. http://www.
healthypeople.gov/2020/topics-objectives/topic/maternal-infant-andchild-health/objectives

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

11. Annus J, Brat T, Diethelm MP, et al.; World Health Organization Special.
Comparative multicentre trial of three IUDs inserted immediately
following delivery of the placenta. Contraception 1980;22:9–18.http://
dx.doi.org/10.1016/0010-7824(80)90112-2
12. Apelo RA, Waszak CS. Postpartum IUD insertions in Manila,
Philippines. Adv Contracept 1985;1:319–28.
13. Baldwin MK, Edelman AB, Lim JY, Nichols MD, Bednarek PH, Jensen
JT. Intrauterine device placement at 3 versus 6weeks postpartum: a
randomized trial. Contraception 2016;93:356–63.http://dx.doi.
org/10.1016/j.contraception.2015.12.006
14. Bonilla Rosales F, Aguilar Zamudio ME, Cázares Montero ML,
Hernández Ortiz ME, Luna Ruiz MA. [Factors for expulsion of
intrauterine device Tcu380A applied immediately postpartum and after
a delayed period]. Rev Med Inst Mex Seguro Soc 2005;43:5–10.
15. Braniff K, Gomez E, Muller R. A randomised clinical trial to assess
satisfaction with the levonorgestrel- releasing intrauterine system inserted
at caesarean section compared to postpartum placement. Aust N Z J
Obstet Gynaecol 2015;55:279–83.http://dx.doi.org/10.1111/ajo.12335
16. Bryant AG, Kamanga G, Stuart GS, Haddad LB, Meguid T, Mhango C.
Immediate postpartum versus 6-week postpartum intrauterine device
insertion: a feasibility study of a randomized controlled trial. Afr J Reprod
Health 2013;17:72–9.
17. Caliskan E, Ozturk N, Dilbaz BO, Dilbaz S. Analysis of risk factors
associated with uterine perforation by intrauterine devices. Eur J Contracep
Reprod 2003;8:150–5.
18. Çelen S, Möröy P, Sucak A, Aktulay A, Danişman N. Clinical outcomes of early
postplacental insertion of intrauterine contraceptive devices. Contraception
2004;69:279–82.http://dx.doi.org/10.1016/j.contraception.2003.12.004
19. Çelen Ş, Sucak A, Yıldız Y, Danışman N. Immediate postplacental insertion
of an intrauterine contraceptive device during cesarean section. Contraception
2011;84:240–3.http://dx.doi.org/10.1016/j.contraception.2011.01.006
20. Chen BA, Reeves MF, Hayes JL, Hohmann HL, Perriera LK, Creinin
MD. Postplacental or delayed insertion of the levonorgestrel intrauterine
device after vaginal delivery: a randomized controlled trial. Obstet Gynecol
2010;116:1079–87.http://dx.doi.org/10.1097/AOG.0b013e3181f73fac
21. Chen JH, Wu SC, Shao WQ, et al. The comparative trial of TCu 380A IUD
and progesterone-releasing vaginal ring used by lactating women. Contraception
1998;57:371–9.http://dx.doi.org/10.1016/S0010-7824(98)00043-2
22. Cohen R, Sheeder J, Arango N, Teal SB, Tocce K. Twelve-month
contraceptive continuation and repeat pregnancy among young mothers
choosing postdelivery contraceptive implants or postplacental
intrauterine devices. Contraception 2016;93:178–83.http://dx.doi.
org/10.1016/j.contraception.2015.10.001
23. Dahlke JD, Terpstra ER, Ramseyer AM, Busch JM, Rieg T, Magann EF.
Postpartum insertion of levonorgestrel—intrauterine system at three
time periods: a prospective randomized pilot study. Contraception
2011;84:244–8.http://dx.doi.org/10.1016/j.contraception.2011.01.007
24. Dias T, Abeykoon S, Kumarasiri S, Gunawardena C, Padeniya T,
D’Antonio F. Use of ultrasound in predicting success of intrauterine
contraceptive device insertion immediately after delivery. Ultrasound
Obstet Gynecol 2015;46:104–8.
25. Elsedeek MS. Puerperal and menstrual bleeding patterns with different
types of contraceptive device fitted during elective cesarean delivery. Int
J Gynaecol Obstet 2012;116:31–4.http://dx.doi.org/10.1016/j.
ijgo.2011.07.036
26. Elsedeek MS. Five-year follow-up of two types of contraceptive device
fitted during elective cesarean delivery. Int J Gynaecol Obstet
2015;130:179–82.http://dx.doi.org/10.1016/j.ijgo.2015.02.031
27. El-Shafei MM, Mashali A, Hassan EO, El-Boghdad L, El-Lakkany N.
Postpartum and postabortion intrauterine device insertion unmet needs
of safe reproductive health: three years experience of Mansoura University
Hospital. J Egypt Soc Obstet Gynecol 2000;26:253–62.

28. Eroğlu K, Akkuzu G, Vural G, et al. Comparison of efficacy and
complications of IUD insertion in immediate postplacental/early
postpartum period with interval period: 1 year follow-up. Contraception
2006;74:376–81.http://dx.doi.org/10.1016/j.contraception.2006.07.003
29. Gueye M, Gaye YF, Diouf AA, et al. Trancesarean intra-uterine device.
Pilot study performed at Dakar teaching hospital. [French]. J Gynecol
Obstet Biol Reprod (Paris) 2013;42:585–90.http://dx.doi.org/10.1016/j.
jgyn.2013.06.003
30. Gupta S, Malik S, Sinha R, Shyamsunder S, Mittal MK. Association of
the Position of the Copper T 380A as Determined by the Ultrasonography
Following its Insertion in the Immediate Postpartum Period with the
Subsequent Complications: An Observational Study. J Obstet Gynaecol
India 2014;64:349–53.http://dx.doi.org/10.1007/s13224-014-0532-5
31. Hagbard L, Ingemanson CA, Sorbe B. Early postpartum insertion
of copper IUD. Contraception 1978;17:355–63.http://dx.doi.
org/10.1016/0010-7824(78)90081-1
32. Hayes JL, Cwiak C, Goedken P, Zieman M. A pilot clinical trial of
ultrasound-guided postplacental insertion of a levonorgestrel intrauterine
device. Contraception 2007;76:292–6.http://dx.doi.org/10.1016/j.
contraception.2007.06.003
33. Jatlaoui TC, Marcus M, Jamieson DJ, Goedken P, Cwiak C. Postplacental
intrauterine device insertion at a teaching hospital. Contraception
2014;89:528–33.http://dx.doi.org/10.1016/j.contraception.2013.10.008
34. Kumar S, Sethi R, Balasubramaniam S, et al. Women’s experience with
postpartum intrauterine contraceptive device use in India. Reprod Health
2014;11:32.http://dx.doi.org/10.1186/1742-4755-11-32
35. Laes E, Lehtovirta P, Weintraub D, Pyörälä T, Luukkainen T. Early
puerperal insertions of copper-T-200. Contraception 1975;11:289–95.
http://dx.doi.org/10.1016/0010-7824(75)90037-2
36. Lara Ricalde R, Menocal Tobías G, Ramos Pérez C, Velázquez Ramírez
N. [Random comparative study between intrauterine device Multiload
Cu375 and TCu 380a inserted in the postpartum period]. Ginecol
Obstet Mex 2006;74:306–11.
37. Lavin P, Bravo C, Waszak C. Comparison of T Cu 200 and Progestasert
IUDs. Contracept Deliv Syst 1983;4:143–7.
38. Lavin P, Waszak C, Bravo C. Preliminary report on a postpartum CuT
200 study, Santiago, Chile. Int J Gynaecol Obstet 1983;21:71–5.http://
dx.doi.org/10.1016/0020-7292(83)90073-5
39. Lester F, Kakaire O, Byamugisha J, et al. Intracesarean insertion of the Copper
T380A versus 6 weeks postcesarean: a randomized clinical trial. Contraception
2015;91:198–203.http://dx.doi.org/10.1016/j.contraception.2014.12.002
40. Letti Müller AL, Lopes Ramos JG, Martins-Costa SH, et al. Transvaginal
ultrasonographic assessment of the expulsion rate of intrauterine devices
inserted in the immediate postpartum period: a pilot study. Contraception
2005;72:192–5.http://dx.doi.org/10.1016/j.contraception.2005.03.014
41. Levi E, Cantillo E, Ades V, Banks E, Murthy A. Immediate postplacental
IUD insertion at cesarean delivery: a prospective cohort study. Contraception
2012;86:102–5.http://dx.doi.org/10.1016/j.contraception.2011.11.019
42. Levi EE, Stuart GS, Zerden ML, Garrett JM, Bryant AG. Intrauterine
device placement during cesarean delivery and continued use 6 months
postpartum: a randomized controlled trial. Obstet Gynecol 2015;126:5–
11.http://dx.doi.org/10.1097/AOG.0000000000000882
43. Mishra S. Evaluation of Safety, Efficacy, and Expulsion of Post-Placental
and Intra-Cesarean Insertion of Intrauterine Contraceptive Devices
(PPIUCD). J Obstet Gynaecol India 2014;64:337–43.http://dx.doi.
org/10.1007/s13224-014-0550-3
44. Morrison C, Waszak C, Katz K, Diabaté F, Mate EM. Clinical outcomes
of two early postpartum IUD insertion programs in Africa. Contraception
1996;53:17–21.http://dx.doi.org/10.1016/0010-7824(95)00254-5
45. Nelson AL, Chen S, Eden R. Intraoperative placement of the Copper
T-380 intrauterine devices in women undergoing elective cesarean
delivery: a pilot study. Contraception 2009;80:81–3.http://dx.doi.
org/10.1016/j.contraception.2009.01.014

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

46. Newton J, Harper M, Chan KK. Immediate post-placental insertion of
intrauterine contraceptive devices. Lancet 1977;310:272–4.http://
dx.doi.org/10.1016/S0140-6736(77)90955-2
47. Prema K, Gayathri TL, Philips FS. Comparative study of early
postpartum, postabortal and interval insertion of Cu T 200 mm2 device.
J Obstet Gynaecol India 1978;28:946–8.
48. Puzey M. Mirena at caesarean section. Eur J Contracep Reprod
2005;10:164–7.
49. Ragab A, Hamed HO, Alsammani MA, et al. Expulsion of Nova-T380,
Multiload 375, and Copper-T380A contraceptive devices inserted during
cesarean delivery. Int J Gynaecol Obstet 2015;130:174–8.http://dx.doi.
org/10.1016/j.ijgo.2015.03.025
50. Shukla M, Qureshi S; Chandrawati. Post-placental intrauterine device
insertion—a five year experience at a tertiary care centre in north India.
Indian J Med Res 2012;136:432–5.
51. Singal S, Bharti R, Dewan R, et al. Clinical Outcome of Postplacental
Copper T 380A Insertion in Women Delivering by Caesarean Section.
J Clin Diagn Res 2014;8:OC01–04.
52. Stuart GS, Bryant AG, O’Neill E, Doherty IA. Feasibility of postpartum
placement of the levonorgestrel intrauterine system more than 6 h after
vaginal birth. Contraception 2012;85:359–62.http://dx.doi.
org/10.1016/j.contraception.2011.08.005
53. Stuart GS, Lesko CR, Stuebe AM, Bryant AG, Levi EE, Danvers AI. A
randomized trial of levonorgestrel intrauterine system insertion 6 to 48 h
compared to 6 weeks after vaginal delivery; lessons learned. Contraception
2015;91:284–8.http://dx.doi.org/10.1016/j.contraception.2014.12.009
54. Thiery M, Van Kets H, Van der Pas H. Immediate post-placental IUD
insertion: the expulsion problem. Contraception 1985;31:331–49.http://
dx.doi.org/10.1016/0010-7824(85)90002-2
55. Van Der Pas MT, Delbeke L, Van Dets H. Comparative performance of
two copper-wired IUDs (ML Cu 250 and T Cu 200: immediate postpartum
and interval insertion. Contracept Deliv Syst 1980;1:27–35.
56. Welkovic S, Costa LO, Faúndes A, de Alencar Ximenes R, Costa CF. Post-partum
bleeding and infection after post-placental IUD insertion. Contraception
2001;63:155–8.http://dx.doi.org/10.1016/S0010-7824(01)00180-9
57. Whitaker AK, Endres LK, Mistretta SQ, Gilliam ML. Postplacental
insertion of the levonorgestrel intrauterine device after cesarean delivery
vs. delayed insertion: a randomized controlled trial. Contraception
2014;89:534–9.http://dx.doi.org/10.1016/j.contraception.2013.12.007
58. Woo CJ, Alamgir H, Potter JE. Women’s experiences after Planned Parenthood’s
exclusion from a family planning program in Texas. Contraception 2016;93:298–
302.http://dx.doi.org/10.1016/j.contraception.2015.12.004
59. Wu SC; Research Group on Failure Causes and Prevention Measures of
Intrauterine Device. [Efficacy of intrauterine device TCu380A when inserted
in four different periods]. Zhonghua Fu Chan Ke Za Zhi 2009;44:431–5.
60. Xu J, Yang X, Gu X, et al. Comparison between two techniques used in
immediate postplacental insertion of TCu 380A intrauterine device:
36-month follow-up. Reprod Contracept 1999;10:156–62.
61. Xu J, Zhuang L, Yu G. [Comparison of two techniques used in immediate
postplacental insertion of TCu 380A intrauterine device: 12 month followup of 910 cases]. Zhonghua Fu Chan Ke Za Zhi 1997;32:354–7.
62. Xu JX, Rivera R, Dunson TR, et al. A comparative study of two techniques
used in immediate postplacental insertion (IPPI) of the Copper T-380A
IUD in Shanghai, People’s Republic of China. Contraception 1996;54:33–
8.http://dx.doi.org/10.1016/0010-7824(96)00117-5
63. Braniff K, Gomez E, Muller R. A randomised clinical trial to assess
satisfaction with the levonorgestrel- releasing intrauterine system inserted
at caesarean section compared to postpartum placement. Aust N Z J
Obstet Gynaecol 2015;55:279–83. http://dx.doi.org/10.1111/ajo.12335
64. Phillips SJ, Tepper NK, Kapp N, Nanda K, Temmerman M, Curtis KM.
Progestogen-only contraceptive use among breastfeeding women: a
systematic review. Contraception 2015;S0010-7824(15)00585-5.
65. Berry-Bibee E, Tepper N, Jatlaoui T, Whiteman M, Jamieson D,
Curtis K. The safety of intrauterine devices in breastfeeding women: a
systematic review. Contraception. In press 2016.

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66. Steenland MW, Tepper NK, Curtis KM, Kapp N. Intrauterine
contraceptive insertion postabortion: a systematic review. Contraception
2011;84:447–64. http://dx.doi.org/10.1016/j.contraception.2011.03.007
67. World Health Organization Collaborative Study of Cardiovascular
Disease and Steroid Hormone Contraception. Cardiovascular disease
and use of oral and injectable progestogen-only contraceptives and
combined injectable contraceptives. Results of an international,
multicenter, case-control study. Contraception 1998;57:315–24. http://
dx.doi.org/10.1016/S0010-7824(98)00041-9.
68. Heinemann LA, Assmann A, DoMinh T, Garbe E. Oral progestogenonly contraceptives and cardiovascular risk: results from the Transnational
Study on Oral Contraceptives and the Health of Young Women. Eur J
Contracept Reprod Health Care 1999;4:67–73. http://dx.doi.
org/10.3109/13625189909064007
69. Vasilakis C, Jick H, del Mar Melero-Montes M. Risk of idiopathic venous
thromboembolism in users of progestagens alone. Lancet 1999;354:1610–
1. http://dx.doi.org/10.1016/S0140-6736(99)04394-9
70. Kingman CE, Kadir RA, Lee CA, Economides DL. The use of
levonorgestrel-releasing intrauterine system for treatment of menorrhagia
in women with inherited bleeding disorders. BJOG 2004;111:1425–8.
http://dx.doi.org/10.1111/j.1471-0528.2004.00305.x
71. Lukes AS, Reardon B, Arepally G. Use of the levonorgestrel-releasing
intrauterine system in women with hemostatic disorders. Fertil Steril
2008;90:673–7. http://dx.doi.org/10.1016/j.fertnstert.2007.07.1315
72. Pisoni CN, Cuadrado MJ, Khamashta MA, Hunt BJ. Treatment of
menorrhagia associated with oral anticoagulation: efficacy and safety of
the levonorgestrel releasing intrauterine device (Mirena coil). Lupus
2006;15:877–80. http://dx.doi.org/10.1177/0961203306071706
73. Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrelreleasing intrauterine system in the management of menorrhagia in
women with hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–
3. http://dx.doi.org/10.1016/j.ajog.2005.05.002
74. Wilson W, Taubert KA, Gewitz M, et al; American Heart Association
Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee;
American Heart Association Council on Cardiovascular Disease in the
Young; American Heart Association Council on Clinical Cardiology;
American Heart Association Council on Cardiovascular Surgery and
Anesthesia; Quality of Care and Outcomes Research Interdisciplinary
Working Group. Prevention of infective endocarditis: guidelines from
the American Heart Association: a guideline from the American Heart
Association Rheumatic Fever, Endocarditis, and Kawasaki Disease
Committee, Council on Cardiovascular Disease in the Young, and the
Council on Clinical Cardiology, Council on Cardiovascular Surgery and
Anesthesia, and the Quality of Care and Outcomes Research
Interdisciplinary Working Group. Circulation 2007;116:1736–54.
http://dx.doi.org/10.1161/CIRCULATIONAHA.106.183095
75. Tepper NK, Paulen ME, Marchbanks PA, Curtis KM. Safety of
contraceptive use among women with peripartum cardiomyopathy: a
systematic review. Contraception 2010;82:95–101. http://dx.doi.
org/10.1016/j.contraception.2010.02.004
76. The Criteria Committee of the New York Heart Association.
Nomenclature and criteria for diagnosis of diseases of the heart and great
vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994.
77. Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures
and breast cancer in a sample of women with systemic lupus
erythematosus. Rheumatology (Oxford) 2004;43:1178–81. http://
dx.doi.org/10.1093/rheumatology/keh282
78. Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated
with abnormal Pap results in systemic lupus erythematosus.
Rheumatology (Oxford) 2004;43:1386–9. http://dx.doi.org/10.1093/
rheumatology/keh331
79. Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin
gene mutation, and thrombosis risk in patients with antiphospholipid
antibodies. J Rheumatol 2002;29:1683–8.

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Recommendations and Reports

80. Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham
risk factors fail to fully account for accelerated atherosclerosis in systemic
lupus erythematosus. Arthritis Rheum 2001;44:2331–7. http://dx.doi.
org/10.1002/1529-0131(200110)44:10<2331::AID-ART395≥3.0.CO;2-I
81. Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women
with systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30.
http://dx.doi.org/10.1093/rheumatology/32.3.227
82. Manzi S, Meilahn EN, Rairie JE, et al. Age-specific incidence rates of
myocardial infarction and angina in women with systemic lupus
erythematosus: comparison with the Framingham Study. Am J Epidemiol
1997;145:408–15. http://dx.doi.org/10.1093/oxfordjournals.aje.
a009122
83. McAlindon T, Giannotta L, Taub N, D’Cruz D, Hughes G. Environmental
factors predicting nephritis in systemic lupus erythematosus. Ann Rheum
Dis 1993;52:720–4. http://dx.doi.org/10.1136/ard.52.10.720
84. McDonald J, Stewart J, Urowitz MB, Gladman DD. Peripheral vascular
disease in patients with systemic lupus erythematosus. Ann Rheum Dis
1992;51:56–60. http://dx.doi.org/10.1136/ard.51.1.56
85. Mintz G, Gutiérrez G, Delezé M, Rodríguez E. Contraception with
progestagens in systemic lupus erythematosus. Contraception
1984;30:29–38. http://dx.doi.org/10.1016/0010-7824(84)90076-3
86. Petri M. Musculoskeletal complications of systemic lupus erythematosus
in the Hopkins Lupus Cohort: an update. Arthritis Care Res
1995;8:137–45. http://dx.doi.org/10.1002/art.1790080305
87. Petri M. Lupus in Baltimore: evidence-based ‘clinical pearls’ from the
Hopkins Lupus Cohort. Lupus 2005;14:970–3. http://dx.doi.
org/10.1191/0961203305lu2230xx
88. Sánchez-Guerrero J, Uribe AG, Jiménez-Santana L, et al. A trial of
contraceptive methods in women with systemic lupus erythematosus. N
Engl J Med 2005;353:2539–49. http://dx.doi.org/10.1056/NEJMoa050817
89. Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and venous
thrombosis after diagnosis of systemic lupus erythematosus. Arthritis
Rheum 2005;53:609–12. http://dx.doi.org/10.1002/art.21314
90. Somers E, Magder LS, Petri M. Antiphospholipid antibodies and
incidence of venous thrombosis in a cohort of patients with systemic
lupus erythematosus. J Rheumatol 2002;29:2531–6.
91. Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo
MA. The bimodal mortality pattern of systemic lupus erythematosus. Am J
Med 1976;60:221–5. http://dx.doi.org/10.1016/0002-9343(76)90431-9
92. Julkunen HA. Oral contraceptives in systemic lupus erythematosus:
side-effects and influence on the activity of SLE. Scand J Rheumatol
1991;20:427–33. http://dx.doi.org/10.3109/03009749109096822
93. Jungers P, Dougados M, Pélissier C, et al. Influence of oral contraceptive
therapy on the activity of systemic lupus erythematosus. Arthritis Rheum
1982;25:618–23. http://dx.doi.org/10.1002/art.1780250603
94. Petri M, Kim MY, Kalunian KC, et al; OC-SELENA Trial. Combined
oral contraceptives in women with systemic lupus erythematosus. N Engl
J Med 2005;353:2550–8. http://dx.doi.org/10.1056/NEJMoa051135
95. Choojitarom K, Verasertniyom O, Totemchokchyakarn K, Nantiruj K,
Sumethkul V, Janwityanujit S. Lupus nephritis and Raynaud’s
phenomenon are significant risk factors for vascular thrombosis in SLE
patients with positive antiphospholipid antibodies. Clin Rheumatol
2008;27:345–51. http://dx.doi.org/10.1007/s10067-007-0721-z
96. Wahl DG, Guillemin F, de Maistre E, Perret C, Lecompte T, Thibaut G.
Risk for venous thrombosis related to antiphospholipid antibodies in
systemic lupus erythematosus—a meta-analysis. Lupus 1997;6:467–73.
http://dx.doi.org/10.1177/096120339700600510
97. Tepper NK, Whiteman MK, Zapata LB, Marchbanks PA, Curtis KM. Safety
of hormonal contraceptives among women with migraine: a systematic review.
Contraception 2016. Epub May 3, 2016. http:// dx.doi.org/10.1016/j.
contraception.2016.04.016
98. Tepper NK, Whiteman MK, Marchbanks PA, James AH, Curtis KM.
Progestin-only contraception and thromboembolism: a systematic review.
Contraception 2016. Epub May 3, 2016. http://dx.doi.org/10.1016/j.
contraception.2016.04.014

99. Pagano HP, Zapata LB, Berry-Bibee EN, Nanda K, Curtis KM. Safety of
hormonal contraception and intrauterine devices among women with
depressive and bipolar disorders: a systematic review. Contraception 2016.
Epub June 27, 2016. http://dx.doi.org/10.1016/j.contraception.2016.06.012
100. Barrington JW, Arunkalaivanan AS, Abdel-Fattah M. Comparison between
the levonorgestrel intrauterine system (LNG-IUS) and thermal balloon
ablation in the treatment of menorrhagia. Eur J Obstet Gynecol Reprod Biol
2003;108:72–4. http://dx.doi.org/10.1016/S0301-2115(02)00408-6
101. Gupta B, Mittal S, Misra R, Deka D, Dadhwal V. Levonorgestrelreleasing intrauterine system vs. transcervical endometrial resection for
dysfunctional uterine bleeding. Int J Gynaecol Obstet 2006;95:261–6.
http://dx.doi.org/10.1016/j.ijgo.2006.07.004
102. Hurskainen R, Teperi J, Rissanen P, et al. Quality of life and costeffectiveness of levonorgestrel-releasing intrauterine system versus
hysterectomy for treatment of menorrhagia: a randomised trial.[see
comment]. Lancet 2001;357:273–7. http://dx.doi.org/10.1016/
S0140-6736(00)03615-1
103. Istre O, Trolle B. Treatment of menorrhagia with the levonorgestrel
intrauterine system versus endometrial resection. Fertil Steril
2001;76:304–9. http://dx.doi.org/10.1016/S0015-0282(01)01909-4
104. Koh SC, Singh K. The effect of levonorgestrel-releasing intrauterine
system use on menstrual blood loss and the hemostatic, fibrinolytic/
inhibitor systems in women with menorrhagia. J Thromb Haemost
2007;5:133–8. http://dx.doi.org/10.1111/j.1538-7836.2006.02243.x
105. Lethaby AE, Cooke I, Rees M. Progesterone/progestogen releasing
intrauterine systems versus either placebo or any other medication for heavy
menstrual bleeding. Cochrane Database Syst Rev 2000;(2):CD002126.
106. Magalhães J, Aldrighi JM, de Lima GR. Uterine volume and menstrual
patterns in users of the levonorgestrel-releasing intrauterine system with
idiopathic menorrhagia or menorrhagia due to leiomyomas. Contraception
2007;75:193–8. http://dx.doi.org/10.1016/j.contraception.2006.11.004
107. Stewart A, Cummins C, Gold L, Jordan R, Phillips W. The
effectiveness of the levonorgestrel-releasing intrauterine system in
menorrhagia: a systematic review. BJOG 2001;108:74–86. http://
dx.doi.org/10.1111/j.1471-0528.2001.00020.x
108. Fedele L, Bianchi S, Zanconato G, Portuese A, Raffaelli R. Use of a
levonorgestrel-releasing intrauterine device in the treatment of
rectovaginal endometriosis. Fertil Steril 2001;75:485–8. http://dx.doi.
org/10.1016/S0015-0282(00)01759-3
109. Lockhat FBE, Emembolu J, Konje JC. The effect of a levonorgestrel intrauterine
system (LNG-IUS) on symptomatic endometriosis. Fertil Steril 2002;77(Suppl
1):S24. http://dx.doi.org/10.1016/S0015-0282(01)03086-2
110. Petta CA, Ferriani RA, Abrao MS, et al. Randomized clinical trial of a
levonorgestrel-releasing intrauterine system and a depot GnRH analogue for
the treatment of chronic pelvic pain in women with endometriosis. Hum
Reprod 2005;20:1993–8. http://dx.doi.org/10.1093/humrep/deh869
111. Vercellini P, Aimi G, Panazza S, De Giorgi O, Pesole A, Crosignani PG.
A levonorgestrel-releasing intrauterine system for the treatment of
dysmenorrhea associated with endometriosis: a pilot study. Fertil Steril
1999;72:505–8. http://dx.doi.org/10.1016/S0015-0282(99)00291-5
112. Vercellini P, Frontino G, De Giorgi O, Aimi G, Zaina B, Crosignani
PG. Comparison of a levonorgestrel-releasing intrauterine device versus
expectant management after conservative surgery for symptomatic
endometriosis: a pilot study. Fertil Steril 2003;80:305–9. http://dx.doi.
org/10.1016/S0015-0282(03)00608-3
113. Gaffield ME, Kapp N, Curtis KM. Combined oral contraceptive and
intrauterine device use among women with gestational trophoblastic
disease. Contraception 2009;80:363–71. http://dx.doi.org/10.1016/j.
contraception.2009.03.022

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114. Whiteman MK, Zapata LB, Tepper NK, Marchbanks PA, Curtis KM.
Use of contraceptive methods among women with endometrial
hyperplasia: a systematic review. Contraception 2010;82:56–63. http://
dx.doi.org/10.1016/j.contraception.2010.02.005
115. Zapata LB, Whiteman MK, Tepper NK, Jamieson DJ, Marchbanks
PA, Curtis KM. Intrauterine device use among women with uterine
fibroids: a systematic review. Contraception 2010;82:41–55. http://
dx.doi.org/10.1016/j.contraception.2010.02.011
116. Tepper NK, Steenland MW, Gaffield ME, Marchbanks PA, Curtis
KM. Retention of intrauterine devices in women who acquire pelvic
inflammatory disease: a systematic review. Contraception 2013;87:655–
60. http://dx.doi.org/10.1016/j.contraception.2012.08.011
117. Faúndes A, Telles E, Cristofoletti ML, Faúndes D, Castro S, Hardy E.
The risk of inadvertent intrauterine device insertion in women carriers
of endocervical Chlamydia trachomatis. Contraception 1998;58:105–
9. http://dx.doi.org/10.1016/S0010-7824(98)00064-X
118. Ferraz do Lago R, Simões JA, Bahamondes L, Camargo RP, Perrotti M,
Monteiro I. Follow-up of users of intrauterine device with and without
bacterial vaginosis and other cervicovaginal infections. Contraception
2003;68:105–9. http://dx.doi.org/10.1016/S0010-7824(03)00109-4
119. Morrison CS, Sekadde-Kigondu C, Miller WC, Weiner DH, Sinei SK.
Use of sexually transmitted disease risk assessment algorithms for
selection of intrauterine device candidates. Contraception 1999;59:97–
106. http://dx.doi.org/10.1016/S0010-7824(99)00006-2
120. Pap-Akeson M, Solheim F, Thorbert G, Akerlund M. Genital tract infections
associated with the intrauterine contraceptive device can be reduced by
inserting the threads into the uterine cavity. Br J Obstet Gynaecol
1992;99:676–9. http://dx.doi.org/10.1111/j.1471-0528.1992.tb13854.x
121. Sinei SK, Schulz KFLP, Lamptey PR, et al. Preventing IUCD-related pelvic
infection: the efficacy of prophylactic doxycycline at insertion. Br J Obstet
Gynaecol 1990;97:412–9. http://dx.doi.org/10.1111/j.1471-0528.1990.
tb01828.x
122. Skjeldestad FE, Halvorsen LE, Kahn H, Nordbø SA, Saake K. IUD users
in Norway are at low risk for genital C. trachomatis infection. Contraception
1996;54:209–12. http://dx.doi.org/10.1016/S0010-7824(96)00190-4
123. Walsh TL, Bernstein GS, Grimes DA, Frezieres R, Bernstein L, Coulson AH;
IUD Study Group. Effect of prophylactic antibiotics on morbidity associated
with IUD insertion: results of a pilot randomized controlled trial. Contraception
1994;50:319–27. http://dx.doi.org/10.1016/0010-7824(94)90019-1
124. Workowski KA, Bolan GA. Sexually transmitted diseases treatment
guidelines, 2015. MMWR Recomm Rep 2015;64(No. RR-03).
125. Jatlaoui TC, Simmons KB, Curtis KM. The safety of intrauterine
contraception initiation among women with current asymptomatic cervical
infections or at increased risk of sexually transmitted infections.
Contraception 2016. Epub June 1, 2016. http://dx.doi.org/10.1016/j.
contraception.2016.05.013
126. Carael M, Van de Perre PH, Lepage PH, et al. Human immunodeficiency
virus transmission among heterosexual couples in Central Africa. AIDS
1988;2:201–5.
127. European Study Group on Heterosexual Transmission of HIV.
Comparison of female to male and male to female transmission of HIV
in 563 stable couples. BMJ 1992;304:809–13. http://dx.doi.
org/10.1136/bmj.304.6830.809
128. Kapiga SH, Lyamuya EF, Lwihula GK, Hunter DJ. The incidence of
HIV infection among women using family planning methods in Dar
es Salaam, Tanzania. AIDS 1998;12:75–84. http://dx.doi.
org/10.1097/00002030-199801000-00009.

MMWR / July 29, 2016 / Vol. 65 / No. 3

129. Kapiga SH, Shao JF, Lwihula GK, Hunter DJ. Risk factors for HIV
infection among women in Dar-es-Salaam, Tanzania. J Acquir Immune
Defic Syndr 1994;7:301–9.
130. Mann JM, Nzilambi N, Piot P, et al. HIV infection and associated risk
factors in female prostitutes in Kinshasa, Zaire. AIDS 1988;2:249–54.
http://dx.doi.org/10.1097/00002030-198808000-00002
131. Martin HL Jr, Nyange PM, Richardson BA, et al. Hormonal
contraception, sexually transmitted diseases, and risk of heterosexual
transmission of human immunodeficiency virus type 1. J Infect Dis
1998;178:1053–9. http://dx.doi.org/10.1086/515654
132. Mali JK, Hunter DJ, Maggwa BN, Tukei PM. Contraceptive use and
the risk of HIV infection in Nairobi, Kenya. Int J Gynaecol Obstet
1995;48:61–7. http://dx.doi.org/10.1016/0020-7292(94)02214-3
133. Nicolosi A, Corrêa Leite ML, Musicco M, Arici C, Gavazzeni G,
Lazzarin A; Italian Study Group on HIV Heterosexual Transmission.
The efficiency of male-to-female and female-to-male sexual transmission
of the human immunodeficiency virus: a study of 730 stable couples.
[comment]. Epidemiology 1994;5:570–5. http://dx.doi.
org/10.1097/00001648-199411000-00003
134. Plourde PJ, Plummer FA, Pepin J, et al. Human immunodeficiency
virus type 1 infection in women attending a sexually transmitted
diseases clinic in Kenya.[comment]. J Infect Dis 1992;166:86–92.
http://dx.doi.org/10.1093/infdis/166.1.86
135. Sinei SK, Fortney JA, Kigondu CS, et al. Contraceptive use and HIV
infection in Kenyan family planning clinic attenders. Int J STD AIDS
1996;7:65–70. http://dx.doi.org/10.1258/0956462961917104
136. Spence MR, Robbins SM, Polansky M, Schable CA. Seroprevalence
of human immunodeficiency virus type I (HIV-1) antibodies in a
family-planning population. Sex Transm Dis 1991;18:143–5. http://
dx.doi.org/10.1097/00007435-199107000-00003
137. Tepper NK, Curtis KM, Nanda K, Jamieson DJ. Safety of intrauterine devices
among women with HIV: a systematic review. Contraception 2016. Epub
June 22, 2016. http://dx.doi.org/0.1016/j.contraception.2016.06.011
138. Grigoryan OR, Grodnitskaya EE, Andreeva EN, Shestakova MV,
Melnichenko GA, Dedov II. Contraception in perimenopausal women
with diabetes mellitus. Gynecol Endocrinol 2006;22:198–206. http://
dx.doi.org/10.1080/09513590600624317
139. Rogovskaya S, Rivera R, Grimes DA, et al. Effect of a levonorgestrel
intrauterine system on women with type 1 diabetes: a randomized trial.
Obstet Gynecol 2005;105:811–5. http://dx.doi.org/10.1097/01.
AOG.0000156301.11939.56
140. Zapata LB, Paulen ME, Cansino C, Marchbanks PA, Curtis KM.
Contraceptive use among women with inflammatory bowel disease: a
systematic review. Contraception 2010;82:72–85. http://dx.doi.
org/10.1016/j.contraception.2010.02.012
141. Paulen ME, Folger SG, Curtis KM, Jamieson DJ. Contraceptive use
among solid organ transplant patients: a systematic review.
Contraception 2010;82:102–12. http://dx.doi.org/10.1016/j.
contraception.2010.02.007
142. Bounds W, Guillebaud J. Observational series on women using the
contraceptive Mirena concurrently with anti-epileptic and other
enzyme-inducing drugs. J Fam Plann Reprod Health Care 2002;28:78–
80. http://dx.doi.org/10.1783/147118902101195992
143. Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens,
reduces lamotrigine serum concentrations. Epilepsia 2005;46:1414–7.
http://dx.doi.org/10.1111/j.1528-1167.2005.10105.x

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix C
Classifications for Progestin-Only Contraceptives
Classifications for progestin-only contraceptives
(POCs) include those for progestin-only implants, depot
medroxyprogesterone acetate (DMPA; 150 mg intramuscularly
or 104 mg subcutaneously), and progestin-only pills (POPs) (Box
C1) (Table C1). POCs do not protect against sexually transmitted
diseases (STDs), including human immunodeficiency virus
(HIV), and women using these methods should be counseled
that consistent and correct use of the male latex condom reduces
the risk for transmission of HIV and other STDs. Use of female
condoms can provide protection from transmission of STDs,
although data are limited.

BOX C1. Categories for classifying progestin-only contraceptives

TABLE C1. Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestin-only pills
Category
Condition

Implants

DMPA

POPs

Clarifications/Evidence/Comments

Clarification: Use of POCs is not required. No known harm to the
woman, the course of her pregnancy, or the fetus occurs if POCs
are inadvertently used during pregnancy. However, the relation
between DMPA use during pregnancy and its effects on the fetus
remains unclear.

1
1
1

2
1
2

1
1
1

1
1

—
—

Personal Characteristics and Reproductive History
Pregnancy

Age
a. Menarche to <18 years
b. 18–45 years
c. >45 years

Parity
a. Nulliparous
b. Parous
Breastfeeding
a. <21 days postpartum

Evidence: Most studies have found that women lose BMD
during DMPA use but recover BMD after discontinuation.
Limited evidence shows a weak association with fracture.
However, one large study suggests that women who choose
DMPA might be at higher risk for fracture before initiation
(1). It is unclear whether adult women with long durations of
DMPA use can regain BMD to baseline levels before entering
menopause and whether adolescents can reach peak bone
mass after discontinuation of DMPA. The relationship between
these changes in BMD during the reproductive years and future
fracture risk is unknown. Studies generally find no effect of
POCs other than DMPA on BMD (1–48).

Evidence: Two small, randomized controlled trials found no
adverse impact on breastfeeding with initiation of etonogestrel
implants within 48 hours postpartum. Other studies found
that initiation of POPs, injectables, and implants at ≤6
weeks postpartum compared with nonhormonal use had
no detrimental effect on breastfeeding outcomes or infant
health, growth, and development in the first year postpartum.
In general, these studies are of poor quality, lack standard
definitions of breastfeeding or outcome measures, and have not
included premature or ill infants (50,51).
Comment: Certain women might be at risk for breastfeeding
difficulties, such as women with previous breastfeeding
difficulties, certain medical conditions, and certain perinatal
complications and those who deliver preterm. For these
women, as for all women, discussions about contraception for
breastfeeding women should include information about risks,
benefits, and alternatives.
See table footnotes on page 49.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition

Implants

b. 21 to <30 days postpartum
i. With other risk factors for VTE
(e.g., age ≥35 years, previous
VTE, thrombophilia, immobility,
transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/
m2, postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
ii. Without other risk factors for VTE

c. 30–42 days postpartum
i. With other risk factors for VTE
(e.g., age ≥35 years, previous
VTE, thrombophilia, immobility,
transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/
m2, postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
ii. Without other risk factors for VTE

DMPA
2

POPs
2

Clarifications/Evidence/Comments
Clarification: Breastfeeding provides important health benefits
for mother and infant. The U.S. Department of Health and Human
Services recommends increasing the proportion of infants initially
breastfed, exclusively breastfed through 6 months of life, and
continuing breastfeeding through at least 1 year of life as key public
health goals (49).
Evidence: Two small, randomized controlled trials found no
adverse impact on breastfeeding with initiation of etonogestrel
implants within 48 hours postpartum. Other studies found
that initiation of POPs, injectables, and implants at ≤6
weeks postpartum compared with nonhormonal use had
no detrimental effect on breastfeeding outcomes or infant
health, growth, and development in the first year postpartum.
In general, these studies are of poor quality, lack standard
definitions of breastfeeding or outcome measures, and have not
included premature or ill infants (50,51).
Comment: Certain women might be at risk for breastfeeding
difficulties, such as women with previous breastfeeding
difficulties, certain medical conditions, and certain perinatal
complications and those who deliver preterm. For these
women, as for all women, discussions about contraception for
breastfeeding women should include information about risks,
benefits, and alternatives.
Clarification: Breastfeeding provides important health benefits
for mother and infant. The U.S. Department of Health and Human
Services recommends increasing the proportion of infants initially
breastfed, exclusively breastfed through 6 months of life, and
continuing breastfeeding through at least 1 year of life as key public
health goals (49).
Evidence: Two small, randomized controlled trials found no
adverse impact on breastfeeding with initiation of etonogestrel
implants within 48 hours postpartum. Other studies found
that initiation of POPs, injectables, and implants at ≤6
weeks postpartum compared with nonhormonal use had
no detrimental effect on breastfeeding outcomes or infant
health, growth, and development in the first year postpartum.
In general, these studies are of poor quality, lack standard
definitions of breastfeeding or outcome measures, and have not
included premature or ill infants (50,51).
Comment: Certain women might be at risk for breastfeeding
difficulties, such as women with previous breastfeeding
difficulties, certain medical conditions, and certain perinatal
complications and those who deliver preterm. For these
women, as for all women, discussions about contraception for
breastfeeding women should include information about risks,
benefits, and alternatives.

d. >42 days postpartum

See table footnotes on page 49.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition
Postpartum (nonbreastfeeding
women)
a. <21 days postpartum
b. 21–42 days postpartum
i. With other risk factors for VTE
(e.g., age ≥35 years, previous
VTE, thrombophilia, immobility,
transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/
m2, postpartum hemorrhage,
postcesarean delivery,
preeclampsia, or smoking)
ii. Without other risk factors for VTE
c. >42 days postpartum
Postabortion
a. First trimester

Implants

DMPA

POPs

Clarifications/Evidence/Comments

—

1
1

—
—

Clarification: POCs may be started immediately postabortion.
Evidence: Limited evidence suggests that no adverse side effects
occur when implants (Norplant) or progestin-only injectables
(NET-EN) are initiated after first trimester abortion (52–55).

b. Second trimester

Clarification: POCs may be started immediately postabortion.

c. Immediate postseptic abortion
Past ectopic pregnancy

1
1

1
2

History of pelvic surgery
Smoking
a. Age <35 years
b. Age ≥35 years
i. <15 cigarettes per day
ii. ≥15 cigarettes per day
Obesity
a. BMI ≥30 kg/m2
b. Menarche to <18 years and BMI
≥30 kg/m2

Clarification: POCs may be started immediately postabortion.
Comment: POP users have a higher absolute rate of ectopic
pregnancy than do users of other POCs but still lower than
women using no method.
—

1
1

1
2

1
1

Evidence: Limited evidence demonstrated no substantial
decrease in effectiveness of oral contraceptives among women
who underwent laparoscopic placement of an adjustable
gastric band (74).

History of bariatric surgery
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Restrictive procedures: decrease
storage capacity of the stomach
(vertical banded gastroplasty,
laparoscopic adjustable gastric band,
or laparoscopic sleeve gastrectomy)
b. Malabsorptive procedures:
decrease absorption of nutrients
and calories by shortening the
functional length of the small
intestine (Roux-en-Y gastric bypass
or biliopancreatic diversion)

—
—
—
—
—
Evidence: Among adult women, generally no association has
been found between baseline weight and weight gain among
DMPA users compared with nonusers. Evidence is mixed for
adolescent DMPA users, with some studies observing greater
weight gain among obese compared with normal weight
users but other studies showing no association; methodologic
differences across studies might account for the differences
in findings. Data on other POC methods and other adverse
outcomes including weight gain are limited (56–73).

Comment: Bariatric surgical procedures involving a
malabsorptive component have the potential to decrease
oral contraceptive effectiveness, perhaps further decreased
by postoperative complications such as long-term diarrhea,
vomiting, or both.
See table footnotes on page 49.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition

Implants

DMPA

POPs

Clarifications/Evidence/Comments

Clarification: When multiple major risk factors exist, risk for
cardiovascular disease might increase substantially. Certain POCs
might increase the risk for thrombosis, although this increase
is substantially less than with COCs. The effects of DMPA might
persist for some time after discontinuation.

Cardiovascular Disease
Multiple risk factors for
atherosclerotic cardiovascular
disease (e.g., older age, smoking,
diabetes, hypertension, low HDL, high
LDL, or high triglyceride levels)

Clarification: The recommendations apply to known preexisting
medical conditions or characteristics. Few if any screening tests
are needed before initiation of contraception. See the U.S. Selected
Practice Recommendations for Contraceptive Use (http://www.cdc.
gov/reproductivehealth/unintendedpregnancy/usspr.htm).
Hypertension
Systolic blood pressure ≥160 mm Hg
or diastolic blood pressure ≥100 mm
Hg are associated with increased risk
for adverse health events as a result of
pregnancy (Box 2).
a. Adequately controlled
hypertension

b. Elevated blood pressure levels
(properly taken measurements)
i. Systolic 140–159 mm Hg or
diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic
≥100 mm Hg

c. Vascular disease

History of high blood pressure
during pregnancy (when current
blood pressure is measurable
and normal)
Deep venous thrombosis/Pulmonary
embolism

a. History of DVT/PE, not receiving
anticoagulant therapy
See table footnotes on page 49.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition

Implants

DMPA

POPs

Clarifications/Evidence/Comments

—

i. Higher risk for recurrent DVT/PE
(one or more risk factors)
• History of estrogen-associated
DVT/PE
• Pregnancy-associated DVT/PE
• Idiopathic DVT/PE
• Known thrombophilia, including
antiphospholipid syndrome
• Active cancer (metastatic, receiving
therapy, or within 6 months after
clinical remission), excluding
nonmelanoma skin cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE
(no risk factors)
b. Acute DVT/PE

c. DVT/PE and established
anticoagulant therapy for at
least 3 months
i. Higher risk for recurrent DVT/PE
(one or more risk factors)
• Known thrombophilia, including
antiphospholipid syndrome
• Active cancer (metastatic, receiving
therapy, or within 6 months after
clinical remission), excluding
nonmelanoma skin cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE
(no risk factors)
d. Family history (first-degree
relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged
immobilization
f. Minor surgery without
immobilization
Known thrombogenic mutations
(e.g., factor V Leiden; prothrombin
mutation; and protein S, protein C,
and antithrombin deficiencies)
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Superficial venous disorders
a. Varicose veins
b. Superficial venous thrombosis
(acute or history)
Current and history of ischemic
Initiation
heart disease
2
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Stroke (history of cerebrovascular
Initiation
accident)
2
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Valvular heart disease
Complicated valvular heart disease
is associated with increased risk for
adverse health events as a result of
pregnancy (Box 2).
a. Uncomplicated

Evidence: No direct evidence exists on use of POCs among
women with acute DVT/PE. Although findings on the risk for
venous thrombosis with use of POCs in otherwise healthy
women is inconsistent, any small increased risk is substantially
less than that with COCs (75–77).
Evidence: No direct evidence exists on use of POCs among
women with DVT/PE receiving anticoagulant therapy. Although
findings on the risk for venous thrombosis with use of POCs is
inconsistent in otherwise healthy women, any small increased
risk is substantially less than that with COCs (75–77).
Limited evidence indicates that intramuscular injections of
DMPA in women receiving chronic anticoagulation therapy does
not pose a significant risk for hematoma at the injection site or
increase the risk for heavy or irregular vaginal bleeding (78).

—

2
1

—
—

—

1
1

Continuation
3

Initiation
2

Continuation Comment: Concern exists about hypoestrogenic effects
and reduced HDL levels, particularly among users of DMPA.
3
However, little concern exists about these effects with regard
to POPs. The effects of DMPA might persist for some time
after discontinuation.

Continuation
3

Initiation
2

Clarification: Routine screening is not appropriate because of
the rarity of the conditions and the high cost of screening.

—
—

—

See table footnotes on page 49.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition
b. Complicated (pulmonary
hypertension, risk for atrial
fibrillation, or history of subacute
bacterial endocarditis)
Peripartum cardiomyopathy
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Normal or mildly impaired cardiac
function (New York Heart Association
Functional Class I or II: patients
with no limitation of activities or
patients with slight, mild limitation
of activity) (80)
i. <6 months
ii. ≥6 months
b. Moderately or severely impaired
cardiac function (New York Heart
Association Functional Class III or IV:
patients with marked limitation of
activity or patients who should be at
complete rest) (80)

Implants

DMPA

POPs

Clarifications/Evidence/Comments

—

Evidence: No direct evidence exists on the safety of POCs
among women with peripartum cardiomyopathy. Limited
indirect evidence from noncomparative studies of women
with cardiac disease demonstrated few cases of hypertension,
thromboembolism, and heart failure in women with cardiac
disease using POPs and DMPA (79).
Comment: Progestin-only implants might induce cardiac
arrhythmias in healthy women; women with peripartum
cardiomyopathy have a high incidence of cardiac arrhythmias.
1
1
2

1
1
2

Initiation

Continuation

Clarification: Persons with SLE are at increased risk for ischemic
heart disease, stroke, and VTE. Categories assigned to such
conditions in U.S. MEC should be the same for women with SLE who
have these conditions. For all subconditions of SLE, classifications
are based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must be
modified in the presence of such risk factors. Many women with
SLE can be considered good candidates for most contraceptive
methods, including hormonal contraceptives (81–99).
Evidence: Antiphospholipid antibodies are associated with a
higher risk for both arterial and venous thrombosis (100,101).

b. Severe thrombocytopenia

Clarification: Persons with SLE are at increased risk for ischemic
heart disease, stroke, and VTE. Categories assigned to such
conditions in U.S. MEC should be the same for women with SLE who
have these conditions. For all subconditions of SLE, classifications
are based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must be
modified in the presence of such risk factors. Many women with
SLE can be considered good candidates for most contraceptive
methods, including hormonal contraceptives (81–99).
Comment: Severe thrombocytopenia increases the risk for
bleeding. POCs might be useful in treating menorrhagia
in women with severe thrombocytopenia. However, given
the increased or erratic bleeding that might be seen on
initiation of DMPA and its irreversibility for 11–13 weeks after
administration, initiation of this method in women with severe
thrombocytopenia should be done with caution.

c. Immunosuppressive therapy

See table footnotes on page 49.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition

Implants

.
d. None of the above

Rheumatoid arthritis
a. Receiving immunosuppressive
therapy

DMPA
Initiation
2

Continuation
2

2/3

POPs

Clarifications/Evidence/Comments

Clarification (DMPA): DMPA use among women receiving longterm corticosteroid therapy with a history of, or with risk factors for,
nontraumatic fractures is classified as category 3. Otherwise, DMPA
use for women with rheumatoid arthritis is classified as category 2.
Evidence: Limited evidence shows no consistent pattern of
improvement or worsening of rheumatoid arthritis with use of
oral contraceptives, progesterone, or estrogen (102).

b. Not receiving immunosuppressive
therapy

Evidence: Limited evidence shows no consistent pattern of
improvement or worsening of rheumatoid arthritis with use of
oral contraceptives, progesterone, or estrogen (102).

—
Evidence: No studies directly examined the risk for stroke
among women with migraine using POCs (103). Limited
evidence demonstrated that women using POPs, DMPA, or
implants do not have an increased risk for ischemic stroke
compared with nonusers (104).

Comment: Menstrual migraine is a subtype of migraine without
aura. For more information, see The International Headache
Society Classification, 3rd edition (http://www.ihs-classification.
org/_downloads/mixed/International-Headache-ClassificationIII-ICHD-III-2013-Beta.pdf ).

Clarification: If a woman is taking anticonvulsants, see
Drug Interactions section. Certain anticonvulsants lower
POC effectiveness.

1
1

2
2

1
1

Neurologic Conditions
Headaches
a. Nonmigraine (mild or severe)
b. Migraine
i. Without aura (This category
of migraine includes
menstrual migraine.)
ii. With aura

Epilepsy
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Multiple sclerosis
a. With prolonged immobility
b. Without prolonged immobility

Evidence: Limited evidence suggests that use of COCs or oral
contraceptives (type not specified) among women with multiple
sclerosis does not worsen the clinical course of disease (105).
Comment: Women with multiple sclerosis might have
compromised bone health from disease-related disability,
immobility, and use of corticosteroids. Use of DMPA, which
has been associated with small changes in BMD, might
be of concern.

Depressive Disorders
Depressive disorders

Clarification: If a woman is taking psychotropic medications or
St. John’s wort, see Drug Interactions section.
Evidence: The frequency of psychiatric hospitalizations for
women with bipolar disorder or depression did not significantly
differ among women using DMPA, LNG-IUD, Cu-IUD, or
sterilization (106).

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without
heavy bleeding

b. Heavy or prolonged bleeding
(includes regular and irregular
patterns)

Clarification: Unusually heavy bleeding should raise the
suspicion of a serious underlying condition.

See table footnotes on page 49.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Implants

DMPA

POPs

Clarifications/Evidence/Comments
Clarification: If pregnancy or an underlying pathological
condition (e.g., pelvic malignancy) is suspected, it must be
evaluated and the category adjusted after evaluation.
Comment: POCs might cause irregular bleeding patterns,
which might mask symptoms of underlying pathologic
conditions. The effects of DMPA might persist for some time
after discontinuation.
—
—

Endometriosis
Benign ovarian tumors
(including cysts)
Severe dysmenorrhea
Gestational trophoblastic disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Suspected gestational
trophoblastic disease (immediate
postevacuation)
i. Uterine size first trimester
ii. Uterine size second trimester
b. Confirmed gestational
trophoblastic disease (after initial
evacuation and during monitoring)
i. Undetectable/nonpregnant β–
hCG levels
ii. Decreasing β–hCG levels
iii. Persistently elevated β-hCG
levels or malignant disease,
with no evidence or suspicion of
intrauterine disease
iv. Persistently elevated β-hCG
levels or malignant disease,
with evidence or suspicion of
intrauterine disease
Cervical ectropion
Cervical intraepithelial neoplasia

1
1

1
2

1
1

—
Evidence: Among women with persistent human papillomavirus
infection, long-term DMPA use (≥5 years) might increase the risk
for carcinoma in situ and invasive carcinoma (107).

Cervical cancer
(awaiting treatment)

Comment: Theoretical concern exists that POC use might affect
prognosis of the existing disease. While awaiting treatment,
women may use POCs. In general, treatment of this condition
can render a woman sterile.

2
1
1

4
3

Clarification: Evaluation should be pursued as early as possible.
—
—
Comment: Breast cancer is a hormonally sensitive tumor, and
the prognosis for women with current or recent breast cancer
might worsen with POC use.

1
1

—
Comment: While awaiting treatment, women may use POCs. In
general, treatment of this condition renders a woman sterile.

Comment: While awaiting treatment, women may use POCs. In
general, treatment of this condition can render a woman sterile.

Comment: POCs do not appear to cause growth of uterine fibroids.

Breast disease
Breast cancer is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer
d. Breast cancer
i. Current
ii. Past and no evidence of current
disease for 5 years
Endometrial hyperplasia
Endometrial cancer
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Ovarian cancer
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Uterine fibroids

—
Clarification: For all subconditions of gestational trophoblastic
disease, classifications are based on the assumption that women
are under close medical supervision because of the need for
monitoring of β-hCG levels for appropriate disease surveillance.

See table footnotes on page 49.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition
Pelvic inflammatory disease
a. Past PID
i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID
Sexually transmitted diseases
a. Current purulent cervicitis or
chlamydial infection or gonococcal
infection
b. Vaginitis (including Trichomonas
vaginalis and bacterial vaginosis)
c. Other factors related to STDs

Implants

DMPA

POPs

Clarifications/Evidence/Comments
Comment: Whether POCs, like COCs, reduce the risk for PID
among women with STDs is unknown; however, they do not
protect against HIV or lower genital tract STDs.

1
1
1

—

Clarification (DMPA): Some studies suggest that women
using progestin-only injectable contraception might be at
increased risk for HIV acquisition; other studies do not show this
association. CDC reviewed all available evidence and agreed
that the data were not sufficiently conclusive to change current
guidance. However, because of the inconclusive nature of the
body of evidence on possible increased risk for HIV acquisition,
women using progestin-only injectable contraception should
be strongly advised to also always use condoms (male or
female) and take other HIV preventive measures. Expansion
of contraceptive method mix and further research on the
relationship between hormonal contraception and HIV infection
are essential. These recommendations will be continually
reviewed in light of new evidence.

HIV
High risk for HIV

Evidence: Overall, evidence does not support an association
between oral contraceptives and risk for HIV acquisition,
evidence is inconsistent regarding an association between
DMPA and increased risk for HIV acquisition, and no studies have
suggested an increased risk for HIV acquisition with etonogestrel
implants although data are limited (108).
HIV infection
For women with HIV infection who
are not clinically well or not using ARV
therapy, this condition is associated
with increased risk for adverse health
events as a result of pregnancy (Box 2).

Clarification: Drug interactions might exist between hormonal
contraceptives and ARV drugs; see Drug Interactions section.
Evidence: Overall, evidence does not support an association
between POC use and progression of HIV. Limited direct
evidence on an association between POC use and transmission
of HIV to noninfected partners, as well as studies measuring
genital viral shedding as a proxy for infectivity, have had mixed
results. Studies measuring whether hormonal contraceptive
methods affect plasma HIV viral load generally have found no
effect (109–111).

Other Infections
Schistosomiasis
Schistosomiasis with fibrosis of the
liver is associated with increased risk
for adverse health events as a result of
pregnancy (Box 2).
a. Uncomplicated

b. Fibrosis of the liver (if severe, see
Cirrhosis section)
Tuberculosis
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Nonpelvic
b. Pelvic
Malaria

Evidence: Among women with uncomplicated schistosomiasis,
limited evidence showed that DMPA use had no adverse effects
on liver function (112).
—
Clarification: If a woman is taking rifampin, see Drug
Interactions section. Rifampin is likely to decrease the
effectiveness of some POCs.

1
1
1

—

See table footnotes on page 49.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition

Implants

DMPA

POPs

Clarifications/Evidence/Comments

Evidence: POCs had no adverse effects on serum lipid levels
in women with a history of gestational diabetes in two small
studies (113,114). Limited evidence is inconsistent about the
development of noninsulin-dependent diabetes among users of
POCs with a history of gestational diabetes (115–118).

2
2

c. Nephropathy, retinopathy, or
neuropathy

Comment: Concern exists about hypoestrogenic effects and
reduced HDL levels, particularly among users of DMPA. The
effects of DMPA might persist for some time after discontinuation.
Some POCs might increase the risk for thrombosis, although this
increase is substantially less than with COCs.

d. Other vascular disease or diabetes
of >20 years’ duration

1
1
1

—
—
—

Evidence: Risk for disease relapse among women with IBD using
oral contraceptives (most studies did not specify formulation)
did not increase significantly from that for nonusers (123).

b. Nonvascular disease
i. Non-insulin dependent
ii. Insulin dependent

Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Evidence: Among women with insulin-dependent or non–
insulin-dependent diabetes, limited evidence on use of POCs
(POPs, DMPA, and LNG implant) suggests that these methods
have little effect on short-term or long-term diabetes control
(e.g., glycosylated hemoglobin levels), hemostatic markers, or
lipid profile (119–122).

Gastrointestinal Conditions
Inflammatory bowel disease
(ulcerative colitis or Crohn’s disease)

Comment: Absorption of POPs among women with IBD might be
reduced if the woman has substantial malabsorption caused by
severe disease or small bowel surgery.
Women with IBD have a higher prevalence of osteoporosis and
osteopenia than the general population. Use of DMPA, which has
been associated with small changes in BMD, might be of concern.
Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic
History of cholestasis
a. Pregnancy related
b. Past COC related

2
2
2
2

—
—
—
—

1
2

1
1
1

—
—
—

1
3

—
—

—
Comment: Theoretical concern exists that a history of COCrelated cholestasis might predict subsequent cholestasis with
POC use. However, this has not been documented.

See table footnotes on page 49.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition
Liver tumors
Hepatocellular adenoma and
malignant liver tumors are associated
with increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Benign
i. Focal nodular hyperplasia

ii. Hepatocellular adenoma

b. Malignant (hepatoma)

Implants

DMPA

POPs

Clarifications/Evidence/Comments

Evidence: Limited direct evidence suggests that hormonal
contraceptive use does not influence either progression or
regression of liver lesions among women with focal nodular
hyperplasia (124).

Comment: No evidence is available about hormonal
contraceptive use among women with hepatocellular adenoma.
COC use in healthy women is associated with development and
growth of hepatocellular adenoma; whether other hormonal
contraceptives have similar effects is not known.
—

Respiratory Conditions
Cystic fibrosis
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).

Clarification: Persons with cystic fibrosis are at increased risk for
diabetes, liver disease, gallbladder disease, and VTE (particularly
related to use of central venous catheters) and are frequently
prescribed antibiotics. Categories assigned to such conditions
in U.S. MEC should be the same for women with cystic fibrosis
who have these conditions. For cystic fibrosis, classifications are
based on the assumption that no other conditions are present;
these classifications must be modified in the presence of such
conditions.
Clarification: Certain drugs to treat cystic fibrosis (e.g.,
lumacaftor) might reduce effectiveness of hormonal
contraceptives, including oral, injectable, transdermal, and
implantable contraceptives.
Evidence: Limited evidence suggests that use of COCs or oral
contraceptives (type not specified) among women with cystic
fibrosis is not associated with worsening of disease severity. Very
limited evidence suggests that cystic fibrosis does not impair the
effectiveness of hormonal contraception (125).
Comment: Women with cystic fibrosis have a higher prevalence
of osteopenia, osteoporosis, and fragility fractures than the
general population. Use of DMPA, which has been associated
with small changes in BMD, might be of concern.

Anemias
Thalassemia
Sickle cell disease
This condition is associated with
increased risk for adverse health
events as a result of pregnancy (Box 2).
Iron deficiency anemia

1
1

—
Evidence: Among women with sickle cell disease, POC use did
not have adverse effects on hematologic parameters and, in some
studies, was beneficial with respect to clinical symptoms (126–133).

Comment: Changes in the menstrual pattern associated with
POC use have little effect on hemoglobin levels.

—

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition

Implants

DMPA

POPs

Clarifications/Evidence/Comments

Drug Interactions
Antiretroviral therapy

Comment: These recommendations generally are for ARV agents
used alone. However, most women receiving ARV therapy
are using multiple drugs in combination. In general, whether
interactions between ARVs and hormonal contraceptives differ
when ARVs are given alone or in combination is unknown.

1
1
1
1
1
1
1

Evidence: NRTIs do not appear to have significant risk for
interactions with hormonal contraceptive methods (134–139).

Clarification: Evidence suggests drug interactions between EFV
and certain hormonal contraceptives. These interactions might
reduce the effectiveness of the hormonal contraceptive.

ii. Etravirine (ETR)
iii. Nevirapine (NVP)

1
1

iv. Rilpivirine (RPV)

Evidence: One study found that women using etonogestrel
implants with EFV had a higher pregnancy rate than women
not using ARVs, although confidence intervals overlapped
and absolute pregnancy rates were still lower than for other
hormonal methods; another study found that etonogestrel
levels were decreased and 5% of women had presumptive
ovulation while using etonogestrel implants with EFV (140,141).
Three studies of women using LNG implants showed increased
pregnancy rates for women using EFV-containing ARV therapy
compared with no ARV use, although absolute pregnancy
rates were still lower than for other hormonal methods in one
study (141–143); another study of LNG implant users found
no difference in pregnancy rates with EFV compared with
no EFV (144).No significant effects were found on pregnancy
rates, DMPA levels, EFV levels, or HIV disease progression in
women using DMPA and EFV compared with DMPA alone
(141,144–148). No significant effects were found on HIV disease
progression in women using LNG implants and EFV compared
with no ARVs (143). No data have assessed effectiveness
of contraceptive implants during later years of use when
progestin concentrations are lower and risk for failure from drug
interactions might be greater.
—
Evidence: Five studies found no significant increase in
pregnancy rates among women using implants and NVP
compared with implants alone (141–144,149). Four studies
found no significant increase in pregnancy rates among
women using DMPA or other contraceptive injectables and NVP
compared with DMPA or other contraceptive injectables alone
(141,144,147,150). One study found no ovulations or changes
in DMPA concentrations (145). No effect was found on HIV
disease progression with use of NVP and DMPA or LNG implants
(143,145,147–149,151). No data have assessed effectiveness
of contraceptive implants during later years of use when
progestin concentrations are lower and risk for failure from drug
interactions might be greater.
—

See table footnotes on page 49.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Implants

DMPA

POPs

Clarifications/Evidence/Comments

Clarification: Theoretically, drug interactions might occur
between certain ritonavir-boosted protease inhibitors and
certain hormonal contraceptives that might reduce the
effectiveness of the hormonal contraceptive. Any potential effect
on contraceptive effectiveness is likely to be lower with DMPA
than with other POCs because of the higher dose of DMPA.
Evidence: One pharmacokinetic study demonstrated increased
progestin concentrations with use of POPs and ATV/r compared
with POPs alone (152).

ii. Ritonavir-boosted darunavir
(DRV/r)

iii. Ritonavir-boosted fosamprenavir
(FPV/r)

iv. Ritonavir-boosted lopinavir
(LPV/r)

Evidence: One study demonstrated no pregnancies, no
ovulations, no change in LPV/r level, and no change in HIV
disease progression in women using DMPA (153); another study
found a small increase in pregnancy rate in women using DMPA
with LPV/r compared with no ARV therapy, however confidence
intervals overlapped (141). Two studies found no increased risk for
pregnancy in women using implants (141,142). Two studies found
contraceptive hormones increased in women using LPV/r with
DMPA or etonogestrel implants (140,153).

v. Ritonavir-boosted saquinavir
(SQV/r)

vi. Ritonavir-boosted tipranavir
(TPV/r)

Comment: When ATV is administered with Cobicistat,
theoretical concern exists for a drug interaction with hormonal
contraceptives. Cobicistat is an inhibitor of CYP3A and CYP2D6
and could theoretically increase contraceptive hormone levels.
However, its effects on CYP enzymes and drug levels might vary
when combined with other ARVs.

ii. Fosamprenavir (FPV)

iii. Indinavir (IDV)

Clarification: Theoretical concern exists that interactions
between FPV and hormonal contraceptives leading to decreased
levels of FPV might diminish effectiveness of the ARV drug. The
drug interaction likely involves CYP3A4 pathways; POCs have
less effect on CYP3A4 enzymes than CHCs.
—

d. Protease inhibitors without
ritonavir
i. Atazanavir (ATV)

See table footnotes on page 49.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition
iv. Nelfinavir (NFV)

Implants

DMPA

POPs

Clarifications/Evidence/Comments
Clarification: Theoretically, drug interactions might occur
between certain protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Any potential effect on contraceptive
effectiveness is likely to be lower with DMPA than with other
POCs because of the higher dose of DMPA. Concern exists that
interactions between NFV and POCs might decrease NFV levels.
Evidence: One study found no pregnancies, no ovulations, no
change in DMPA concentrations and no change in HIV disease
progression with use of DMPA and NFV compared with DMPA
alone; NFV concentrations were decreased with concomitant
DMPA use (145,147).

e. CCR5 co-receptor antagonists
i. Maraviroc (MVC)
f. HIV integrase strand transfer
inhibitors
i. Raltegravir (RAL)
ii. Dolutegravir (DTG)
iii. Elvitegravir (EVG)

g. Fusion inhibitors
i. Enfuvirtide
Anticonvulsant therapy
a. Certain anticonvulsants
(phenytoin, carbamazepine,
barbiturates, primidone, topiramate,
and oxcarbazepine)

1
1
1

—
—
Comment: When EVG is administered with Cobicistat,
theoretical concern exists for a drug interaction with hormonal
contraceptives. Cobicistat is an inhibitor of CYP3A and CYP2D6
and could theoretically increase contraceptive hormone levels.
However, its effects on CYP enzymes and drug levels may vary
when combined with other ARVs.

—
—
Clarification: Although the interaction of certain anticonvulsants
with POPs and etonogestrel implants is not harmful to women, it is
likely to reduce the effectiveness of POPs and etonogestrel implants.
Whether increasing the hormone dose of POPs alleviates this concern
remains unclear. Use of other contraceptives should be encouraged
for women who are long-term users of any of these drugs. Use of
DMPA is a category 1 because its effectiveness is not decreased by
use of certain anticonvulsants.
Evidence: Use of certain anticonvulsants might decrease the
effectiveness of POCs (154–156).

b. Lamotrigine
Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampin or rifabutin therapy

Evidence: No drug interactions have been reported among
women with epilepsy receiving lamotrigine and POCs (157).

1
1
1
2

1
1
1
1

1
1
1
3

—
—
—
Clarification: Although the interaction of rifampin or rifabutin
with POPs and etonogestrel implants is not harmful to women,
it is likely to reduce the effectiveness of POPs and etonogestrel
implants. Use of other contraceptives should be encouraged for
women who are long-term users of any of these drugs. Use of
DMPA is a category 1 because its effectiveness is not decreased
by use of rifampin or rifabutin. Whether increasing the hormone
dose of POPs alleviates this concern remains unclear.

See table footnotes on page 49.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE C1. (Continued) Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestinonly pills
Category
Condition

Implants

DMPA

POPs

Psychotropic medications

Clarifications/Evidence/Comments
Comment: For many common psychotropic agents, limited
or no theoretical concern exits for clinically significant drug
interactions when co-administered with hormonal contraceptives.
However, either no or very limited data exist examining potential
interactions for these classes of medications.

a. SSRIs

Evidence: No evidence specifically examined the use of POCs
with SSRIs. Limited clinical and pharmacokinetic data do not
demonstrate concern for SSRIs decreasing the effectiveness
of oral contraceptives. Limited evidence suggests that for
women taking SSRIs, the use of hormonal contraceptives was
not associated with differences in effectiveness of the SSRI for
treatment or in adverse events when compared with women not
taking hormonal contraceptives (158).
Comment: Drugs that are inhibitors of CYP3A4 or CYP2C9
theoretically have the potential to increase levels of
contraceptive steroid, which might increase adverse events.
Fluvoxamine is an SSRI known to be a moderate inhibitor of both
3A4 and 2C9; however, no clinical or pharmacokinetic studies
were identified to explore potential drug-drug interactions.

St. John’s wort

Evidence: No evidence specifically examined the use of POCs
with St John’s wort. Although clinical data are limited, studies with
pharmacokinetic and pharmacodynamics outcomes raise concern
that St. John’s wort might decrease effectiveness of hormonal
contraceptives, including increased risk for breakthrough bleeding
and ovulation and increased metabolism of estrogen and
progestin. Any interactions might be dependent on the dose of
St John’s wort, and the concentration of active ingredients across
types of St. John’s wort preparations may vary (159).
Comment: Any potential effect on contraceptive effectiveness
is likely to be lower with DMPA than with other POCs because of
the higher dose of DMPA.

Abbreviations: ARV = antiretroviral; BMD = bone mineral density; BMI = body mass index; COC = combined oral contraceptive; DMPA = depot medroxyprogesterone acetate; DVT = deep
venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; HIV = human immunodeficiency virus; IBD = inflammatory bowel disease; LDL = low-density
lipoprotein; LNG = levonorgestrel; NA = not applicable; NET-EN = norethisterone enantate; PE = pulmonary embolism; PID = pelvic inflammatory disease; POC = progestin-only contraceptive;
POP = progestin-only pill; SSRI = selective serotonin reuptake inhibitor; STD = sexually transmitted disease; VTE = venous thromboembolism.

References
1. Lanza LL, McQuay LJ, Rothman KJ, et al. Use of depot medroxyprogesterone
acetate contraception and incidence of bone fracture. Obstet Gynecol
2013;121:593–600. http://dx.doi.org/10.1097/AOG.0b013e318283d1a1
2. Harel Z, Riggs S, Vaz R, Flanagan P, Harel D, Machan JT. Bone accretion
in adolescents using the combined estrogen and progestin transdermal
contraceptive method Ortho Evra: a pilot study. J Pediatr Adolesc Gynecol
2010;23:23–31. http://dx.doi.org/10.1016/j.jpag.2009.04.008
3. Kaunitz AM, Miller PD, Rice VM, Ross D, McClung MR. Bone mineral
density in women aged 25–35 years receiving depot medroxyprogesterone
acetate: recovery following discontinuation. Contraception 2006;74:90–9.
http://dx.doi.org/10.1016/j.contraception.2006.03.010
4. Kaunitz AM, Arias R, McClung M. Bone density recovery after depot
medroxyprogesterone acetate injectable contraception use. Contraception
2008;77:67–76. http://dx.doi.org/10.1016/j.contraception.2007.10.005
5. Kaunitz AM, Darney PD, Ross D, Wolter KD, Speroff L. Subcutaneous
DMPA vs. intramuscular DMPA: a 2-year randomized study of
contraceptive efficacy and bone mineral density. Contraception
2009;80:7–17. http://dx.doi.org/10.1016/j.contraception.2009.02.005
6. Lappe JM, Stegman MR, Recker RR. The impact of lifestyle factors on
stress fractures in female Army recruits. Osteoporos Int 2001;12:35–42.
http://dx.doi.org/10.1007/s001980170155
7. Lara-Torre E, Edwards CP, Perlman S, Hertweck SP. Bone mineral density in
adolescent females using depot medroxyprogesterone acetate. J Pediatr Adolesc
Gynecol 2004;17:17–21. http://dx.doi.org/10.1016/j.jpag.2003.11.017

8. Lopez LM, Chen M, Mullins S, Curtis KM, Helmerhorst FM. Steroidal
contraceptives and bone fractures in women: evidence from observational
studies. Cochrane Database Syst Rev 2012;8:CD009849.
9. Lopez LM, Grimes DA, Schulz KF, Curtis KM. Steroidal contraceptives: effect
on bone fractures in women. Cochrane Database Syst Rev 2011;(7):CD006033.
10. Meier C, Brauchli YB, Jick SS, Kraenzlin ME, Meier CR. Use of depot
medroxyprogesterone acetate and fracture risk. J Clin Endocrinol Metab
2010;95:4909–16. http://dx.doi.org/10.1210/jc.2010-0032
11. Merki-Feld GS, Neff M, Keller PJ. A 2-year prospective study on the
effects of depot medroxyprogesterone acetate on bone mass-response to
estrogen and calcium therapy in individual users. Contraception
2003;67:79–86. http://dx.doi.org/10.1016/S0010-7824(02)00460-2
12. Monteiro-Dantas C, Espejo-Arce X, Lui-Filho JF, Fernandes AM, Monteiro I,
Bahamondes L. A three-year longitudinal evaluation of the forearm bone density
of users of etonogestrel- and levonorgestrel-releasing contraceptive implants.
Reprod Health 2007;4:11. http://dx.doi.org/10.1186/1742-4755-4-11
13. Naessen T, Olsson SE, Gudmundson J. Differential effects on
bone density of progestogen-only methods for contraception in
premenopausal women. Contraception 1995;52:35–9. http://dx.doi.
org/10.1016/0010-7824(95)00121-P
14. Sanches L, Marchi NM, Castro S, Juliato CT, Villarroel M, Bahamondes L.
Forearm bone mineral density in postmenopausal former users of depot
medroxyprogesterone acetate. Contraception 2008;78:365–9. http://
dx.doi.org/10.1016/j.contraception.2008.07.013
15. Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Injectable hormone
contraception and bone density: results from a prospective study. Epidemiology
2002;13:581–7. http://dx.doi.org/10.1097/00001648-200209000-00015

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

16. Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Change in
bone mineral density among adolescent women using and discontinuing
depot medroxyprogesterone acetate contraception. Arch Pediatr Adolesc
Med 2005;159:139–44. http://dx.doi.org/10.1001/archpedi.159.2.139
17. Segall-Gutierrez P, Agarwal R, Ge M, Lopez C, Hernandez G, Stanczyk
FZ. A pilot study examining short-term changes in bone mineral density
among class 3 obese users of depot-medroxyprogesterone acetate. Eur J
Contracept Reprod Health Care 2013;18:199–205. http://dx.doi.org/
10.3109/13625187.2013.774358
18. Tang OS, Tang G, Yip PS, Li B. Further evaluation on long-term depotmedroxyprogesterone acetate use and bone mineral density: a longitudinal
cohort study. Contraception 2000;62:161–4. http://dx.doi.org/10.1016/
S0010-7824(00)00168-2
19. Vestergaard P, Rejnmark L, Mosekilde L. The effects of depot
medroxyprogesterone acetate and intrauterine device use on fracture risk
in Danish women. Contraception 2008;78:459–64. http://dx.doi.
org/10.1016/j.contraception.2008.07.014
20. Viola AS, Castro S, Marchi NM, Bahamondes MV, Viola CF, Bahamondes
L. Long-term assessment of forearm bone mineral density in postmenopausal
former users of depot medroxyprogesterone acetate. Contraception
2011;84:122–7. http://dx.doi.org/10.1016/j.contraception.2010.11.007
21. Walsh JS, Eastell R, Peel NF. Depot medroxyprogesterone acetate use
after peak bone mass is associated with increased bone turnover but no
decrease in bone mineral density. Fertil Steril 2010;93:697–701. http://
dx.doi.org/10.1016/j.fertnstert.2008.10.004
22. Wetmore CM, Ichikawa L, LaCroix AZ, Ott SM, Scholes D. Association
between caffeine intake and bone mass among young women: potential
effect modification by depot medroxyprogesterone acetate use.
Osteoporos Int 2008;19:519–27. http://dx.doi.org/10.1007/
s00198-007-0473-2
23. Wong AY, Tang LC, Chin RK. Levonorgestrel-releasing intrauterine system
(Mirena) and depot medroxyprogesterone acetate (Depoprovera) as long-term
maintenance therapy for patients with moderate and severe endometriosis: a
randomised controlled trial. Aust N Z J Obstet Gynaecol 2010;50:273–9.
http://dx.doi.org/10.1111/j.1479-828X.2010.01152.x
24. Yang KY, Kim YS, Ji YI, Jung MH. Changes in bone mineral density of
users of the levonorgestrel-releasing intrauterine system. J Nippon Med
Sch 2012;79:190–4. http://dx.doi.org/10.1272/jnms.79.190
25. Zhang MH, Zhang W, Zhang AD, Yang Y, Gai L. Effect of depot
medroxyprogesterone acetate on bone mineral density in adolescent
women. Chin Med J (Engl) 2013;126:4043–7.
26. Bahamondes MV, Monteiro I, Castro S, Espejo-Arce X, Bahamondes
L. Prospective study of the forearm bone mineral density of long-term
users of the levonorgestrel-releasing intrauterine system. Hum Reprod
2010;25:1158–64. http://dx.doi.org/10.1093/humrep/deq043
27. Banks E, Berrington A, Casabonne D. Overview of the relationship between
use of progestogen-only contraceptives and bone mineral density. BJOG
2001;108:1214–21. http://dx.doi.org/10.1111/j.1471-0528.2001.00296.x
28. Beerthuizen R, van Beek A, Massai R, Mäkäräinen L, Hout J, Bennink HC.
Bone mineral density during long-term use of the progestagen contraceptive
implant Implanon compared to a non-hormonal method of contraception.
Hum Reprod 2000;15:118–22. http://dx.doi.org/10.1093/humrep/15.1.118
29. Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral density
in adolescents using norethisterone enanthate, depot-medroxyprogesterone
acetate or combined oral contraceptives for contraception. Contraception
2007;75:438–43. http://dx.doi.org/10.1016/j.contraception.2007.02.001
30. Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral
density in a cohort of adolescents during use of norethisterone enanthate,
depot-medroxyprogesterone acetate or combined oral contraceptives
and after discontinuation of norethisterone enanthate. Contraception
2009;79:345–9. http://dx.doi.org/10.1016/j.contraception.2008.11.009
31. Berenson AB, Breitkopf CR, Grady JJ, Rickert VI, Thomas A. Effects
of hormonal contraception on bone mineral density after 24 months of
use. Obstet Gynecol 2004;103:899–906. http://dx.doi.org/10.1097/01.
AOG.0000117082.49490.d5

MMWR / July 29, 2016 / Vol. 65 / No. 3

32. Berenson AB, Rahman M, Breitkopf CR, Bi LX. Effects of depot
medroxyprogesterone acetate and 20-microgram oral contraceptives on
bone mineral density. Obstet Gynecol 2008;112:788–99. http://dx.doi.
org/10.1097/AOG.0b013e3181875b78
33. Busen NH, Britt RB, Rianon N. Bone mineral density in a cohort of
adolescent women using depot medroxyprogesterone acetate for one to
two years. J Adolesc Health 2003;32:257–9. http://dx.doi.org/10.1016/
S1054-139X(02)00567-0
34. Caird LE, Reid-Thomas V, Hannan WJ, Gow S, Glasier AF. Oral
progestogen-only contraception may protect against loss of bone mass
in breast-feeding women. Clin Endocrinol (Oxf ) 1994;41:739–45.
http://dx.doi.org/10.1111/j.1365-2265.1994.tb02788.x
35. Clark MK, Sowers M, Levy B, Nichols S. Bone mineral density loss and
recovery during 48 months in first-time users of depot medroxyprogesterone
acetate. Fertil Steril 2006;86:1466–74. http://dx.doi.org/10.1016/j.
fertnstert.2006.05.024
36. Cromer BA, Lazebnik R, Rome E, et al. Double-blinded randomized
controlled trial of estrogen supplementation in adolescent girls who receive
depot medroxyprogesterone acetate for contraception. Am J Obstet
Gynecol 2005;192:42–7. http://dx.doi.org/10.1016/j.ajog.2004.07.041
37. Cromer BA, Blair JM, Mahan JD, Zibners L, Naumovski Z. A
prospective comparison of bone density in adolescent girls receiving
depot medroxyprogesterone acetate (Depo-Provera), levonorgestrel
(Norplant), or oral contraceptives. J Pediatr 1996;129:671–6. http://
dx.doi.org/10.1016/S0022-3476(96)70148-8
38. Cromer BA, Bonny AE, Stager M, et al. Bone mineral density in
adolescent females using injectable or oral contraceptives: a 24-month
prospective study. Fertil Steril 2008;90:2060–7. http://dx.doi.
org/10.1016/j.fertnstert.2007.10.070
39. Cromer BA, Stager M, Bonny A, et al. Depot medroxyprogesterone acetate,
oral contraceptives and bone mineral density in a cohort of adolescent girls. J
Adolesc Health 2004;35:434–41. http://dx.doi.org/10.1016/j.
jadohealth.2004.07.005
40. Cundy T, Ames R, Horne A, et al. A randomized controlled trial of estrogen
replacement therapy in long-term users of depot medroxyprogesterone
acetate. J Clin Endocrinol Metab 2003;88:78–81. http://dx.doi.
org/10.1210/jc.2002-020874
41. Cundy T, Cornish J, Evans MC, Roberts H, Reid IR. Recovery of bone
density in women who stop using medroxyprogesterone acetate. BMJ
1994;308:247–8. http://dx.doi.org/10.1136/bmj.308.6923.247
42. Cundy T, Cornish J, Roberts H, Reid IR. Menopausal bone loss in
long-term users of depot medroxyprogesterone acetate contraception.
Am J Obstet Gynecol 2002;186:978–83. http://dx.doi.org/10.1067/
mob.2002.122420
43. Di X, Li Y, Zhang C, Jiang J, Gu S. Effects of levonorgestrel-releasing subdermal
contraceptive implants on bone density and bone metabolism. Contraception
1999;60:161–6. http://dx.doi.org/10.1016/S0010-7824(99)00080-3
44. Díaz S, Reyes MV, Zepeda A, et al. Norplant® implants and progesterone
vaginal rings do not affect maternal bone turnover and density during
lactation and after weaning. Hum Reprod 1999;14:2499–505. http://
dx.doi.org/10.1093/humrep/14.10.2499
45. Gai L, Zhang J, Zhang H, Gai P, Zhou L, Liu Y. The effect of depot
medroxyprogesterone acetate (DMPA) on bone mineral density (BMD)
and evaluating changes in BMD after discontinuation of DMPA in
Chinese women of reproductive age. Contraception 2011;83:218–22.
http://dx.doi.org/10.1016/j.contraception.2010.07.027
46. Bahamondes L, Espejo-Arce X, Hidalgo MM, Hidalgo-Regina C, TeatinJuliato C, Petta CA. A cross-sectional study of the forearm bone density
of long-term users of levonorgestrel-releasing intrauterine system. Hum
Reprod 2006;21:1316–9. http://dx.doi.org/10.1093/humrep/dei457
47. Bahamondes L, Monteiro-Dantas C, Espejo-Arce X, et al. A prospective
study of the forearm bone density of users of etonorgestrel- and
levonorgestrel-releasing contraceptive implants. Hum Reprod
2006;21:466–70. http://dx.doi.org/10.1093/humrep/dei358

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

48. Pitts SA, Feldman HA, Dorale A, Gordon CM. Bone mineral density,
fracture, and vitamin D in adolescents and young women using depot
medroxyprogesterone acetate. J Pediatr Adolesc Gynecol 2012;25:23–6.
http://dx.doi.org/10.1016/j.jpag.2011.07.014
49. US Department of Health and Human Services. Healthy people 2020:
maternal, infant, and child health objectives. Washington, DC: US
Department of Health and Human Services; 2015. http://www.
healthypeople.gov/2020/topics-objectives/topic/maternal-infant-andchild-health/objectives
50. Braga GC, Ferriolli E, Quintana SM, Ferriani RA, Pfrimer K, Vieira CS.
Immediate postpartum initiation of etonogestrel-releasing implant: a
randomized controlled trial on breastfeeding impact. Contraception
2015;92:536–42. http://dx.doi.org/10.1016/j.contraception.2015.07.009
51. Phillips SJ, Tepper NK, Kapp N, Nanda K, Temmerman M, Curtis KM.
Progestogen-only contraceptive use among breastfeeding women: a
systematic review. Contraception 2015;S0010-7824(15)00585-5.
52. Kurunmäki H. Contraception with levonorgestrel-releasing subdermal
capsules, Norplant, after pregnancy termination. Contraception
1983;27:473–82. http://dx.doi.org/10.1016/0010-7824(83)90044-6
53. Kurunmäki H, Toivonen J, Lähteenmäki PL, Luukkainen T. Immediate
postabortal contraception with Norplant: levonorgestrel, gonadotropin,
estradiol, and progesterone levels over two postabortal months and return
of fertility after removal of Norplant capsules. Contraception
1984;30:431–42. http://dx.doi.org/10.1016/0010-7824(84)90035-0.
54. Lähteenmäki P, Toivonen J, Lähteenmäki PL. Postabortal contraception
with norethisterone enanthate injections. Contraception 1983;27:553–
62 http://dx.doi.org/10.1016/0010-7824(83)90020-3
55. Ortayli N, Bulut A, Sahin T, Sivin I. Immediate postabortal contraception
with the levonorgestrel intrauterine device, Norplant, and traditional
methods. Contraception 2001;63:309–14. http://dx.doi.org/10.1016/
S0010-7824(01)00212-8
56. Beksinska ME, Smit JA, Kleinschmidt I, Milford C, Farley TM. Prospective
study of weight change in new adolescent users of DMPA, NET-EN, COCs,
nonusers and discontinuers of hormonal contraception. Contraception
2010;81:30–4. http://dx.doi.org/10.1016/j.contraception.2009.07.007
57. Bender NM, Segall-Gutierrez P, Najera SO, Stanczyk FZ, Montoro M,
Mishell DR Jr. Effects of progestin-only long-acting contraception on
metabolic markers in obese women. Contraception 2013;88:418–25.
http://dx.doi.org/10.1016/j.contraception.2012.12.007
58. Berenson AB, Rahman M. Changes in weight, total fat, percent body
fat, and central-to-peripheral fat ratio associated with injectable and oral
contraceptive use. Am J Obstet Gynecol 2009;200:329.e1–8. http://
dx.doi.org/10.1016/j.ajog.2008.12.052
59. Bonny AE, Secic M, Cromer B. Early weight gain related to later weight
gain in adolescents on depot medroxyprogesterone acetate. Obstet Gynecol
2011;117:793–7. http://dx.doi.org/10.1097/AOG.0b013e31820f387c.
60. Bonny AE, Ziegler J, Harvey R, Debanne SM, Secic M, Cromer BA.
Weight gain in obese and nonobese adolescent girls initiating depot
medroxyprogesterone, oral contraceptive pills, or no hormonal
contraceptive method. Arch Pediatr Adolesc Med 2006;160:40–5 http://
dx.doi.org/10.1001/archpedi.160.1.40
61. Clark MK, Dillon JS, Sowers M, Nichols S. Weight, fat mass, and central
distribution of fat increase when women use depot-medroxyprogesterone
acetate for contraception. Int J Obes 2005;29:1252–8. http://dx.doi.
org/10.1038/sj.ijo.0803023
62. Gerlach LS, Saldaña SN, Wang Y, Nick TG, Spigarelli MG. Retrospective
review of the relationship between weight change and demographic factors
following initial depot medroxyprogesterone acetate injection in adolescents.
Clin Ther 2011;33:182–7. http://dx.doi.org/10.1016/j.clinthera.2011.02.008
63. Jain J, Jakimiuk AJ, Bode FR, Ross D, Kaunitz AM. Contraceptive
efficacy and safety of DMPA-SC. Contraception 2004;70:269–75.
http://dx.doi.org/10.1016/j.contraception.2004.06.011
64. Kozlowski KJ, Rickert VI, Hendon A, Davis P. Adolescents and Norplant:
preliminary findings of side effects. J Adolesc Health 1995;16:373–8.
http://dx.doi.org/10.1016/S1054-139X(94)00029-E

65. Le YC, Rahman M, Berenson AB. Early weight gain predicting later weight
gain among depot medroxyprogesterone acetate users. Obstet Gynecol
2009;114:279–84. http://dx.doi.org/10.1097/AOG.0b013e3181af68b2
66. Leiman G. Depo-medroxyprogesterone acetate as a contraceptive agent:
its effect on weight and blood pressure. Am J Obstet Gynecol
1972;114:97–102. http://dx.doi.org/10.1016/0002-9378(72)90296-7.
67. Lopez LM, Grimes DA, Chen M, et al. Hormonal contraceptives for
contraception in overweight or obese women. Cochrane Database Syst
Rev 2013;4:CD008452.
68. Mangan SA, Larsen PG, Hudson S. Overweight teens at increased risk
for weight gain while using depot medroxyprogesterone acetate. J Pediatr
Adolesc Gynecol 2002;15:79–82. http://dx.doi.org/10.1016/
S1083-3188(01)00147-4
69. Nyirati CM, Habash DL, Shaffer LE. Weight and body fat changes in
postpartum depot-medroxyprogesterone acetate users. Contraception
2013;88:169–76. http://dx.doi.org/10.1016/j.contraception.2012.10.016
70. Pantoja M, Medeiros T, Baccarin MC, Morais SS, Bahamondes L,
Fernandes AM. Variations in body mass index of users of depotmedroxyprogesterone acetate as a contraceptive. Contraception
2010;81:107–11. http://dx.doi.org/10.1016/j.contraception.2009.07.008
71. Risser WL, Gefter LR, Barratt MS, Risser JM. Weight change in
adolescents who used hormonal contraception. J Adolesc Health
1999;24:433–6. http://dx.doi.org/10.1016/S1054-139X(98)00151-7
72. Segall-Gutierrez P, Xiang AH, Watanabe RM, et al. Deterioration in
cardiometabolic risk markers in obese women during depot
medroxyprogesterone acetate use. Contraception 2012;85:36–41. http://
dx.doi.org/10.1016/j.contraception.2011.04.016
73. Westhoff C, Jain JK, Milsom I, Ray A. Changes in weight with depot
medroxyprogesterone acetate subcutaneous injection 104 mg/0.65 mL.
Contraception 2007;75:261–7. http://dx.doi.org/10.1016/j.
contraception.2006.12.009
74. Paulen ME, Zapata LB, Cansino C, Curtis KM, Jamieson DJ. Contraceptive
use among women with a history of bariatric surgery: a systematic review.
Contraception 2010;82:86–94. http://dx.doi.org/10.1016/j.
contraception.2010.02.008
75. World Health Organization Collaborative Study of Cardiovascular
Disease and Steroid Hormone Contraception. Cardiovascular disease
and use of oral and injectable progestogen-only contraceptives and
combined injectable contraceptives. Results of an international,
multicenter, case-control study. Contraception 1998;57:315–24 http://
dx.doi.org/10.1016/S0010-7824(98)00041-9
76. Heinemann LA, Assmann A, DoMinh T, Garbe E. Oral progestogenonly contraceptives and cardiovascular risk: results from the Transnational
Study on Oral Contraceptives and the Health of Young Women. Eur J
Contracept Reprod Health Care 1999;4:67–73. http://dx.doi.
org/10.3109/13625189909064007
77. Vasilakis C, Jick H, del Mar Melero-Montes M. Risk of idiopathic venous
thromboembolism in users of progestagens alone. Lancet 1999;354:1610–1.
http://dx.doi.org/10.1016/S0140-6736(99)04394-9
78. Sönmezer M, Atabekoğlu C, Cengiz B, Dökmeci F, Cengiz SD. Depotmedroxyprogesterone acetate in anticoagulated patients with previous
hemorrhagic corpus luteum. Eur J Contracept Reprod Health Care
2005;10:9–14. http://dx.doi.org/10.1080/13625180400020952
79. Tepper NK, Paulen ME, Marchbanks PA, Curtis KM. Safety of
contraceptive use among women with peripartum cardiomyopathy: a
systematic review. Contraception 2010;82:95–101. http://dx.doi.
org/10.1016/j.contraception.2010.02.004
80. The Criteria Committee of the New York Heart Association.
Nomenclature and criteria for diagnosis of diseases of the heart and great
vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994.
81. Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures
and breast cancer in a sample of women with systemic lupus erythematosus.
Rheumatology (Oxford) 2004;43:1178–81. http://dx.doi.org/10.1093/
rheumatology/keh282

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

82. Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated
with abnormal Pap results in systemic lupus erythematosus.
Rheumatology (Oxford) 2004;43:1386–9. http://dx.doi.org/10.1093/
rheumatology/keh331
83. Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin
gene mutation, and thrombosis risk in patients with antiphospholipid
antibodies. J Rheumatol 2002;29:1683–8.
84. Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham
risk factors fail to fully account for accelerated atherosclerosis in systemic
lupus erythematosus. Arthritis Rheum 2001;44:2331–7. http://dx.doi.
org/10.1002/1529-0131(200110)44:10<2331::AID-ART395≥3.0.CO;2-I
85. Julkunen HA. Oral contraceptives in systemic lupus erythematosus:
side-effects and influence on the activity of SLE. Scand J Rheumatol
1991;20:427–33. http://dx.doi.org/10.3109/03009749109096822
86. Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women
with systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30.
http://dx.doi.org/10.1093/rheumatology/32.3.227
87. Jungers P, Dougados M, Pélissier C, et al. Influence of oral contraceptive
therapy on the activity of systemic lupus erythematosus. Arthritis Rheum
1982;25:618–23. http://dx.doi.org/10.1002/art.1780250603
88. Manzi S, Meilahn EN, Rairie JE, et al. Age-specific incidence rates of
myocardial infarction and angina in women with systemic lupus
erythematosus: comparison with the Framingham Study. Am J Epidemiol
1997;145:408–15. http://dx.doi.org/10.1093/oxfordjournals.aje.a009122
89. McAlindon T, Giannotta L, Taub N, D’Cruz D, Hughes G. Environmental
factors predicting nephritis in systemic lupus erythematosus. Ann Rheum
Dis 1993;52:720–4. http://dx.doi.org/10.1136/ard.52.10.720
90. McDonald J, Stewart J, Urowitz MB, Gladman DD. Peripheral vascular
disease in patients with systemic lupus erythematosus. Ann Rheum Dis
1992;51:56–60. http://dx.doi.org/10.1136/ard.51.1.56
91. Mintz G, Gutiérrez G, Delezé M, Rodríguez E. Contraception with
progestagens in systemic lupus erythematosus. Contraception
1984;30:29–38. http://dx.doi.org/10.1016/0010-7824(84)90076-3
92. Petri M. Musculoskeletal complications of systemic lupus erythematosus
in the Hopkins Lupus Cohort: an update. Arthritis Care Res
1995;8:137–45. http://dx.doi.org/10.1002/art.1790080305
93. Petri M. Lupus in Baltimore: evidence-based ‘clinical pearls’ from the
Hopkins Lupus Cohort. Lupus 2005;14:970–3. http://dx.doi.
org/10.1191/0961203305lu2230xx
94. Petri M, Kim MY, Kalunian KC, et al; OC-SELENA Trial. Combined
oral contraceptives in women with systemic lupus erythematosus. N Engl
J Med 2005;353:2550–8. http://dx.doi.org/10.1056/NEJMoa051135
95. Sánchez-Guerrero J, Uribe AG, Jiménez-Santana L, et al. A trial of
contraceptive methods in women with systemic lupus erythematosus. N
Engl J Med 2005;353:2539–49. http://dx.doi.org/10.1056/NEJMoa050817
96. Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and venous
thrombosis after diagnosis of systemic lupus erythematosus. Arthritis
Rheum 2005;53:609–12. http://dx.doi.org/10.1002/art.21314
97. Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrel-releasing
intrauterine system in the management of menorrhagia in women with
hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–3. http://dx.doi.
org/10.1016/j.ajog.2005.05.002
98. Somers E, Magder LS, Petri M. Antiphospholipid antibodies and
incidence of venous thrombosis in a cohort of patients with systemic
lupus erythematosus. J Rheumatol 2002;29:2531–6.
99. Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo
MA. The bimodal mortality pattern of systemic lupus erythematosus. Am J
Med 1976;60:221–5. http://dx.doi.org/10.1016/0002-9343(76)90431-9

MMWR / July 29, 2016 / Vol. 65 / No. 3

100. Choojitarom K, Verasertniyom O, Totemchokchyakarn K, Nantiruj K,
Sumethkul V, Janwityanujit S. Lupus nephritis and Raynaud’s phenomenon
are significant risk factors for vascular thrombosis in SLE patients with
positive antiphospholipid antibodies. Clin Rheumatol 2008;27:345–51.
http://dx.doi.org/10.1007/s10067-007-0721-z
101. Wahl DG, Guillemin F, de Maistre E, Perret C, Lecompte T, Thibaut
G. Risk for venous thrombosis related to antiphospholipid antibodies
in systemic lupus erythematosus—a meta-analysis. Lupus 1997;6:467–
73. http://dx.doi.org/10.1177/096120339700600510
102. Farr SL, Folger SG, Paulen ME, Curtis KM. Safety of contraceptive methods
for women with rheumatoid arthritis: a systematic review. Contraception
2010;82:64–71. http://dx.doi.org/10.1016/j.contraception.2010.02.003
103. Tepper NK, Whiteman MK, Zapata LB, Marchbanks PA, Curtis KM.
Safety of hormonal contraceptives among women with migraine: a
systematic review. Contraception 2016. Epub May 3, 2016. http://
dx.doi.org/10.1016/j.contraception.2016.04.016
104. Tepper NK, Whiteman MK, Marchbanks PA, James AH, Curtis KM.
Progestin-only contraception and thromboembolism: a systematic
review. Contraception 2016. Epub May 3, 2016. http://dx.doi.
org/10.1016/j.contraception.2016.04.014
105. Zapata LB, Oduyebo T, Whiteman MK, Marchbanks PA, Curtis KM.
Contraceptive use among women with multiple sclerosis: a systematic
review. Contraception. In press 2016.
106. Pagano HP, Zapata LB, Berry-Bibee EN, Nanda K, Curtis KM. Safety of
hormonal contraception and intrauterine devices among women with
depressive and bipolar disorders: a systematic review. Contraception 2016.
Epub June 27, 2016. http://dx.doi.org/10.1016/j.contraception.2016.06.012
107. Smith JS, Green J, Berrington de Gonzalez A, et al. Cervical cancer and
use of hormonal contraceptives: a systematic review. Lancet 2003;361:1159–
67. http://dx.doi.org/10.1016/S0140-6736(03)12949-2.
108. Polis CB, Phillips SJ, Curtis KM, et al. Hormonal contraceptive
methods and risk of HIV acquisition in women: a systematic review
of epidemiological evidence. Contraception 2014;90:360–90 http://
dx.doi.org/10.1016/j.contraception.2014.07.009
109. Phillips SJ, Curtis KM, Polis CB. Effect of hormonal contraceptive
methods on HIV disease progression: a systematic review. AIDS
2013;27:787–94. http://dx.doi.org/10.1097/QAD.0b013e32835bb672
110. Polis CB, Phillips SJ, Curtis KM. Hormonal contraceptive use and
female-to-male HIV transmission: a systematic review of the
epidemiologic evidence. AIDS 2013;27:493–505. http://dx.doi.
org/10.1097/QAD.0b013e32835ad539
111. Phillips SJ, Polis CB, Curtis KM. The safety of hormonal contraceptives
for women living with HIV and their sexual partners. Contraception
2016;93:11–6 http://dx.doi.org/10.1016/j.contraception.2015.10.002.
112. Tagy AH, Saker ME, Moussa AA, Kolgah A. The effect of low-dose
combined oral contraceptive pills versus injectable contraceptive (Depot
Provera) on liver function tests of women with compensated bilharzial
liver fibrosis. Contraception 2001;64:173–6. http://dx.doi.org/10.1016/
S0010-7824(01)00248-7
113. Pyörälä T, Vähäpassi J, Huhtala M. The effect of lynestrenol and
norethindrone on the carbohydrate and lipid metabolism in subjects
with gestational diabetes. Ann Chir Gynaecol 1979;68:69–74.
114. Rådberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies in
gestational diabetic women during contraceptive treatment: effects on
glucose tolerance and fatty acid composition of serum lipids. Gynecol
Obstet Invest 1982;13:17–29. http://dx.doi.org/10.1159/000299480

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

115. Kjos SL, Peters RK, Xiang A, Thomas D, Schaefer U, Buchanan TA.
Contraception and the risk of type 2 diabetes mellitus in Latina women
with prior gestational diabetes mellitus. JAMA 1998;280:533–8. http://
dx.doi.org/10.1001/jama.280.6.533
116. Nelson AL, Le MH, Musherraf Z, Vanberckelaer A. Intermediate-term
glucose tolerance in women with a history of gestational diabetes:
natural history and potential associations with breastfeeding and
contraception. Am J Obstet Gynecol 2008;198:699.e1–8.
117. Xiang AH, Kawakubo M, Buchanan TA, Kjos SL. A longitudinal study
of lipids and blood pressure in relation to method of contraception in
Latino women with prior gestational diabetes mellitus. Diabetes Care
2007;30:1952–8. http://dx.doi.org/10.2337/dc07-0180
118. Xiang AH, Kawakubo M, Kjos SL, Buchanan TA. Long-acting injectable
progestin contraception and risk of type 2 diabetes in Latino women
with prior gestational diabetes mellitus. Diabetes Care 2006;29:613–7.
http://dx.doi.org/10.2337/diacare.29.03.06.dc05-1940
119. Diab KM, Zaki MM. Contraception in diabetic women: comparative
metabolic study of Norplant, depot medroxyprogesterone acetate, low dose
oral contraceptive pill and CuT380A. J Obstet Gynaecol Res 2000;26:17–
26. http://dx.doi.org/10.1111/j.1447-0756.2000.tb01195.x
120. Lunt H, Brown LJ. Self-reported changes in capillary glucose
and insulin requirements during the menstrual cycle. Diabet
Med 1996;13:525–30. http://dx.doi.org/10.1002/
(SICI)1096-9136(199606)13:6<525::AID-DIA123≥3.0.CO;2-D
121. Rådberg T, Gustafson A, Skryten A, Karlsson K. Oral contraception
in diabetic women. A cross-over study on serum and high density
lipoprotein (HDL) lipids and diabetes control during progestogen and
combined estrogen/progestogen contraception. Horm Metab Res
1982;14:61–5.
122. Skouby SO, Mølsted-Pedersen L, Kühl C, Bennet P. Oral contraceptives
in diabetic women: metabolic effects of four compounds with different
estrogen/progestogen profiles. Fertil Steril 1986;46:858–64 http://
dx.doi.org/10.1016/S0015-0282(16)49825-0.
123. Zapata LB, Paulen ME, Cansino C, Marchbanks PA, Curtis KM.
Contraceptive use among women with inflammatory bowel disease: a
systematic review. Contraception 2010;82:72–85. http://dx.doi.
org/10.1016/j.contraception.2010.02.012
124. Kapp N, Curtis KM. Hormonal contraceptive use among women with
liver tumors: a systematic review. Contraception 2009;80:387–90.
http://dx.doi.org/10.1016/j.contraception.2009.01.021
125. Whiteman MK, Oduyebo T, Zapata LB, Walker S, Curtis KM.
Contraceptive safety among women with cystic fibrosis: a systematic
review. Contraception 2016. Epub June 7, 2016. http://dx.doi.
org/10.1016/j.contraception.2016.05.016
126. Adadevoh BK, Isaacs WA.The effect of megestrol acetate on sickling. Am J Med Sci
1973;265:367–70. http://dx.doi.org/10.1097/00000441-197305000-00002
127. Barbosa IC, Ladipo OA, Nascimento ML, et al. Carbohydrate
metabolism in sickle cell patients using a subdermal implant containing
nomegestrol acetate (Uniplant). Contraception 2001;63:263–5. http://
dx.doi.org/10.1016/S0010-7824(01)00202-5
128. de Abood M, de Castillo Z, Guerrero F, Espino M, Austin KL. Effect
of Depo-Provera or Microgynon on the painful crises of sickle cell
anemia patients. Contraception 1997;56:313–6. http://dx.doi.
org/10.1016/S0010-7824(97)00156-X
129. De Ceulaer K, Hayes R, Gruber C, Serjeant GR. Medroxyprogesterone
acetate and homozygous sickle-cell disease. Lancet 1982;320:229–31.
http://dx.doi.org/10.1016/S0140-6736(82)90320-8

130. Howard RJ, Lillis C, Tuck SM. Contraceptives, counselling, and
pregnancy in women with sickle cell disease. BMJ 1993;306:1735–7.
http://dx.doi.org/10.1136/bmj.306.6894.1735
131. Ladipo OA, Falusi AG, Feldblum PJ, Osotimehin BO, Otolorin EO,
Ojengbede OA. Norplant use by women with sickle cell disease. Int J Gynaecol
Obstet 1993;41:85–7. http://dx.doi.org/10.1016/0020-7292(93)90159-T
132. Nascimento ML, Ladipo OA, Coutinho EM. Nomegestrol acetate
contraceptive implant use by women with sickle cell disease. Clin
Pharmacol Ther 1998;64:433–8. http://dx.doi.org/10.1016/
S0009-9236(98)90074-1
133. Yoong WC, Tuck SM, Yardumian A. Red cell deformability in oral
contraceptive pill users with sickle cell anaemia. Br J Haematol 1999;104:868–
70. http://dx.doi.org/10.1046/j.1365-2141.1999.01255.x
134. Aweeka FT, Rosenkranz SL, Segal Y, et al; NIAID AIDS Clinical Trials
Group. The impact of sex and contraceptive therapy on the plasma
and intracellular pharmacokinetics of zidovudine. AIDS 2006;20:1833–
41. http://dx.doi.org/10.1097/01.aids.0000244202.18629.36
135. Kearney BP, Mathias A. Lack of effect of tenofovir disoproxil fumarate
on pharmacokinetics of hormonal contraceptives. Pharmacotherapy
2009;29:924–9. http://dx.doi.org/10.1592/phco.29.8.924
136. Todd CS, Deese J, Wang M, et al; FEM-PrEP Study Group. Sino-implant
(II)® continuation and effect of concomitant tenofovir disoproxil
fumarate-emtricitabine use on plasma levonorgestrel concentrations
among women in Bondo, Kenya. Contraception 2015;91:248–52.
http://dx.doi.org/10.1016/j.contraception.2014.10.008
137. Murnane PM, Heffron R, Ronald A, et al; Partners PrEP Study Team.
Pre-exposure prophylaxis for HIV-1 prevention does not diminish the
pregnancy prevention effectiveness of hormonal contraception. AIDS
2014;28:1825–30. http://dx.doi.org/10.1097/QAD.0000000000000290
138. Kasonde M, Niska RW, Rose C, et al. Bone mineral density changes among
HIV-uninfected young adults in a randomised trial of pre-exposure
prophylaxis with tenofovir-emtricitabine or placebo in Botswana. PLoS
One 2014;9:e90111. http://dx.doi.org/10.1371/journal.pone.0090111
139. Callahan R, Nanda K, Kapiga S, et al; FEM-PrEP Study Group.
Pregnancy and contraceptive use among women participating in the
FEM-PrEP trial. J Acquir Immune Defic Syndr 2015;68:196–203.
http://dx.doi.org/10.1097/QAI.0000000000000413
140. Vieira CS, Bahamondes MV, de Souza RM, et al. Effect of antiretroviral
therapy including lopinavir/ritonavir or efavirenz on etonogestrelreleasing implant pharmacokinetics in HIV-positive women. J Acquir
Immune Defic Syndr 2014;66:378–85. http://dx.doi.org/10.1097/
QAI.0000000000000189
141. Patel RC, Onono M, Gandhi M, et al. Pregnancy rates in HIV-positive
women using contraceptives and efavirenz-based or nevirapine-based
antiretroviral therapy in Kenya: a retrospective cohort study. Lancet HIV
2015;2:e474–82. http://dx.doi.org/10.1016/S2352-3018(15)00184-8
142. Perry SH, Swamy P, Preidis GA, Mwanyumba A, Motsa N, Sarero HN.
Implementing the Jadelle implant for women living with HIV in a
resource-limited setting: concerns for drug interactions leading to
unintended pregnancies. AIDS 2014;28:791–3. http://dx.doi.
org/10.1097/QAD.0000000000000177
143. Scarsi KK, Darin KM, Nakalema S, et al. Unintended pregnancies
observed with combined use of the levonorgestrel contraceptive implant
and efavirenz-based antiretroviral therapy: a three-arm pharmacokinetic
evaluation over 48 weeks. Clin Infect Dis 2015;62:675–82. http://
dx.doi.org/10.1093/cid/civ1001

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Recommendations and Reports

144. Pyra M, Heffron R, Mugo NR, et al; Partners in Prevention HSVHIV
Transmission Study and Partners PrEP Study Teams. Effectiveness of
hormonal contraception in HIV-infected women using antiretroviral
therapy. AIDS 2015;29:2353–9. http://dx.doi.org/10.1097/
QAD.0000000000000827
145. Cohn SE, Park JG, Watts DH, et al; ACTG A5093 Protocol Team. Depomedroxyprogesterone in women on antiretroviral therapy: effective
contraception and lack of clinically significant interactions. Clin Pharmacol
Ther 2007;81:222–7. http://dx.doi.org/10.1038/sj.clpt.6100040
146. Nanda K, Amaral E, Hays M, Viscola MA, Mehta N, Bahamondes L.
Pharmacokinetic interactions between depot medroxyprogesterone
acetate and combination antiretroviral therapy. Fertil Steril
2008;90:965–71. http://dx.doi.org/10.1016/j.fertnstert.2007.07.1348
147. Watts DH, Park JG, Cohn SE, et al. Safety and tolerability of depot
medroxyprogesterone acetate among HIV-infected women on
antiretroviral therapy: ACTG A5093. Contraception 2008;77:84–90.
http://dx.doi.org/10.1016/j.contraception.2007.10.002
148. Polis CB, Nakigozi G, Ssempijja V, et al. Effect of injectable
contraceptive use on response to antiretroviral therapy among women
in Rakai, Uganda. Contraception 2012;86:725–30. http://dx.doi.
org/10.1016/j.contraception.2012.05.001
149. Hubacher D, Liku J, Kiarie J, et al. Effect of concurrent use of antiretroviral therapy and levonorgestrel sub-dermal implant for contraception
on CD4 counts: a prospective cohort study in Kenya. J Int AIDS Soc
2013;16:18448. http://dx.doi.org/10.7448/IAS.16.1.18448
150. Myer L, Carter RJ, Katyal M, Toro P, El-Sadr WM, Abrams EJ. Impact
of antiretroviral therapy on incidence of pregnancy among HIV-infected
women in Sub-Saharan Africa: a cohort study. PLoS Med
2010;7:e1000229. http://dx.doi.org/10.1371/journal.pmed.1000229
151. Day S, Graham SM, Masese LN, et al. A prospective cohort study of
the effect of depot medroxyprogesterone acetate on detection of plasma
and cervical HIV-1 in women initiating and continuing antiretroviral
therapy. J Acquir Immune Defic Syndr 2014;66:452–6. http://dx.doi.
org/10.1097/QAI.0000000000000187

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152. DuBois BN, Atrio J, Stanczyk FZ, Cherala G. Increased exposure of
norethindrone in HIV+ women treated with ritonavir-boosted
atazanavir therapy. Contraception 2015;91:71–5. http://dx.doi.
org/10.1016/j.contraception.2014.08.009
153. Luque AE, Cohn SE, Park JG, et al. Depot medroxyprogesterone acetate
in combination with a twice-daily lopinavir-ritonavir-based regimen
in HIV-infected women showed effective contraception and a lack of
clinically significant interactions, with good safety and tolerability:
results of the ACTG 5283 study. Antimicrob Agents Chemother
2015;59:2094–101. http://dx.doi.org/10.1128/AAC.04701-14
154. Odlind V, Olsson SE. Enhanced metabolism of levonorgestrel during
phenytoin treatment in a woman with Norplant implants. Contraception
1986;33:257–61. http://dx.doi.org/10.1016/0010-7824(86)90018-1
155. Schindlbeck C, Janni W, Friese K. Failure of Implanon contraception
in a patient taking carbamazepin for epilepsia. Arch Gynecol Obstet
2006;273:255–6. http://dx.doi.org/10.1007/s00404-005-0064-4
156. Shane-McWhorter L, Cerveny JD, MacFarlane LL, Osborn C.
Enhanced metabolism of levonorgestrel during phenobarbital treatment
and resultant pregnancy. Pharmacotherapy 1998;18:1360–4.
157. Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens,
reduces lamotrigine serum concentrations. Epilepsia 2005;46:1414–7.
http://dx.doi.org/10.1111/j.1528-1167.2005.10105.x
158. Berry-Bibee E, Kim MJ, Simmons K, Pagano P, Curtis K. Drug
interactions between hormonal contraceptives and psychotropic drugs:
a systematic review. Contraception. In press 2016.
159. Berry-Bibee E, Kim MJ, Tepper N, Riley H, Curtis K. The safety of
St. John’s wort and hormonal contraceptives: a systematic review.
Contraception. In press 2016.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix D
Classifications for Combined Hormonal Contraceptives
Combined hormonal contraceptives (CHCs) include lowdose (containing ≤35 µg ethinyl estradiol) combined oral
contraceptives (COCs), the combined hormonal patch, and
the combined vaginal ring (Box D1) (Table D1). Limited
information is available about the safety of the combined
hormonal patch and combined vaginal ring among women
with specific medical conditions. Evidence indicates that the
combined hormonal patch and the combined vaginal ring
provide comparable safety and pharmacokinetic profiles to
COCs with similar hormone formulations (1–33). Pending
further studies, the evidence available for recommendations
about COCs applies to the recommendations for the combined
hormonal patch and vaginal ring. Therefore, the patch and
ring should have the same categories as COCs, except where
noted. Therefore, the assigned categories should be considered
a preliminary best judgement, which will be reevaluated as new
data become available.

BOX D1. Categories for classifying combined hormonal contraceptives

1 = A condition for which there is no restriction for the
use of the contraceptive method.
2 = A condition for which the advantages of using the
method generally outweigh the theoretical or proven risks.
3 = A condition for which the theoretical or proven risks
usually outweigh the advantages of using the method.
4 = A condition that represents an unacceptable health
risk if the contraceptive method is used.
COCs, the patch, and the ring do not protect against
sexually transmitted diseases (STDs), including human
immunodeficiency virus (HIV), and women using these methods
should be counseled that consistent and correct use of the male
latex condom reduces the risk for transmission of HIV and other
STDs. Use of female condoms can provide protection from
transmission of STDs, although data are limited

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Recommendations and Reports

TABLE D1. Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

Clarifications/Evidence/Comments

Clarification: Use of CHCs is not required. No known harm to the woman, the course of
her pregnancy, or the fetus occurs if CHCs are inadvertently used during pregnancy.

Personal Characteristics and Reproductive History
Pregnancy
Age
a. Menarche to <40 years
b. ≥40 years

1
2

Evidence: Evidence is inconsistent about whether CHC use affects fracture risk
(34–45), although three recent studies show no effect (34,35,45). CHC use might
decrease BMD in adolescents, especially in those choosing very low-dose
formulations (COCs containing <30 µg ethinyl estradiol) (46–59). CHC use has little to
no effect on BMD in premenopausal women (60–74) and might preserve bone mass
in those who are perimenopausal (75–83). BMD is a surrogate marker for fracture risk
that might not be valid for premenopausal women and therefore might not
accurately predict current or future (postmenopausal) fracture risk (84–86).
Comment: The risk for cardiovascular disease increases with age and might
increase with CHC use. In the absence of other adverse clinical conditions, CHCs
can be used until menopause.

Parity
a. Nulliparous
b. Parous
Breastfeeding
a. <21 days postpartum

1
1

—
—

Clarification: Breastfeeding provides important health benefits for mother and
infant. The U.S. Department of Health and Human Services recommends increasing
the proportion of infants initially breastfed, exclusively breastfed through 6 months
of life, and continuing breastfeeding through at least 1 year of life as key public
health goals (87).
Evidence: Clinical studies demonstrate conflicting results regarding effects on
breastfeeding continuation or exclusivity in women exposed to COCs during
lactation. No consistent effects on infant growth or illness have been reported.
Adverse health outcomes or manifestations of exogenous estrogen in infants
exposed to CHCs through breast milk have not been demonstrated; however,
studies have been inadequately designed to determine whether a risk for either
serious or subtle long-term effects exists (88).
Evidence: One study examined use of CHCs during the postpartum period and
found that VTE rates were higher for CHC users compared with nonusers at all time
points postpartum (89). Rates were significantly different only after 13 weeks
postpartum; however, the numbers needed to harm were lowest in the first 6
weeks postpartum. VTE risk is increased during pregnancy and the postpartum
period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to
near baseline levels by 42 days postpartum (90–94).
Comment: Certain women might be at risk for breastfeeding difficulties, such as
women with previous breastfeeding difficulties, certain medical conditions, or
certain perinatal complications, and those who deliver preterm. For these women,
as for all women, discussions about contraception for breastfeeding women should
include information about risks, benefits, and alternatives.

b. 21 to <30 days postpartum
i. With other risk factors for VTE (e.g., age ≥35 years, previous VTE,
thrombophilia, immobility, transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/m2, postpartum hemorrhage,
postcesarean delivery, preeclampsia, or smoking)

Clarification: Breastfeeding provides important health benefits for mother and
infant. The U.S. Department of Health and Human Services recommends increasing
the proportion of infants initially breastfed, exclusively breastfed through 6 months
of life, and continuing breastfeeding through at least 1 year of life as key public
health goals (87).
Clarification: For women with other risk factors for VTE, these risk factors might
increase the classification to a category 4.
Evidence: Clinical studies demonstrate conflicting results regarding effects on
breastfeeding continuation or exclusivity in women exposed to COCs during
lactation. No consistent effects on infant growth or illness have been reported.
Adverse health outcomes or manifestations of exogenous estrogen in infants
exposed to CHCs through breast milk have not been demonstrated; however,
studies have been inadequately designed to determine whether a risk for either
serious or subtle long-term effects exists (88).
Evidence: One study examined use of CHCs during the postpartum period and
found that VTE rates were higher for CHC users compared with nonusers at all time
points postpartum (89). Rates were significantly different only after 13 weeks
postpartum; however, the numbers needed to harm were lowest in the first 6
weeks postpartum. VTE risk is increased during pregnancy and the postpartum
period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to
near baseline levels by 42 days postpartum (90–94).
Comment: Certain women might be at risk for breastfeeding difficulties, such as
women with previous breastfeeding difficulties, certain medical conditions, or
certain perinatal complications, and those who deliver preterm. For these women,
as for all women, discussions about contraception for breastfeeding women should
include information about risks, benefits, and alternatives.

See table footnotes on page 69.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition
ii. Without other risk factors for VTE

Category CHCs

Clarifications/Evidence/Comments

c. 30–42 days postpartum
i. With other risk factors for VTE (e.g., age ≥35 years, previous VTE,
thrombophilia, immobility, transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/m2, postpartum hemorrhage,
postcesarean delivery, preeclampsia, or smoking)

Clarification: Breastfeeding provides important health benefits for mother and
infant. The U.S. Department of Health and Human Services recommends increasing
the proportion of infants initially breastfed, exclusively breastfed through 6 months
of life, and continuing breastfeeding through at least 1 year of life as key public
health goals (87).
Clarification: For women with other risk factors for VTE, these risk factors might
increase the classification to a category 4.
Evidence: Clinical studies demonstrate conflicting results regarding effects on
breastfeeding continuation or exclusivity in women exposed to COCs during
lactation. No consistent effects on infant growth or illness have been reported.
Adverse health outcomes or manifestations of exogenous estrogen in infants
exposed to CHCs through breast milk have not been demonstrated; however,
studies have been inadequately designed to determine whether a risk for either
serious or subtle long-term effects exists (88).
Evidence: One study examined use of CHCs during the postpartum period and
found that VTE rates were higher for CHC users compared with nonusers at all time
points postpartum (89). Rates were significantly different only after 13 weeks
postpartum; however, the numbers needed to harm were lowest in the first 6
weeks postpartum. VTE risk is increased during pregnancy and the postpartum
period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to
near baseline levels by 42 days postpartum (90–94).
Comment: Certain women might be at risk for breastfeeding difficulties, such as
women with previous breastfeeding difficulties, certain medical conditions, or
certain perinatal complications, and those who deliver preterm. For these women,
as for all women, discussions about contraception for breastfeeding women should
include information about risks, benefits, and alternatives.

See table footnotes on page 69.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition
ii. Without other risk factors for VTE

Category CHCs

Clarifications/Evidence/Comments

d. >42 days postpartum

Postpartum (nonbreastfeeding women)
a. <21 days postpartum

ii. Without other risk factors for VTE

c. >42 days postpartum

Evidence: One study examined use of CHCs during the postpartum period and
found that VTE rates were higher for CHC users compared with nonusers at all time
points postpartum (89). Rates were significantly different only after 13 weeks
postpartum; however, the numbers needed to harm were lowest in the first 6
weeks postpartum. VTE risk is increased during pregnancy and the postpartum
period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to
near baseline levels by 42 days postpartum (90–94). Risk for pregnancy during the
first 21 days postpartum is very low but increases after that point; ovulation before
first menses is common (95).

Clarification: For women with other risk factors for VTE, these risk factors might
increase the classification to a category 4.
Evidence: One study examined use of CHCs during the postpartum period and
found that VTE rates were higher for CHC users compared with nonusers at all time
points postpartum (89). Rates were significantly different only after 13 weeks
postpartum; however, the numbers needed to harm were lowest in the first 6
weeks postpartum. VTE risk is increased during pregnancy and the postpartum
period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to
near baseline levels by 42 days postpartum (90–94).

See table footnotes on page 69.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic abortion

1
1
1

Past ectopic pregnancy

History of pelvic surgery
Smoking
a. Age <35 years
b. Age ≥35 years
i. <15 cigarettes per day
ii. ≥15 cigarettes per day
Obesity
a. BMI ≥30 kg/m2
b. Menarche to <18 years and BMI ≥30 kg/m2

History of bariatric surgery
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Restrictive procedures: decrease storage capacity of the stomach
(vertical banded gastroplasty, laparoscopic adjustable gastric band, or
laparoscopic sleeve gastrectomy)
b. Malabsorptive procedures: decrease absorption of nutrients and
calories by shortening the functional length of the small intestine
(Roux-en-Y gastric bypass or biliopancreatic diversion)

Clarifications/Evidence/Comments
Clarification: CHCs may be started immediately postabortion.

2
3
4
2
2

Evidence: Women who started taking COCs immediately after first trimester
medical or surgical abortion did not experience more side effects or adverse
vaginal bleeding outcomes or clinically significant changes in coagulation
parameters than did women who used a placebo, an IUD, a nonhormonal
contraceptive method, or delayed COC initiation (96–102). Limited evidence on
women using the ring immediately after first trimester medical or surgical abortion
found no serious adverse events and no infection related to use of the combined
vaginal ring during 3 cycles of follow-up postabortion (103).
Comment: The risk for future ectopic pregnancy is increased among women who
have had an ectopic pregnancy in the past. CHCs protect against pregnancy in
general, including ectopic gestation.
—
Evidence: COC users who smoked were at increased risk for cardiovascular
diseases, especially myocardial infarction, compared with those who did not
smoke. Studies also showed an increased risk for myocardial infarction with
increasing number of cigarettes smoked per day (104–116).
Evidence: Obese women who use COCs are more likely than obese women who do
not use COCs to experience VTE. Research examining the interaction between
COCs and BMI on VTE risk is limited, particularly for women in the highest BMI
categories (BMI ≥35 kg/m2). Although the absolute risk for VTE in otherwise
healthy women of reproductive age is small, obese women are at 2–3 times higher
risk for VTE than normal weight women regardless of COC use. Limited evidence
suggests that obese women who use COCs do not have a higher risk for acute
myocardial infarction or stroke than do obese nonusers (117). Limited evidence
suggests that effectiveness of some COC formulations might decrease with
increasing BMI, however the observed reductions in effectiveness are minimal and
evidence is conflicting (118–125). Effectiveness of the patch might be reduced in
women >90 kg (126). Limited evidence suggests obese women are no more likely
to gain weight during COC or vaginal ring use than normal weight or overweight
women (117,127).

Evidence: Limited evidence demonstrated no substantial decrease in effectiveness
of oral contraceptives among women who underwent laparoscopic placement of
an adjustable gastric band (128).

COCs: 3
Patch and ring: 1

Evidence: Limited evidence demonstrated no substantial decrease in effectiveness
of oral contraceptives among women who underwent a biliopancreatic diversion;
however, evidence from pharmacokinetic studies reported conflicting results of
oral contraceptive effectiveness among women who underwent a jejunoileal
bypass (128).
Comment: Bariatric surgical procedures involving a malabsorptive component
have the potential to decrease oral contraceptive effectiveness, perhaps further
decreased by postoperative complications, such as long-term diarrhea or vomiting.

Cardiovascular Disease
Multiple risk factors for atherosclerotic cardiovascular disease (e.g.,
older age, smoking, diabetes, hypertension, low HDL, high LDL, or high
triglyceride levels)

3/4

Clarification: When a woman has multiple major risk factors, any of which alone
would substantially increase her risk for cardiovascular disease, use of CHCs might
increase her risk to an unacceptable level. However, a simple addition of categories
for multiple risk factors is not intended; for example, a combination of two
category 2 risk factors might not necessarily warrant a higher category.
Clarification: The recommendations apply to known preexisting medical
conditions or characteristics. Few if any screening tests are needed before initiation
of contraception. See the U.S. Selected Practice Recommendations for Contraceptive
Use (http://www.cdc.gov/reproductivehealth/unintendedpregnancy/usspr.htm).

See table footnotes on page 69.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

Hypertension
Systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100
mm Hg are associated with increased risk for adverse health events as a
result of pregnancy (Box 2).
a. Adequately controlled hypertension

Clarifications/Evidence/Comments

Clarification: For all categories of hypertension, classifications are based on the
assumption that no other risk factors exist for cardiovascular disease. When
multiple risk factors do exist, risk for cardiovascular disease might increase
substantially. A single reading of blood pressure level is not sufficient to classify a
woman as hypertensive.
Clarification: Women adequately treated for hypertension are at reduced risk for
acute myocardial infarction and stroke compared with untreated women.
Although no data exist, CHC users with adequately controlled and monitored
hypertension should be at reduced risk for acute myocardial infarction and stroke
compared with untreated hypertensive CHC users.
Evidence: Among women with hypertension, COC users were at higher risk than
nonusers for stroke, acute myocardial infarction, and peripheral arterial disease
(104,106,113–116,129–143). Discontinuation of COCs in women with hypertension
might improve blood pressure control (144).

b. Elevated blood pressure levels
(properly taken measurements)
i. Systolic 140–159 mm Hg or diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic ≥100 mm Hg
c. Vascular disease

3
4
4

History of high blood pressure during pregnancy (when current blood
pressure is measurable and normal)

Deep venous thrombosis/Pulmonary embolism
a. History of DVT/PE, not receiving anticoagulant therapy
i. Higher risk for recurrent DVT/PE (one or more risk factors)
• History of estrogen-associated DVT/PE
• Pregnancy-associated DVT/PE
• Idiopathic DVT/PE
• Known thrombophilia, including antiphospholipid syndrome
• Active cancer (metastatic, receiving therapy, or within 6 months
after clinical remission), excluding nonmelanoma skin cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE (no risk factors)
b. Acute DVT/PE
c. DVT/PE and established anticoagulant therapy for at least 3 months
i. Higher risk for recurrent DVT/PE (one or more risk factors)
• Known thrombophilia, including antiphospholipid syndrome
• Active cancer (metastatic, receiving therapy, or within 6 months
after clinical remission), excluding nonmelanoma skin cancer
• History of recurrent DTV/PE
ii. Lower risk for recurrent DVT/PE (no risk factors)
d. Family history (first-degree relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged immobilization
f. Minor surgery without immobilization
Known thrombogenic mutations (e.g., factor V Leiden; prothrombin
mutation; and protein S, protein C, and antithrombin deficiencies)
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
Superficial venous disorders
a. Varicose veins

Evidence: Women with a history of high blood pressure in pregnancy who also
used COCs had a higher risk for myocardial infarction and VTE than did COC users
who did not have a history of high blood pressure during pregnancy. The absolute
risks for acute myocardial infarction and VTE in this population remained small
(115,130,142,143,145–151).

—

3
4

—
—
Clarification: Women using anticoagulant therapy are at risk for gynecologic
complications of therapy, such as hemorrhagic ovarian cysts and severe
menorrhagia. Hormonal contraceptive methods can be of benefit in preventing or
treating these complications. When a contraceptive method is used as a therapy,
rather than solely to prevent pregnancy, the risk/benefit ratio might differ and
should be considered on a case-by-case basis.

3
2
4
2
1
4

Comment: Some conditions that increase the risk for DTV/PE are heritable.
—
—
—
Clarification: Routine screening is not appropriate because of the rarity of the
conditions and the high cost of screening.
Evidence: Among women with thrombogenic mutations, COC users had a twofold
to twentyfold higher risk for thrombosis than did nonusers (152–175).

Evidence: One study suggested that among women with varicose veins, the rate of
VTE and superficial venous thrombosis was higher in oral contraceptive users
compared with nonusers; however, statistical significance was not reported and
the number of events was small (176).

See table footnotes on page 69.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition
b. Superficial venous thrombosis (acute or history)

Current and history of ischemic heart disease
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
Stroke (history of cerebrovascular accident)
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
Valvular heart disease
Complicated valvular heart disease is associated with increased risk for
adverse health events as a result of pregnancy (Box 2).
a. Uncomplicated
b. Complicated (pulmonary hypertension, risk for atrial fibrillation, or
history of subacute bacterial endocarditis)
Peripartum cardiomyopathy
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Normal or mildly impaired cardiac function (New York Heart
Association Functional Class I or II: patients with no limitation of
activities or patients with slight, mild limitation of activity) (178)
i. <6 months
ii. ≥6 months
b. Moderately or severely impaired cardiac function (New York Heart
Association Functional Class III or IV: patients with marked limitation of
activity or patients who should be at complete rest) (178)

Category CHCs

Clarifications/Evidence/Comments

Clarification: Superficial venous thrombosis might be associated with an increased risk
for VTE. If a woman has risk factors for concurrent DVT (e.g., known thrombophilia or
cancer) or has current or history of DVT, see recommendations for DVT/PE. Superficial
venous thrombosis associated with a peripheral intravenous catheter is less likely to be
associated with additional thrombosis and use of CHCs may be considered.

2
4

Evidence: One study demonstrated that among women with superficial venous
thrombosis, the risk for VTE was higher in oral contraceptive users compared with
nonusers (176).
—

—

—
Comment: Among women with valvular heart disease, CHC use may further
increase the risk for arterial thrombosis; women with complicated valvular heart
disease are at greatest risk.
Evidence: No direct evidence exists about the safety of CHCs among women with
peripartum cardiomyopathy. Limited indirect evidence from noncomparative
studies of women with cardiac disease demonstrated few cases of hypertension
and transient ischemic attack in women with cardiac disease using COCs. No cases
of heart failure were reported (177).

4
3
4

Comment: COCs might increase fluid retention in healthy women; fluid retention
may worsen heart failure in women with peripartum cardiomyopathy. COCs might
induce cardiac arrhythmias in healthy women; women with peripartum
cardiomyopathy have a high incidence of cardiac arrhythmias.

Clarification: Persons with SLE are at increased risk for ischemic heart disease, stroke,
and VTE. Categories assigned to such conditions in U.S. MEC should be the same for
women with SLE who have these conditions. For all subconditions of SLE,
classifications are based on the assumption that no other risk factors for cardiovascular disease are present; these classifications must be modified in the presence of such
risk factors. Many women with SLE can be considered good candidates for most
contraceptive methods, including hormonal contraceptives (179–197).
Evidence: Antiphospholipid antibodies are associated with a higher risk for both
arterial and venous thrombosis (198,199).

b. Severe thrombocytopenia

c. Immunosuppressive therapy

d. None of the above

See table footnotes on page 69.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition
Rheumatoid arthritis
a. Receiving immunosuppressive therapy
b. Not receiving immunosuppressive therapy

Category CHCs

Clarifications/Evidence/Comments

2
2

Evidence: Limited evidence shows no consistent pattern of improvement or
worsening of rheumatoid arthritis with use of oral contraceptives, progesterone, or
estrogen (200).

Neurologic Conditions
Headaches
a. Nonmigraine (mild or severe)

b. Migraine
i. Without aura (This category of migraine includes
menstrual migraine.)
ii. With aura

2
4

Clarification: Classification depends on accurate diagnosis of those severe
headaches that are migraines and those headaches that are not, as well as
diagnosis of ever experiencing aura. Aura is a specific focal neurologic symptom.
For more information about headache classification see The International Headache
Society Classification, 3rd edition (http://www.ihs-classification.org/_downloads/
mixed/International-Headache-Classification-III-ICHD-III-2013-Beta.pdf). Any new
headaches or marked changes in headaches should be evaluated.
Clarification: Classification depends on accurate diagnosis of those severe
headaches that are migraines and those headaches that are not, as well as
diagnosis of ever experiencing aura. Aura is a specific focal neurologic symptom.
For more information about headache classification see The International Headache
Society Classification, 3rd edition (http://www.ihs-classification.org/_downloads/
mixed/International-Headache-Classification-III-ICHD-III-2013-Beta.pdf). Any new
headaches or marked changes in headaches should be evaluated.
Clarification: Classification is for women without any other risk factors for stroke
(e.g., age, hypertension, and smoking).
Evidence: Among women with migraine, oral contraceptive use is associated with
about a threefold increased risk for ischemic stroke compared with nonuse,
although most studies did not specify migraine type or oral contraceptive
formulation. The only study to examine migraine type found that the risk for
ischemic stroke among women with migraine with aura was increased to a similar
level among both oral contraceptive users and nonusers, compared with women
without migraine (201). The risk for ischemic stroke is increased among women
using COCs, compared with women not using COCs (104,202). The risk for ischemic
stroke is also increased among women with migraine with aura, compared with
women without migraine (203–205). One older meta-analysis found that migraine
without aura was associated with an increased risk for ischemic stroke, while two
more recent meta-analyses did not find such an association (203–205).
Comment: Menstrual migraine is a subtype of migraine without aura. For more
information, see The International Headache Society Classification, 3rd edition (http://
www.ihs-classification.org/_downloads/mixed/International-HeadacheClassification-III-ICHD-III-2013-Beta.pdf).

Epilepsy
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
Multiple sclerosis
a. With prolonged immobility
b. Without prolonged immobility

3
1

Clarification: If a woman is taking anticonvulsants, see Drug Interactions section.
Certain anticonvulsants lower COC effectiveness. The extent to which patch or ring
use is similar to COC use in this regard remains unclear.
Evidence: Limited evidence suggests that use of COCs or oral contraceptives (type
not specified) among women with multiple sclerosis does not worsen the clinical
course of disease (206).
Comment: No data exist that evaluate the increased risk for VTE among women
with multiple sclerosis using CHCs. However, women with multiple sclerosis are at
higher risk than unaffected women for VTE.

Depressive Disorders
Depressive disorders

Clarification: If a woman is receiving psychotropic medications or St. John’s wort,
see Drug Interactions section.
Evidence: COC use was not associated with increased depressive symptoms in
women with depression or scoring above threshold levels on a validated
depression screening instrument compared with baseline or with nonusers with
depression. One small study of women with bipolar disorder found that oral
contraceptives did not significantly change mood across the menstrual cycle (207).

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without heavy bleeding
b. Heavy or prolonged bleeding (includes regular and
irregular patterns)

Comment: Irregular menstrual bleeding patterns are common among healthy women.

Clarification: Unusually heavy bleeding should raise the suspicion of a serious
underlying condition.
Evidence: A Cochrane Collaboration Review identified one randomized controlled
trial evaluating the effectiveness of COC use compared with naproxen and danazol
in treating menorrhagia. Women with menorrhagia did not report worsening of
the condition or any adverse events related to COC use (208).

See table footnotes on page 69.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition
Unexplained vaginal bleeding
(suspicious for serious condition) before evaluation

Category CHCs
2

Clarifications/Evidence/Comments
Clarification: If pregnancy or an underlying pathological condition (e.g., pelvic
malignancy) is suspected, it must be evaluated and the category adjusted
after evaluation.
Comment: No conditions that cause vaginal bleeding will be worsened in the
short-term by use of CHCs.

Endometriosis

Benign ovarian tumors (including cysts)
Severe dysmenorrhea

1
1

Gestational trophoblastic disease
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Suspected gestational trophoblastic disease (immediate
postevacuation)
i. Uterine size first trimester
ii. Uterine size second trimester
b. Confirmed gestational trophoblastic disease (after initial evacuation
and during monitoring)
i. Undetectable/nonpregnant β-hCG levels
ii. Decreasing β-hCG levels
iii. Persistently elevated β-hCG levels or malignant disease, with no
evidence or suspicion of intrauterine disease
iv. Persistently elevated β-hCG levels or malignant disease, with
evidence or suspicion of intrauterine disease
Cervical ectropion

Evidence: A Cochrane Collaboration Review identified one randomized controlled
trial evaluating the effectiveness of COC use compared with a gonadotropinreleasing hormone analog in treating the symptoms of endometriosis. Women
with endometriosis did not report worsening of the condition or any adverse
events related to COC use (209).
Evidence: Risk for side effects with COC use was not higher among women with
dysmenorrhea than among women not using COCs. Some COC users had a
reduction in pain and bleeding (210,211).
Clarification: For all subconditions of gestational trophoblastic disease,
classifications are based on the assumption that women are under close medical
supervision because of the need for monitoring of β-hCG levels for appropriate
disease surveillance.

1
1

1
1
1

Evidence: After molar pregnancy evacuation, the balance of evidence found COC use
did not increase the risk for postmolar trophoblastic disease, and β–hCG levels
regressed more rapidly in some COC users than in nonusers (212). Limited evidence
suggests that use of COCs during chemotherapy does not significantly affect the
regression or treatment of postmolar trophoblastic disease compared with women
who used a nonhormonal contraceptive method or DMPA during chemotherapy (212).

1
1

Comment: Cervical ectropion is not a risk factor for cervical cancer, and restriction
of CHC use is unnecessary.

Cervical intraepithelial neoplasia

Evidence: Among women with persistent human papillomavirus infection,
long-term COC use (≥5 years) might increase the risk for carcinoma in situ and
invasive carcinoma (213). Limited evidence on women with low-grade squamous
intraepithelial lesions found use of the vaginal ring did not worsen the condition (9).

Cervical cancer (awaiting treatment)

Comment: Theoretical concern exists that CHC use might affect prognosis of the
existing disease. While awaiting treatment, women may use CHCs. In general,
treatment of this condition can render a woman sterile.

Breast disease
Breast cancer is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer

2
1
1

Clarification: The woman should be evaluated as early as possible.
—
Evidence: Women with breast cancer susceptibility genes (e.g., BRCA1 and BRCA2)
have a higher baseline risk for breast cancer than women without these genes. The
baseline risk for breast cancer is also higher among women with a family history of
breast cancer than among those who do not have such a history. However,
evidence does not suggest that the increased risk for breast cancer among women
with either a family history of breast cancer or breast cancer susceptibility genes is
modified by the use of COCs (214–231).

d. Breast cancer
i. Current
ii. Past and no evidence of current disease for 5 years
Endometrial hyperplasia
Endometrial cancer
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).

4
3
1
1

Comment: Breast cancer is a hormonally sensitive tumor, and the prognosis for
women with current or recent breast cancer might worsen with CHC use.
—
Comment: COC use reduces the risk for endometrial cancer; whether patch or ring
use reduces the risk for endometrial cancer is not known. While awaiting
treatment, women may use CHCs. In general, treatment of this condition renders a
woman sterile.

Ovarian cancer
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).

Comment: COC use reduces the risk for ovarian cancer; whether patch or ring use
reduces the risk for ovarian cancer is not known. While awaiting treatment, women
may use CHCs. In general, treatment of this condition can render a woman sterile.

Uterine fibroids

Comment: COCs do not appear to cause growth of uterine fibroids, and patch and
ring also are not expected to cause growth.

See table footnotes on page 69.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

Pelvic inflammatory disease
a. Past PID
i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID
Sexually transmitted diseases
a. Current purulent cervicitis or chlamydial infection or gonococcal
infection
b. Vaginitis (including Trichomonas vaginalis and bacterial vaginosis)
c. Other factors related to STDs

1
1
1

Clarifications/Evidence/Comments
Comment: COCs might reduce the risk for PID among women with STDs but do
not protect against HIV or lower genital tract STDs. Whether use of patch or ring
reduces the risk for PID among women with STDs is unknown; however, they do
not protect against HIV or lower genital tract STDs.

—

1
1

—
—

HIV
High risk for HIV

Evidence: Overall, evidence does not support an association between oral
contraceptives and risk for HIV acquisition (232).

Clarification: Drug interactions might exist between hormonal contraceptives and
ARV drugs; see Drug Interactions section.
Evidence: Overall, evidence does not support an association between COC use and
progression of HIV. Limited direct evidence does not support an association
between COC use and transmission of HIV to noninfected partners; studies
measuring genital viral shedding as a proxy for infectivity have had mixed results.
Studies measuring whether hormonal contraceptive methods affect plasma HIV
viral load generally have found no effect (233–235).

Other Infections
Schistosomiasis
Schistosomiasis with fibrosis of the liver is associated with increased risk
for adverse health events as a result of pregnancy (Box 2).
a. Uncomplicated
b. Fibrosis of the liver (if severe, see Cirrhosis section)
Tuberculosis
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Nonpelvic
b. Pelvic
Malaria

1
1

1
1
1

Evidence: Among women with uncomplicated schistosomiasis, COC use had no
adverse effects on liver function (236–242).
—
Clarification: If a woman is taking rifampin, see Drug Interactions section. Rifampin
is likely to decrease COC effectiveness. The extent to which patch or ring use is
similar to COC use in this regard remains unclear.

—

b. Nonvascular disease
i. Non-insulin dependent
ii. Insulin dependent

c. Nephropathy, retinopathy, or neuropathy
d. Other vascular disease or diabetes of >20 years’ duration
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Evidence: The development of non–insulin-dependent diabetes in women with a
history of gestational diabetes is not increased by use of COCs (243–250). Likewise,
lipid levels appear to be unaffected by COC use (251–253).

2
2

Evidence: Among women with insulin-dependent or non–insulin-dependent
diabetes, COC use had limited effect on daily insulin requirements and no effect on
long-term diabetes control (e.g., glycosylated hemoglobin levels) or progression to
retinopathy. Changes in lipid profile and hemostatic markers were limited, and
most changes remained within normal values (254–263).

3/4

Clarification: The category should be assessed according to the severity of the condition.

3/4

Clarification: The category should be assessed according to the severity of the condition.

1
1
1

—
—
—

2/3

Clarification: For women with mild IBD and with no other risk factor for VTE, the
benefits of CHC use generally outweigh the risks (category 2). However, for women
with IBD who are at increased risk for VTE (e.g., those with active or extensive
disease, surgery, immobilization, corticosteroid use, vitamin deficiencies, or fluid
depletion), the risks of CHC use generally outweigh the benefits (category 3).

Gastrointestinal Conditions
Inflammatory bowel disease (ulcerative colitis or Crohn’s disease)

Evidence: Risk for disease relapse was not significantly higher among women with
IBD using oral contraceptives (most studies did not specify type) than among
nonusers (264). Absorption of COCs among women with mild ulcerative colitis and
no or small ileal resections was similar to the absorption among healthy women
(264). Findings might not apply to women with Crohn’s disease or more extensive
bowel resections. No data exist that evaluate the increased risk for VTE among
women with IBD using CHCs. However, women with IBD are at higher risk than
unaffected women for VTE (264).
See table footnotes on page 69.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic
History of cholestasis
a. Pregnancy related

2
3
3
2
2

b. Past COC related
Viral hepatitis
a. Acute or flare

Clarifications/Evidence/Comments
Comment: CHCs might cause a small increased risk for gallbladder disease. CHCs
might worsen existing gallbladder disease.

Comment: History of pregnancy-related cholestasis might predict an increased risk
for COC-related cholestasis.
Comment: History of COC-related cholestasis predicts an increased risk with
subsequent COC use.

3
Initiation
3/4

Continuation
2
Clarification (initiation): The category should be assessed according to the severity
of the condition.
Evidence: Data suggest that in women with chronic hepatitis, COC use does not
increase the rate or severity of cirrhotic fibrosis, nor does it increase the risk for
hepatocellular carcinoma. For women who are carriers, COC use does not appear
to trigger liver failure or severe dysfunction. Evidence is limited for COC use during
active hepatitis (265).

b. Carrier

Evidence: Data suggest that in women with chronic hepatitis, COC use does not
increase the rate or severity of cirrhotic fibrosis, nor does it increase the risk for
hepatocellular carcinoma. For women who are carriers, COC use does not appear
to trigger liver failure or severe dysfunction. Evidence is limited for COC use during
active hepatitis (265).

c. Chronic

Cirrhosis
Severe cirrhosis is associated with increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Mild (compensated)
b. Severe (decompensated)
Liver tumors
Hepatocellular adenoma and malignant liver tumors are associated with
increased risk for adverse health events as a result of pregnancy (Box 2).
a. Benign
i. Focal nodular hyperplasia

ii. Hepatocellular adenoma
b. Malignant (hepatoma)

1
4

—
—

4
4

Respiratory Conditions
Cystic fibrosis
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).

Clarification: Persons with cystic fibrosis are at increased risk for diabetes, liver
disease, gallbladder disease, and VTE (particularly related to use of central venous
catheters) and are frequently prescribed antibiotics. Categories assigned to such
conditions in U.S. MEC should be the same for women with cystic fibrosis who have
these conditions. For cystic fibrosis, classifications are based on the assumption
that no other conditions are present; these classifications must be modified in the
presence of such conditions.
Clarification: Certain drugs to treat cystic fibrosis (e.g., lumacaftor) might reduce
effectiveness of hormonal contraceptives, including oral, injectable, transdermal,
and implantable contraceptives.
Evidence: Limited evidence suggests that use of COCs or oral contraceptives (type
not specified) among women with cystic fibrosis is not associated with worsening
of disease severity. Very limited evidence suggests that cystic fibrosis does not
impair the effectiveness of hormonal contraception (267).

Anemias
Thalassemia

Sickle cell disease
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
Iron deficiency anemia

Comment: Anecdotal evidence from countries where thalassemia is prevalent
indicates that COC use does not worsen the condition.
—

Comment: CHC use might decrease menstrual blood loss.

Solid Organ Transplantation
Solid organ transplantation
This condition is associated with increased risk for adverse health events
as a result of pregnancy (Box 2).
See table footnotes on page 69.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

Clarifications/Evidence/Comments

a. Complicated: graft failure (acute or chronic), rejection, cardiac
allograft vasculopathy

Evidence: Limited evidence of COC and patch users indicated no overall changes in
biochemical measures. However, one study reported discontinuations of COC use in
two (8%) of 26 women as a result of serious medical complications, and in one case
report, a woman developed cholestasis associated with high-dose COC use (268).

b. Uncomplicated

Clarification: Women with Budd-Chiari syndrome should not use CHCs because of
the increased risk for thrombosis.
Evidence: Limited evidence of COC and patch users indicated no overall changes in
biochemical measures. However, one study reported discontinuations of COC use in
two (8%) of 26 women as a result of serious medical complications, and in one case
report, a woman developed cholestasis associated with high-dose COC use (268).

Drug Interactions
Antiretroviral therapy

Comment: These recommendations generally are for ARV agents used alone.
However, most women receiving ARV therapy are using multiple drugs in
combination. In general, whether interactions between ARVs and hormonal
contraceptives differ when ARVs are given alone or in combination is unknown.

1
1
1
1
1
1
1

Evidence: NRTIs do not appear to have significant risk for interactions with
hormonal contraceptive methods (269–274).

Clarification: Evidence suggests drug interactions between EFV and certain
hormonal contraceptives. These interactions might reduce the effectiveness of the
hormonal contraceptive.
Evidence: Two studies suggested that pregnancy rates might be higher among
women using COCs and EFV compared with COCs alone, although one study found
no difference in pregnancy rates (275–277) Two studies found conflicting results on
ovulations in women receiving COCs and EFV compared with EFV alone (278,279).
Two pharmacokinetic studies demonstrated decreases in ethinyl estradiol and
progestin concentrations in women receiving COCs and EFV compared with COCs
alone (279,280). Pharmacokinetic studies demonstrated generally no changes in
EFV concentrations with concomitant COC use (279,280).

ii. Etravirine (ETR)

Evidence: One study demonstrated no clinically relevant pharmacokinetic or
pharmacodynamic changes in women using COCs and ETR compared with COCs
alone (281).

iii. Nevirapine (NVP)

Evidence: Five studies found no significant differences in pregnancy rates among
women using COCs and NVP compared with women using COCs alone (275–
277,282,283). Three studies reported no ovulations among women receiving COCs
and NVP (278,283,284). Two pharmacokinetic studies demonstrated decreased
concentrations of ethinyl estradiol and progestin among women using COCs and
NVP compared with COCs alone, and one study found no change in contraceptive
hormone concentrations (278,284,285). Pharmacokinetic studies demonstrated
generally no changes in NVP concentrations with concomitant COC use
(278,285,286).

iv. Rilpivirine (RPV)

Evidence: One study demonstrated no clinical significant pharmacokinetic
changes or adverse events in women using COCs and RPV compared with COCs
alone (287).

c. Ritonavir-boosted protease inhibitors
i. Ritonavir-boosted atazanavir (ATV/r)

Evidence: One pharmacokinetic study demonstrated decreased estrogen but
increased progestin concentrations in women using COCs and ATV/r compared
with COCs alone (288).
ii. Ritonavir-boosted darunavir (DRV/r)

Clarification: Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal contraceptives that
might reduce the effectiveness of the hormonal contraceptive.
Evidence: One pharmacokinetic study demonstrated no change in follicle-stimulating hormone or luteinizing hormone but decreases in ethinyl estradiol and
norethindrone in women using COCs with DRV/r compared with COCs alone (289).

See table footnotes on page 69.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition
iii. Ritonavir-boosted fosamprenavir (FPV/r)

Category CHCs
2

Clarifications/Evidence/Comments
Clarification: Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal contraceptives that
might reduce the effectiveness of the hormonal contraceptive.
Evidence: Information from the package label states that both ethinyl estradiol
and norethindrone concentrations decreased with concurrent administration of
COCs and FPV/r (290).

iv. Ritonavir-boosted lopinavir (LPV/r)

Evidence: One study demonstrated a non-significant increase in pregnancy rates
among women using COCs and LPV/r compared with COCs alone (275). One study
demonstrated no ovulations in women using the combined hormonal patch and
LPV/r compared with combined hormonal patch alone; ethinyl estradiol
concentrations for COC and patch users decreased but norelgestromin concentrations increased with use of the patch (291).

v. Ritonavir-boosted saquinavir (SQV/r)

Clarification: Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal contraceptives that
might reduce the effectiveness of the hormonal contraceptive.
Evidence: One pharmacokinetic study demonstrated no change in SQV
concentrations in women using COC and SQV compared with COCs alone (292).

iv. Ritonavir-boosted tipranavir (TPV/r)

Clarification: Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal contraceptives that
might reduce the effectiveness of the hormonal contraceptive.
Evidence: Information from the package label states that ethinyl estradiol
concentrations decrease but norethindrone concentrations increased with
concurrent administration of COCs and TPV/r (293).

d. Protease inhibitors without ritonavir
i. Atazanavir (ATV)

Clarification: Theoretical concern exists that increased levels of ethinyl estradiol
because of interactions with ATV might increase the risk for adverse events.
Evidence: Information from the package label states that there are inconsistent
changes in ethinyl estradiol concentrations and increases in progestin concentrations with concurrent administration of two different COCs and ATV (294).
Comment: When ATV is administered with Cobicistat, theoretical concern exists for
a drug interaction with hormonal contraceptives. Cobicistat is an inhibitor of
CYP3A and CYP2D6 and could theoretically increase contraceptive hormone levels.
However, its effects on CYP enzymes and drug levels may vary when combined
with other ARVs.

ii. Fosamprenavir (FPV)

Clarification: Concern exists that interactions between FPV and hormonal
contraceptives leading to decreased levels of FPV might diminish effectiveness of
the ARV drug.
Evidence: Information from the package label states that amprenavir concentrations decreased with concurrent administration of COCs and amprenavir.
Norethindrone concentrations increased and ethinyl estradiol concentrations did
not change (290).

iii. Indinavir (IDV)

Evidence: One small study found no pregnancies in women using COCs and IDV (277).

iv. Nelfinavir (NFV)

Clarification: Evidence suggests drug interactions between certain protease
inhibitors and certain hormonal contraceptives. These interactions might reduce
the effectiveness of the hormonal contraceptive.
Evidence: One small study suggested that women using COCs and NFV may have
had higher pregnancy rates than those using COCs alone (277).

e. CCR5 co-receptor antagonists
i. Maraviroc (MVC)
f. HIV integrase strand transfer inhibitors
i. Raltegravir (RAL)

ii. Dolutegravir (DTG)

Evidence: COC concentrations were not altered by co-administration with MVC (295).

Evidence: One pharmacokinetic study demonstrated increased concentrations of
norgestimate and no change in ethinyl estradiol among women using COCs and
RAL compared with COCs alone (296).

Evidence: One study demonstrated no clinically relevant pharmacokinetic or
pharmacodynamic changes in women using COCs and DTG compared with COCs
alone (297).

See table footnotes on page 69.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

iii. Elvitegravir (EVG)

Clarifications/Evidence/Comments
Evidence: Information from the package label states that ethinyl estradiol
concentrations decreased and norgestimate concentrations increased with
concurrent administration of COCs and EVG (298).
Comment: When ATV is administered with Cobicistat, theoretical concern exists for
a drug interaction with hormonal contraceptives. Cobicistat is an inhibitor of
CYP3A and CYP2D6 and could theoretically increase contraceptive hormone levels.
However, its effects on CYP enzymes and drug levels may vary when combined
with other ARVs.

g. Fusion inhibitors
i. Enfuvirtide
Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin, carbamazepine, barbiturates,
primidone, topiramate, oxcarbazepine)

1
3

—
Clarification: Although the interaction of certain anticonvulsants with CHCs is not
harmful to women, it is likely to reduce the effectiveness of CHCs. Use of other
contraceptives should be encouraged for women who are long-term users of any
of these drugs. When a COC is chosen, a preparation containing a minimum of 30
µg ethinyl estradiol should be used.
Evidence: Use of certain anticonvulsants might decrease the effectiveness of COCs
(299–302).

b. Lamotrigine

Clarification: The recommendation for lamotrigine applies only for situations
where lamotrigine monotherapy is taken concurrently with COCs. Anticonvulsant
treatment regimens that combine lamotrigine and non–enzyme-inducing
antiepileptic drugs (e.g., sodium valproate) do not interact with COCs.
Evidence: Pharmacokinetic studies show levels of lamotrigine decrease
significantly during COC use (303–307). Some women who used both COCs and
lamotrigine experienced increased seizure activity in one trial (303).

Antimicrobial therapy
a. Broad-spectrum antibiotics

Evidence: Most broad-spectrum antibiotics do not affect the contraceptive
effectiveness of COCs (308–344), patch (345), or ring (346).

b. Antifungals

Evidence: Studies of antifungal agents have shown no clinically significant
pharmacokinetic interactions with COCs (347–356), or ring (357).

c. Antiparasitics

Evidence: Studies of antiparasitic agents have shown no clinically significant
pharmacokinetic interactions with COCs (236,358–362).

d. Rifampin or rifabutin therapy

Clarification: Although the interaction of rifampin or rifabutin therapy with CHCs is
not harmful to women, it is likely to reduce the effectiveness of CHCs. Use of other
contraceptives should be encouraged for women who are long-term users of
either of these drugs. When a COC is chosen, a preparation containing a minimum
of 30 µg ethinyl estradiol should be used.
Evidence: The balance of the evidence suggests that rifampin reduces the
effectiveness of COCs (363–378). Data on rifabutin are limited, but effects on
metabolism of COCs are less than with rifampin, and small studies have not shown
evidence of ovulation (365,372).

Psychotropic medications

Comment: For many common psychotropic agents, limited or no theoretical
concern exists for clinically significant drug interactions when co-administered
with hormonal contraceptives. However, either no or very limited data exist
examining potential interactions for these classes of medications. For psychotropic
agents that are CYP1A2 substrates, such as duloxetine, mirtazapine, ziprasidone,
olanzapine, clomipramine, imipramine, and amitriptyline, co-administration with
CHCs could theoretically yield increased concentrations of the psychotropic drug.
For agents with narrow therapeutic windows, such as tricyclic antidepressants,
increased drug concentrations might pose safety concerns that could necessitate
closer monitoring.

a. SSRIs

Evidence: Limited clinical and pharmacokinetic data do not demonstrate concern
for SSRIs decreasing the effectiveness of oral contraceptives. Limited evidence
suggests that for women taking SSRIs, the use of hormonal contraceptives was not
associated with differences in effectiveness of the SSRI for treatment or in adverse
events when compared with women not taking hormonal contraceptives (379).
Comment: Drugs that are inhibitors of CYP3A4 or CYP2C9 theoretically have the
potential to increase levels of contraceptive steroids which might increase adverse
events. Fluvoxamine is an SSRI known to be a moderate inhibitor of both CYP3A4
and CYP2C9; however, no clinical or pharmacokinetic studies were identified to
explore potential drug-drug interactions.

See table footnotes on page 69.

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TABLE D1. (Continued) Classifications for combined hormonal contraceptives, including pill, patch, and ring
Condition

Category CHCs

St. John’s wort

Clarifications/Evidence/Comments

Evidence: Although clinical data are limited, studies with pharmacokinetic and
pharmacodynamics outcomes raise concern that St. John’s wort might decrease
effectiveness of hormonal contraceptives, including increased risk for breakthrough bleeding and ovulation and increased metabolism of estrogen and
progestins. Any interactions might be dependent on the dose of St John’s wort,
and the concentration of active ingredients across types of St. John’s wort
preparations may vary (380).

Abbreviations: ARV = antiretroviral; BMD = bone mineral density; BMI = body mass index; CHC = combined hormonal contraceptive; COC = combined oral contraceptive; DVT = deep venous
thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; HIV = human immunodeficiency virus; IBD = inflammatory bowel disease; LDL = low-density lipoprotein;
PE = pulmonary embolism; PID = pelvic inflammatory disease; SLE = systemic lupus erythematosus; SSRI = selective serotonin reuptake inhibitor; STD = sexually transmitted infection;
VTE = venous thromboembolism.

References
1. Abrams LS, Skee DM, Natarajan J, Wong FA, Lasseter KC. Multipledose pharmacokinetics of a contraceptive patch in healthy women
participants. Contraception 2001;64:287–94. http://dx.doi.
org/10.1016/S0010-7824(01)00273-6
2. Ahrendt HJ, Nisand I, Bastianelli C, et al. Efficacy, acceptability and
tolerability of the combined contraceptive ring, NuvaRing, compared
with an oral contraceptive containing 30 microg of ethinyl estradiol and
3 mg of drospirenone. Contraception 2006;74:451–7. http://dx.doi.
org/10.1016/j.contraception.2006.07.004
3. Audet M-C, Moreau M, Koltun WD, et al; ORTHO EVRA/EVRA
004 Study Group. Evaluation of contraceptive efficacy and cycle control
of a transdermal contraceptive patch vs an oral contraceptive: a
randomized controlled trial. JAMA 2001;285:2347–54. http://dx.doi.
org/10.1001/jama.285.18.2347
4. Bjarnadóttir RI, Tuppurainen M, Killick SR. Comparison of cycle control
with a combined contraceptive vaginal ring and oral levonorgestrel/
ethinyl estradiol. Am J Obstet Gynecol 2002;186:389–95. http://dx.doi.
org/10.1067/mob.2002.121103
5. Boonyarangkul A, Taneepanichskul S. Comparison of cycle control and side
effects between transdermal contraceptive patch and an oral contraceptive
in women older than 35 years. J Med Assoc Thai 2007;90:1715–9.
6. Burkman RT. The transdermal contraceptive patch: a new approach to
hormonal contraception. Int J Fertil Womens Med 2002;47:69–76.
7. Cole JA, Norman H, Doherty M, Walker AM. Venous thromboembolism,
myocardial infarction, and stroke among transdermal contraceptive
system users. Obstet Gynecol 2007;109:339–46. http://dx.doi.
org/10.1097/01.AOG.0000250968.82370.04
8. Devineni D, Skee D, Vaccaro N, et al. Pharmacokinetics and
pharmacodynamics of a transdermal contraceptive patch and an oral
contraceptive. J Clin Pharmacol 2007;47:497–509. http://dx.doi.
org/10.1177/0091270006297919.
9. Dieben TO, Roumen FJ, Apter D. Efficacy, cycle control, and user
acceptability of a novel combined contraceptive vaginal ring. Obstet
Gynecol 2002;100:585–93.
10. Dittrich R, Parker L, Rosen JB, Shangold G, Creasy GW, Fisher AC;
Ortho Evra/Evra 001 Study Group. Transdermal contraception:
evaluation of three transdermal norelgestromin/ethinyl estradiol doses
in a randomized, multicenter, dose-response study. Am J Obstet Gynecol
2002;186:15–20. http://dx.doi.org/10.1067/mob.2002.118844
11. Duijkers I, Killick S, Bigrigg A, Dieben TO. A comparative study on
the effects of a contraceptive vaginal ring NuvaRing and an oral
contraceptive on carbohydrate metabolism and adrenal and thyroid
function. Eur J Contracept Reprod Health Care 2004;9:131–40. http://
dx.doi.org/10.1080/13625180400007199
12. Duijkers IJ, Klipping C, Verhoeven CH, Dieben TO. Ovarian function with
the contraceptive vaginal ring or an oral contraceptive: a randomized study.
Hum Reprod 2004;19:2668–73. http://dx.doi.org/10.1093/humrep/deh493

13. Elkind-Hirsch KE, Darensbourg C, Ogden B, Ogden LF, Hindelang P.
Contraceptive vaginal ring use for women has less adverse metabolic
effects than an oral contraceptive. Contraception 2007;76:348–56.
http://dx.doi.org/10.1016/j.contraception.2007.08.001
14. Hedon B, Helmerhorst FM, Cronje HS, Shangold GA, Fisher AC,
Creasy GW. Comparison of efficacy, cycle control, compliance, and
safety in users of a contraceptive patch versus an oral contraceptive. Int
J Gynaecol Obstet 2000;70(Suppl 2):B78. http://dx.doi.org/10.1016/
S0020-7292(00)85161-9
15. Jick S, Kaye JA, Li L, Jick H. Further results on the risk of nonfatal
venous thromboembolism in users of the contraceptive transdermal
patch compared to users of oral contraceptives containing norgestimate
and 35 microg of ethinyl estradiol. Contraception 2007;76:4–7. http://
dx.doi.org/10.1016/j.contraception.2007.03.003
16. Jick SS, Jick H. Cerebral venous sinus thrombosis in users of four
hormonal contraceptives: levonorgestrel-containing oral contraceptives,
norgestimate-containing oral contraceptives, desogestrel-containing oral
contraceptives and the contraceptive patch. Contraception 2006;74:290–
2. http://dx.doi.org/10.1016/j.contraception.2006.05.071
17. Jick SS, Jick H. The contraceptive patch in relation to ischemic stroke
and acute myocardial infarction. Pharmacotherapy 2007;27:218–20.
http://dx.doi.org/10.1592/phco.27.2.218
18. Jick SS, Kaye JA, Russmann S, Jick H. Risk of nonfatal venous
thromboembolism in women using a contraceptive transdermal patch
and oral contraceptives containing norgestimate and 35 microg of ethinyl
estradiol. Contraception 2006;73:223–8. http://dx.doi.org/10.1016/j.
contraception.2006.01.001
19. Magnusdóttir EM, Bjarnadóttir RI, Onundarson PT, et al. The contraceptive
vaginal ring (NuvaRing) and hemostasis: a comparative study. Contraception
2004;69:461–7. http://dx.doi.org/10.1016/j.contraception.2003.12.010
20. Massai R, Mäkäräinen L, Kuukankorpi A, Klipping C, Duijkers I, Dieben
T. The combined contraceptive vaginal ring and bone mineral density in
healthy pre-menopausal women. Hum Reprod 2005;20:2764–8. http://
dx.doi.org/10.1093/humrep/dei117
21. Milsom I, Lete I, Bjertnaes A, et al. Effects on cycle control and bodyweight
of the combined contraceptive ring, NuvaRing, versus an oral contraceptive
containing 30 µg ethinyl estradiol and 3 mg drospirenone. Hum Reprod
2006;21:2304–11. http://dx.doi.org/10.1093/humrep/del162
22. Oddsson K, Leifels-Fischer B, de Melo NR, et al. Efficacy and safety of
a contraceptive vaginal ring (NuvaRing) compared with a combined oral
contraceptive: a 1-year randomized trial. Contraception 2005;71:176–
82. http://dx.doi.org/10.1016/j.contraception.2004.09.001
23. Pierson RA, Archer DF, Moreau M, Shangold GA, Fisher AC, Creasy GW.
Ortho Evra/Evra versus oral contraceptives: follicular development and
ovulation in normal cycles and after an intentional dosing error. Fertil Steril
2003;80:34–42. http://dx.doi.org/10.1016/S0015-0282(03)00556-9
24. Radowicki S, Skórzewska K, Szlendak K. Safety evaluation of a
transdermal contraceptive system with an oral contraceptive [Polish].
Ginekol Pol 2005;76:884–9.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

25. Sabatini R, Cagiano R. Comparison profiles of cycle control, side effects
and sexual satisfaction of three hormonal contraceptives. Contraception
2006;74:220–3. http://dx.doi.org/10.1016/j.contraception.2006.03.022
26. Smallwood GH, Meador ML, Lenihan JP, Shangold GA, Fisher AC, Creasy
GW; ORTHO EVRA/EVRA 002 Study Group. Efficacy and safety of a
transdermal contraceptive system. Obstet Gynecol 2001;98:799–805.
27. Timmer CJ, Mulders TM. Pharmacokinetics of etonogestrel and ethinylestradiol
released from a combined contraceptive vaginal ring. Clin Pharmacokinet
2000;39:233–42. http://dx.doi.org/10.2165/00003088-200039030-00005
28. Tuppurainen M, Klimscheffskij R, Venhola M, Dieben TO. The
combined contraceptive vaginal ring (NuvaRing) and lipid metabolism:
a comparative study. Contraception 2004;69:389–94. http://dx.doi.
org/10.1016/j.contraception.2004.01.004
29. Urdl W, Apter D, Alperstein A, et al; ORTHO EVRA/EVRA 003 Study
Group. Contraceptive efficacy, compliance and beyond: factors related
to satisfaction with once-weekly transdermal compared with oral
contraception. Eur J Obstet Gynecol Reprod Biol 2005;121:202–10.
http://dx.doi.org/10.1016/j.ejogrb.2005.01.021
30. van den Heuvel MW, van Bragt AJM, Alnabawy AKM, Kaptein MCJ.
Comparison of ethinylestradiol pharmacokinetics in three hormonal
contraceptive formulations: the vaginal ring, the transdermal patch and
an oral contraceptive. Contraception 2005;72:168–74. http://dx.doi.
org/10.1016/j.contraception.2005.03.005
31. Veres S, Miller L, Burington B. A comparison between the vaginal ring
and oral contraceptives. Obstet Gynecol 2004;104:555–63. http://
dx.doi.org/10.1097/01.AOG.0000136082.59644.13
32. White T, Ozel B, Jain JK, Stanczyk FZ. Effects of transdermal and oral
contraceptives on estrogen-sensitive hepatic proteins. Contraception
2006;74:293–6. http://dx.doi.org/10.1016/j.contraception.2006.04.005
33. Zieman M, Guillebaud J, Weisberg E, Shangold GA, Fisher AC, Creasy GW.
Contraceptive efficacy and cycle control with the Ortho Evra/Evra transdermal
system: the analysis of pooled data. Fertil Steril 2002;77(Suppl 2):S13–8.
http://dx.doi.org/10.1016/S0015-0282(01)03275-7
34. Memon S, Iversen L, Hannaford PC. Is the oral contraceptive pill
associated with fracture in later life? New evidence from the Royal College
of General Practitioners Oral Contraception Study. Contraception
2011;84:40–7. http://dx.doi.org/10.1016/j.contraception.2010.11.019
35. Vestergaard P, Rejnmark L, Mosekilde L. Fracture risk in very young
women using combined oral contraceptives. Contraception 2008;78:358–
64. http://dx.doi.org/10.1016/j.contraception.2008.06.010
36. Vestergaard P, Rejnmark L, Mosekilde L. Oral contraceptive use and risk
of fractures. Contraception 2006;73:571–6. http://dx.doi.org/10.1016/j.
contraception.2006.01.006
37. Barad D, Kooperberg C, Wactawski-Wende J, Liu J, Hendrix SL, Watts
NB. Prior oral contraception and postmenopausal fracture: a Women’s
Health Initiative observational cohort study. Fertil Steril 2005;84:374–
83. http://dx.doi.org/10.1016/j.fertnstert.2005.01.132
38. Michaëlsson K, Baron JA, Farahmand BY, Ljunghall S. Influence of
parity and lactation on hip fracture risk. Am J Epidemiol 2001;153:1166–
72. http://dx.doi.org/10.1093/aje/153.12.1166
39. Michaëlsson K, Baron JA, Farahmand BY, Persson I, Ljunghall S. Oralcontraceptive use and risk of hip fracture: a case-control study. Lancet
1999;353:1481–4. http://dx.doi.org/10.1016/S0140-6736(98)09044-8
40. La Vecchia C, Tavani A, Gallus S. Oral contraceptives and risk of
hip fractures. Lancet 1999;354:335–6. http://dx.doi.org/10.1016/
S0140-6736(05)75239-9
41. Vessey M, Mant J, Painter R. Oral contraception and other factors in relation
to hospital referral for fracture. Findings in a large cohort study. Contraception
1998;57:231–5. http://dx.doi.org/10.1016/S0010-7824(98)00026-2
42. O’Neill TW, Marsden D, Adams JE, Silman AJ. Risk factors, falls, and
fracture of the distal forearm in Manchester, UK. J Epidemiol Community
Health 1996;50:288–92. http://dx.doi.org/10.1136/jech.50.3.288
43. Mallmin H, Ljunghall S, Persson I, Bergström R. Risk factors for fractures
of the distal forearm: a population-based case-control study. Osteoporos
Int 1994;4:298–304. http://dx.doi.org/10.1007/BF01622186

MMWR / July 29, 2016 / Vol. 65 / No. 3

44. Cooper C, Hannaford P, Croft P, Kay CR. Oral contraceptive pill use
and fractures in women: a prospective study. Bone 1993;14:41–5. http://
dx.doi.org/10.1016/8756-3282(93)90254-8
45. Meier C, Brauchli YB, Jick SS, Kraenzlin ME, Meier CR. Use of depot
medroxyprogesterone acetate and fracture risk. J Clin Endocrinol Metab
2010;95:4909–16. http://dx.doi.org/10.1210/jc.2010-0032
46. Cibula D, Skrenkova J, Hill M, Stepan JJ. Low-dose estrogen combined
oral contraceptives may negatively influence physiological bone mineral
density acquisition during adolescence. Eur J Endocrinol 2012;166:1003–
11. http://dx.doi.org/10.1530/EJE-11-1047
47. Gai L, Jia Y, Zhang M, et al. Effect of two kinds of different combined oral
contraceptives use on bone mineral density in adolescent women. Contraception
2012;86:332–6. http://dx.doi.org/10.1016/j.contraception.2012.01.009
48. Scholes D, Hubbard RA, Ichikawa LE, et al. Oral contraceptive use and
bone density change in adolescent and young adult women: a prospective
study of age, hormone dose, and discontinuation. J Clin Endocrinol
Metab 2011;96:E1380–7. http://dx.doi.org/10.1210/jc.2010-3027
49. Lattakova M, Borovsky M, Payer J, Killinger Z. Oral contraception
usage in relation to bone mineral density and bone turnover in adolescent
girls. Eur J Contracept Reprod Health Care 2009;14:207–14. http://
dx.doi.org/10.1080/13625180902838828
50. Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral
density in a cohort of adolescents during use of norethisterone enanthate,
depot-medroxyprogesterone acetate or combined oral contraceptives
and after discontinuation of norethisterone enanthate. Contraception
2009;79:345–9. http://dx.doi.org/10.1016/j.contraception.2008.11.009
51. Pikkarainen E, Lehtonen-Veromaa M, Möttönen T, Kautiainen H, Viikari
J. Estrogen-progestin contraceptive use during adolescence prevents bone
mass acquisition: a 4-year follow-up study. Contraception 2008;78:226–
31. http://dx.doi.org/10.1016/j.contraception.2008.05.002
52. Cromer BA, Bonny AE, Stager M, et al. Bone mineral density in adolescent
females using injectable or oral contraceptives: a 24-month prospective study.
Fertil Steril 2008;90:2060–7. http://dx.doi.org/10.1016/j.fertnstert.2007.10.070
53. Berenson AB, Rahman M, Breitkopf CR, Bi LX. Effects of depot
medroxyprogesterone acetate and 20-µg oral contraceptives on bone
mineral density. Obstet Gynecol 2008;112:788–99. http://dx.doi.
org/10.1097/AOG.0b013e3181875b78
54. Harel Z, Riggs S, Vaz R, Flanagan P, Harel D, Machan JT. Bone accretion
in adolescents using the combined estrogen and progestin transdermal
contraceptive method Ortho Evra: a pilot study. J Pediatr Adolesc
Gynecol 2010;23:23–31. http://dx.doi.org/10.1016/j.jpag.2009.04.008
55. Cobb KL, Bachrach LK, Sowers M, et al. The effect of oral contraceptives
on bone mass and stress fractures in female runners. Med Sci Sports Exerc
2007;39:1464–73. http://dx.doi.org/10.1249/mss.0b013e318074e532
56. Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral density
in adolescents using norethisterone enanthate, depot-medroxyprogesterone
acetate or combined oral contraceptives for contraception. Contraception
2007;75:438–43. http://dx.doi.org/10.1016/j.contraception.2007.02.001
57. Lara-Torre E, Edwards CP, Perlman S, Hertweck SP. Bone mineral density in
adolescent females using depot medroxyprogesterone acetate. J Pediatr Adolesc
Gynecol 2004;17:17–21. http://dx.doi.org/10.1016/j.jpag.2003.11.017
58. Cromer BA, Blair JM, Mahan JD, Zibners L, Naumovski Z. A
prospective comparison of bone density in adolescent girls receiving
depot medroxyprogesterone acetate (Depo-Provera), levonorgestrel
(Norplant), or oral contraceptives. J Pediatr 1996;129:671–6. http://
dx.doi.org/10.1016/S0022-3476(96)70148-8
59. Polatti F, Perotti F, Filippa N, Gallina D, Nappi RE. Bone mass and long-term
monophasic oral contraceptive treatment in young women. Contraception
1995;51:221–4. http://dx.doi.org/10.1016/0010-7824(95)00036-A
60. Sørdal T, Grob P, Verhoeven C. Effects on bone mineral density of a monophasic
combined oral contraceptive containing nomegestrol acetate/17ß-estradiol in
comparison to levonorgestrel/ethinylestradiol. Acta Obstet Gynecol Scand
2012;91:1279–85. http://dx.doi.org/10.1111/j.1600-0412.2012.01498.x

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

61. Gargano V, Massaro M, Morra I, Formisano C, Di Carlo C, Nappi C.
Effects of two low-dose combined oral contraceptives containing
drospirenone on bone turnover and bone mineral density in young fertile
women: a prospective controlled randomized study. Contraception
2008;78:10–5. http://dx.doi.org/10.1016/j.contraception.2008.01.016
62. Nappi C, Di Spiezio Sardo A, Greco E, Tommaselli GA, Giordano E,
Guida M. Effects of an oral contraceptive containing drospirenone on
bone turnover and bone mineral density. Obstet Gynecol 2005;105:53–
60. http://dx.doi.org/10.1097/01.AOG.0000148344.26475.fc
63. Berenson AB, Radecki CM, Grady JJ, Rickert VI, Thomas A. A
prospective, controlled study of the effects of hormonal contraception
on bone mineral density. Obstet Gynecol 2001;98:576–82.
64. Berenson AB, Breitkopf CR, Grady JJ, Rickert VI, Thomas A. Effects
of hormonal contraception on bone mineral density after 24 months of
use. Obstet Gynecol 2004;103:899–906. http://dx.doi.org/10.1097/01.
AOG.0000117082.49490.d5
65. Elgán C, Samsioe G, Dykes AK. Influence of smoking and oral
contraceptives on bone mineral density and bone remodeling in young
women: a 2-year study. Contraception 2003;67:439–47. http://dx.doi.
org/10.1016/S0010-7824(03)00048-9
66. Elgán C, Dykes AK, Samsioe G. Bone mineral density changes in young
women: a two year study. Gynecol Endocrinol 2004;19:169–77. http://
dx.doi.org/10.1080/09513590400012119
67. Endrikat J, Mih E, Düsterberg B, et al. A 3-year double-blind, randomized,
controlled study on the influence of two oral contraceptives containing either
20 µg or 30 µg ethinylestradiol in combination with levonorgestrel on bone
mineral density. Contraception 2004;69:179–87. http://dx.doi.org/10.1016/j.
contraception.2003.10.002
68. Paoletti AM, Orrù M, Lello S, et al. Short-term variations in bone
remodeling markers of an oral contraception formulation containing
3 mg of drospirenone plus 30 microg of ethinyl estradiol: observational
study in young postadolescent women. Contraception 2004;70:293–8.
http://dx.doi.org/10.1016/j.contraception.2004.04.004
69. Nappi C, Di Spiezio Sardo A, Acunzo G, et al. Effects of a low-dose and
ultra-low-dose combined oral contraceptive use on bone turnover and
bone mineral density in young fertile women: a prospective controlled
randomized study. Contraception 2003;67:355–9. http://dx.doi.
org/10.1016/S0010-7824(03)00025-8
70. Reed SD, Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM.
Longitudinal changes in bone density in relation to oral contraceptive
use. Contraception 2003;68:177–82. http://dx.doi.org/10.1016/
S0010-7824(03)00147-1
71. Cobb KL, Kelsey JL, Sidney S, Ettinger B, Lewis CE. Oral contraceptives
and bone mineral density in white and black women in CARDIA.
Coronary Risk Development in Young Adults. Osteoporos Int
2002;13:893–900. http://dx.doi.org/10.1007/s001980200123
72. Burr DB, Yoshikawa T, Teegarden D, et al. Exercise and oral contraceptive
use suppress the normal age-related increase in bone mass and strength
of the femoral neck in women 18–31 years of age. Bone 2000;27:855–63.
http://dx.doi.org/10.1016/S8756-3282(00)00403-8
73. Recker RR, Davies KM, Hinders SM, Heaney RP, Stegman MR, Kimmel
DB. Bone gain in young adult women. JAMA 1992;268:2403–8. http://
dx.doi.org/10.1001/jama.1992.03490170075028
74. Mazess RB, Barden HS. Bone density in premenopausal women: effects
of age, dietary intake, physical activity, smoking, and birth-control pills.
Am J Clin Nutr 1991;53:132–42.
75. Gambacciani M, Cappagli B, Lazzarini V, Ciaponi M, Fruzzetti F,
Genazzani AR. Longitudinal evaluation of perimenopausal bone loss:
effects of different low dose oral contraceptive preparations on bone
mineral density. Maturitas 2006;54:176–80. http://dx.doi.org/10.1016/j.
maturitas.2005.10.007
76. Gambacciani M, Spinetti A, Taponeco F, Cappagli B, Piaggesi L,
Fioretti P. Longitudinal evaluation of perimenopausal vertebral bone
loss: effects of a low-dose oral contraceptive preparation on bone mineral
density and metabolism. Obstet Gynecol 1994;83:392–6.

77. Gambacciani M, Spinetti A, Cappagli B, et al. Hormone replacement
therapy in perimenopausal women with a low dose oral contraceptive
preparation: effects on bone mineral density and metabolism. Maturitas
1994;19:125–31. http://dx.doi.org/10.1016/0378-5122(94)90062-0
78. Gambacciani M, Cappagli B, Ciaponi M, Benussi C, Genazzani AR. Hormone
replacement therapy in perimenopause: effect of a low dose oral contraceptive
preparation on bone quantitative ultrasound characteristics. Menopause
1999;6:43–8. http://dx.doi.org/10.1097/00042192-199906010-00009
79. Volpe A, Malmusi S, Zanni AL, Landi S, Cagnacci A. Oral contraceptives
and bone metabolism. Eur J Contracept Reprod Health Care
1997;2:225–8. http://dx.doi.org/10.3109/13625189709165298
80. Hansen MA, Overgaard K, Riis BJ, Christiansen C. Potential risk factors
for development of postmenopausal osteoporosis—examined over a
12-year period. Osteoporos Int 1991;1:95–102. http://dx.doi.
org/10.1007/BF01880450
81. Shargil AA. Hormone replacement therapy in perimenopausal women
with a triphasic contraceptive compound: a three-year prospective study.
Int J Fertil 1985;30:15, 18–28.
82. Taechakraichana N, Limpaphayom K, Ninlagarn T, Panyakhamlerd K,
Chaikittisilpa S, Dusitsin N. A randomized trial of oral contraceptive
and hormone replacement therapy on bone mineral density and coronary
heart disease risk factors in postmenopausal women. Obstet Gynecol
2000;95:87–94.
83. Taechakraichana N, Jaisamrarn U, Panyakhamlerd K, Chaikittisilpa S,
Limpaphayom K. Difference in bone acquisition among hormonally
treated postmenopausal women with normal and low bone mass. J Med
Assoc Thai 2001;84(Suppl 2):S586–92.
84. Grimes DA, Schulz KF. Surrogate end points in clinical research:
hazardous to your health. Obstet Gynecol 2005;105:1114–8. http://
dx.doi.org/10.1097/01.AOG.0000157445.67309.19
85. Schönau E. The peak bone mass concept: is it still relevant? Pediatr Nephrol
2004;19:825–31. http://dx.doi.org/10.1007/s00467-004-1465-5
86. Cohen A, Shane E. Treatment of premenopausal women with low bone
mineral density. Curr Osteoporos Rep 2008;6:39–46. http://dx.doi.
org/10.1007/s11914-008-0007-7
87. US Department of Health and Human Services. Healthy people 2020:
maternal, infant, and child health objectives. Washington, DC: US
Department of Health and Human Services; 2015. http://www.
healthypeople.gov/2020/topics-objectives/topic/maternal-infant-andchild-health/objectives.
88. Tepper NK, Phillips SJ, Kapp N, Gaffield ME, Curtis KM. Combined
hormonal contraceptive use among breastfeeding women: an updated
systematic review. Contraception 2015;S0010-7824(15)00218-8.
89. Petersen JF, Bergholt T, Nielsen AK, Paidas MJ, Løkkegaard EC.
Combined hormonal contraception and risk of venous thromboembolism
within the first year following pregnancy. Danish nationwide historical
cohort 1995–2009. Thromb Haemost 2014;112:73–8. http://dx.doi.
org/10.1160/TH13-09-0797
90. Jackson E, Curtis KM, Gaffield ME. Risk of venous thromboembolism
during the postpartum period: a systematic review. Obstet Gynecol
2011;117:691–703. http://dx.doi.org/10.1097/AOG.0b013e31820ce2db
91. Kamel H, Navi BB, Sriram N, Hovsepian DA, Devereux RB, Elkind MS.
Risk of a thrombotic event after the 6-week postpartum period. N Engl J
Med 2014;370:1307–15. http://dx.doi.org/10.1056/NEJMoa1311485
92. Sultan AA, Tata LJ, West J, et al. Risk factors for first venous
thromboembolism around pregnancy: a population-based cohort study
from the United Kingdom. Blood 2013;121:3953–61. http://dx.doi.
org/10.1182/blood-2012-11-469551
93. Sultan AA, West J, Tata LJ, Fleming KM, Nelson-Piercy C, Grainge MJ.
Risk of first venous thromboembolism in and around pregnancy: a
population-based cohort study. Br J Haematol 2012;156:366–73. http://
dx.doi.org/10.1111/j.1365-2141.2011.08956.x

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Recommendations and Reports

94. Tepper NK, Boulet SL, Whiteman MK, et al. Postpartum venous
thromboembolism: incidence and risk factors. Obstet Gynecol
2014;123:987–96. http://dx.doi.org/10.1097/AOG.0000000000000230
95. Jackson E, Glasier A. Return of ovulation and menses in postpartum
nonlactating women: a systematic review. Obstet Gynecol 2011;117:657–
62. http://dx.doi.org/10.1097/AOG.0b013e31820ce18c
96. Lähteenmäki P. Influence of oral contraceptives on immediate
postabortal pituitary-ovarian function. Acta Obstet Gynecol Scand
Suppl 1978;76:1–43.
97. Lähteenmäki P, Rasi V, Luukkainen T, Myllyä G. Coagulation factors
in women using oral contraceptives or intrauterine contraceptive devices
immediately after abortion. Am J Obstet Gynecol 1981;141:175–9.
98. Martin CW, Brown AH, Baird DT. A pilot study of the effect of methotrexate
or combined oral contraceptive on bleeding patterns after induction of
abortion with mifepristone and a prostaglandin pessary. Contraception
1998;58:99–103. http://dx.doi.org/10.1016/S0010-7824(98)00072-9
99. Niswonger JW, London GD, Anderson GV, Wolfe L. Oral
contraceptives during immediate postabortal period. Obstet Gynecol
1968;32:325–7.
100. Peterson WF. Contraceptive therapy following therapeutic abortion:
an analysis. Obstet Gynecol 1974;44:853–7.
101. Tang OS, Gao PP, Cheng L, Lee SW, Ho PC. A randomized double-blind
placebo-controlled study to assess the effect of oral contraceptive pills on
the outcome of medical abortion with mifepristone and misoprostol. Hum
Reprod 1999;14:722–5. http://dx.doi.org/10.1093/humrep/14.3.722
102. Tang OS, Xu J, Cheng L, Lee SW, Ho PC. The effect of contraceptive pills
on the measured blood loss in medical termination of pregnancy by
mifepristone and misoprostol: a randomized placebo controlled trial. Hum
Reprod 2002;17:99–102. http://dx.doi.org/10.1093/humrep/17.1.99
103. Fine PM, Tryggestad J, Meyers NJ, Sangi-Haghpeykar H. Safety and
acceptability with the use of a contraceptive vaginal ring after surgical
or medical abortion. Contraception 2007;75:367–71. http://dx.doi.
org/10.1016/j.contraception.2007.01.009
104. Gillum LA, Mamidipudi SK, Johnston SC. Ischemic stroke risk with
oral contraceptives: a meta-analysis. JAMA 2000;284:72–8. http://
dx.doi.org/10.1001/jama.284.1.72
105. Jick SS, Walker AM, Stergachis A, Jick H. Oral contraceptives and
breast cancer. Br J Cancer 1989;59:618–21. http://dx.doi.org/10.1038/
bjc.1989.125
106. Khader YS, Rice J, John L, Abueita O. Oral contraceptives use and the
risk of myocardial infarction: a meta-analysis. Contraception
2003;68:11–7. http://dx.doi.org/10.1016/S0010-7824(03)00073-8
107. Lawson DH, Davidson JF, Jick H. Oral contraceptive use and venous
thromboembolism: absence of an effect of smoking. BMJ 1977;2:729–
30. http://dx.doi.org/10.1136/bmj.2.6089.729
108. Lidegaard O, Edström B, Kreiner S. Oral contraceptives and venous
thromboembolism. A case-control study. Contraception 1998;57:291–
301. http://dx.doi.org/10.1016/S0010-7824(98)00033-X
109. Nightingale AL, Lawrenson RA, Simpson EL, Williams TJ, MacRae
KD, Farmer RD. The effects of age, body mass index, smoking and
general health on the risk of venous thromboembolism in users of
combined oral contraceptives. Eur J Contracept Reprod Health Care
2000;5:265–74. http://dx.doi.org/10.1080/13625180008500402
110. Petitti DB, Wingerd J, Pellegrin F, Ramcharan S. Risk of vascular disease
in women. Smoking, oral contraceptives, noncontraceptive estrogens,
and other factors. JAMA 1979;242:1150–4. http://dx.doi.org/10.1001/
jama.1979.03300110022020

MMWR / July 29, 2016 / Vol. 65 / No. 3

111. Rosenberg L, Palmer JR, Rao RS, Shapiro S. Low-dose oral contraceptive
use and the risk of myocardial infarction. Arch Intern Med
2001;161:1065–70. http://dx.doi.org/10.1001/archinte.161.8.1065
112. Straneva P, Hinderliter A, Wells E, Lenahan H, Girdler S. Smoking,
oral contraceptives, and cardiovascular reactivity to stress. Obstet
Gynecol 2000;95:78–83.
113. Tanis BC, van den Bosch MA, Kemmeren JM, et al. Oral contraceptives
and the risk of myocardial infarction. N Engl J Med 2001;345:1787–
93. http://dx.doi.org/10.1056/NEJMoa003216
114. Van den Bosch MA, Kemmeren JM, Tanis BC, et al. The RATIO study:
oral contraceptives and the risk of peripheral arterial disease in young
women. J Thromb Hemost 2003;1:439–44.
115. World Health Organization Collaborative Study of Cardiovascular
Disease and Steroid Hormone Contraception. Venous thromboembolic
disease and combined oral contraceptives: results of international
multicentre case-control study. Lancet 1995;346:1575–82. http://
dx.doi.org/10.1016/S0140-6736(95)91926-0
116. Collaborative Group for the Study of Stroke in Young Women. Oral
contraceptives and stroke in young women. Associated risk factors. JAMA
1975;231:718–22. http://dx.doi.org/10.1001/jama.1975.03240190022010
117. Horton LG, Simmons KB, Curtis KM. Combined hormonal
contraceptive use among obese women and risk for cardiovascular events:
a systematic review. Contraception 2016. Epub June 1, 2016. http://
dx.doi.org/10.1016/j.contraception.2016.05.014
118. Brunner Huber LR, Hogue CJ, Stein AD, Drews C, Zieman M. Body
mass index and risk for oral contraceptive failure: a case-cohort study
in South Carolina. Ann Epidemiol 2006;16:637–43. http://dx.doi.
org/10.1016/j.annepidem.2006.01.001
119. Brunner Huber LR, Toth JL. Obesity and oral contraceptive failure:
findings from the 2002 National Survey of Family Growth. Am J
Epidemiol 2007;166:1306–11. http://dx.doi.org/10.1093/aje/kwm221
120. Brunner LR, Hogue CJ. The role of body weight in oral contraceptive failure:
results from the 1995 national survey of family growth. Ann Epidemiol
2005;15:492–9. http://dx.doi.org/10.1016/j.annepidem.2004.10.009
121. Holt VL, Cushing-Haugen KL, Daling JR. Body weight and risk of
oral contraceptive failure. Obstet Gynecol 2002;99:820–7.
122. Holt VL, Scholes D, Wicklund KG, Cushing-Haugen KL, Daling JR. Body
mass index, weight, and oral contraceptive failure risk. Obstet Gynecol
2005;105:46–52. http://dx.doi.org/10.1097/01.AOG.0000149155.11912.52
123. Trussell J, Schwarz EB, Guthrie K. Obesity and oral contraceptive pill
failure. Contraception 2009;79:334–8. http://dx.doi.org/10.1016/j.
contraception.2008.11.017
124. Vessey M. Oral contraceptive failures and body weight: findings in a
large cohort study. J Fam Plann Reprod Health Care 2001;27:90–1.
http://dx.doi.org/10.1783/147118901101195092
125. Yamazaki M, Dwyer K, Sobhan M, et al. Effect of obesity on the
effectiveness of hormonal contraceptives: an individual participant data
meta-analysis. Contraception 2015;92:445–52. http://dx.doi.
org/10.1016/j.contraception.2015.07.016
126. Zieman M, Guillebaud J, Weisberg E, Shangold GA, Fisher AC, Creasy
GW. Contraceptive efficacy and cycle control with the Ortho Evra/Evra
transdermal system: the analysis of pooled data. Fertil Steril 2002;77(Suppl
2):S13–8. http://dx.doi.org/10.1016/S0015-0282(01)03275-7
127. O’Connell KJ, Osborne LM, Westhoff C. Measured and reported
weight change for women using a vaginal contraceptive ring vs. a lowdose oral contraceptive. Contraception 2005;72:323–7. http://dx.doi.
org/10.1016/j.contraception.2005.05.008

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128. Paulen ME, Zapata LB, Cansino C, Curtis KM, Jamieson DJ.
Contraceptive use among women with a history of bariatric surgery: a
systematic review. Contraception 2010;82:86–94. http://dx.doi.
org/10.1016/j.contraception.2010.02.008
129. Lidegaard Ø, Edström B, Kreiner S. Oral contraceptives and venous
thromboembolism: a five-year national case-control study. Contraception
2002;65:187–96. http://dx.doi.org/10.1016/S0010-7824(01)00307-9
130. Croft P, Hannaford PC. Risk factors for acute myocardial infarction
in women: evidence from the Royal College of General Practitioners’
oral contraception study. BMJ 1989;298:165–8. http://dx.doi.
org/10.1136/bmj.298.6667.165
131. D’Avanzo B, La Vecchia C, Negri E, Parazzini F, Franceschi S. Oral
contraceptive use and risk of myocardial infarction: an Italian casecontrol study. J Epidemiol Community Health 1994;48:324–5. http://
dx.doi.org/10.1136/jech.48.3.324
132. Dunn NR, Faragher B, Thorogood M, et al. Risk of myocardial
infarction in young female smokers. Heart 1999;82:581–3. http://
dx.doi.org/10.1136/hrt.82.5.581
133. Hannaford PC, Croft PR, Kay CR. Oral contraception and stroke.
Evidence from the Royal College of General Practitioners’ Oral
Contraception Study. Stroke 1994;25:935–42. http://dx.doi.
org/10.1161/01.STR.25.5.935
134. Heinemann LA, Lewis MA, Spitzer WO, Thorogood M, GuggenmoosHolzmann I, Bruppacher R; Transnational Research Group on Oral
Contraceptives and the Health of Young Women. Thromboembolic
stroke in young women. A European case-control study on oral
contraceptives. Contraception 1998;57:29–37. http://dx.doi.
org/10.1016/S0010-7824(97)00204-7
135. Kemmeren JM, Tanis BC, van den Bosch MA, et al. Risk of Arterial
Thrombosis in Relation to Oral Contraceptives (RATIO) study: oral
contraceptives and the risk of ischemic stroke. Stroke 2002;33:1202–8.
http://dx.doi.org/10.1161/01.STR.0000015345.61324.3F
136. Lewis MA, Heinemann LA, Spitzer WO, MacRae KD, Bruppacher R.
The use of oral contraceptives and the occurrence of acute myocardial
infarction in young women. Results from the Transnational Study on
Oral Contraceptives and the Health of Young Women. Contraception
1997;56:129–40. http://dx.doi.org/10.1016/S0010-7824(97)00118-2
137. Lidegaard O. Oral contraception and risk of a cerebral thromboembolic
attack: results of a case-control study. BMJ 1993;306:956–63. http://
dx.doi.org/10.1136/bmj.306.6883.956
138. Lidegaard O. Oral contraceptives, pregnancy and the risk of cerebral
thromboembolism: the influence of diabetes, hypertension, migraine
and previous thrombotic disease. Br J Obstet Gynaecol 1995;102:153–
9. http://dx.doi.org/10.1111/j.1471-0528.1995.tb09070.x
139. Lubianca JN, Faccin CS, Fuchs FD. Oral contraceptives: a risk factor for
uncontrolled blood pressure among hypertensive women. Contraception
2003;67:19–24. http://dx.doi.org/10.1016/S0010-7824(02)00429-8
140. Narkiewicz K, Graniero GR, D’Este D, Mattarei M, Zonzin P, Palatini P.
Ambulatory blood pressure in mild hypertensive women taking oral
contraceptives. A case-control study. Am J Hypertens 1995;8:249–53.
http://dx.doi.org/10.1016/0895-7061(95)96212-3
141. Siritho S, Thrift AG, McNeil JJ, You RX, Davis SM, Donnan GA;
Melbourne Risk Factor Study (MERFS) Group. Risk of ischemic stroke
among users of the oral contraceptive pill: The Melbourne Risk Factor
Study (MERFS) Group. Stroke 2003;34:1575–80. http://dx.doi.
org/10.1161/01.STR.0000077925.16041.6B

142. WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Ischaemic stroke and combined oral
contraceptives: results of an international, multicentre, case-control
study. Lancet 1996;348:498–505. http://dx.doi.org/10.1016/
S0140-6736(95)12393-8
143. WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Acute myocardial infarction and combined
oral contraceptives: results of an international multicentre case-control
study. Lancet 1997;349:1202–9. http://dx.doi.org/10.1016/
S0140-6736(97)02358-1
144. Lubianca JN, Moreira LB, Gus M, Fuchs FD. Stopping oral
contraceptives: an effective blood pressure-lowering intervention in
women with hypertension. J Hum Hypertens 2005;19:451–5. http://
dx.doi.org/10.1038/sj.jhh.1001841
145. Aberg H, Karlsson L, Melander S. Studies on toxaemia of pregnancy with
special reference to blood pressure. II. Results after 6–11 years’ follow-up. Ups
J Med Sci 1978;83:97–102. http://dx.doi.org/10.3109/03009737809179119
146. Carmichael SM, Taylor MM, Ayers CR. Oral contraceptives,
hypertension, and toxemia. Obstet Gynecol 1970;35:371–6.
147. Meinel H, Ihle R, Laschinski M. [Effect of hormonal contraceptives
on blood pressure following pregnancy-induced hypertension].
Zentralbl Gynakol 1987;109:527–31.
148. Pritchard JA, Pritchard SA. Blood pressure response to estrogen-progestin oral
contraceptive after pregnancy-induced hypertension. Am J Obstet Gynecol
1977;129:733–9 http://dx.doi.org/10.1016/0002-9378(77)90390-8.
149. Sibai BM, Taslimi MM, el-Nazer A, Amon E, Mabie BC, Ryan GM.
Maternal-perinatal outcome associated with the syndrome of hemolysis,
elevated liver enzymes, and low platelets in severe preeclampsiaeclampsia. Am J Obstet Gynecol 1986;155:501–7. http://dx.doi.
org/10.1016/0002-9378(86)90266-8
150. Sibai BM, Ramadan MK, Chari RS, Friedman SA. Pregnancies
complicated by HELLP syndrome (hemolysis, elevated liver enzymes,
and low platelets): subsequent pregnancy outcome and long-term
prognosis. Am J Obstet Gynecol 1995;172:125–9. http://dx.doi.
org/10.1016/0002-9378(95)90099-3
151. WHO Collaborative Study of Cardiovascular Disease and Steroid
Hormone Contraception. Haemorrhagic stroke, overall stroke risk,
and combined oral contraceptives: results of an international,
multicentre, case-control study. Lancet 1996;348:505–10. http://
dx.doi.org/10.1016/S0140-6736(95)12394-6
152. Sidney S, Petitti DB, Soff GA, Cundiff DL, Tolan KK, Quesenberry
CP Jr. Venous thromboembolic disease in users of low-estrogen
combined estrogen-progestin oral contraceptives. Contraception
2004;70:3–10. http://dx.doi.org/10.1016/j.contraception.2004.02.010
153. Andersen BS, Olsen J, Nielsen GL, et al. Third generation oral
contraceptives and heritable thrombophilia as risk factors of non-fatal
venous thromboembolism. Thromb Haemost 1998;79:28–31.
154. Aznar J, Mira Y, Vayá A, et al. Factor V Leiden and prothrombin
G20210A mutations in young adults with cryptogenic ischemic stroke.
Thromb Haemost 2004;91:1031–4.
155. Bennet L, Odeberg H. Resistance to activated protein C, highly
prevalent amongst users of oral contraceptives with venous
thromboembolism. J Intern Med 1998;243:27–32. http://dx.doi.
org/10.1046/j.1365-2796.1998.00310.x
156. Bloemenkamp KW, Rosendaal FR, Helmerhorst FM, Vandenbroucke
JP. Higher risk of venous thrombosis during early use of oral contraceptives
in women with inherited clotting defects.[comment]. Arch Intern Med
2000;160:49–52. http://dx.doi.org/10.1001/archinte.160.1.49

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Recommendations and Reports

157. Bloemenkamp KW, Helmerhorst FM, Rosendaal FR, Vandenbroucke
JP, Büller HR. Enhancement by factor V Leiden mutation of risk of
deep-vein thrombosis associated with oral contraceptives containing a
third-generation progestagen. Lancet 1995;346:1593–6. http://dx.doi.
org/10.1016/S0140-6736(95)91929-5
158. de Bruijn SF, Stam J, Koopman MM, Vandenbroucke JP; The Cerebral
Venous Sinus Thrombosis Study Group. Case-control study of risk of
cerebral sinus thrombosis in oral contraceptive users and in [correction
of who are] carriers of hereditary prothrombotic conditions. BMJ
1998;316:589–92. http://dx.doi.org/10.1136/bmj.316.7131.589
159. Emmerich J, Rosendaal FR, Cattaneo M, et al; Study Group for PooledAnalysis in Venous Thromboembolism. Combined effect of factor V
Leiden and prothrombin 20210A on the risk of venous
thromboembolism—pooled analysis of 8 case-control studies including
2310 cases and 3204 controls. Thromb Haemost 2001;86:809–16.
160. Gadelha T, André C, Jucá AA, Nucci M. Prothrombin 20210A and
oral contraceptive use as risk factors for cerebral venous thrombosis.
Cerebrovasc Dis 2005;19:49–52. http://dx.doi.org/10.1159/000081911
161. Legnani C, Palareti G, Guazzaloca G, et al. Venous thromboembolism
in young women; role of thrombophilic mutations and oral
contraceptive use. Eur Heart J 2002;23:984–90. http://dx.doi.
org/10.1053/euhj.2001.3082
162. Martinelli I, Battaglioli T, Bucciarelli P, Passamonti SM, Mannucci
PM. Risk factors and recurrence rate of primary deep vein thrombosis
of the upper extremities. Circulation 2004;110:566–70. http://dx.doi.
org/10.1161/01.CIR.0000137123.55051.9B
163. Martinelli I, Sacchi E, Landi G, Taioli E, Duca F, Mannucci PM. High
risk of cerebral-vein thrombosis in carriers of a prothrombin-gene
mutation and in users of oral contraceptives.[comment]. N Engl J Med
1998;338:1793–7. http://dx.doi.org/10.1056/NEJM199806183382502
164. Martinelli I, Taioli E, Bucciarelli P, Akhavan S, Mannucci PM.
Interaction between the G20210A mutation of the prothrombin gene
and oral contraceptive use in deep vein thrombosis. Arterioscler Thromb
Vasc Biol 1999;19:700–3. http://dx.doi.org/10.1161/01.ATV.19.3.700
165. Middeldorp S, Meinardi JR, Koopman MM, et al. A prospective
study of asymptomatic carriers of the factor V Leiden mutation
to determine the incidence of venous thromboembolism.
[comment]. Ann Intern Med 2001;135:322–7. http://dx.doi.
org/10.7326/0003-4819-135-5-200109040-00008
166. Pabinger I, Schneider B; The GTH Study Group on Natural Inhibitors.
Thrombotic risk of women with hereditary antithrombin III-, protein C- and
protein S-deficiency taking oral contraceptive medication. Thromb Haemost
1994;71:548–52.
167. Pezzini A, Grassi M, Iacoviello L, et al. Inherited thrombophilia and stratification
of ischaemic stroke risk among users of oral contraceptives. J Neurol Neurosurg
Psychiatry 2007;78:271–6. http://dx.doi.org/10.1136/jnnp.2006.101675
168. Santamaría A, Mateo J, Oliver A, et al. Risk of thrombosis associated
with oral contraceptives of women from 97 families with inherited
thrombophilia: high risk of thrombosis in carriers of the G20210A
mutation of the prothrombin gene. Haematologica 2001;86:965–71.
169. Slooter AJ, Rosendaal FR, Tanis BC, Kemmeren JM, van der Graaf Y,
Algra A. Prothrombotic conditions, oral contraceptives, and the risk
of ischemic stroke. J Thromb Haemost 2005;3:1213–7. http://dx.doi.
org/10.1111/j.1538-7836.2005.01442.x
170. Spannagl M, Heinemann LA, Schramm W. Are factor V Leiden carriers
who use oral contraceptives at extreme risk for venous thromboembolism?
Eur J Contracept Reprod Health Care 2000;5:105–12. http://dx.doi.
org/10.1080/13625180008500383

MMWR / July 29, 2016 / Vol. 65 / No. 3

171. van Boven HH, Vandenbroucke JP, Briët E, Rosendaal FR. Gene-gene
and gene-environment interactions determine risk of thrombosis in families
with inherited antithrombin deficiency. Blood 1999;94:2590–4.
172. van Vlijmen EF, Brouwer JL, Veeger NJ, Eskes TK, de Graeff PA, van
der Meer J. Oral contraceptives and the absolute risk of venous
thromboembolism in women with single or multiple thrombophilic
defects: results from a retrospective family cohort study. Arch Intern
Med 2007;167:282–9. http://dx.doi.org/10.1001/archinte.167.3.282
173. Vandenbroucke JP, Koster T, Rosendaal FR, Briët E, Reitsma PH, Bertina RM.
Increased risk of venous thrombosis in oral-contraceptive users who are carriers
of factor V Leiden mutation.[comment]. Lancet 1994;344:1453–7. http://
dx.doi.org/10.1016/S0140-6736(94)90286-0
174. Vayá A, Mira Y, Mateo J, et al. Prothrombin G20210A mutation and
oral contraceptive use increase upper-extremity deep vein thrombotic
risk. Thromb Haemost 2003;89:452–7.
175. Martinelli I, Battaglioli T, Burgo I, Di Domenico S, Mannucci PM.
Oral contraceptive use, thrombophilia and their interaction in young
women with ischemic stroke. Haematologica 2006;91:844–7.
176. Tepper NK, Marchbanks PA, Curtis KM. Superficial venous disease
and combined hormonal contraceptives: a systematic review.
Contraception 2015;S0010-7824(15)00128-6.
177. Tepper NK, Paulen ME, Marchbanks PA, Curtis KM. Safety of
contraceptive use among women with peripartum cardiomyopathy: a
systematic review. Contraception 2010;82:95–101. http://dx.doi.
org/10.1016/j.contraception.2010.02.004
178. The Criteria Committee of the New York Heart Association.
Nomenclature and criteria for diagnosis of diseases of the heart and
great vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994.
179. Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures
and breast cancer in a sample of women with systemic lupus
erythematosus. Rheumatology (Oxford) 2004;43:1178–81. http://
dx.doi.org/10.1093/rheumatology/keh282
180. Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated
with abnormal Pap results in systemic lupus erythematosus.
Rheumatology (Oxford) 2004;43:1386–9. http://dx.doi.org/10.1093/
rheumatology/keh331
181. Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin
gene mutation, and thrombosis risk in patients with antiphospholipid
antibodies. J Rheumatol 2002;29:1683–8.
182. Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham
risk factors fail to fully account for accelerated atherosclerosis in systemic
lupus erythematosus. Arthritis Rheum 2001;44:2331–7. http://dx.doi.
org/10.1002/1529-0131(200110)44:10<2331::AID-ART395≥3.0.CO;2-I
183. Julkunen HA. Oral contraceptives in systemic lupus erythematosus:
side-effects and influence on the activity of SLE. Scand J Rheumatol
1991;20:427–33. http://dx.doi.org/10.3109/03009749109096822
184. Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women
with systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30.
http://dx.doi.org/10.1093/rheumatology/32.3.227
185. Jungers P, Dougados M, Pélissier C, et al. Influence of oral contraceptive
therapy on the activity of systemic lupus erythematosus. Arthritis
Rheum 1982;25:618–23. http://dx.doi.org/10.1002/art.1780250603
186. Manzi S, Meilahn EN, Rairie JE, et al. Age-specific incidence rates of
myocardial infarction and angina in women with systemic lupus
erythematosus: comparison with the Framingham Study. Am J Epidemiol
1997;145:408–15. http://dx.doi.org/10.1093/oxfordjournals.aje.a009122

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Recommendations and Reports

187. McAlindon T, Giannotta L, Taub N, D’Cruz D, Hughes G.
Environmental factors predicting nephritis in systemic lupus
erythematosus. Ann Rheum Dis 1993;52:720–4. http://dx.doi.
org/10.1136/ard.52.10.720
188. McDonald J, Stewart J, Urowitz MB, Gladman DD. Peripheral vascular
disease in patients with systemic lupus erythematosus. Ann Rheum
Dis 1992;51:56–60. http://dx.doi.org/10.1136/ard.51.1.56
189. Mintz G, Gutiérrez G, Delezé M, Rodríguez E. Contraception with
progestagens in systemic lupus erythematosus. Contraception
1984;30:29–38. http://dx.doi.org/10.1016/0010-7824(84)90076-3
190. Petri M. Musculoskeletal complications of systemic lupus erythematosus
in the Hopkins Lupus Cohort: an update. Arthritis Care Res
1995;8:137–45. http://dx.doi.org/10.1002/art.1790080305
191. Petri M. Lupus in Baltimore: evidence-based ‘clinical pearls’ from the
Hopkins Lupus Cohort. Lupus 2005;14:970–3. http://dx.doi.
org/10.1191/0961203305lu2230xx
192. Petri M, Kim MY, Kalunian KC, et al; OC-SELENA Trial. Combined
oral contraceptives in women with systemic lupus erythematosus. N Engl
J Med 2005;353:2550–8. http://dx.doi.org/10.1056/NEJMoa051135
193. Sánchez-Guerrero J, Uribe AG, Jiménez-Santana L, et al. A trial of
contraceptive methods in women with systemic lupus erythematosus. N
Engl J Med 2005;353:2539–49. http://dx.doi.org/10.1056/NEJMoa050817
194. Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and venous
thrombosis after diagnosis of systemic lupus erythematosus. Arthritis
Rheum 2005;53:609–12. http://dx.doi.org/10.1002/art.21314
195. Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrelreleasing intrauterine system in the management of menorrhagia in
women with hemostatic disorders. Am J Obstet Gynecol
2005;193:1361–3. http://dx.doi.org/10.1016/j.ajog.2005.05.002
196. Somers E, Magder LS, Petri M. Antiphospholipid antibodies and
incidence of venous thrombosis in a cohort of patients with systemic
lupus erythematosus. J Rheumatol 2002;29:2531–6.
197. Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo
MA. The bimodal mortality pattern of systemic lupus erythematosus. Am J
Med 1976;60:221–5. http://dx.doi.org/10.1016/0002-9343(76)90431-9
198. Choojitarom K, Verasertniyom O, Totemchokchyakarn K, Nantiruj
K, Sumethkul V, Janwityanujit S. Lupus nephritis and Raynaud’s
phenomenon are significant risk factors for vascular thrombosis in SLE
patients with positive antiphospholipid antibodies. Clin Rheumatol
2008;27:345–51. http://dx.doi.org/10.1007/s10067-007-0721-z
199. Wahl DG, Guillemin F, de Maistre E, Perret C, Lecompte T, Thibaut
G. Risk for venous thrombosis related to antiphospholipid antibodies
in systemic lupus erythematosus—a meta-analysis. Lupus 1997;6:467–
73. http://dx.doi.org/10.1177/096120339700600510
200. Farr SL, Folger SG, Paulen ME, Curtis KM. Safety of contraceptive methods
for women with rheumatoid arthritis: a systematic review. Contraception
2010;82:64–71. http://dx.doi.org/10.1016/j.contraception.2010.02.003
201. Tepper NK, Whiteman MK, Zapata LB, Marchbanks PA, Curtis KM. Safety
of hormonal contraceptives among women with migraine: a systematic review.
Contraception 2016. Epub May 3, 2016. http:// dx.doi.org/10.1016/j.
contraception.2016.04.016
202. Xu Z, Li Y, Tang S, Huang X, Chen T. Current use of oral contraceptives
and the risk of first-ever ischemic stroke: A meta-analysis of
observational studies. Thromb Res 2015;136:52–60. http://dx.doi.
org/10.1016/j.thromres.2015.04.021
203. Etminan M, Takkouche B, Isorna FC, Samii A. Risk of ischaemic stroke
in people with migraine: systematic review and meta-analysis of
observational studies. BMJ 2005;330:63. http://dx.doi.org/10.1136/
bmj.38302.504063.8F

204. Schürks M, Rist PM, Bigal ME, Buring JE, Lipton RB, Kurth T.
Migraine and cardiovascular disease: systematic review and metaanalysis. BMJ 2009;339:b3914. http://dx.doi.org/10.1136/bmj.b3914
205. Spector JT, Kahn SR, Jones MR, Jayakumar M, Dalal D, Nazarian S.
Migraine headache and ischemic stroke risk: an updated meta-analysis. Am
J Med 2010;123:612–24. http://dx.doi.org/10.1016/j.amjmed.2009.12.021
206. Zapata LB, Oduyebo T, Whiteman MK, Marchbanks PA, Curtis KM.
Contraceptive use among women with multiple sclerosis: a systematic
review. Contraception. In press 2016.
207. Pagano HP, Zapata LB, Berry-Bibee EN, Nanda K, Curtis KM. Safety of
hormonal contraception and intrauterine devices among women with
depressive and bipolar disorders: a systematic review. Contraception 2016.
Epub June 27, 2016. http://dx.doi.org/10.1016/j.contraception.2016.06.012
208. Iyer V, Farquhar C, Jepson R. Oral contraceptive pills for heavy
menstrual bleeding. Cochrane Database Syst Rev 2000;(2):CD000154.
209. Davis L, Kennedy SS, Moore J, Prentice A. Oral contraceptives for
pain associated with endometriosis. Cochrane Database Syst Rev
2007;(3):CD001019.
210. Hendrix SL, Alexander NJ. Primary dysmenorrhea treatment with a
desogestrel-containing low-dose oral contraceptive. Contraception
2002;66:393–9. http://dx.doi.org/10.1016/S0010-7824(02)00414-6
211. Proctor ML, Roberts H, Farquhar CM. Combined oral contraceptive
pill (OCP) as treatment for primary dysmenorrhoea. Cochrane
Database Syst Rev 2001;(4):CD002120.
212. Gaffield ME, Kapp N, Curtis KM. Combined oral contraceptive and
intrauterine device use among women with gestational trophoblastic
disease. Contraception 2009;80:363–71. http://dx.doi.org/10.1016/j.
contraception.2009.03.022
213. Smith JS, Green J, Berrington de Gonzalez A, et al. Cervical cancer and
use of hormonal contraceptives: a systematic review. Lancet 2003;361:1159–
67. http://dx.doi.org/10.1016/S0140-6736(03)12949-2
214. Black MM, Barclay THC, Polednak A, Kwon CS, Leis HP Jr,
Pilnik S. Family history, oral contraceptive usage, and breast cancer.
Cancer 1983;51:2147–51. http://dx.doi.org/10.1002/10970142(19830601)51:11<2147::AID-CNCR2820511133≥3.0.CO;2-X
215. Brinton LA, Hoover R, Szklo M, Fraumeni JF Jr. Oral contraceptives
and breast cancer. Int J Epidemiol 1982;11:316–22. http://dx.doi.
org/10.1093/ije/11.4.316
216. Brohet RM, Goldgar DE, Easton DF, et al. Oral contraceptives and
breast cancer risk in the international BRCA1/2 carrier cohort study:
a report from EMBRACE, GENEPSO, GEO-HEBON, and the
IBCCS Collaborating Group. J Clin Oncol 2007;25:3831–6. http://
dx.doi.org/10.1200/JCO.2007.11.1179
217. Claus EB, Stowe M, Carter D. Oral contraceptives and the risk of
ductal breast carcinoma in situ. Breast Cancer Res Treat 2003;81:129–
36. http://dx.doi.org/10.1023/A:1025728524310
218. Collaborative Group on Hormonal Factors in Breast Cancer. Familial
breast cancer: collaborative reanalysis of individual data from 52
epidemiological studies including 58,209 women with breast cancer
and 101,986 women without the disease. Lancet 2001;358:1389–99.
http://dx.doi.org/10.1016/S0140-6736(01)06524-2
219. Grabrick DM, Hartmann LC, Cerhan JR, et al. Risk of breast cancer with oral
contraceptive use in women with a family history of breast cancer.[comment].
JAMA 2000;284:1791–8. http://dx.doi.org/10.1001/jama.284.14.1791
220. Gronwald J, Byrski T, Huzarski T, et al. Influence of selected lifestyle
factors on breast and ovarian cancer risk in BRCA1 mutation carriers
from Poland. Breast Cancer Res Treat 2006;95:105–9. http://dx.doi.
org/10.1007/s10549-005-9051-5

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Recommendations and Reports

221. Haile RW, Thomas DC, McGuire V, et al; kConFab Investigators;
Ontario Cancer Genetics Network Investigators. BRCA1 and BRCA2
mutation carriers, oral contraceptive use, and breast cancer before
age 50. Cancer Epidemiol Biomarkers Prev 2006;15:1863–70. http://
dx.doi.org/10.1158/1055-9965.EPI-06-0258
222. Harris NV, Weiss NS, Francis AM, Polissar L. Breast cancer in relation to
patterns of oral contraceptive use. Am J Epidemiol 1982;116:643–51.
223. Hennekens CH, Speizer FE, Lipnick RJ, et al. A case-control study of
oral contraceptive use and breast cancer. J Natl Cancer Inst
1984;72:39–42.
224. Jernström H, Loman N, Johannsson OT, Borg A, Olsson H. Impact of
teenage oral contraceptive use in a population-based series of early-onset
breast cancer cases who have undergone BRCA mutation testing. Eur J
Cancer 2005;41:2312–20. http://dx.doi.org/10.1016/j.ejca.2005.03.035
225. Marchbanks PA, McDonald JA, Wilson HG, et al. Oral contraceptives
and the risk of breast cancer. N Engl J Med 2002;346:2025–32. http://
dx.doi.org/10.1056/NEJMoa013202
226. Milne RL, Knight JA, John EM, et al. Oral contraceptive use and risk
of early-onset breast cancer in carriers and noncarriers of BRCA1 and
BRCA2 mutations. Cancer Epidemiol Biomarkers Prev 2005;14:350–6.
http://dx.doi.org/10.1158/1055-9965.EPI-04-0376
227. Narod SA, Dubé MP, Klijn J, et al. Oral contraceptives and the risk of
breast cancer in BRCA1 and BRCA2 mutation carriers. J Natl Cancer
Inst 2002;94:1773–9. http://dx.doi.org/10.1093/jnci/94.23.1773
228. Rosenberg L, Palmer JR, Rao RS, et al. Case-control study of oral
contraceptive use and risk of breast cancer. Am J Epidemiol 1996;143:25–
37. http://dx.doi.org/10.1093/oxfordjournals.aje.a008654
229. Silvera SA, Miller AB, Rohan TE. Oral contraceptive use and risk of
breast cancer among women with a family history of breast cancer: a
prospective cohort study. Cancer Causes Control 2005;16:1059–63.
http://dx.doi.org/10.1007/s10552-005-0343-1
230. Ursin G, Henderson BE, Haile RW, et al. Does oral contraceptive use
increase the risk of breast cancer in women with BRCA1/BRCA2
mutations more than in other women? Cancer Res 1997;57:3678–81.
231. Ursin G, Ross RK, Sullivan-Halley J, Hanisch R, Henderson B,
Bernstein L. Use of oral contraceptives and risk of breast cancer in
young women. Breast Cancer Res Treat 1998;50:175–84. http://dx.doi.
org/10.1023/A:1006037823178
232. Polis CB, Phillips SJ, Curtis KM, et al. Hormonal contraceptive
methods and risk of HIV acquisition in women: a systematic review
of epidemiological evidence. Contraception 2014;90:360–90. http://
dx.doi.org/10.1016/j.contraception.2014.07.009
233. Polis CB, Phillips SJ, Curtis KM. Hormonal contraceptive use and
female-to-male HIV transmission: a systematic review of the
epidemiologic evidence. AIDS 2013;27:493–505. http://dx.doi.
org/10.1097/QAD.0b013e32835ad539
234. Phillips SJ, Polis CB, Curtis KM. The safety of hormonal contraceptives
for women living with HIV and their sexual partners. Contraception
2016;93:11–6 http://dx.doi.org/10.1016/j.contraception.2015.10.002.
235. Phillips SJ, Curtis KM, Polis CB. Effect of hormonal contraceptive
methods on HIV disease progression: a systematic review. AIDS
2013;27:787–94. http://dx.doi.org/10.1097/QAD.0b013e32835bb672
236. el-Raghy I, Back DJ, Osman F, Orme ML, Fathalla M. Contraceptive
steroid concentrations in women with early active schistosomiasis: lack
of effect of antischistosomal drugs. Contraception 1986;33:373–7.
http://dx.doi.org/10.1016/0010-7824(86)90099-5
237. Gad-el-Mawla N, Abdallah A. Liver function in bilharzial females
receiving contraceptive pills. Acta Hepatosplenol 1969;16:308–10.

MMWR / July 29, 2016 / Vol. 65 / No. 3

238. Gad-el-Mawla N, el-Roubi O, Sabet S, Abdallah A. Plasma lipids and
lipoproteins in bilharzial females during oral contraceptive therapy. J Egypt
Med Assoc 1972;55:137–47.
239. Shaaban MM, Hammad WA, Falthalla MF, et al. Effects of oral
contraception on liver function tests and serum proteins in women
with active schistosomiasis. Contraception 1982;26:75–82. http://
dx.doi.org/10.1016/0010-7824(82)90174-3
240. Shaaban MM, Ghaneimah SA, Mohamed MA, Abdel-Chani S, Mostafa
SA. Effect of oral contraception on serum bile acid. Int J Gynaecol Obstet
1984;22:111–5. http://dx.doi.org/10.1016/0020-7292(84)90023-7
241. Sy FS, Osteria TS, Opiniano V, Gler S. Effect of oral contraceptive on liver
function tests of women with schistosomiasis in the Philippines. Contraception
1986;34:283–94. http://dx.doi.org/10.1016/0010-7824(86)90009-0
242. Tagy AH, Saker ME, Moussa AA, Kolgah A. The effect of low-dose
combined oral contraceptive pills versus injectable contraceptive (Depot
Provera) on liver function tests of women with compensated bilharzial
liver fibrosis. Contraception 2001;64:173–6. http://dx.doi.org/10.1016/
S0010-7824(01)00248-7
243. Beck P, Wells SA. Comparison of the mechanisms underlying
carbohydrate intolerance in subclinical diabetic women during
pregnancy and during post-partum oral contraceptive steroid treatment.
J Clin Endocrinol Metab 1969;29:807–18. http://dx.doi.org/10.1210/
jcem-29-6-807
244. Kjos SL, Peters RK, Xiang A, Thomas D, Schaefer U, Buchanan TA.
Contraception and the risk of type 2 diabetes mellitus in Latina women
with prior gestational diabetes mellitus. JAMA 1998;280:533–8. http://
dx.doi.org/10.1001/jama.280.6.533
245. Kung AW, Ma JT, Wong VC, et al. Glucose and lipid metabolism with triphasic
oral contraceptives in women with history of gestational diabetes. Contraception
1987;35:257–69. http://dx.doi.org/10.1016/0010-7824(87)90027-8
246. Rådberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies in
gestational diabetic women during contraceptive treatment: effects on
glucose tolerance and fatty acid composition of serum lipids. Gynecol
Obstet Invest 1982;13:17–29. http://dx.doi.org/10.1159/000299480
247. Skouby SO, Andersen O, Kühl C. Oral contraceptives and insulin
receptor binding in normal women and those with previous gestational
diabetes. Am J Obstet Gynecol 1986;155:802–7. http://dx.doi.
org/10.1016/S0002-9378(86)80024-2
248. Skouby SO, Andersen O, Saurbrey N, Kühl C. Oral contraception and
insulin sensitivity: in vivo assessment in normal women and women
with previous gestational diabetes. J Clin Endocrinol Metab
1987;64:519–23. http://dx.doi.org/10.1210/jcem-64-3-519
249. Skouby SO, Mølsted-Pedersen L, Kühl C. Low dosage oral
contraception in women with previous gestational diabetes. Obstet
Gynecol 1982;59:325–8.
250. Xiang AH, Kawakubo M, Kjos SL, Buchanan TA. Long-acting injectable
progestin contraception and risk of type 2 diabetes in Latino women
with prior gestational diabetes mellitus. Diabetes Care 2006;29:613–7.
http://dx.doi.org/10.2337/diacare.29.03.06.dc05-1940
251. Kjos SL, Shoupe D, Douyan S, et al. Effect of low-dose oral contraceptives on
carbohydrate and lipid metabolism in women with recent gestational diabetes:
results of a controlled, randomized, prospective study. Am J Obstet Gynecol
1990;163:1822–7. http://dx.doi.org/10.1016/0002-9378(90)90757-X
252. Rådberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies in
women with previous gestational diabetes during contraceptive
treatment: effects on serum lipids and high density lipoproteins. Acta
Endocrinol (Copenh) 1982;101:134–9.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

253. Skouby SO, Kühl C, Mølsted-Pedersen L, Petersen K, Christensen MS.
Triphasic oral contraception: metabolic effects in normal women and those
with previous gestational diabetes. Am J Obstet Gynecol 1985;153:495–
500. http://dx.doi.org/10.1016/0002-9378(85)90460-0
254. Beck P, Arnett DM, Alsever RN, Eaton RP. Effect of contraceptive steroids on
arginine- stimulated glucagon and insulin secretion in women. II. Carbohydrate
and lipid physiology in insulin-dependent diabetics. Metabolism 1976;25:23–
31 http://dx.doi.org/10.1016/0026-0495(76)90156-6.
255. Diab KM, Zaki MM. Contraception in diabetic women: comparative
metabolic study of Norplant, depot medroxyprogesterone acetate, low dose
oral contraceptive pill and CuT380A. J Obstet Gynaecol Res 2000;26:17–
26. http://dx.doi.org/10.1111/j.1447-0756.2000.tb01195.x
256. Garg SK, Chase HP, Marshall G, Hoops SL, Holmes DL, Jackson WE.
Oral contraceptives and renal and retinal complications in young women
with insulin-dependent diabetes mellitus. JAMA 1994;271:1099–102.
http://dx.doi.org/10.1001/jama.1994.03510380055037
257. Grigoryan OR, Grodnitskaya EE, Andreeva EN, Shestakova MV,
Melnichenko GA, Dedov II. Contraception in perimenopausal women
with diabetes mellitus. Gynecol Endocrinol 2006;22:198–206. http://
dx.doi.org/10.1080/09513590600624317
258. Margolis KL, Adami H-O, Luo J, Ye W, Weiderpass E. A prospective study of
oral contraceptive use and risk of myocardial infarction among Swedish women.
Fertil Steril 2007;88:310–6. http://dx.doi.org/10.1016/j.fertnstert.2006.11.206
259. Petersen KR, Skouby SO, Jespersen J. Balance of coagulation activity
with fibrinolysis during use of oral contraceptives in women with
insulin-dependent diabetes mellitus. Int J Fertil Menopausal Stud
1995;40(Suppl 2):105–11.
260. Petersen KR, Skouby SO, Sidelmann J, Jespersen J. Assessment of
endothelial function during oral contraception in women with insulindependent diabetes mellitus. Metabolism 1994;43:1379–83. http://
dx.doi.org/10.1016/0026-0495(94)90031-0
261. Rådberg T, Gustafson A, Skryten A, Karlsson K. Oral contraception in
diabetic women. A cross-over study on serum and high density lipoprotein
(HDL) lipids and diabetes control during progestogen and combined
estrogen/progestogen contraception. Horm Metab Res 1982;14:61–5.
262. Skouby SO, Jensen BM, Kühl C, Mølsted-Pedersen L, Svenstrup B,
Nielsen J. Hormonal contraception in diabetic women: acceptability
and influence on diabetes control and ovarian function of a nonalkylated
estrogen/progestogen compound. Contraception 1985;32:23–31.
http://dx.doi.org/10.1016/0010-7824(85)90113-1
263. Skouby SO, Mølsted-Pedersen L, Kühl C, Bennet P. Oral contraceptives
in diabetic women: metabolic effects of four compounds with different
estrogen/progestogen profiles. Fertil Steril 1986;46:858–64 http://
dx.doi.org/10.1016/S0015-0282(16)49825-0.
264. Zapata LB, Paulen ME, Cansino C, Marchbanks PA, Curtis KM.
Contraceptive use among women with inflammatory bowel disease: A
systematic review. Contraception 2010;82:72–85. http://dx.doi.
org/10.1016/j.contraception.2010.02.012
265. Kapp N, Tilley IB, Curtis KM. The effects of hormonal contraceptive
use among women with viral hepatitis or cirrhosis of the liver: a
systematic review. Contraception 2009;80:381–6. http://dx.doi.
org/10.1016/j.contraception.2009.04.007
266. Kapp N, Curtis KM. Hormonal contraceptive use among women with
liver tumors: a systematic review. Contraception 2009;80:387–90.
http://dx.doi.org/10.1016/j.contraception.2009.01.021
267. Whiteman MK, Oduyebo T, Zapata LB, Walker S, Curtis KM.
Contraceptive safety among women with cystic fibrosis: a systematic review.
Contraception 2016. Epub June 7, 2016. http://dx.doi.org/10.1016/j.
contraception.2016.05.016

268. Paulen ME, Folger SG, Curtis KM, Jamieson DJ. Contraceptive use among
solid organ transplant patients: a systematic review. Contraception
2010;82:102–12. http://dx.doi.org/10.1016/j.contraception.2010.02.007
269. Aweeka FT, Rosenkranz SL, Segal Y, et al; NIAID AIDS Clinical Trials
Group. The impact of sex and contraceptive therapy on the plasma
and intracellular pharmacokinetics of zidovudine. AIDS 2006;20:1833–
41. http://dx.doi.org/10.1097/01.aids.0000244202.18629.36
270. Kearney BP, Mathias A. Lack of effect of tenofovir disoproxil fumarate
on pharmacokinetics of hormonal contraceptives. Pharmacotherapy
2009;29:924–9. http://dx.doi.org/10.1592/phco.29.8.924
271. Todd CS, Deese J, Wang M, et al; FEM-PrEP Study Group. Sino-implant
(II)® continuation and effect of concomitant tenofovir disoproxil
fumarate-emtricitabine use on plasma levonorgestrel concentrations
among women in Bondo, Kenya. Contraception 2015;91:248–52.
http://dx.doi.org/10.1016/j.contraception.2014.10.008
272. Murnane PM, Heffron R, Ronald A, et al; Partners PrEP Study Team.
Pre-exposure prophylaxis for HIV-1 prevention does not diminish the
pregnancy prevention effectiveness of hormonal contraception. AIDS
2014;28:1825–30. http://dx.doi.org/10.1097/QAD.0000000000000290
273. Kasonde M, Niska RW, Rose C, et al. Bone mineral density changes
among HIV-uninfected young adults in a randomised trial of preexposure prophylaxis with tenofovir-emtricitabine or placebo in
Botswana. PLoS One 2014;9:e90111. http://dx.doi.org/10.1371/
journal.pone.0090111
274. Callahan R, Nanda K, Kapiga S, et al; FEM-PrEP Study Group.
Pregnancy and contraceptive use among women participating in the
FEM-PrEP trial. J Acquir Immune Defic Syndr 2015;68:196–203.
http://dx.doi.org/10.1097/QAI.0000000000000413
275. Patel RC, Onono M, Gandhi M, et al. Pregnancy rates in HIV-positive
women using contraceptives and efavirenz-based or nevirapine-based
antiretroviral therapy in Kenya: a retrospective cohort study. Lancet HIV
2015;2:e474–82. http://dx.doi.org/10.1016/S2352-3018(15)00184-8
276. Pyra M, Heffron R, Mugo NR, et al; Partners in Prevention HSV/HIV
Transmission Study and Partners PrEP Study Teams. Effectiveness of hormonal
contraception in HIV-infected women using antiretroviral therapy. AIDS
2015;29:2353–9. http://dx.doi.org/10.1097/QAD.0000000000000827
277. Clark RA, Theall K. Population-based study evaluating association
between selected antiretroviral therapies and potential oral contraceptive
failure. J Acquir Immune Defic Syndr 2004;37:1219–20. http://dx.doi.
org/10.1097/01.qai.0000136724.15758.ae
278. Landolt NK, Phanuphak N, Ubolyam S, et al. Efavirenz, in contrast
to nevirapine, is associated with unfavorable progesterone and
antiretroviral levels when coadministered with combined oral
contraceptives. J Acquir Immune Defic Syndr 2013;62:534–9. http://
dx.doi.org/10.1097/QAI.0b013e31827e8f98
279. Sevinsky H, Eley T, Persson A, et al. The effect of efavirenz on the
pharmacokinetics of an oral contraceptive containing ethinyl estradiol
and norgestimate in healthy HIV-negative women. Antivir Ther
2011;16:149–56. http://dx.doi.org/10.3851/IMP1725
280. Landolt NK, Phanuphak N, Ubolyam S, et al. Significant decrease of
ethinylestradiol with nevirapine, and of etonogestrel with efavirenz in
HIV-positive women. J Acquir Immune Defic Syndr 2014;66:e50–2.
281. Schöller-Gyüre M, Kakuda TN, Woodfall B, et al. Effect of steady-state
etravirine on the pharmacokinetics and pharmacodynamics of
ethinylestradiol and norethindrone. Contraception 2009;80:44–52.
http://dx.doi.org/10.1016/j.contraception.2009.01.009

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Recommendations and Reports

282. Myer L, Carter RJ, Katyal M, Toro P, El-Sadr WM, Abrams EJ. Impact
of antiretroviral therapy on incidence of pregnancy among HIV-infected
women in Sub-Saharan Africa: a cohort study. PLoS Med 2010;7:e1000229.
http://dx.doi.org/10.1371/journal.pmed.1000229
283. Nanda K, Delany-Moretlwe S, Dubé K, et al. Nevirapine-based
antiretroviral therapy does not reduce oral contraceptive effectiveness.
AIDS 2013;27(Suppl 1):S17–25. http://dx.doi.org/10.1097/
QAD.0000000000000050
284. Stuart GS, Moses A, Corbett A, et al. Combined oral contraceptives and
antiretroviral PK/PD in Malawian women: pharmacokinetics and
pharmacodynamics of a combined oral contraceptive and a generic
combined formulation antiretroviral in Malawi. J Acquir Immune Defic
Syndr 2011;58:e40–3. http://dx.doi.org/10.1097/QAI.0b013e31822b8bf8
285. Mildvan D, Yarrish R, Marshak A, et al. Pharmacokinetic interaction between
nevirapine and ethinyl estradiol/norethindrone when administered concurrently
to HIV-infected women. J Acquir Immune Defic Syndr 2002;29:471–7.
http://dx.doi.org/10.1097/00042560-200204150-00007
286. Muro E, Droste JA, Hofstede HT, Bosch M, Dolmans W, Burger DM.
Nevirapine plasma concentrations are still detectable after more than 2 weeks
in the majority of women receiving single-dose nevirapine: implications for
intervention studies. J Acquir Immune Defic Syndr 2005;39:419–2. http://
dx.doi.org/10.1097/01.qai.0000167154.37357.f9
287. Crauwels HM, van Heeswijk RP, Buelens A, Stevens M, Hoetelmans RM.
Lack of an effect of rilpivirine on the pharmacokinetics of ethinylestradiol
and norethindrone in healthy volunteers. Int J Clin Pharmacol Ther
2014;52:118–28. http://dx.doi.org/10.5414/CP201943
288. Zhang J, Chung E, Yones C, et al. The effect of atazanavir/ritonavir
on the pharmacokinetics of an oral contraceptive containing ethinyl
estradiol and norgestimate in healthy women. Antivir Ther
2011;16:157–64. http://dx.doi.org/10.3851/IMP1724
289. Sekar VJ, Lefebvre E, Guzman SS, et al. Pharmacokinetic interaction
between ethinyl estradiol, norethindrone and darunavir with low-dose
ritonavir in healthy women. Antivir Ther 2008;13:563–9.
290. Glaxo Smith Kline. Lexiva (fosamprenavir calcium) [Package insert].
Research Triangle Park, NC: Glaxo Smith Kline; 2015.
291. Vogler MA, Patterson K, Kamemoto L, et al. Contraceptive efficacy of
oral and transdermal hormones when co-administered with protease
inhibitors in HIV-1-infected women: pharmacokinetic results of ACTG
trial A5188. J Acquir Immune Defic Syndr 2010;55:473–82. http://
dx.doi.org/10.1097/QAI.0b013e3181eb5ff5
292. Fröhlich M, Burhenne J, Martin-Facklam M, et al. Oral
contraception does not alter single dose saquinavir pharmacokinetics
in women. Br J Clin Pharmacol 2004;57:244–52 http://dx.doi.
org/10.1111/j.1365-2125.2003.01983.x.
293. Boehringer Ingelheim Pharmaceuticals. Aptivus (tipranavir) [Package
insert]. Ridgefield, CT; 2005.
294. Bristol-Myers Squibb. Reyataz (atazanavir sulfate) [Package insert].
Princeton, NJ; 2003.
295. Abel S, Russell D, Whitlock LA, Ridgway CE, Muirhead GJ. Effect of
maraviroc on the pharmacokinetics of midazolam, lamivudine/
zidovudine, and ethinyloestradiol/levonorgestrel in healthy volunteers.
Br J Clin Pharmacol 2008;65(Suppl 1):19–26. http://dx.doi.
org/10.1111/j.1365-2125.2008.03132.x
296. Anderson MS, Hanley WD, Moreau AR, et al. Effect of raltegravir on
estradiol and norgestimate plasma pharmacokinetics following oral
contraceptive administration in healthy women. Br J Clin Pharmacol
2011;71:616–20. http://dx.doi.org/10.1111/j.1365-2125.2010.03885.x

MMWR / July 29, 2016 / Vol. 65 / No. 3

297. Song IH, Borland J, Chen S, Wajima T, Peppercorn AF, Piscitelli SC.
Dolutegravir has no effect on the pharmacokinetics of oral contraceptives
with norgestimate and ethinyl estradiol. Ann Pharmacother 2015;49:784–
9. http://dx.doi.org/10.1177/1060028015580637
298. Gilead Sciences. Vitekta (elvitegravir) [Package insert]. Foster City, CA; 2012.
299. Back DJ, Bates M, Bowden A, et al. The interaction of phenobarbital and
other anticonvulsants with oral contraceptive steroid therapy. Contraception
1980;22:495–503. http://dx.doi.org/10.1016/0010-7824(80)90102-X
300. Doose DR, Wang SS, Padmanabhan M, Schwabe S, Jacobs D, Bialer
M. Effect of topiramate or carbamazepine on the pharmacokinetics of
an oral contraceptive containing norethindrone and ethinyl estradiol
in healthy obese and nonobese female subjects. Epilepsia 2003;44:540–
9. http://dx.doi.org/10.1046/j.1528-1157.2003.55602.x
301. Fattore C, Cipolla G, Gatti G, et al. Induction of ethinylestradiol and
levonorgestrel metabolism by oxcarbazepine in healthy women. Epilepsia
1999;40:783–7. http://dx.doi.org/10.1111/j.1528-1157.1999.tb00779.x
302. Rosenfeld WE, Doose DR, Walker SA, Nayak RK. Effect of topiramate
on the pharmacokinetics of an oral contraceptive containing norethindrone
and ethinyl estradiol in patients with epilepsy. Epilepsia 1997;38:317–23.
http://dx.doi.org/10.1111/j.1528-1157.1997.tb01123.x
303. Christensen J, Petrenaite V, Atterman J, et al. Oral contraceptives
induce lamotrigine metabolism: evidence from a double-blind,
placebo-controlled trial. Epilepsia 2007;48:484–9. http://dx.doi.
org/10.1111/j.1528-1167.2007.00997.x
304. Contin M, Albani F, Ambrosetto G, et al. Variation in lamotrigine
plasma concentrations with hormonal contraceptive monthly cycles in
patients with epilepsy. Epilepsia 2006;47:1573–5. http://dx.doi.
org/10.1111/j.1528-1167.2006.00558.x
305. Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens,
reduces lamotrigine serum concentrations. Epilepsia 2005;46:1414–7.
http://dx.doi.org/10.1111/j.1528-1167.2005.10105.x
306. Sabers A, Buchholt JM, Uldall P, Hansen EL. Lamotrigine plasma levels
reduced by oral contraceptives. Epilepsy Res 2001;47:151–4. http://
dx.doi.org/10.1016/S0920-1211(01)00305-9
307. Sabers A, Ohman I, Christensen J, Tomson T. Oral contraceptives
reduce lamotrigine plasma levels. Neurology 2003;61:570–1. http://
dx.doi.org/10.1212/01.WNL.0000076485.09353.7A
308. Back DJ, Breckenridge AM, MacIver M, et al. The effects of ampicillin
on oral contraceptive steroids in women. Br J Clin Pharmacol
1982;14:43–8. http://dx.doi.org/10.1111/j.1365-2125.1982.tb04932.x
309. Back DJ, Grimmer SF, Orme ML, Proudlove C, Mann RD,
Breckenridge AM. Evaluation of Committee on Safety of Medicines
yellow card reports on oral contraceptive-drug interactions with
anticonvulsants and antibiotics. Br J Clin Pharmacol 1988;25:527–32.
http://dx.doi.org/10.1111/j.1365-2125.1988.tb03341.x
310. Back DJ, Tjia J, Martin C, et al. The lack of interaction between
temafloxacin and combined oral contraceptive steroids. Contraception
1991;43:317–23. http://dx.doi.org/10.1016/0010-7824(91)90070-V
311. Bacon JF, Shenfield GM. Pregnancy attributable to interaction between
tetracycline and oral contraceptives. BMJ 1980;280:293. http://dx.doi.
org/10.1136/bmj.280.6210.293
312. Bainton R. Interaction between antibiotic therapy and contraceptive
medication. Oral Surg Oral Med Oral Pathol 1986;61:453–5. http://
dx.doi.org/10.1016/0030-4220(86)90385-3
313. Bollen M. Use of antibiotics when taking the oral contraceptive pill.
[comment]. Aust Fam Physician 1995;24:928–9.
314. Bromham DR, Cartmill RS. Knowledge and use of secondary
contraception among patients requesting termination of pregnancy.
BMJ 1993;306:556–7. http://dx.doi.org/10.1136/bmj.306.6877.556

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Recommendations and Reports

315. Côté J. Interaction of griseofulvin and oral contraceptives.[comment].
J Am Acad Dermatol 1990;22:124–5. http://dx.doi.org/10.1016/
S0190-9622(08)80010-2
316. Csemiczky G, Alvendal C, Landgren BM. Risk for ovulation in women
taking a low-dose oral contraceptive (Microgynon) when receiving
antibacterial treatment with a fluoroquinolone (ofloxacin). Adv
Contracept 1996;12:101–9. http://dx.doi.org/10.1007/BF01849631
317. de Groot AC, Eshuis H, Stricker BH. Inefficacy of oral contraception
during use of minocycline [Dutch]. Ned Tijdschr Geneeskd
1990;134:1227–9.
318. DeSano EA Jr, Hurley SC. Possible interactions of antihistamines and
antibiotics with oral contraceptive effectiveness. Fertil Steril
1982;37:853–4 http://dx.doi.org/10.1016/S0015-0282(16)46350-8.
319. Donley TG, Smith RF, Roy B. Reduced oral contraceptive effectiveness
with concurrent antibiotic use: a protocol for prescribing antibiotics
to women of childbearing age. Compendium 1990;11:392–6.
320. Friedman CI, Huneke AL, Kim MH, Powell J. The effect of ampicillin
on oral contraceptive effectiveness. Obstet Gynecol 1980;55:33–7.
321. Grimmer SF, Allen WL, Back DJ, Breckenridge AM, Orme M, Tjia J. The
effect of cotrimoxazole on oral contraceptive steroids in women. Contraception
1983;28:53–9. http://dx.doi.org/10.1016/S0010-7824(83)80005-5
322. Helms SE, Bredle DL, Zajic J, Jatjoura D, Brodell RT, Krishnarao I.
Oral contraceptive failure rates and oral antibiotics. J Am Acad Dermatol
1997;36:705–10. http://dx.doi.org/10.1016/S0190-9622(97)80322-2
323. Hempel E, Böhm W, Carol W, Klinger G. [Enzyme induction by drugs
and hormonal contraception]. Zentralbl Gynakol 1973;95:1451–7.
324. Hempel E, Zorn C, Graf K. [Effect of chemotherapy agents and
antibiotics on hormonal contraception]. Z Arztl Fortbild (Jena)
1978;72:924–6.
325. Hetényi G. Possible interactions between antibiotics and oral
contraceptives. Ther Hung 1989;37:86–9.
326. Hughes BR, Cunliffe WJ. Interactions between the oral contraceptive
pill and antibiotics.[comment]. Br J Dermatol 1990;122:717–8. http://
dx.doi.org/10.1111/j.1365-2133.1990.tb07299.x
327. Joshi JV, Joshi UM, Sankholi GM, et al. A study of interaction
of low-dose combination oral contraceptive with Ampicillin and
Metronidazole. Contraception 1980;22:643–52. http://dx.doi.
org/10.1016/0010-7824(80)90089-X
328. Kakouris H, Kovacs GT. Pill failure and nonuse of secondary
precautions. Br J Fam Plann 1992;18:41–4.
329. Kakouris H, Kovacs GT. How common are predisposing factors to pill
failure among pill users? Br J Fam Plann 1994;20:33–5.
330. Kovacs GT, Riddoch G, Duncombe P, et al. Inadvertent pregnancies
in oral contraceptive users. Med J Aust 1989;150:549–51.
331. Lequeux A. [Pregnancy under oral contraceptives after treatment with
tetracycline]. Louv Med 1980;99:413–4.
332. London BM, Lookingbill DP. Frequency of pregnancy in acne patients taking
oral antibiotics and oral contraceptives. Arch Dermatol 1994;130:392–3.
http://dx.doi.org/10.1001/archderm.1994.01690030128027
333. Maggiolo F, Puricelli G, Dottorini M, Caprioli S, Bianchi W, Suter F.
The effect of ciprofloxacin on oral contraceptive steroid treatments.
Drugs Exp Clin Res 1991;17:451–4.
334. Murphy AA, Zacur HA, Charache P, Burkman RT. The effect of
tetracycline on levels of oral contraceptives. Am J Obstet Gynecol
1991;164:28–33. http://dx.doi.org/10.1016/0002-9378(91)90617-Z
335. Neely JL, Abate M, Swinker M, D’Angio R. The effect of doxycycline
on serum levels of ethinyl estradiol, norethindrone, and endogenous
progesterone. Obstet Gynecol 1991;77:416–20.

336. Pillans PI, Sparrow MJ. Pregnancy associated with a combined oral
contraceptive and itraconazole.[comment]. N Z Med J 1993;106:436.
337. Scholten PC, Droppert RM, Zwinkels MG, Moesker HL, Nauta JJ,
Hoepelman IM. No interaction between ciprofloxacin and an oral
contraceptive. Antimicrob Agents Chemother 1998;42:3266–8.
338. Silber TJ. Apparent oral contraceptive failure associated with antibiotic
administration. J Adolesc Health Care 1983;4:287–9. http://dx.doi.
org/10.1016/S0197-0070(83)80014-X
339. Sparrow MJ. Pill method failures. N Z Med J 1987;100:102–5.
340. Sparrow MJ. Pregnancies in reliable pill takers. N Z Med J
1989;102:575–7.
341. Sparrow MJ. Pill method failures in women seeking abortion: fourteen
years experience. N Z Med J 1998;111:386–8.
342. van Dijke CP, Weber JC. Interaction between oral contraceptives and
griseofulvin. Br Med J (Clin Res Ed) 1984;288:1125–6. http://dx.doi.
org/10.1136/bmj.288.6424.1125-a
343. Wermeling DP, Chandler MH, Sides GD, Collins D, Muse KN.
Dirithromycin increases ethinyl estradiol clearance without allowing
ovulation. Obstet Gynecol 1995;86:78–84. http://dx.doi.
org/10.1016/0029-7844(95)00075-3
344. Young LK, Farquhar CM, McCowan LM, Roberts HE, Taylor J. The
contraceptive practices of women seeking termination of pregnancy in
an Auckland clinic. N Z Med J 1994;107:189–92.
345. Abrams LS, Skee D, Natarajan J, Wong FA. Pharmacokinetic overview
of Ortho Evra/Evra. Fertil Steril 2002;77(Suppl 2):S3–12. http://
dx.doi.org/10.1016/S0015-0282(01)03261-7
346. Dogterom P, van den Heuvel MW, Thomsen T. Absence of
pharmacokinetic interactions of the combined contraceptive vaginal
ring NuvaRing with oral amoxicillin or doxycycline in two randomised
trials. Clin Pharmacokinet 2005;44:429–38. http://dx.doi.
org/10.2165/00003088-200544040-00007
347. Devenport MH, Crook D, Wynn V, Lees LJ. Metabolic effects of lowdose fluconazole in healthy female users and non-users of oral
contraceptives. Br J Clin Pharmacol 1989;27:851–9. http://dx.doi.
org/10.1111/j.1365-2125.1989.tb03449.x
348. Hilbert J, Messig M, Kuye O, Friedman H. Evaluation of interaction
between fluconazole and an oral contraceptive in healthy women.
Obstet Gynecol 2001;98:218–23.
349. Kovács I, Somos P, Hámori M. Examination of the potential interaction
between ketoconazole (Nizoral) and oral contraceptives with special
regard to products of low hormone content (Rigevidon, anteovin).
Ther Hung 1986;34:167–70.
350. Lunell NO, Pschera H, Zador G, Carlström K. Evaluation of the
possible interaction of the antifungal triazole SCH 39304 with oral
contraceptives in normal healthy women. Gynecol Obstet Invest
1991;32:91–7. http://dx.doi.org/10.1159/000293003
351. McDaniel PA, Caldroney RD. Oral contraceptives and griseofulvin
interactions. Drug Intell Clin Pharm 1986;20:384.
352. Meyboom RH, van Puijenbroek EP, Vinks MH, Lastdrager CJ.
Disturbance of withdrawal bleeding during concomitant use of
itraconazole and oral contraceptives. N Z Med J 1997;110:300.
353. Rieth H, Sauerbrey N. [Interaction studies with fluconazole, a new
triazole antifungal drug]. Wien Med Wochenschr 1989;139:370–4.
354. Sinofsky FE, Pasquale SA. The effect of fluconazole on circulating
ethinyl estradiol levels in women taking oral contraceptives. Am J
Obstet Gynecol 1998;178:300–4. http://dx.doi.org/10.1016/
S0002-9378(98)80016-1

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Recommendations and Reports

355. van Puijenbroek EP, Feenstra J, Meyboom RH. [Pill cycle disturbance
in simultaneous use of itraconazole and oral contraceptives]. Ned
Tijdschr Geneeskd 1998;142:146–9.
356. Van Puijenbroek EP, Egberts AC, Meyboom RH, Leufkens HG.
Signalling possible drug-drug interactions in a spontaneous reporting
system: delay of withdrawal bleeding during concomitant use of oral
contraceptives and itraconazole. Br J Clin Pharmacol 1999;47:689–93.
http://dx.doi.org/10.1046/j.1365-2125.1999.00957.x
357. Verhoeven CH, van den Heuvel MW, Mulders TM, Dieben TO. The
contraceptive vaginal ring, NuvaRing, and antimycotic co-medication.
Contraception 2004;69:129–32. http://dx.doi.org/10.1016/j.
contraception.2003.10.001
358. Back DJ, Breckenridge AM, Grimmer SF, Orme ML, Purba HS.
Pharmacokinetics of oral contraceptive steroids following the administration
of the antimalarial drugs primaquine and chloroquine. Contraception
1984;30:289–95. http://dx.doi.org/10.1016/0010-7824(84)90092-1
359. Croft AM, Herxheimer A. Adverse effects of the antimalaria drug, mefloquine:
due to primary liver damage with secondary thyroid involvement? BMC Public
Health 2002;2:6. http://dx.doi.org/10.1186/1471-2458-2-6
360. Karbwang J, Looareesuwan S, Back DJ, Migasana S, Bunnag D,
Breckenridge AM. Effect of oral contraceptive steroids on the clinical
course of malaria infection and on the pharmacokinetics of mefloquine
in Thai women. Bull World Health Organ 1988;66:763–7.
361. McGready R, Stepniewska K, Seaton E, et al. Pregnancy and use of
oral contraceptives reduces the biotransformation of proguanil to
cycloguanil. Eur J Clin Pharmacol 2003;59:553–7. http://dx.doi.
org/10.1007/s00228-003-0651-x
362. Wanwimolruk S, Kaewvichit S, Tanthayaphinant O, Suwannarach C,
Oranratnachai A. Lack of effect of oral contraceptive use on the
pharmacokinetics of quinine. Br J Clin Pharmacol 1991;31:179–81.
http://dx.doi.org/10.1111/j.1365-2125.1991.tb05509.x
363. Back DJ, Breckenridge AM, Crawford F, et al. The effect of rifampicin
on norethisterone pharmacokinetics. Eur J Clin Pharmacol
1979;15:193–7. http://dx.doi.org/10.1007/BF00563105
364. Back DJ, Breckenridge AM, Crawford FE, et al. The effect of rifampicin
on the pharmacokinetics of ethynylestradiol in women. Contraception
1980;21:135–43. http://dx.doi.org/10.1016/0010-7824(80)90125-0
365. Barditch-Crovo P, Trapnell CB, Ette E, et al. The effects of rifampin
and rifabutin on the pharmacokinetics and pharmacodynamics of a
combination oral contraceptive. Clin Pharmacol Ther 1999;65:428–38.
http://dx.doi.org/10.1016/S0009-9236(99)70138-4

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366. Bolt HM, Bolt M, Kappus H. Interaction of rifampicin treatment with
pharmacokinetics and metabolism of ethinyloestradiol in man. Acta
Endocrinol (Copenh) 1977;85:189–97.
367. Gupta KC, Ali MY. Failure of oral contraceptive with rifampicin. Med
J Zambia 1980;15:23.
368. Hirsch A. [Letter: Sleeping pills]. Nouv Presse Med 1973;2:2957.
369. Hirsch A, Tillement JP, Chretien J. Effets contrariants de la rifampicine
sur les contraceptifs oraux: a propos de trois grossesses non desiree chez
trois malades. Rev Fr Mal Respir 1975;2:174–82.
370. Joshi JV, Joshi UM, Sankolli GM, et al. A study of interaction of a low-dose
combination oral contraceptive with anti-tubercular drugs. Contraception
1980;21:617–29. http://dx.doi.org/10.1016/0010-7824(80)90034-7
371. Kropp R. [Rifampicin and oral contraceptives (author’s transl)]. Prax
Pneumol 1974;28:270–2.
372. LeBel M, Masson E, Guilbert E, et al. Effects of rifabutin and rifampicin on
the pharmacokinetics of ethinylestradiol and norethindrone. J Clin Pharmacol
1998;38:1042–50. http://dx.doi.org/10.1177/009127009803801109
373. Meyer B, Müller F, Wessels P, Maree J. A model to detect interactions
between roxithromycin and oral contraceptives. Clin Pharmacol Ther
1990;47:671–4. http://dx.doi.org/10.1038/clpt.1990.92
374. Nocke-Finck L, Breuer H, Reimers D. Dtsch Med Wochenschr
1973;98:1521–3. http://dx.doi.org/10.1055/s-0028-1107071
375. Piguet B, Muglioni JF, Chaline G. [Letter: Oral contraception and
rifampicin]. Nouv Presse Med 1975;04:115–6.
376. Reimers D, Jezek A. [The simultaneous use of rifampicin and other
antitubercular agents with oral contraceptives]. Prax Pneumol
1971;25:255–62.
377. Skolnick JL, Stoler BS, Katz DB, Anderson WH. Rifampin, oral
contraceptives, and pregnancy. JAMA 1976;236:1382. http://dx.doi.
org/10.1001/jama.1976.03270130044027
378. Szoka PR, Edgren RA. Drug interactions with oral contraceptives:
compilation and analysis of an adverse experience report database. Fertil
Steril 1988;49(Suppl 2):31S–8S.
379. Berry-Bibee E, Kim MJ, Simmons K, Pagano P, Curtis K. Drug
interactions between hormonal contraceptives and psychotropic drugs:
a systematic review. Contraception. In press 2016.
380. Berry-Bibee E, Kim MJ, Tepper N, Riley H, Curtis K. The safety of
St John’s wort and hormonal contraceptives: a systematic review.
Contraception. In press 2016.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix E
Classifications for Barrier Methods
Classifications for barrier contraceptive methods include
those for condoms, which include male latex condoms, male
polyurethane condoms, and female condoms; spermicides; and
diaphragm with spermicide or cervical cap (Box E1) (Table E1).
Women with conditions that make pregnancy an unacceptable
risk should be advised that barrier methods for pregnancy
prevention might not be appropriate for those who cannot
use them consistently and correctly because of the relatively
higher typical-use failure rates of these methods. Women
should be counseled that consistent and correct use of the
male latex condom reduces the risk for transmission of human
immunodeficiency virus (HIV) and other sexually transmitted
diseases (STDs). Use of female condoms can provide protection
from transmission of STDs, although data are limited.

BOX E1. Categories for classifying barrier methods

TABLE E1. Classifications for barrier methods, including condoms, spermicides, diaphragms (with spermicide), and cap
Category
Condition

Condom

Spermicide

Diaphragm (with
spermicide)/Cap

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy

Age
a. Menarche to <40 years
b. ≥40 years
Parity
a. Nulliparous
b. Parous

1
1

1
2

Postpartum (breastfeeding and nonbreastfeeding)
a. <6 weeks postpartum

1
1

1
1
1

1
1

b. ≥6 weeks postpartum
Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic abortion
Past ectopic pregnancy
History of pelvic surgery
Smoking
a. Age <35 years
b. Age ≥35 years
i. <15 cigarettes per day
ii. ≥15 cigarettes per day
Obesity
a. BMI ≥30 kg/m2
b. Menarche to <18 years and BMI ≥30 kg/m2

Clarification: None of these methods are relevant for
contraception during known pregnancy. However, for
women who remain at risk for STDs/HIV during
pregnancy, the correct and consistent use of condoms is
recommended.
—
—
—
Clarification: Risk for cervical cap failure is higher in
parous women than in nulliparous women.
Clarification: Diaphragm and cap are unsuitable until
uterine involution is complete.
—
—
Clarification: Diaphragm and cap are unsuitable until 6
weeks after second trimester abortion.
—
—
—
—
—
—
Comment: Severe obesity might make diaphragm and
cap placement difficult.

See table footnotes on page 87.

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Recommendations and Reports

TABLE E1. (Continued) Classifications for barrier methods, including condoms, spermicides, diaphragms (with spermicide), and cap
Category
Condition
History of bariatric surgery
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Restrictive procedures: decrease storage capacity of the
stomach (vertical banded gastroplasty, laparoscopic
adjustable gastric band, or laparoscopic sleeve
gastrectomy)
b. Malabsorptive procedures: decrease absorption of
nutrients and calories by shortening the functional length
of the small intestine (Roux-en-Y gastric bypass or
biliopancreatic diversion)

Condom

Spermicide

Diaphragm (with
spermicide)/Cap

Clarifications/Evidence/Comments

—

1
1
1
1

—
—
—
—

—

1
1

—
—

1
1

—
—

1
1
1

—
—
—

Cardiovascular Disease
Multiple risk factors for atherosclerotic cardiovascular
disease (e.g., older age, smoking, diabetes, hypertension,
low HDL, high LDL, or high triglyceride levels)
Hypertension
Systolic blood pressure ≥160 mm Hg or diastolic blood
pressure ≥100 mm Hg are associated with increased risk for
adverse health events as a result of pregnancy (Box 2).
a. Adequately controlled hypertension
b. Elevated blood pressure levels
(properly taken measurements)
i. Systolic 140–159 mm Hg or diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic ≥100 mm Hg
c. Vascular disease
History of high blood pressure during pregnancy (when
current blood pressure is measurable and normal)
Deep venous thrombosis/Pulmonary embolism
a. History of DVT/PE, not receiving anticoagulant therapy
i. Higher risk for recurrent DVT/PE (one or more risk
factors)
• History of estrogen-associated DVT/PE
• Pregnancy-associated DVT/PE
• Idiopathic DVT/PE
• Known thrombophilia, including antiphospholipid
syndrome
• Active cancer (metastatic, receiving therapy, or within
6 months after clinical remission), excluding
nonmelanoma skin cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE (no risk factors)
b. Acute DVT/PE
c. DVT/PE and established anticoagulant therapy for at
least 3 months
i. Higher risk for recurrent DVT/PE (one or more risk
factors)
• Known thrombophilia, including antiphospholipid
syndrome
• Active cancer (metastatic, receiving therapy, or within
6 months after clinical remission), excluding
nonmelanoma skin cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE (no risk factors)
d. Family history (first-degree relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged immobilization
f. Minor surgery without immobilization
See table footnotes on page 87.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE E1. (Continued) Classifications for barrier methods, including condoms, spermicides, diaphragms (with spermicide), and cap
Category
Condition
Known thrombogenic mutations (e.g., factor V Leiden;
prothrombin mutation; or protein S, protein C, and
antithrombin deficiencies)
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Superficial venous disorders
a. Varicose veins
b. Superficial venous thrombosis (acute or history)
Current and history of ischemic heart disease
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Stroke (history of cerebrovascular accident)
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Valvular heart disease
Complicated valvular heart disease is associated with
increased risk for adverse health events as a result of
pregnancy (Box 2).
a. Uncomplicated
b. Complicated (pulmonary hypertension, risk for atrial
fibrillation, or history of subacute bacterial endocarditis)
Peripartum cardiomyopathy
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Normal or mildly impaired cardiac function (New York
Heart Association Functional Class I or II: patients with no
limitation of activities or patients with slight, mild
limitation of activity) (1)
i. <6 months
ii. ≥6 months
b. Moderately or severely impaired cardiac function (New
York Heart Association Functional Class III or IV: patients
with marked limitation of activity or patients who should
be at complete rest) (1)

Condom

Spermicide

Diaphragm (with
spermicide)/Cap

1
1
1

—
—
—

—

1
1

1
2

—
—

1
1
1

—
—
—

1
1
1
1

—
—
—
—

1
1

—
—

1
1

—
—

—

Clarification: If pregnancy or an underlying pathological
condition (e.g., pelvic malignancy) is suspected, it must
be evaluated and the category adjusted after evaluation.

Clarifications/Evidence/Comments
Clarification: Routine screening is not appropriate
because of the rarity of the conditions and the high cost
of screening.

Rheumatic Diseases
Systemic lupus erythematosus
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Positive (or unknown) antiphospholipid antibodies
b. Severe thrombocytopenia
c. Immunosuppressive therapy
d. None of the above
Rheumatoid arthritis
a. Receiving immunosuppressive therapy
b. Not receiving immunosuppressive therapy

Neurologic Conditions
Headaches
a. Nonmigraine (mild or severe)
b. Migraine
i. Without aura (This category of migraine includes
menstrual migraine.)

ii. With aura
Epilepsy
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Multiple sclerosis
a. With prolonged immobility
b. Without prolonged immobility

Comment: Menstrual migraine is a subtype of migraine
without aura. For more information see The International
Headache Society Classification, 3rd edition (http://www.
ihs-classification.org/_downloads/mixed/InternationalHeadache-Classification-III-ICHD-III-2013-Beta.pdf).
—
—

Depressive Disorders
Depressive disorders

Reproductive Tract Infections and Disorders
Unexplained vaginal bleeding
(suspicious for serious condition) before evaluation
See table footnotes on page 87.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE E1. (Continued) Classifications for barrier methods, including condoms, spermicides, diaphragms (with spermicide), and cap
Category
Condition

Condom

Spermicide

Diaphragm (with
spermicide)/Cap

Clarifications/Evidence/Comments

1
1
1

—
—
—

1
1

—
—

1
1
1

—
—
—

Endometriosis
Benign ovarian tumors (including cysts)
Severe dysmenorrhea
Gestational trophoblastic disease
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Suspected gestational trophoblastic disease
(immediate postevacuation)
i. Uterine size first trimester
ii. Uterine size second trimester
b. Confirmed gestational trophoblastic disease
(after initial evacuation and during monitoring)
i. Undetectable/nonpregnant β–hCG levels
ii. Decreasing β–hCG levels
iii. Persistently elevated β-hCG levels or malignant
disease, with no evidence or suspicion of intrauterine
disease
iv. Persistently elevated β-hCG levels or malignant
disease, with evidence or suspicion of intrauterine
disease
Cervical ectropion
Cervical intraepithelial neoplasia

—

1
1

—
Clarification: The cap should not be used. Diaphragm use
has no restrictions.

Cervical cancer (awaiting treatment)

Clarification: The cap should not be used. Diaphragm use
has no restrictions.
Comment: Repeated and high-dose use of the spermicide
nonoxynol-9 can cause vaginal and cervical irritation or
abrasions.

Breast disease
Breast cancer is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Undiagnosed mass
b. Benign breast disease
c. Family history of cancer
d. Breast cancer
i. Current
ii. Past and no evidence of current disease for 5 years
Endometrial hyperplasia
Endometrial cancer
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Ovarian cancer
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Uterine fibroids
Anatomical abnormalities

Pelvic inflammatory disease
a. Past PID
i. With subsequent pregnancy
ii. Without subsequent pregnancy
b. Current PID
Sexually transmitted diseases
a. Current purulent cervicitis or chlamydial infection or
gonococcal infection
b. Vaginitis (including Trichomonas vaginalis and bacterial
vaginosis)
c. Other factors related to STDs

1
1
1

—
—
—

1
1
1
1

—
—
—
—

—

1
1

1
NA

—
Clarification: The diaphragm cannot be used in certain
cases of prolapse. Cap use is not appropriate for a woman
with markedly distorted cervical anatomy.

1
1
1

—
—
—

—

Evidence: Repeated and high-dose use of the spermicide
nonoxynol-9 was associated with increased risk for
genital lesions, which might increase the risk for HIV
infection (2).

HIV
High risk for HIV

Comment: Diaphragm use is assigned category 4 because
of concerns about the spermicide, not the diaphragm.
See table footnotes on page 87.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE E1. (Continued) Classifications for barrier methods, including condoms, spermicides, diaphragms (with spermicide), and cap
Category
Condition
HIV infection
For women with HIV infection who are not clinically well or
not receiving ARV therapy, this condition is associated with
increased risk for adverse health events as a result of
pregnancy (Box 2).

Condom

Spermicide

Diaphragm (with
spermicide)/Cap

Comment: Use of spermicides or diaphragms (with
spermicide) can disrupt the cervical mucosa, which might
increase viral shedding and HIV transmission to
noninfected sex partners.

Clarifications/Evidence/Comments

Other Infections
Schistosomiasis
Schistosomiasis with fibrosis of the liver is associated with
increased risk for adverse health events as a result of
pregnancy (Box 2).
a. Uncomplicated
b. Fibrosis of the liver
Tuberculosis
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Nonpelvic
b. Pelvic
Malaria
History of toxic shock syndrome

1
1

—
—

1
1
1
1

1
1
1
3

—
—
—
Comment: Toxic shock syndrome has been reported in
association with contraceptive sponge and diaphragm use.

Urinary tract infection

Comment: Use of diaphragms and spermicides might
increase risk for urinary tract infection.

—

1
1
1
1

—
—
—
—

1
1
1

—
—
—

—

1
1
1
1

—
—
—
—

1
1

—
—

1
1
1

—
—
—

1
1

—
—

Endocrine Conditions
Diabetes
Insulin-dependent diabetes; diabetes with nephropathy,
retinopathy, or neuropathy; diabetes with other vascular
disease; or diabetes of >20 years’ duration are associated
with increased risk for adverse health events as a result of
pregnancy (Box 2).
a. History of gestational disease
b. Nonvascular disease
i. Non-insulin dependent
ii. Insulin dependent
c. Nephropathy, retinopathy, or neuropathy
d. Other vascular disease or diabetes of >20 years’
duration
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

Gastrointestinal Conditions
Inflammatory bowel disease
(ulcerative colitis or Crohn’s disease)
Gallbladder disease
a. Symptomatic
i. Treated by cholecystectomy
ii. Medically treated
iii. Current
b. Asymptomatic
History of cholestasis
a. Pregnancy related
b. Past COC related
Viral hepatitis
a. Acute or flare
b. Carrier
c. Chronic
Cirrhosis
Severe cirrhosis is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Mild (compensated)
b. Severe (decompensated)
See table footnotes on page 87.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

TABLE E1. (Continued) Classifications for barrier methods, including condoms, spermicides, diaphragms (with spermicide), and cap
Category
Condition
Liver tumors
Hepatocellular adenoma and malignant liver tumors are
associated with increased risk for adverse health events as a
result of pregnancy (Box 2).
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma
b. Malignant (hepatoma)

Condom

Spermicide

Diaphragm (with
spermicide)/Cap

Clarifications/Evidence/Comments

1
1
1

—
—
—

—

1
1

—
—

—

Respiratory Conditions
Cystic fibrosis
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).

Anemias
Thalassemia
Sickle cell disease
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
Iron deficiency anemia

Solid Organ Transplantation
Solid organ transplantation
This condition is associated with increased risk for adverse
health events as a result of pregnancy (Box 2).
a. Complicated: graft failure (acute or chronic), rejection,
or cardiac allograft vasculopathy
b. Uncomplicated

Drug Interactions
Antiretroviral therapy
a. Nucleoside reverse transcriptase inhibitors (NRTIs)
i. Abacavir (ABC)
ii. Tenofovir (TDF)
iii. Zidovudine (AZT)
iv. Lamivudine (3TC)
v. Didanosine (DDI)
vi. Emtricitabine (FTC)
vii. Stavudine (D4T)
b. Nonnucleoside reverse transcriptase inhibitors (NNRTIs)
i. Efavirenz (EFV)
ii. Etravirine (ETR)
iii. Nevirapine (NVP)
iv. Rilpivirine (RPV)
c. Ritonavir-boosted protease inhibitors
i. Ritonavir-boosted atazanavir (ATV/r)
ii. Ritonavir-boosted darunavir (DRV/r)
iii. Ritonavir-boosted fosamprenavir (FPV/r)
iv. Ritonavir-boosted lopinavir (LPV/r)
v. Ritonavir-boosted saquinavir (SQV/r)
vi. Ritonavir-boosted tipranavir (TPV/r)
d. Protease inhibitors without ritonavir
i. Atazanavir (ATV)
ii. Fosamprenavir (FPV)
iii. Indinavir (IDV)
iv. Nelfinavir (NFV)
e. CCR5 co-receptor antagonists
i. Maraviroc (MVC)
f. HIV integrase strand transfer inhibitors
i. Raltegravir (RAL)
ii. Dolutegravir (DTG)
iii. Elvitegravir (EVG)
g. Fusion inhibitors
i. Enfuvirtide
Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin, carbamazepine,
barbiturates, primidone, topiramate, or oxcarbazepine)
b. Lamotrigine

Clarification: No drug interaction between ARV therapy
and barrier method use is known. However, HIV infection
is classified as category 3 for spermicides and diaphragms
(see HIV section).

1
1
1
1
1
1
1

3
3
3
3
3
3
3

1
1
1
1

3
3
3
3

1
1
1
1
1
1

3
3
3
3
3
3

1
1
1
1

3
3
3
3

1
1
1

3
3
3

—

See table footnotes on page 87.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE E1. (Continued) Classifications for barrier methods, including condoms, spermicides, diaphragms (with spermicide), and cap
Category
Condition
Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampin or rifabutin therapy
Psychotropic medications
a. SSRIs
St. John’s wort
Allergy to latex

Condom

Spermicide

Diaphragm (with
spermicide)/Cap

Clarifications/Evidence/Comments

1
1
1
1

—
—
—
—

1
1
3

1
1
1

1
1
3

—
—
Clarification: The condition of allergy to latex does not
apply to plastic condoms/diaphragms.

Abbreviations: ARV = antiretroviral; BMI = body mass index; COC = combined oral contraceptive; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density
lipoprotein; HIV = human immunodeficiency virus; LDL = low-density lipoprotein; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease; SSRI = selective serotonin
reuptake inhibitor; STD = sexually transmitted disease.

References
1. The Criteria Committee of the New York Heart Association. Nomenclature
and criteria for diagnosis of diseases of the heart and great vessels. 9th ed.
Boston, MA: Little, Brown and Co; 1994.

2. Wilkinson D, Ramjee G, Tholandi M, Rutherford G. Nonoxynol-9 for
preventing vaginal acquisition of HIV infection by women from men.
Cochrane Database Syst Rev 2002;4(CD003936):CD003936.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Appendix F
Classifications for Fertility Awareness–Based Methods
Fertility awareness–based (FAB) methods of family planning
involve identifying the fertile days of the menstrual cycle,
whether by observing fertility signs such as cervical secretions
and basal body temperature or by monitoring cycle days
(Box F1) (Table F1). FAB methods can be used in combination
with abstinence or barrier methods during the fertile time. If
barrier methods are used, see the Classifications for Barrier
Methods (Appendix E).
No medical conditions worsen because of FAB methods.
In general, FAB methods can be used without concern for
health effects in persons who choose them. However, several
conditions make their use more complex. The existence of
these conditions suggests that 1) use of these methods should
be delayed until the condition is corrected or resolved, or
2) persons using FAB methods need special counseling, and
a provider with particular training in use of these methods is
generally necessary to ensure correct use.
Women with conditions that make pregnancy an unacceptable
risk should be advised that FAB methods might not be
appropriate for them because of the relatively higher typical-use
failure rates of these methods. Symptoms-based and calendarbased methods do not protect against sexually transmitted
diseases (STDs), including human immunodeficiency virus
(HIV), and women using these methods should be counseled
that consistent and correct use of the male latex condom reduces
the risk for transmission of HIV and other STDs. Use of female
condoms can provide protection from transmission of STDs,
although data are limited.

MMWR / July 29, 2016 / Vol. 65 / No. 3

BOX F1. Definitions for terms associated with fertility awareness–
based methods

• Symptoms-based methods: FAB methods based on
observation of fertility signs (e.g., cervical secretions or basal
body temperature) such as the cervical mucus method, the
symptothermal method, and the TwoDay method.
• Calendar-based methods: FAB methods based on
calendar calculations such as the calendar rhythm
method and the standard days method.
• Accept: No medical reason exists to deny the particular
FAB method to a woman in this circumstance.
• Caution: The method normally is provided in a routine
setting but with extra preparation and precautions. For
FAB methods, this usually means that special counseling
might be needed to ensure correct use of the method by
a woman in this circumstance.
• Delay: Use of this method should be delayed until the
condition is evaluated or corrected. Alternative
temporary methods of contraception should be offered.
Abbreviation: FAB = fertility awareness–based.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE F1. Fertility awareness–based methods, including symptoms-based and calendar-based methods
Category
Condition

Symptoms-based
method

Calendar-based
method

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy
Life stage
a. Postmenarche
b. Perimenopause
Breastfeeding

Caution
Caution

Clarification: FAB methods are not relevant during pregnancy.
Comment: Menstrual irregularities are common in postmenarche and perimenopause
and might complicate the use of FAB methods.
Comment: Use of FAB methods when breastfeeding might be less effective than when
not breastfeeding.

a. <6 weeks postpartum
b. ≥6 weeks

Delay
Caution

Delay
Delay

Comment: Women who are primarily breastfeeding and are amenorrheic are unlikely to
have sufficient ovarian function to produce detectable fertility signs and hormonal changes
during the first 6 months postpartum. However, the likelihood of resumption of fertility
increases with time postpartum and with substitution of breast milk by other foods.

c. After menses begin

Caution

Clarification: When the woman notices fertility signs, particularly cervical secretions, she
can use a symptoms-based method. First postpartum menstrual cycles in breastfeeding
women vary significantly in length. Return to regularity takes several cycles. When she has
had at least three postpartum menses and her cycles are regular again, she can use a
calendar-based method. When she has had at least four postpartum menses and her most
recent cycle lasted 26–32 days, she can use the standard days method. Before that time, a
barrier method should be offered if the woman plans to use a FAB method later.

Delay

Clarification: Nonbreastfeeding women are not likely to have detectable fertility signs
or hormonal changes before 4 weeks postpartum. Although the risk for pregnancy is
low, ovulation before first menses is common; therefore, a method appropriate for the
postpartum period should be offered.

b. ≥4 weeks

Delay

Clarification: Nonbreastfeeding women are likely to have sufficient ovarian function to
produce detectable fertility signs, hormonal changes, or both at this time; likelihood
increases rapidly with time postpartum. Women can use calendar-based methods as
soon as they have completed three postpartum menses. Methods appropriate for the
postpartum period should be offered before that time.

Postabortion

Caution

Delay

Clarification: After abortion, women are likely to have sufficient ovarian function to
produce detectable fertility signs, hormonal changes, or both; likelihood increases with
time postabortion. Women can start using calendar-based methods after they have had
at least one postabortion menses (e.g., women who before this pregnancy primarily had
cycles of 26–32 days can then use the standard days method). Methods appropriate for
the postabortion period should be offered before that time.

Irregular vaginal bleeding

Delay

Clarification: Presence of this condition makes FAB methods unreliable. Therefore,
barrier methods should be recommended until the bleeding pattern is compatible with
proper method use. The condition should be evaluated and treated as necessary.

Vaginal discharge

Delay

Clarification: Because vaginal discharge makes recognition of cervical secretions
difficult, the condition should be evaluated and treated if needed before providing
methods based on cervical secretions.

Caution /Delay

Caution/Delay

Caution
Delay

Accept
Accept

Postpartum (nonbreastfeeding women)
a. <4 weeks

Reproductive Tract Infections and Disorders

Other
Use of drugs that affect cycle regularity,
hormones, or fertility signs

Diseases that elevate body temperature
a. Chronic diseases
b. Acute diseases

Clarification: Use of certain mood-altering drugs such as lithium, tricyclic antidepressants, and antianxiety therapies, as well as certain antibiotics and anti-inflammatory
drugs, might alter cycle regularity or affect fertility signs. The condition should be
carefully evaluated and a barrier method offered until the degree of effect has been
determined or the drug is no longer being used.
Clarification: Elevated temperatures might make basal body temperature difficult to interpret
but have no effect on cervical secretions. Thus, use of a method that relies on temperature
should be delayed until the acute febrile disease abates. Temperature-based methods are not
appropriate for women with chronically elevated temperatures. In addition, some chronic
diseases interfere with cycle regularity, making calendar-based methods difficult to interpret.

Abbreviations: FAB = fertility awareness–based; NA = not applicable.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Appendix G
Lactational Amenorrhea Method
The Bellagio Consensus provided the scientific basis for
defining the conditions under which breastfeeding can be used
safely and effectively for birth-spacing purposes; programmatic
guidelines were developed at a meeting of family planning
experts for its use as a method of family planning, and the
method was then given the name the lactational amenorrhea
method (1,2). These guidelines include the following three
criteria, all of which must be met to ensure adequate protection
from an unplanned pregnancy: 1) amenorrhea; 2) fully or
nearly fully breastfeeding (no interval of >4–6 hours between
breastfeeds); and 3) <6 months postpartum.
All major medical organizations recommend exclusive
breastfeeding for the first 6 months of life, with continuing
breastfeeding through the first year and beyond for as long as
mutually desired (3). No medical conditions exist for which
use of the lactational amenorrhea method for contraception is
restricted. However, breastfeeding might not be recommended
for women or infants with certain conditions.
Women with conditions that make pregnancy an unacceptable
risk should be advised that the lactational amenorrhea method
might not be appropriate for them because of its relatively higher
typical-use failure rates. The lactational amenorrhea method does
not protect against sexually transmitted diseases (STDs), including
human immunodeficiency virus (HIV), and women using this
method should be counseled that consistent and correct use of
the male latex condom reduces the risk for transmission of HIV
and other STDs. Use of female condoms can provide protection
from transmission of STDs, although data are limited.
References
1. Kennedy KI, Rivera R, McNeilly AS. Consensus statement on the use of
breastfeeding as a family planning method. Contraception 1989;39:477–
96. http://dx.doi.org/10.1016/0010-7824(89)90103-0
2. Labbok M, Cooney K, Coly S. Guidelines: breastfeeding, family planning,
and the Lactational Amenorrhea Method-LAM. Washington, DC: Institute
for Reproductive Health; 1994.
3. American Academy of Pediatrics Section on Breastfeeding. Breastfeeding
and the use of human milk [Policy statement]. Pediatrics 2012;129:e827–
41. http://dx.doi.org/10.1542/peds.2011-3552

MMWR / July 29, 2016 / Vol. 65 / No. 3

HIV Infection
HIV can be transmitted from mother to infant through
breastfeeding. Therefore, in the United States, where
replacement feeding is affordable, feasible, acceptable,
sustainable, and safe, breastfeeding for women with HIV is
not recommended (3,4).

Other Medical Conditions
The American Academy of Pediatrics (AAP) also recommends
against breastfeeding for women with active untreated
tuberculosis disease, untreated brucellosis, varicella, H1N1
influenza, or positivity for human T-cell lymphotropic virus
types I or II or for those who have herpes simplex lesions on
a breast. In addition, infants with classic galactosemia should
not breastfeed (3).

Medication Used During Breastfeeding
AAP recommends that the benefits of breastfeeding outweigh
the risk of exposure to most therapeutic agents via human
milk. More information about specific drugs and radioactive
compounds is provided by AAP (5) and LactMed (http://
toxnet.nlm.nih.gov).

4. Perinatal HIV Guidelines Working Group. Public Service Task Force
recommendations for use of antiretroviral drugs in pregnant HIV-infected women
for maternal health and interventions to reduce perinatal HIV transmission in
the United States. Rockville, MD: Public Health Service Task Force; 2009.
5. Sachs HC; Committee On Drugs. The transfer of drugs and therapeutics
into human breast milk: an update on selected topics. Pediatrics
2013;132:e796–809. http://dx.doi.org/10.1542/peds.2013-1985

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix H
Coitus Interruptus (Withdrawal)
Coitus interruptus, also known as withdrawal, is a traditional
family planning method in which the man completely removes
his penis from the vagina and away from the external genitalia
of the female partner before he ejaculates. Coitus interruptus
prevents sperm from entering the woman’s vagina, thereby
preventing contact between spermatozoa and the ovum.
This method might be appropriate for couples
• who are highly motivated and able to use this method
effectively;
• with religious or philosophical reasons for not using other
methods of contraception;
• who need contraception immediately and have entered
into a sexual act without alternative methods available;
• who need a temporary method while awaiting the start of
another method; or
• who have intercourse infrequently.

Some benefits of coitus interruptus are that the method, if used
correctly, does not affect breastfeeding and is always available
for primary use or use as a back-up method. In addition, coitus
interruptus involves no economic cost or use of chemicals and
has no directly associated health risks. Coitus interruptus does not
protect against sexually transmitted diseases (STDs), including
human immunodeficiency virus (HIV), and women using this
method should be counseled that consistent and correct use of the
male latex condom reduces the risk for transmission of HIV and
other STDs. Use of female condoms can provide protection from
transmission of STDs, although data are limited.
Coitus interruptus is unforgiving of incorrect use, and its
effectiveness depends on the willingness and ability of the couple
to use withdrawal with every act of intercourse. Women with
conditions that make pregnancy an unacceptable risk should be
advised that coitus interruptus might not be appropriate for them
because of its relatively higher typical-use failure rates.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Appendix I
Female and Male Sterilization
Tubal sterilization for women and vasectomy for men are
permanent, safe, and highly effective methods of contraception.
In general, no medical conditions absolutely restrict a person’s
eligibility for sterilization (with the exception of known
allergy or hypersensitivity to any materials used to complete
the sterilization method). However, certain conditions
place a woman at high surgical risk; in these cases, careful
consideration should be given to the risks and benefits of
other acceptable alternatives, including long-acting, highly
effective, reversible methods and vasectomy. Female and male
sterilization do not protect against sexually transmitted diseases
(STDs), including human immunodeficiency virus (HIV),
and women using these methods should be counseled that
consistent and correct use of the male latex condom reduces
the risk for transmission of HIV and other STDs. Use of female
condoms can provide protection from transmission of STDs,
although data are limited.
Because these methods are intended to be irreversible,
persons who choose sterilization should be certain that they
want to prevent pregnancy permanently. Most persons who

MMWR / July 29, 2016 / Vol. 65 / No. 3

choose sterilization remain satisfied with their decision.
However, a small proportion of women regret this decision
(1%–26% from different studies, with higher rates of regret
reported by women who were younger at sterilization) (1,2).
Regret among men about vasectomy has been reported to be
approximately 5% (3), similar to the proportion of women
who report regretting their husbands’ vasectomy (6%) (4).
Therefore, all persons should be appropriately counseled about
the permanency of sterilization and the availability of highly
effective, reversible methods of contraception.
References
1. Hillis SD, Marchbanks PA, Tylor LR, Peterson HB. Poststerilization
regret: findings from the United States Collaborative Review of
Sterilization. Obstet Gynecol 1999;93:889–95.
2. Peterson HB. Sterilization. Obstet Gynecol 2008;111:189–203. http://
dx.doi.org/10.1097/01.AOG.0000298621.98372.62
3. Ehn BE, Liljestrand J. A long-term follow-up of 108 vasectomized men.
Good counselling routines are important. Scand J Urol Nephrol
1995;29:477–81. http://dx.doi.org/10.3109/00365599509180030
4. Jamieson DJ, Kaufman SC, Costello C, Hillis SD, Marchbanks PA,
Peterson HB; US Collaborative Review of Sterilization Working Group.
A comparison of women’s regret after vasectomy versus tubal sterilization.
Obstet Gynecol 2002;99:1073–9.

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

Appendix J
Classifications for Emergency Contraception
A copper-containing intrauterine device (Cu-IUD) can be
used within 5 days of unprotected intercourse as an emergency
contraceptive. However, when the time of ovulation can be
estimated, the Cu-IUD can be inserted beyond 5 days after
intercourse, if necessary, as long as the insertion does not occur
>5 days after ovulation. The eligibility criteria for interval
Cu-IUD insertion also apply for the insertion of Cu-IUDs as
emergency contraception (Box J1) (Table J1).
Classifications for emergency contraceptive pills (ECPs) are
given for ulipristal acetate (UPA), levonorgestrel (LNG), and
combined oral contraceptives (COCs). Cu-IUDs, UPA, LNG,
and COCs do not protect against sexually transmitted diseases
(STDs), including human immunodeficiency virus (HIV),
and women using these methods should be counseled that
consistent and correct use of the male latex condom reduces

BOX J1. Categories for classifying emergency contraception

TABLE J1. Classifications for emergency contraception, including the copper-containing intrauterine device, ulipristal acetate, levonorgestrel,
and combined oral contraceptives*
Category
Condition

Cu-IUD

UPA

LNG

COC

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History
Pregnancy

Clarification (IUD): The IUD is not indicated during pregnancy and should
not be used because of the risk for serious pelvic infection and septic
spontaneous abortion.
Clarification (ECPs): Although this method is not indicated for a woman with
a known or suspected pregnancy, no harm to the woman, the course of her
pregnancy, or the fetus if ECPs are inadvertently used is known to exist.
Evidence: Evidence suggests that poor pregnancy outcomes are rare
among pregnant women who used ECPs during conception cycle or early in
pregnancy (1).

Breastfeeding

Past ectopic pregnancy
History of bariatric surgery
This condition is associated with increased risk for
adverse health events as a result of pregnancy (Box 2).
a. Restrictive procedures: decrease storage capacity
of the stomach (vertical banded gastroplasty,
laparoscopic adjustable gastric band, or laparoscopic
sleeve gastrectomy)
b. Malabsorptive procedures: decrease absorption of
nutrients and calories by shortening the functional
length of the small intestine (Roux-en-Y gastric
bypass or biliopancreatic diversion)

Clarification (UPA): Breastfeeding is not recommended for 24 hours after
taking UPA because it is excreted in breast milk, with highest concentrations in the first 24 hours, and maximum maternal serum levels are reached
1–3 hours after administration. Mean UPA concentrations in breast milk
decrease markedly from 0 to 24–48 hours and then slowly decrease over 5
days (2). Breast milk should be expressed and discarded for 24 hours after
taking UPA.
Evidence: Breastfeeding outcomes do not seem to differ between women
exposed to LNG and those who are not exposed. One pharmacokinetic
study demonstrated that LNG passes to breast milk but in minimal
quantities (1).
—

—

Comment: Bariatric surgical procedures involving a malabsorptive
component have the potential to decrease oral contraceptive effectiveness,
perhaps further decreased by postoperative complications such as
long-term diarrhea, vomiting, or both. Because of these malabsorptive
concerns, an emergency IUD might be more appropriate than ECPs.

See table footnotes on page 94.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE J1. (Continued) Classifications for emergency contraception, including the copper-containing intrauterine device, ulipristal acetate,
levonorgestrel, and combined oral contraceptives*
Category
Condition

Cu-IUD

UPA

LNG

COC

Clarifications/Evidence/Comments

2
1

1
1

—

Clarification: Recurrent ECP use is an indication that the woman requires
further counseling about other contraceptive options. Frequently repeated
ECP use might be harmful for women with conditions classified as 2, 3, or 4
for CHC or POC use.

Cardiovascular Disease
History of severe cardiovascular disease (ischemic
heart disease, cerebrovascular attack, or other
thromboembolic conditions)
This condition is associated with increased risk for
adverse health events as a result of pregnancy (Box 2).

Comment: The duration of ECP use is less than that of regular use of COCs
or POPs and thus would be expected to have less clinical impact.

Rheumatic Diseases
Rheumatoid arthritis
a. Receiving immunosuppressive therapy
b. Not receiving immunosuppressive therapy

—
—

Neurologic Conditions
Migraine

Comment: The duration of ECP use is less than that of regular use of COCs
and thus would be expected to have less clinical impact.

Gastrointestinal Conditions
Inflammatory bowel disease (ulcerative colitis or
Crohn’s disease)
Severe liver disease (including jaundice)
This condition is associated with increased risk for
adverse health events as a result of pregnancy (Box 2).

—
Comment: The duration of ECP use is less than that of regular use of COCs
or POPs and thus would be expected to have less clinical impact.

Solid Organ Transplantation
Solid organ transplantation
This condition is associated with increased risk for
adverse health events as a result of pregnancy (Box 2).
a. Complicated: graft failure (acute or chronic),
rejection, or cardiac allograft vasculopathy
b. Uncomplicated

Other
Repeated ECP use

Evidence: In one case-control study, risk for ectopic pregnancy compared
with intrauterine pregnancy did not increase after repeated use of LNG
ECPs compared with nonuse (1).
Sexual assault

Clarification (IUD): Women who have experienced sexual assault are at
increased risk for STDs. According to CDC STD treatment guidelines, routine
presumptive treatment of chlamydia, gonorrhea, and trichomonas is
recommended after sexual assault (3). Women with current purulent
cervicitis or chlamydial infection or gonococcal infection should not
undergo IUD insertion (category 4).

Obesity (BMI ≥30 kg/m2)

Clarification (ECPs): ECPs might be less effective among women with BMI
≥30 kg/m2 than among women with BMI <25 kg/m2. Despite this, no safety
concerns exist.
Evidence: Limited evidence from secondary data analyses suggests that
women with BMI ≥30 kg/m2 experience an increased risk for pregnancy
after use of LNG compared with women with BMI <25 kg/m2. Two analyses
suggest obese women might also experience an increased risk for
pregnancy after use of UPA compared with nonobese women, although
this increase was not significant in one study (4).

CYP3A4 inducers (e.g., bosentan, carbamazepine,
felbamate, griseofulvin, oxcarbazepine, phenytoin,
rifampin, St. John’s wort, topiramate, efavirenz, and
lumacaftor)

Clarification (ECPs): Strong CYP3A4 inducers might reduce the effectiveness of ECPs.
Evidence: According to labelling information, rifampin markedly decreases
UPA levels by ≥90%, which might decrease its efficacy (2). Therefore,
theoretical concerns extend to use of other CYP3A4 inducers as well as to
COC and LNG ECPs, which have metabolic pathways similar to those of UPA.
A small pharmacokinetic study found that concomitant efavirenz use
decreased LNG levels in women taking LNG ECPs (0.75 mg) by 56%
compared with LNG ECPs alone (5).

Abbreviations: BMI = body mass index; CHC = combined hormonal contraceptive; COC = combined hormonal contraceptive; Cu-IUD = copper-containing intrauterine device; ECP = emergency
contraceptive pill; HIV = human immunodeficiency virus; IUD = intrauterine device; LNG = levonorgestrel; NA = not applicable; POC = progestin-only contraceptive; POP = progestin-only
pill; STD = sexually transmitted disease; UPA = ulipristal acetate.

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

References
1. Jatlaoui TC, Riley H, Curtis KM. Safety data for levonorgestrel, ulipristal
acetate and Yuzpe regimens for emergency contraception. Contraception
2016;93:93–112. http://dx.doi.org/10.1016/j.contraception.2015.11.001
2. Watson Pharmaceuticals. Ella [Prescribing information]. Morristown, NJ; 2010.
https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/022474s000lbl.pdf
3. Workowski KA, Bolan GA. Sexually transmitted diseases treatment
guidelines, 2015. MMWR Recomm Rep 2015;64(No. RR-03).

4. Jatlaoui TC, Curtis KM. Safety and effectiveness data for emergency
contraceptive pills among women with obesity: a systematic review.
Contraception 2016. Epub May 24, 2016. http://dx.doi.org/10.1016/j.
contraception.2016.05.002
5. Carten ML, Kiser JJ, Kwara A, Mawhinney S, Cu-Uvin S. Pharmacokinetic
interactions between the hormonal emergency contraception,
levonorgestrel (Plan B), and efavirenz. Infect Dis Obstet Gynecol
2012;2012:137192.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

Recommendations and Reports

Appendix K
Summary of Classifications for Hormonal Contraceptive Methods and Intrauterine Devices
Health-care providers can use the summary table as a quick
reference guide to the classifications for hormonal contraceptive
methods and intrauterine contraception to compare classifications
across these methods (Box K1) (Table K1). See the respective
appendix for each method for clarifications to the numeric
categories, as well as for summaries of the evidence and additional
comments. Hormonal contraceptives and intrauterine devices
do not protect against sexually transmitted diseases (STDs),
including human immunodeficiency virus (HIV), and women
using these methods should be counseled that consistent and
correct use of the male latex condom reduces the risk for
transmission of HIV and other STDs. Use of female condoms
can provide protection from transmission of STDs, although
data are limited.

BOX K1. Categories for classifying hormonal contraceptives and
intrauterine devices

TABLE K1. Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

LNG-IUD

Implants

DMPA

POP

CHCs

4*
Menarche to
<20 years: 2
≥20 years: 1

NA*
Menarche to
<18 years: 1
18–45 years: 1
>45 years: 1

NA*
Menarche to
<18 years: 2
18–45 years: 1
>45 years: 2

NA*
Menarche to
<18 years: 1
18–45 years: 1
>45 years: 1

NA*
Menarche to
<40 years: 1
≥40 years: 2

2
1

1
1

—

—
—

1*
1*

2*
2*

Personal Characteristics And Reproductive History
Pregnancy
Age

Parity
a. Nulliparous
b. Parous
Breastfeeding
a. <21 days postpartum
b. 21 to <30 days postpartum
i. With other risk factors for VTE (e.g.,
age ≥35 years, previous VTE,
thrombophilia, immobility,
transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage,
postcesarean delivery, preeclampsia,
or smoking)
ii. Without other risk factors for VTE
c. 30–42 days postpartum
i. With other risk factors for VTE (e.g.,
age ≥35 years, previous VTE,
thrombophilia, immobility,
transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage,
postcesarean delivery, preeclampsia,
or smoking)
ii. Without other risk factors for VTE
d. >42 days postpartum
See table footnotes on page 103.

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US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE K1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
Postpartum (nonbreastfeeding
women)
a. <21 days postpartum
b. 21–42 days postpartum
i. With other risk factors for VTE (e.g.,
age ≥35 years, previous VTE,
thrombophilia, immobility,
transfusion at delivery, peripartum
cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage,
postcesarean delivery, preeclampsia,
or smoking)
ii. Without other risk factors for VTE
c. >42 days postpartum
Postpartum (including cesarean
delivery)
a. <10 minutes after delivery of the
placenta
i. Breastfeeding
ii. Nonbreastfeeding
b. 10 minutes after delivery of the
placenta to <4 weeks (breastfeeding
or nonbreastfeeding)
c. ≥4 weeks (breastfeeding or
nonbreastfeeding)
d. Postpartum sepsis
Postabortion
a. First trimester
b. Second trimester
c. Immediate postseptic abortion
Past ectopic pregnancy
History of pelvic surgery (see
Postpartum [Including Cesarean
Delivery] section)
Smoking
a. Age <35 years
b. Age ≥35 years
i. <15 cigarettes per day
ii. ≥15 cigarettes per day
Obesity
a. BMI ≥30 kg/m2
b. Menarche to <18 years and BMI
≥30 kg/m2
History of bariatric surgery
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Restrictive procedures: decrease
storage capacity of the stomach
(vertical banded gastroplasty,
laparoscopic adjustable gastric band,
or laparoscopic sleeve gastrectomy)
b. Malabsorptive procedures:
decrease absorption of nutrients and
calories by shortening the functional
length of the small intestine
(Roux-en-Y gastric bypass or
biliopancreatic diversion)

Cu-IUD

LNG-IUD

Implants

DMPA

POP

CHCs

—

—
—

1
1

2
1

1*
1*
2*

2*
1*
2*

—
—
—

—

1*
2*
4
1
1

1*
1*
1*
1
1

1*
1*
1*
2
1

1*
1*
1*
1
1

1
1

3
4

1
1

1
2

1
1

2
2

COCs: 3
Patch and ring: 1

3/4*

See table footnotes on page 103.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE K1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
b. Elevated blood pressure levels
(properly taken measurements)
i. Systolic 140–159 mm Hg or
diastolic 90–99 mm Hg
ii. Systolic ≥160 mm Hg or diastolic
≥100 mm Hg
c. Vascular disease
History of high blood pressure during
pregnancy (when current blood
pressure is measurable and normal)
Deep venous thrombosis/
Pulmonary embolism
a. History of DVT/PE, not receiving
anticoagulant therapy
i. Higher risk for recurrent DVT/PE
(one or more risk factors)
• History of estrogen-associated
DVT/PE
• Pregnancy-associated DVT/PE
• Idiopathic DVT/PE
• Known thrombophilia, including
antiphospholipid syndrome
• Active cancer (metastatic,
receiving therapy, or within
6 months after clinical remission),
excluding nonmelanoma skin
cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE
(no risk factors)
b. Acute DVT/PE
c. DVT/PE and established anticoagulant therapy for at least 3 months
i. Higher risk for recurrent DVT/PE
(one or more risk factors)
• Known thrombophilia, including
antiphospholipid syndrome
• Active cancer (metastatic,
receiving therapy, or within
6 months after clinical remission),
excluding nonmelanoma skin
cancer
• History of recurrent DVT/PE
ii. Lower risk for recurrent DVT/PE
(no risk factors)
d. Family history (first-degree
relatives)
e. Major surgery
i. With prolonged immobilization
ii. Without prolonged
immobilization
f. Minor surgery without
immobilization
Known thrombogenic mutations (e.g.,
factor V Leiden; prothrombin mutation;
and protein S, protein C, and
antithrombin deficiencies)
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
Superficial venous disorders
a. Varicose veins
b. Superficial venous thrombosis
(acute or history)
Current and history of ischemic
heart disease
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).

Cu-IUD

LNG-IUD

Implants

DMPA

POP

CHCs

1*
1

2*
1

3*
1

2*
1

4*
2

1
1

2
1

4
2

1
1

1
3*

Initiation Continuation
2
3

Initiation Continuation Initiation Continuation
2
3
2
3

See table footnotes on page 103.

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US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE K1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
Stroke (history of cerebrovascular
accident)
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
Valvular heart disease
Complicated valvular heart disease is
associated with increased risk for
adverse health events as a result of
pregnancy (Box 2).
a. Uncomplicated
b. Complicated (pulmonary
hypertension, risk for atrial fibrillation,
or history of subacute bacterial
endocarditis)
Peripartum cardiomyopathy
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Normal or mildly impaired cardiac
function (New York Heart Association
Functional Class I or II: patients with no
limitation of activities or patients with
slight, mild limitation of activity) (1)
i. <6 months
ii. ≥6 months
b. Moderately or severely impaired
cardiac function (New York Heart
Association Functional Class III or IV:
patients with marked limitation of
activity or patients who should be at
complete rest) (1).

Cu-IUD

LNG-IUD

1
1

2
2
2

Implants

DMPA

POP

CHCs

Initiation Continuation
2
3

1
1

2
4

1
1
2

4
3
4

Initiation Continuation
2
3

Rheumatic Diseases
Initiation Continuation
Systemic lupus erythematosus
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Positive (or unknown) antiphospho1*
1*
3*
lipid antibodies
b. Severe thrombocytopenia
3*
2*
2*
c. Immunosuppressive therapy
2*
1*
2*
d. None of the above
1*
1*
2*
Rheumatoid arthritis
Initiation Continuation Initiation Continuation
a. Receiving immunosuppressive
2
1
2
1
therapy
b. Not receiving immunosuppressive
1
1
therapy

Initiation Continuation

2*
2*
2*

3*
2*
2*

2*
2*
2*

2/3*

Neurologic Conditions
Headaches
a. Nonmigraine (mild or severe)
b. Migraine
i. Without aura (This category of
migraine includes menstrual
migraine.)
ii. With aura
Epilepsy
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
Multiple sclerosis
a. With prolonged immobility
b. Without prolonged immobility

1
1

1
1*

4*
1*

1
1

2
2

1
1

3
1

Initiation Continuation
1
1

Depressive Disorders
Depressive disorders

Reproductive Tract Infections and Disorders
Vaginal bleeding patterns
a. Irregular pattern without heavy
bleeding
b. Heavy or prolonged bleeding
(includes regular and irregular
patterns)

1
2*

See table footnotes on page 103.

US Department of Health and Human Services/Centers for Disease Control and Prevention

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Recommendations and Reports

TABLE K1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

Unexplained vaginal bleeding
Initiation Continuation
(suspicious for serious condition)
4*
2*
before evaluation
Endometriosis
2
Benign ovarian tumors (including
1
cysts)
Severe dysmenorrhea
2
Gestational trophoblastic disease
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Suspected gestational trophoblastic
disease (immediate postevacuation)
i. Uterine size first trimester
1*
ii. Uterine size second trimester
2*
b. Confirmed gestational trophoblas- Initiation Continuation
tic disease (after initial evacuation and
during monitoring)
i. Undetectable/nonpregnant β-hCG
1*
1*
levels
ii. Decreasing β-hCG levels
2*
1*
iii. Persistently elevated β-hCG levels
2*
1*
or malignant disease, with no
evidence or suspicion of intrauterine
disease
iv. Persistently elevated β-hCG levels
4*
2*
or malignant disease, with evidence
or suspicion of intrauterine disease
Cervical ectropion
1
Cervical intraepithelial neoplasia
1
Cervical cancer (awaiting treatment)
Initiation Continuation
4
2
Breast disease
Breast cancer is associated with
increased risk of adverse health events
as a result of pregnancy (Box 2).
a. Undiagnosed mass
1
b. Benign breast disease
1
c. Family history of cancer
1
d. Breast cancer
i. Current
1
ii. Past and no evidence of current
1
disease for 5 years
Endometrial hyperplasia
1
Initiation Continuation
Endometrial cancer
This condition is associated with
increased risk for adverse health events
4
2
as a result of pregnancy (Box 2).
1
Ovarian cancer
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
Uterine fibroids
2
Anatomical abnormalities
a. Distorted uterine cavity (any
4
congenital or acquired uterine
abnormality distorting the uterine
cavity in a manner that is incompatible with IUD insertion)
2
b. Other abnormalities (including
cervical stenosis or cervical
lacerations) not distorting the uterine
cavity or interfering with IUD insertion
Pelvic inflammatory disease
a. Past PID
Initiation Continuation
i. With subsequent pregnancy
1
1
ii. Without subsequent pregnancy
2
2
b. Current PID
4
2*

LNG-IUD

Implants

DMPA

POP

CHCs

Initiation Continuation
4*
2*

1
1

1*
1*

1*
2*
Initiation Continuation

2*
2*

1*
1*

1
2
Initiation Continuation
4
2

1
2

1
1

1
2

2
1
1

2*
1
1

4
3

—

Initiation Continuation
1
1
2
2
4
2*

1
1
1

1
Initiation Continuation
4

See table footnotes on page 103.

100

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Recommendations and Reports

TABLE K1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition
Sexually transmitted diseases
a. Current purulent cervicitis or
chlamydial infection or gonococcal
infection
b. Vaginitis (including Trichomonas
vaginalis and bacterial vaginosis)
c. Other factors related to STDs

Cu-IUD

LNG-IUD

Initiation Continuation Initiation Continuation
4
2*
4
2*

Implants

DMPA

POP

CHCs

1
1*

1*
1*

1
1*

HIV
High risk for HIV
HIV infection
For women with HIV infection who are
not clinically well or not receiving ARV
therapy, this condition is associated
with increased risk for adverse health
events as a result of pregnancy (Box 2).
a. Clinically well receiving ARV
therapy
b. Not clinically well or not receiving
ARV therapy

Initiation Continuation Initiation Continuation
2
2
2
2
—
—
—
—

—

1
1

1*
1*
1

Other Infections
Schistosomiasis
Schistosomiasis with fibrosis of the liver
is associated with increased risk for
adverse health events as a result of
pregnancy (Box 2).
a. Uncomplicated
1
1
b. Fibrosis of the liver (if severe, see
1
1
Cirrhosis)
Initiation Continuation Initiation Continuation
Tuberculosis
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Nonpelvic
1
1
1
1
b. Pelvic
4
3
4
3
Malaria
1
1

Endocrine Conditions
Diabetes
Insulin-dependent diabetes; diabetes
with nephropathy, retinopathy, or
neuropathy; diabetes with other
vascular disease; or diabetes of
>20 years’ duration are associated with
increased risk of adverse health events
as a result of pregnancy (Box 2).
a. History of gestational disease
b. Nonvascular disease
i. Non-insulin dependent
ii. Insulin dependent
c. Nephropathy, retinopathy, or
neuropathy
d. Other vascular disease or diabetes
of >20 years’ duration
Thyroid disorders
a. Simple goiter
b. Hyperthyroid
c. Hypothyroid

1
1
1

2
2
2

2
2
3

2
2
2

2
2
3/4*

3/4*

1
1
1

2/3*

1
1
1
1

2
2
2
2

2
3
3
2

1
1

1
2

2
3

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Recommendations and Reports

TABLE K1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

Viral hepatitis
a. Acute or flare
b. Carrier
c. Chronic
Cirrhosis
Severe cirrhosis is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Mild (compensated)
b. Severe (decompensated)
Liver tumors
Hepatocellular adenoma and malignant
liver tumors are associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
a. Benign
i. Focal nodular hyperplasia
ii. Hepatocellular adenoma
b. Malignant (hepatoma)

LNG-IUD

Implants

DMPA

POP

CHCs

1
1
1

Initiation Continuation
3/4*
2
1
1
1
1

1
1

1
3

1
4

1
1
1

2
3
3

2
4
4

2
2

1
1

1
2

Respiratory Conditions
Cystic fibrosis
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).

Anemias
Thalassemia
Sickle cell disease
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
Iron-deficiency anemia

Solid Organ Transplantation
Initiation Continuation Initiation Continuation
Solid organ transplantation
This condition is associated with
increased risk for adverse health events
as a result of pregnancy (Box 2).
3
2
3
2
a. Complicated: graft failure (acute or
chronic), rejection, or cardiac allograft
vasculopathy
b. Uncomplicated
2
2
2
2

Initiation Continuation Initiation Continuation

1/2*
1/2*
1/2*
1/2*
1/2*
1/2*
1/2*

1*
1*
1*
1*
1*
1*
1*

1/2*
1/2*
1/2*
1/2*
1/2*
1/2*
1/2*

1*
1*
1*
1*
1*
1*
1*

1
1
1
1
1
1
1

1/2*
1/2*
1/2*
1/2*

1*
1*
1*
1*

1/2*
1/2*
1/2*
1/2*

1*
1*
1*
1*

2*
1
1
1

1*
1
1
1

2*
1
1
1

1/2*

See table footnotes on page 103.

102

MMWR / July 29, 2016 / Vol. 65 / No. 3

US Department of Health and Human Services/Centers for Disease Control and Prevention

Recommendations and Reports

TABLE K1. (Continued) Summary of classifications for hormonal contraceptive methods and intrauterine devices
Condition

Cu-IUD

d. Protease inhibitors without
ritonavir
i. Atazanavir (ATV)
ii. Fosamprenavir (FPV)
iii. Indinavir (IDV)
iv. Nelfinavir (NFV)
e. CCR5 co-receptor antagonists
i. Maraviroc (MVC)
f. HIV integrase strand transfer
inhibitors
i. Raltegravir (RAL)
ii. Dolutegravir (DTG)
iii. Elvitegravir (EVG)
g. Fusion inhibitors
i. Enfuvirtide
Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin,
carbamazepine, barbiturates,
primidone, topiramate, and
oxcarbazepine)
b. Lamotrigine
Antimicrobial therapy
a. Broad-spectrum antibiotics
b. Antifungals
c. Antiparasitics
d. Rifampin or rifabutin therapy
Psychotropic medications
a. SSRIs
St. John’s wort

LNG-IUD

Implants

DMPA

POP

CHCs

1/2*
1/2*
1/2*
1/2*

1*
1*
1*
1*

1/2*
1/2*
1/2*
1/2*

1*
1*
1*
1*

1
2*
1
2*

1
2*
1
1*

1
2*
1
2*

2*
3*
1
2*

1/2*

1/2*
1/2*
1/2*

1*
1*
1*

1/2*
1/2*
1/2*

1*
1*
1*

1
1
1

1/2*

1
1
1
1

1
1
1
2*

1
1
1
1*

1
1
1
3*

1
1

1
2

1
1

1
2

Abbreviations: BMI = body mass index; COC = combined oral contraceptive; Cu-IUD = copper-containing IUD; DMPA = depot medroxyprogesterone acetate;
DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; HIV = human immunodeficiency virus.; IUD = intrauterine
device; LDL = low-density lipoprotein; LNG-IUD = levonorgestrel-releasing IUD; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease;
POP = progestin-only pill; SSRI = selective serotonin reuptake inhibitor; STD = sexually transmitted disease.
* Consult the appendix for this contraceptive method for a clarification to this classification.

US Department of Health and Human Services/Centers for Disease Control and Prevention

MMWR / July 29, 2016 / Vol. 65 / No. 3

103

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Morbidity and Mortality Weekly Report
Recommendations and Reports / Vol. 63 / No. 4

April 25, 2014

Providing Quality Family Planning Services
Recommendations of CDC and the U.S. Office of Population Affairs

Continuing Education Examination available at http://www.cdc.gov/mmwr/cme/conted.html.

U.S. Department of Health and Human Services
Centers for Disease Control and Prevention

Recommendations and Reports

CONTENTS
Introduction ............................................................................................................1
Methods....................................................................................................................3
Contraceptive Services ........................................................................................7
Pregnancy Testing and Counseling ............................................................. 13
Clients Who Want to Become Pregnant ..................................................... 14
Basic Infertility Services.................................................................................... 15
Preconception Health Services ..................................................................... 16
Sexually Transmitted Disease Services ....................................................... 18
Related Preventive Health Services ............................................................. 20
Summary of Recommendations for Providing Family Planning and
Related Preventive Health Services ........................................................... 21
Conducting Quality Improvement............................................................... 21
Conclusion ............................................................................................................ 25
Appendix A ........................................................................................................... 30
Appendix B ........................................................................................................... 35
Appendix C ........................................................................................................... 45
Appendix D........................................................................................................... 47
Appendix E............................................................................................................ 48
Appendix F............................................................................................................ 51

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Recommendations and Reports

Providing Quality Family Planning Services
Recommendations of CDC and the U.S. Office of Population Affairs
Prepared by
Loretta Gavin, PhD,1 Susan Moskosky, MS,2 Marion Carter, PhD,1 Kathryn Curtis, PhD,1 Evelyn Glass, MSPH,2 Emily Godfrey,
MD,1 Arik Marcell, MD,3 Nancy Mautone-Smith, MSW,2 Karen Pazol, PhD,1 Naomi Tepper, MD,1 Lauren Zapata, PhD1
1Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, CDC
2Office of Population Affairs, US Department of Health and Human Services, Rockville, Maryland
3The Johns Hopkins University and the Male Training Center for Family Planning and Reproductive Health, Baltimore, Maryland

Summary
This report provides recommendations developed collaboratively by CDC and the Office of Population Affairs (OPA) of the
U.S. Department of Health and Human Services (HHS). The recommendations outline how to provide quality family planning
services, which include contraceptive services, pregnancy testing and counseling, helping clients achieve pregnancy, basic infertility
services, preconception health services, and sexually transmitted disease services. The primary audience for this report is all current
or potential providers of family planning services, including those working in service sites that are dedicated to family planning
service delivery as well as private and public providers of more comprehensive primary care.
The United States continues to face substantial challenges to improving the reproductive health of the U.S. population. Nearly
one half of all pregnancies are unintended, with more than 700,000 adolescents aged 15–19 years becoming pregnant each year
and more than 300,000 giving birth. One of eight pregnancies in the United States results in preterm birth, and infant mortality
rates remain high compared with those of other developed countries.
This report can assist primary care providers in offering family planning services that will help women, men, and couples achieve
their desired number and spacing of children and increase the likelihood that those children are born healthy. The report provides
recommendations for how to help prevent and achieve pregnancy, emphasizes offering a full range of contraceptive methods for
persons seeking to prevent pregnancy, highlights the special needs of adolescent clients, and encourages the use of the family planning
visit to provide selected preventive health services for women, in accordance with the recommendations for women issued by the
Institute of Medicine and adopted by HHS.

Introduction
The United States continues to face challenges to improving
the reproductive health of the U.S. population. Nearly half (49%)
of all pregnancies are unintended (1). Although adolescent birth
rates declined by more than 61% during 1991–2012, the United
States has one of the highest adolescent pregnancy rates in the
developed world, with >700,000 adolescents aged 15–19 years
becoming pregnant each year and >300,000 giving birth (2,3).
Approximately one of eight pregnancies in the United States
results in a preterm birth, and infant mortality rates remain high
compared with other developed countries (3,4). Moreover, all
of these outcomes affect racial and ethnic minority populations
disproportionately (1–4).
Corresponding preparers: Loretta Gavin, PhD, Division of Reproductive
Health, National Center for Chronic Disease Prevention and Health
Promotion, CDC. Telephone: 770-488-6284; E-mail: [email protected];
Susan Moskosky, MS, Office of Population Affairs, US Department of
Health and Human Services. Telephone: 240-453-2818; E-mail:
[email protected].

Family planning services can help address these and other public
health challenges by providing education, counseling, and medical
services (5). Family planning services include the following:
t providing contraception to help women and men plan
and space births, prevent unintended pregnancies, and
reduce the number of abortions;
t offering pregnancy testing and counseling;
t helping clients who want to conceive;
t providing basic infertility services;
t providing preconception health services to improve infant
and maternal outcomes and improve women’s and men’s
health; and
t providing sexually transmitted disease (STD) screening
and treatment services to prevent tubal infertility and
improve the health of women, men, and infants.
This report provides recommendations developed
collaboratively by CDC and the Office of Population Affairs
(OPA) of the U.S. Department of Health and Human Services
(HHS). The recommendations outline how to provide family
planning services by:

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

t defining a core set of family planning services for women
and men,
t describing how to provide contraceptive and other clinical
services, serve adolescents, and perform quality
improvements, and
t encouraging the use of the family planning visit to provide
selected preventive health services for women, in accordance
with the recommendations for women issued by the
Institute of Medicine (IOM) and adopted by HHS (6).
The collaboration between CDC and OPA drew on the
strengths of both agencies. CDC has a long-standing history of
developing evidence-based recommendations for clinical care,
and OPA’s Title X Family Planning Program (7) has served as
the national leader in direct family planning service delivery
since the Title X program was established in 1970.
This report provides recommendations for providing care to
clients of reproductive age who are in need of family planning
services. These recommendations are intended for all current
or potential providers of family planning services, including
those funded by the Title X program.

Current Context of Family
Planning Services
Women of reproductive age often report that their family
planning provider is also their usual source of health care (8).
As the U.S. health-care system evolves in response to increased
efforts to expand health insurance coverage, contain costs, and
emphasize preventive care (9), providers of family planning
services will face new challenges and opportunities in care
delivery. For example, they will have increased opportunities
to serve new clients and to serve as gateways for their clients to
other essential health-care services. In addition, primary care
and other providers who provide a range of health-care services
will be expected to integrate family planning services for all
persons of reproductive age, including those whose primary
reason for their health-care visit might not be family planning.
Strengthened, multidirectional care coordination also will be
needed to improve health outcomes. For example, this type
of care coordination will be needed with clients referred to
specialist care after initial screening at a family planning visit,
as well as with specialists referring clients with family planning
needs to family planning providers.

Defining Quality in Family
Planning Service Delivery
The central premise underpinning these recommendations
is that improving the quality of family planning services will
lead to improved reproductive health outcomes (10–12). IOM

MMWR / April 25, 2014 / Vol. 63 / No. 4

defines health-care quality as the extent to which health-care
services improve health outcomes in a manner that is consistent
with current professional knowledge (10,13). According to
IOM, quality health care has the following attributes:
t Safety. These recommendations integrate other CDC
recommendations about which contraceptive methods can
be provided safely to women with various medical
conditions, and integrate CDC and U.S. Preventive
Services Task Force (USPSTF) recommendations on STD,
preconception, and related preventive health services.
t Effectiveness. These recommendations support offering
a full range of Food and Drug Administration
(FDA)–approved contraceptive methods as well as
counseling that highlights the effectiveness of contraceptive
methods overall and, in specific patient situations, draws
attention to the effectiveness of specific clinical preventive
health services and identifies clinical preventive health
services for which the potential harms outweigh the
benefits (i.e., USPSTF “D” recommendations).
t Client-centered approach. These recommendations
encourage taking a client-centered approach by
1) highlighting that the client’s primary purpose for
visiting the service site must be respected, 2) noting the
importance of confidential services and suggesting ways
to provide them, 3) encouraging the availability of a broad
range of contraceptive methods so that clients can make
a selection based on their individual needs and preferences,
and 4) reinforcing the need to deliver services in a
culturally competent manner so as to meet the needs of
all clients, including adolescents, those with limited
English proficiency, those with disabilities, and those who
are lesbian, gay, bisexual, transgender, or questioning their
sexual identity (LGBTQ). Organizational policies,
governance structures, and individual attitudes and
practices all contribute to the cultural competence of a
health-care entity and its staff. Cultural competency within
a health-care setting refers to attitudes, practices, and
policies that enable professionals to work effectively in
cross-cultural situations (14–16).
t Timeliness. These recommendations highlight the
importance of ensuring that services are provided to clients
in a timely manner.
t Efficiency. These recommendations identify a core set of
services that providers can focus on delivering, as well as
ways to maximize the use of resources.
t Accessibility. These recommendations address how to
remove barriers to contraceptive use, use the family planning
visit to provide access to a broader range of primary care
and behavioral health services, use the primary care visit to

Recommendations and Reports

provide access to contraceptive and other family planning
services, and strengthen links to other sources of care.
t Equity. These recommendations highlight the need for
providers of family planning services to deliver highquality care to all clients, including adolescents, LGBTQ
persons, racial and ethnic minorities, clients with limited
English proficiency, and persons living with disabilities.
t Value. These recommendations highlight services (i.e.,
contraception and other clinical preventive services) that
have been shown to be very cost-effective (17–19).

Methods
Recommendations Development Process
The recommendations were developed jointly under the
auspices of CDC’s Division of Reproductive Health and
OPA, in consultation with a wide range of experts and key
stakeholders. More information about the processes used to
conduct systematic reviews, the role of technical experts in
reviewing the evidence, and the process of using the evidence
to develop recommendations is provided (Appendix A). A
multistage process was used to develop the recommendations
that drew on established procedures for developing clinical
guidelines (20,21). First, an Expert Work Group* was formed
comprising family planning clinical providers, program
administrators, and representatives from relevant federal
agencies and professional medical associations to help define
the scope of the recommendations. Next, literature about
three priority topics (i.e., counseling and education, serving
adolescents, and quality improvement) was reviewed by using
the USPSTF methodology for conducting systematic reviews
(22). The results were presented to three technical panels†
comprising subject matter experts (one panel for each priority
topic) who considered the quality of the evidence and made
suggestions for what recommendations might be supported on
the basis of the evidence. In a separate process, existing clinical
recommendations on women’s and men’s preventive services
were compiled from more than 35 federal and professional
medical associations, and these results were presented to two
technical panels of subject matter experts, one that addressed
women’s clinical services and one that addressed men’s clinical
services. The panels provided individual feedback about
which clinical preventive services should be offered in a family
planning setting and which clinical recommendations should
receive the highest consideration.
* A list of the members of the Expert Work Group appears on page 52.
† A list of the members of the technical panels appears on pages 52 and 53.

CDC and OPA used the input from the subject matter
experts to develop a set of core recommendations and asked
the Expert Work Group to review them. The members of
the Expert Work Group were more familiar with the family
planning service delivery context than the members of the
Technical Panel and thus could better comment on the
feasibility and appropriateness of the recommendations,
as well as the supporting evidence. The Expert Work
Group considered the core recommendations by using the
following criteria: 1) the quality of the evidence; 2) the
positive and negative consequences of implementing the
recommendations on health outcomes, costs or cost-savings,
and implementation challenges; and 3) the relative importance
of these consequences, (e.g., the likelihood that implementation
of the recommendation will have a substantial effect on health
outcomes might be considered more than the logistical
challenges of implementing it) (20). In certain cases, when
the evidence from the literature reviews was inconclusive or
incomplete, recommendations were made on the basis of expert
opinion. Finally, CDC and OPA staff considered the individual
feedback from Expert Work Group members when finalizing
the core recommendations and writing the recommendations
document. A description of how the recommendations link
to the evidence is provided together with the rationale for the
inclusion of each recommendation in this report (Appendix B).
The evidence used to prepare these recommendations
will appear in background papers that will be published
separately. Resources that will help providers implement the
recommendations will be provided through a web-based tool
kit that will be available at http://www.hhs.gov/opa.

Audience for the Recommendations
The primary audience for this report is all providers or
potential providers of family planning services to clients of
reproductive age, including providers working in clinics that
are dedicated to family planning service delivery, as well as
private and public providers of more comprehensive primary
care. Providers of dedicated family planning services might be
less familiar with the specific recommendations for the delivery
of preconception services. Providers of more comprehensive
primary care might be less familiar with the delivery of
contraceptive services, pregnancy testing and counseling, and
services to help clients achieve pregnancy.
This report can be used by medical directors to write clinical
protocols that describe how care should be provided. Job aids
and other resources for use in service sites are being developed
and will be made available when ready through OPA’s website
(http://www.hhs.gov/opa).

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

In this report, the term “provider” refers to any staff member
who is involved in providing family planning services to a
client. This includes physicians, physician assistants, nurse
practitioners, nurse-midwives, nursing staff, and health
educators. The term “service site” represents the numerous
settings in which family planning services are delivered, which
include freestanding service sites, community health centers,
private medical facilities, and hospitals. A list of special terms
used in this report is provided (Box 1).
The recommendations are designed to guide general clinical
practice; however, health-care providers always should consider
the individual clinical circumstances of each person seeking
family planning services. Similarly, these recommendations
might need to be adapted to meet the needs of particular
populations, such as clients who are HIV-positive or who are
substance users.

Organization of the Recommendations
This report is divided into nine sections. An initial section
provides an overview of steps to assess the needs of a client
and decide what family planning services to offer. Subsequent
sections describe how to provide each of the following services:
contraceptive services, pregnancy testing and counseling, helping
clients achieve pregnancy, basic infertility services, preconception
health services, STD services and related preventive health services.
A final section on quality improvement describes actions that all
providers of family planning services should consider to ensure
that services are of high quality. More detailed information about
selected topics addressed in the recommendations is provided
(Appendices A–F).
These recommendations focus on the direct delivery of care
to individual clients. However, parallel steps might need to be
taken to maintain the systems required to support the provision of
quality services for all clients (e.g., record-keeping procedures that
preserve client confidentiality, procedures that improve efficiency
and reduce clients’ wait time, staff training to ensure that all clients
are treated with respect, and the establishment and maintenance
of a strong system of care coordination and referrals).

Client Care
Family planning services are embedded within a broader
framework of preventive health services (Figure 1). In this
report, health services are divided into three main categories:
t Family planning services. These include contraceptive
services for clients who want to prevent pregnancy and space
births, pregnancy testing and counseling, assistance to achieve
pregnancy, basic infertility services, STD services (including
HIV/AIDS), and other preconception health services (e.g.,
screening for obesity, smoking, and mental health). STD/HIV

MMWR / April 25, 2014 / Vol. 63 / No. 4

BOX 1. Definitions of quality terms used in this report

Accessible. The timely use of personal health services
to achieve the best possible health outcomes.*
Client-centered. Care is respectful of, and responsive
to, individual client preferences, needs, and values; client
values guide all clinical decisions.†
Effective. Services are based on scientific knowledge and
provided to all who could benefit and are not provided to
those not likely to benefit.†
Efficient. Waste is avoided, including waste of equipment,
supplies, ideas, and energy.†
Equitable. Care does not vary in quality because of the
personal characteristics of clients (e.g., sex, race/ethnicity,
geographic location, insurance status, or socioeconomic
status).†
Evidence-based. The process of integrating sciencebased interventions with community preferences to
improve the health of populations.§
Health-care quality. The degree to which health-care
services for individuals and populations increase the
likelihood of desired health outcomes and are consistent
with current professional knowledge.†
Process. Whether services are provided correctly and
completely and how clients perceive the care they receive.¶
Safe. Avoids injuries to clients from the care that is
intended to help them.†
Structure. The characteristics of the settings in which
providers deliver health care, including material resources,
human resources, and organizational structure.¶
Timely. Waits and sometimes harmful delays for both
those who receive and those who provide care are reduced.†
Value. The care provides good return relative to the costs
involved, such as a return on investment or a reduction in
the per capita cost of health care.*
* Source: Institute of Medicine. Future directions for the national healthcare
quality and disparities reports. Ulmer C, Bruno M, Burke S, eds.
Washington, DC: The National Academies Press; 2010.
† Source: Institute of Medicine. Crossing the quality chasm: a new health
system for the 21st century. Committee on Quality of Health Care in
America, ed. Washington, DC: National Academies of Science; 2001.
§ Source: Kohatsu ND, Robinson JG, Torner JC. Evidence-based public
health: an evolving concept. Am J Prev Med 2004;27:417–21.
¶ Source: Donabedian A. The quality of care. JAMA 1988;260:1743–8.

and other preconception health services are considered family
planning services because they improve women’s and men’s
health and can influence a person’s ability to conceive or to
have a healthy birth outcome.
t Related preventive health services. These include services
that are considered to be beneficial to reproductive health,

Recommendations and Reports

FIGURE 1. Family planning and related and other preventive health
services

Family planning services
t$POUSBDFQUJWFTFSWJDFT
t1SFHOBODZUFTUJOHBOE
DPVOTFMJOH
t"DIJFWJOHQSFHOBODZ
t#BTJDJOGFSUJMJUZTFSWJDFT
t1SFDPODFQUJPOIFBMUI
t4FYVBMMZUSBOTNJUUFE
EJTFBTFTFSWJDFT

Related preventive
health services
FH
TDSFFOJOHGPSCSFBTU
BOEDFSWJDBMDBODFS

Other preventive
health services
FH
TDSFFOJOHGPSMJQJE
EJTPSEFST

are closely linked to family planning services, and are
appropriate to deliver in the context of a family planning visit
but that do not contribute directly to achieving or preventing
pregnancy (e.g., breast and cervical cancer screening).
t Other preventive health services. These include
preventive health services for women that were not
included above (6), as well as preventive services for men.
Screening for lipid disorders, skin cancer, colorectal cancer,
or osteoporosis are examples of this type of service.
Although important in the context of primary care, these
have no direct link to family planning services.
Providers of family planning services should be trained and
equipped to offer all family planning and related preventive
health services so that they can provide optimal care to clients,
with referral for specialist care, as needed. Other preventive
health services should be available either on-site or by referral,
but these recommendations do not address this category
of services. Information about preventive services that are
beyond the scope of this report is available at http://www.
uspreventiveservicestaskforce.org.

Determining the Client’s Need for Services
These recommendations apply to two types of encounters
with women and men of reproductive age. In the first type of
encounter, the primary reason for a client’s visit to a healthcare provider is related to preventing or achieving pregnancy,

(i.e., contraceptive services, pregnancy testing and counseling,
or becoming pregnant). Other aspects of managing pregnancy
(e.g., prenatal and delivery care ) are not addressed in these
recommendations. For clients seeking to prevent or achieve
pregnancy, providers should assess whether the client needs
other related services and offer them to the client. In the second
type of encounter, the primary reason for a client’s visit to a
health-care provider is not related to preventing or achieving
pregnancy. For example, the client might come in for acute
care (e.g., a male client coming in for STD symptoms or as
a contact of a person with an STD), for chronic care, or for
another preventive service. In this situation, providers not only
should address the client’s primary reason for the visit but also
assess the client’s need for services related to preventing or
achieving pregnancy.
A clinical pathway of family planning services for women and
men of reproductive age is provided (Figure 2). The following
questions can help providers determine what family planning
services are most appropriate for a given visit.
t What is the client’s reason for the visit? It is essential to
understand the client’s goals for the visit and address those
needs to the extent possible.
t Does the client have another source of primary health
care? Understanding whether a provider is the main source
of primary care for a client will help identify what
preventive services a provider should offer. If a provider is
the client’s main source of primary care, it will be
important to assess the client’s needs for the other services
listed in this report. If the client receives ongoing primary
care from another provider, the provider should confirm
that the client’s preventive health needs are met while
avoiding the delivery of duplicative services.
t What is the client’s reproductive life plan? An assessment
should be made of the client’s reproductive life plan, which
outlines personal goals about becoming pregnant (23–25)
(Box 2).The provider should avoid making assumptions
about the client’s needs based on his or her characteristics,
such as sexual orientation or disabilities. For clients whose
initial reason for coming to the service site was not related to
preventing or achieving pregnancy, asking questions about
his or her reproductive life plan might help identify unmet
reproductive health-care needs. Identifying a need for
contraceptive services might be particularly important given
the high rate of unintended pregnancy in the United States.
– If the client does not want a child at this time and is
sexually active, then offer contraceptive services.
– If the client desires pregnancy testing, then provide
pregnancy testing and counseling.
– If the client wants to have a child now, then provide
services to help the client achieve pregnancy.

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Recommendations and Reports

FIGURE 2. Clinical pathway of family planning services for women and men of reproductive age
Determine the need for services among
female and male clients of reproductive age
tAssess reason for visit
tAssess source of primary care
tAssess reproductive life plan

Reason for visit is related to
preventing or achieving
pregnancy

Initial reason for visit is not
related to preventing or
achieving pregnancy
tAcute care
tChronic care management
tPreventive services

Contraceptive
services

Pregnancy
testing and
counseling

Achieving
pregnancy

Basic
infertility
services
If needed,
provide
services

Clients also should be
provided these
services, per
clinical recommendations

Clients also should be provided
or referred for these services,
per clinical recommendations

Sexually
transmitted
disease
services

Preconception
health
services

If services are not needed at this
visit, reassess at subsequent visits

Related
preventive
health
services

– If the client wants to have a child and is experiencing
difficulty conceiving, then provide basic infertility services.
t Does the client need preconception health services?
Preconception health services (such as screening for
obesity, smoking, and mental health) are a subset of all
preventive services for women and men. Preconception
health care is intended to promote the health of women
and men of reproductive age before conception, with the
goal of improving pregnancy-related outcomes (24).
Preconception health services are also important because
they improve the health of women and men, even if they
choose not to become pregnant. The federal and
professional medical recommendations cited in this report
should be followed when determining which preconception
health services a client might need.
t Does the client need STD services? The need for STD
services, including HIV/AIDS testing, should be considered

Assess need for services related
to preventing or achieving
pregnancy

MMWR / April 25, 2014 / Vol. 63 / No. 4

at every visit. Many clients requesting contraceptive services
also might meet the criteria for being at risk of one or more
STDs. Screening for chlamydia and gonorrhea is especially
important in a family planning context because these STDs
contribute to tubal infertility if left untreated. STD services
are also necessary to maximize preconception health. The
federal recommendations cited in this report should be
followed when determining which STD services a client
might need. Aspects of managing symptomatic STDs are
not addressed in these recommendations.
t What other related preventive health services does the
client need? Whether the client needs related preventive
health services, such as breast and cervical cancer screening
for female clients, should be assessed. The federal and
professional medical recommendations cited in this report
should be followed when determining which related
preventive health services a client might need.

Recommendations and Reports

BOX 2. Recommended questions to ask when assessing a client’s
reproductive life plan

Providers should discuss a reproductive life plan with
clients receiving contraceptive, pregnancy testing and
counseling, basic infertility, sexually transmitted disease,
and preconception health services in accordance with
CDC’s recommendation that all persons capable of having
a child should have a reproductive life plan.*
Providers should assess the client’s reproductive life plan
by asking the client questions such as:
t Do you have any children now?
t Do you want to have (more) children?
t How many (more) children would you like to have
and when?
* Source: CDC. Recommendations to improve preconception health and
health care—United States: a report of the CDC/ATSDR Preconception
Care Work Group and the Select Panel on Preconception Care. MMWR
2006;55(No. RR-6).

The individual client’s needs should be considered when
determining what services to offer at a given visit. It might not
be feasible to deliver all the needed services in a single visit, and
they might need to be delivered over the course of several visits.
Providers should tailor services to meet the specific needs of
the population they serve. For example, clients who are trying
to achieve pregnancy and those at high risk of unintended
pregnancy should be given higher priority for preconception
health services. In some cases, the provider will deliver the
initial screening service but then refer to another provider for
further diagnosis or follow-up care.
The delivery of preconception, STD, and related preventive
health services should not become a barrier to a client’s ability
to receive services related to preventing or achieving pregnancy.
For these clients, receiving services related to preventing or
achieving pregnancy is the priority; if other family planning
services cannot be delivered at the initial visit, then follow-up
visits should be scheduled.
In addition, professional recommendations for how to
address the needs of diverse clients, such as LGBTQ persons
(26–32) or persons with disabilities (33), should be consulted
and integrated into procedures, as appropriate. For example,
as noted before, providers should avoid making assumptions
about a client’s gender identity, sexual orientation, race,
or ethnicity; all requests for services should be treated
without regard to these characteristics. Similarly, services for
adolescents should be provided in a “youth-friendly” manner,
which means that they are accessible, equitable, acceptable,
appropriate, comprehensive, effective, and efficient for youth,
as recommended by the World Health Organization (34).

Contraceptive Services
Providers should offer contraceptive services to clients who
wish to delay or prevent pregnancy. Contraceptive services
should include consideration of a full range of FDA-approved
contraceptive methods, a brief assessment to identify the
contraceptive methods that are safe for the client, contraceptive
counseling to help a client choose a method of contraception
and use it correctly and consistently, and provision of one or
more selected contraceptive method(s), preferably on site, but
by referral if necessary. Contraceptive counseling is defined as
a process that enables clients to make and follow through on
decisions about their contraceptive use. Education is an integral
component of the contraceptive counseling process that helps
clients to make informed decisions and obtain the information
they need to use contraceptive methods correctly.
Key steps in providing contraceptive services, including
contraceptive counseling and education, have been outlined
(Box 3). These key steps are in accordance with the five principles
of quality counseling (Appendix C). To help a client who is
initiating or switching to a new method of contraception,
providers should follow these steps. These steps most likely will
be implemented iteratively when working with a client and
should help clients adopt, change, or maintain contraceptive use.
Step 1. Establish and maintain rapport with the client.
Providers should strive to establish and maintain rapport.
Strategies to achieve these goals include the following:
t using open-ended questions;
t demonstrating expertise, trustworthiness, and accessibility;
t ensuring privacy and confidentiality;
t explaining how personal information will be used;
t encouraging the client to ask questions and share
information;
t listening to and observing the client; and
t being encouraging and demonstrating empathy and
acceptance.
Step 2. Obtain clinical and social information from
the client. Providers should ask clients about their medical
history to identify methods that are safe. In addition, to learn
more about factors that might influence a client’s choice of a
contraceptive method, providers should confirm the client’s
pregnancy intentions or reproductive life plan, ask about the
client’s contraceptive experiences and preferences, and conduct
a sexual health assessment. When available, standardized tools
should be used.
t Medical history. A medical history should be taken to
ensure that methods of contraception being considered
by a client are safe for that particular client. For a female
client, the medical history should include menstrual
history (including last menstrual period, menstrual
frequency, length and amount of bleeding, and other
MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

BOX 3. Steps in providing contraceptive services, including
contraceptive counseling* and education

t Establish and maintain rapport with the client.
t Obtain clinical and social information from the client.
t Work with the client interactively to select the most
effective and appropriate contraceptive method.
t Conduct a physical assessment related to
contraceptive use, only when warranted.
t Provide the contraceptive method along with
instructions about correct and consistent use, help the
client develop a plan for using the selected method
and for follow up, and confirm client understanding.
* Key principles of providing quality counseling including education have
been outlined (Appendix C).

patterns of uterine/vaginal bleeding), gynecologic and
obstetrical history, contraceptive use, allergies, recent
intercourse, recent delivery, miscarriage, or termination,
and any relevant infectious or chronic health condition
and other characteristics and exposures (e.g., age,
postpartum, and breastfeeding) that might affect the
client’s medical eligibility criteria for contraceptive
methods (35). Clients considering combined hormonal
contraception should be asked about smoking tobacco, in
accordance with CDC guidelines on contraceptive use
(35). Additional details about the methods of contraception
that are safe to use for female clients with specific medical
conditions and characteristics (e.g., hypertension) are
addressed in previously published guidelines (35). For a
male client, a medical history should include use of
condoms, known allergies to condoms, partner use of
contraception, recent intercourse, whether his partner is
currently pregnant or has had a child, miscarriage, or
termination, and the presence of any infectious or chronic
health condition. However, the taking of a medical history
should not be a barrier to making condoms available in
the clinical setting (i.e., a formal visit should not be a
prerequisite for a client to obtain condoms).
t Pregnancy intention or reproductive life plan. Each
client should be encouraged to clarify decisions about her
or his reproductive life plan (i.e., whether the client wants
to have any or more children and, if so, the desired timing
and spacing of those children) (24).
t Contraceptive experiences and preferences. Methodspecific experiences and preferences should be assessed by
asking questions such as, “What method(s) are you
currently using, if any?”; “What methods have you used
in the past?”; “Have you previously used emergency

MMWR / April 25, 2014 / Vol. 63 / No. 4

contraception?”; “Did you use contraception at last sex?”;
“What difficulties did you experience with prior methods
if any (e.g., side effects or noncompliance)?”; “Do you
have a specific method in mind?”; and “Have you discussed
method options with your partner, and does your partner
have any preferences for which method you use?” Male
clients should be asked if they are interested in vasectomy.
t Sexual health assessment. A sexual history and risk
assessment that considers the client’s sexual practices,
partners, past STD history, and steps taken to prevent
STDs (36) is recommended to help the client select the
most appropriate method(s) of contraception. Correct and
consistent condom use is recommended for those at risk
for STDs. CDC recommendations for how to conduct a
sexual health assessment have been summarized (Box 4).
Step 3. Work with the client interactively to select the most
effective and appropriate contraceptive method. Providers
should work with the client interactively to select an effective
and appropriate contraceptive method. Specifically, providers
should educate the client about contraceptive methods that
the client can safely use, and help the client consider potential
barriers to using the method(s) under consideration. Use of
decision aids (e.g., computerized programs that help a client
to identify a range of methods that might be appropriate for
the client based on her physical characteristics such as health
conditions or preferences about side effects) before or while
waiting for the appointment can facilitate and maximize the
utility of the time spent on this step.
Providers should inform clients about all contraceptive
methods that can be used safely. Before the health-care visit,
clients might have only limited information about all or
specific methods of contraception (37). A broad range of
methods, including long-acting reversible contraception (i.e.,
intrauterine devices [IUDs] and implants), should be discussed
with all women and adolescents, if medically appropriate.
Providers are encouraged to present information on potential
reversible methods of contraception by using a tiered approach
(i.e., presenting information on the most effective methods first,
before presenting information on less effective methods) (38,39).
This information should include an explanation that longacting reversible contraceptive methods are safe and effective for
most women, including those who have never given birth and
adolescents (35). Information should be tailored and presented
to ensure a client-centered approach. It is not appropriate to omit
presenting information on a method solely because the method
is not available at the service site. If not all methods are available
at the service site, it is important to have strong referral links in
place to other providers to maximize opportunities for clients
to obtain their preferred method that is medically appropriate.

Recommendations and Reports

BOX 4. Steps in conducting a sexual health assessment*

t Practices: Explore the types of sexual activity in which
the patient engages (e.g., vaginal, anal, or oral sex).
t Pregnancy prevention: Discuss current and future
contraceptive options. Ask about current and previous
use of methods, use of contraception at last sex,
difficulties with contraception, and whether the client
has a particular method in mind.
t Partners: Ask questions to determine the number, gender
(men, women, or both), and concurrency of the patient’s
sex partners (if partner had sex with another partner while
still in a sexual relationship with the patient). It might be
necessary to define the term “partner” to the patient or use
other, relevant terminology.
t Protection from sexually transmitted diseases
(STDs): Ask about condom use, with whom they do
or do not use condoms, and situations that make it
harder or easier to use condoms. Topics such as
monogamy and abstinence also can be discussed.
t Past STD history: Ask about any history of STDs,
including whether their partners have ever had an
STD. Explain that the likelihood of an STD is higher
with a past history of an STD.
* Source: CDC. Sexually transmitted diseases treatment guidelines, 2010.
MMWR 2010;59(No. RR-12).

For clients who have completed childbearing or do not plan
to have children, permanent sterilization (female or male) is an
option that may be discussed. Both female and male sterilization
are safe, are highly effective, and can be performed in an office
or outpatient surgery setting (40,41). Women and men should
be counseled that these procedures are not intended to be
reversible and that other highly effective, reversible methods of
contraception (e.g., implants or IUDs) might be an alternative
if they are unsure about future childbearing. Clients interested
in sterilization should be referred to an appropriate source of
care if the provider does not perform the procedure.
When educating clients about contraceptive methods that
the clients can use safely, providers should ensure that clients
understand the following:
t Method effectiveness. A contraceptive method’s rate of
typical effectiveness, or the percentage of women
experiencing an unintended pregnancy during the first
year of typical use, is an important consideration (Figure 3;
Appendix D) (38,42).
t Correct use of the method. The mode of administration
and understanding how to use the method correctly might
be important considerations for the client when choosing

a method. For example, receiving a contraceptive injection
every 3 months might not be acceptable to a woman who
fears injections. Similarly, oral contraceptives might not
be acceptable to a woman who is concerned that she might
not be able to remember to take a pill every day.
t Noncontraceptive benefits. Many contraceptives have
noncontraceptive benefits, in addition to preventing
pregnancy, such as reducing heavy menstrual bleeding.
Although the noncontraceptive benefits are not generally
the major determinant for selecting a method, awareness
of these benefits can help clients decide between two or
more suitable methods and might enhance the client’s
motivation to use the method correctly and consistently.
t Side effects. Providers should inform the client about risks
and side effects of the method(s) under consideration, help
the client understand that certain side effects of contraceptive
methods might disappear over time, and encourage the
client to weigh the experience of coping with side effects
against the experience and consequences of an unintended
pregnancy. The provider should be prepared to discuss and
correct misperceptions about side effects. Clients also should
be informed about warning signs for rare, but serious,
adverse events with specific contraceptive methods, such as
stroke and venous thromboembolism with use of combined
hormonal methods.
t Protection from STDs, including HIV. Clients should
be informed that contraceptive methods other than
condoms offer no protection against STDs, including
HIV. Condoms, when used correctly and consistently,
help reduce the risk of STDs, including HIV, and provide
protection against pregnancy. Dual protection (i.e.,
protection from both pregnancy and STDs) is important
for clients at risk of contracting an STD, such as those
with multiple or potentially infected partner(s). Dual
protection can be achieved through correct and consistent
use of condoms with every act of sexual intercourse, or
correct and consistent use of a condom to prevent infection
plus another form of contraception to prevent pregnancy.
(For more information about preventing and treating
STDs, see STD Services.)
When educating clients about the range of contraceptive
methods, providers should ensure that clients have information
that is medically accurate, balanced, and provided in a
nonjudgmental manner. To assist clients in making informed
decisions, providers should educate clients in a manner that
can be readily understood and retained. The content, format,
method, and medium for delivering education should be
evidence-based (see Appendix E).
When working with male clients, when appropriate, providers
should discuss information about female-controlled methods

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

FIGURE 3. The typical effectiveness of Food and Drug Administration–approved contraceptive methods

(including emergency contraception) encourage discussion of
contraception with partners, and provide information about how
partners can access contraceptive services. Male clients should
also be reminded that condoms should be used correctly and
consistently to reduce risk of STDs, including HIV.
When working with any client, encourage partner
communication about contraception, as well as understanding
partner barriers (e.g., misperceptions about side effects) and
facilitators (e.g., general support) of contraceptive use (43–46).
46
The provider should help the client consider potential
barriers to using the method(s) under consideration. This
includes consideration of the following factors:
t Social-behavioral factors. Social-behavioral factors might
influence the likelihood of correct and consistent use of

MMWR / April 25, 2014 / Vol. 63 / No. 4

contraception (47). Providers should help the client
consider the advantages and disadvantages of the
method(s) being considered, the client’s feelings about
using the method(s), how her or his partner is likely to
respond, the client’s peers’ perceptions of the method(s),
and the client’s confidence in being able to use the method
correctly and consistently (e.g., using a condom during
every act of intercourse or remembering to take a pill every
day) (37).
t Intimate partner violence and sexual violence. Current
and past intimate partner sexual or domestic violence
might impede the correct and consistent use of
contraception, and might be a consideration when
(47–
47 49
49). For example, an IUD might
choosing a method (47–49).

Recommendations and Reports

be preferred because it does not require the partner’s
participation. The medical history might provide
information on signs of current or past violence and, if
not, providers should ask clients about relationship issues
that might be potential barriers to contraceptive use. In
addition, clients experiencing intimate partner violence
or sexual violence should be referred for appropriate care.
t Mental health and substance use behaviors. Mental health
(e.g., depression, anxiety disorders, and other mental
disorders) and substance use behaviors (e.g., alcohol use,
prescription abuse, and illicit drug use) might affect a client’s
ability to correctly and consistently use contraception
(47,50). The medical history might provide information
about the signs of such conditions or behaviors, and if not,
providers should ask clients about substance use behaviors
or mental health disorders, such as depression or anxiety,
that might interfere with the motivation or ability to follow
through with contraceptive use. If needed, clients with
mental health disorders or risky substance use behaviors
should be referred for appropriate care.
Step 4. Conduct a physical assessment related to
contraceptive use, when warranted. Most women will need
no or few examinations or laboratory tests before starting a
method of contraception. Guidance on necessary examinations
and tests related to initiation of contraception is available (42).
A list of assessments that need to be conducted when providing
reversible contraceptive services to a female client seeking to
initiate or switch to a new method of reversible contraception is
provided (Table 1) (42). Clinical evaluation of a client electing
permanent sterilization should be guided by the clinician who
performs the procedure. Recommendations for contraceptive
use are available (42). Key points include the following:
t Blood pressure should be taken before initiating the use
of combined hormonal contraception.
t Providers should assess the current pregnancy status of
clients receiving contraception (42), which provides
guidance on how to be reasonably certain that a woman
is not pregnant at the time of contraception initiation. In
most cases, a detailed history provides the most accurate
assessment of pregnancy risk in a woman about to start
using a contraceptive method. Routine pregnancy testing
for every woman is not necessary.
t Weight measurement is not needed to determine medical
eligibility for any method of contraception because all
methods generally can be used among obese women.
However, measuring weight and calculating BMI at baseline
might be helpful for monitoring any changes and counseling
women who might be concerned about weight change
perceived to be associated with their contraceptive method.

t Unnecessary medical procedures and tests might create
logistical, emotional, or economic barriers to contraceptive
access for some women, particularly adolescents and lowincome women, who have high rates of unintended
pregnancies (1,51,52). For both adolescent and adult
female clients, the following examinations and tests are
not needed routinely to provide contraception safely to a
healthy client (although they might be needed to address
other non-contraceptive health needs) (42):
– pelvic examinations, unless inserting an intrauterine
device (IUD) or fitting a diaphragm;
– cervical cytology or other cancer screening, including
clinical breast exam;
– human immunodeficiency virus (HIV) screening; and
– laboratory tests for lipid, glucose, liver enzyme, and
hemoglobin levels or thrombogenic mutations.
For male clients, no physical examination needs to be
performed before distributing condoms.
Step 5. Provide the contraceptive method along with
instructions about correct and consistent use, help the
client develop a plan for using the selected method and for
follow-up, and confirm client understanding.
t A broad range of FDA-approved contraceptive methods
should be available onsite. Referrals for methods not
available onsite should be provided for clients who indicate
they prefer those methods. When providing contraception,
providers should instruct the client about correct and
consistent use and employ the following strategies to
facilitate a client’s use of contraception:
– Provide onsite dispensing;
– Begin contraception at the time of the visit rather than
waiting for next menses (also known as “quick start”) if
the provider can reasonably be certain that the client is
not pregnant (42). A provider can be reasonably certain
that a woman is not pregnant if she has no symptoms or
signs of pregnancy and meets any one of the following
criteria (42,53):
º is ≤7 days after the start of normal menses,
º has not had sexual intercourse since the start of last
normal menses,
º has been using a reliable method of contraception
correctly and consistently,
º is ≤7 days after spontaneous or induced abortion,
º is within 4 weeks postpartum,
º is fully or nearly fully breastfeeding (exclusively
breastfeeding or the vast majority [≥85%] of feeds are
breastfeeds), amenorrheic, and <6 months postpartum;
– Provide or prescribe multiple cycles (ideally a full year’s
supply) of oral contraceptive pills, the patch, or the ring

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Recommendations and Reports

TABLE 1. Assessments to conduct when a female client is initiating a new method of reversible contraception

Examination
Blood pressure
Weight (BMI) (weight [kg]/height [m]2)
Clinical breast examination
Bimanual examination and cervical
inspection
Laboratory test
Glucose
Lipids
Liver enzymes
Hemoglobin
Thrombogenic mutations
Cervical cytology (Papanicolaou smear)
STD screening with laboratory tests
HIV screening with laboratory tests

Combined
hormonal
Progestincontraception only pills

Diaphragm or
cervical
cap
Spermicide

Cu-IUD and
LNG-IUD

Implant

Injectable

C
—†
C
A

C
—†
C
C

A*
—†
C
C

C
—†
C
C

C
C
C
C

C
C
C
A§

C
C
C
C

C
C
C
C
C
C
—¶
C

C
C
C
C
C
C
C
C

Condom

Source: CDC. U.S. selected practice recommendations for contraceptive use 2013. MMWR 2013;62(No. RR-5).
Abbreviations: A = Class A: essential and mandatory in all circumstances for safe and effective use of the contraceptive method; B = Class B: contributes substantially
to safe and effective use, but implementation might be considered within the public health and/or service context (the risk of not performing an examination or test
should be balanced against the benefits of making the contraceptive method available); C = Class C: does not contribute substantially to safe and effective use of the
contraceptive method; Cu-IUD = copper-containing intrauterine device; LNG-IUD = levonorgestrel releasing intrauterine device.
* In cases in which access to health care might be limited, the blood pressure measurement can be obtained by the woman in a nonclinical setting (e.g., pharmacy
or fire station) and self-reported to the provider.
† Weight (BMI) measurement is not needed to determine medical eligibility for any methods of contraception because all methods can be used (U.S. Medical Eligibility
Criteria 1) or generally can be used (U.S. Medical Eligibility Criteria 2) among obese women (Source: CDC. U.S. medical eligibility criteria for contraceptive use 2010.
MMWR 2010;59[No. RR-4]). However, measuring weight and calculating BMI at baseline might be helpful for monitoring any changes and counseling women who
might be concerned about weight change perceived to be associated with their contraceptive method.
§ A bimanual examination (not cervical inspection) is needed for diaphragm fitting.
¶ Most women do not require additional STD screening at the time of IUD insertion, if they have already been screened according to CDC’s STD treatment guidelines
(Sources: CDC. STD treatment guidelines. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cdc.gov/std/treatment.
CDC. Sexually transmitted diseases treatment guidelines, 2010. MMWR. 2010;59[No. RR-12]). If a woman has not been screened according to guidelines, screening
can be performed at the time of IUD insertion and insertion should not be delayed. Women with purulent cervicitis or current chlamydial infection or gonorrhea
should not undergo IUD insertion (U.S. Medical Eligibility Criteria 4). Women who have a very high individual likelihood of STD exposure (e.g., those with a currently
infected partner) generally should not undergo IUD insertion (U.S. Medical Eligibility Criteria 3) (Source: CDC. U.S. medical eligibility criteria for contraceptive use
2010. MMWR 2010;59[No. RR-4]). For these women, IUD insertion should be delayed until appropriate testing and treatment occurs.

to minimize the number of times a client has to return to
the service site;
– Make condoms easily and inexpensively available; and
– If a client chooses a method that is not available on-site
or the same day, provide the client another method to
use until she or he can start the chosen method.
t Help the client develop a plan for using the selected
method. Using a method incorrectly or inconsistently and
having gaps in contraceptive protection because of method
switching both increase the likelihood of an unintended
pregnancy (37). After the method has been provided, or
a plan put into place to obtain the chosen method,
providers should help the client develop an action plan
for using the selected method.
Providers should encourage clients to anticipate reasons
why they might not use their chosen method(s) correctly or
consistently, and help them develop strategies to deal with
these possibilities. For example, for a client selecting oral
contraceptive pills who might forget to take a pill, the provider
can work with the client to identify ways to routinize daily
pill taking (e.g., use of reminder systems such as daily text

MMWR / April 25, 2014 / Vol. 63 / No. 4

messages or cell phone alarms). Providers also may inform
clients about the availability of emergency contraceptive pills
and may provide clients an advance supply of emergency
contraceptive pills on-site or by prescription, if requested.
Side effects (e.g., irregular vaginal bleeding) are a primary
reason for method discontinuation (54), so providers
should discuss ways the client might deal with potential side
effects to increase satisfaction with the method and improve
continuation (42).
t Develop a plan for follow-up. Providers should discuss an
appropriate follow-up plan with the client to meet their
individual needs, considering the client’s risk for
discontinuation. Follow-up provides an opportunity to
inquire about any initial difficulties the client might be
experiencing, and might reinforce the perceived accessibility
of the provider and increase rapport. Alternative modes
of follow-up other than visits to the service site, such as
telephone, e-mail, or text messaging, should be considered
(assuming confidentiality can be assured), as needed.
As noted previously, if a client chooses a method that
is not available on-site or during the visit, the provider

Recommendations and Reports

should schedule a follow-up visit with the client or provide
a referral for her or him to receive the method. The client
should be provided another method to use until she or he
can start the chosen method.
t Confirm the client’s understanding. Providers should assess
whether the client understands the information that was
presented. The client’s understanding of the most
important information about her or his chosen
contraceptive method should be documented in the
medical record (e.g., by a checkbox or written statement).
The teach-back method may be used to confirm the client’s
understanding by asking the client to repeat back messages
about risks and benefits and appropriate method use and
follow-up. If providers assess the client’s understanding, then
the check box or written statement can be used in place of a
written method-specific informed consent form. Topics that
providers may consider having the client repeat back include
the following: typical method effectiveness; how to use the
method correctly; protection from STDs; warning signs
for rare, but serious, adverse events and what to do if they
experience a warning sign; and when to return for follow-up.
Provide Counseling for Returning Clients
When serving contraceptive clients who return for ongoing
care related to contraception, providers should ask if the
client has any concerns with the method and assess its use.
The provider should assess any changes in the client’s medical
history, including changes in risk factors and medications that
might affect safe use of the contraceptive method. If the client
is using the method correctly and consistently and there are no
concerns about continued use, an appropriate follow-up plan
should be discussed and more contraceptive supplies given
(42). If the client or provider has concerns about the client’s
correct or consistent use of the method, the provider should
ask if the client would be interested in considering a different
method of contraception. If the client is interested, the steps
described above should be followed.
Counseling Adolescent Clients
Providers should give comprehensive information to
adolescent clients about how to prevent pregnancy (55–57).
This information should clarify that avoiding sex (i.e.,
abstinence) is an effective way to prevent pregnancy and STDs.
If the adolescent indicates that she or he will be sexually active,
providers should give information about contraception and
help her or him to choose a method that best meets her or his
individual needs, including the use of condoms to reduce the
risk of STDs. Long-acting reversible contraception is a safe
and effective option for many adolescents, including those
who have not been pregnant or given birth (35).

Providers of family planning services should offer confidential
services to adolescents and observe all relevant state laws and
any legal obligations, such as notification or reporting of child
abuse, child molestation, sexual abuse, rape, or incest, as well
as human trafficking (58,59). Confidentiality is critical for
adolescents and can greatly influence their willingness to access
and use services (60–67). As a result, multiple professional
medical associations have emphasized the importance of
providing confidential services to adolescents (68–70).
Providers should encourage and promote communication
between the adolescent and his or her parent(s) or guardian(s)
about sexual and reproductive health (71–86). Adolescents
who come to the service site alone should be encouraged to
talk to their parents or guardians. Educational materials and
programs can be provided to parents or guardians that help
them talk about sex and share their values with their child
(72,87). When both parent or guardian and child have agreed,
joint discussions can address family values and expectations
about dating, relationships, and sexual behavior.
In a given year, approximately 20% of adolescent births
represent repeat births (88), so in addition to providing
postpartum contraception, providers should refer pregnant
and parenting adolescents to home visiting and other programs
that have been demonstrated to provide needed support and
reduce rates of repeat teen pregnancy (89–94).
Services for adolescents should be provided in a “youthfriendly” manner, which means that they are accessible,
equitable, acceptable, appropriate, comprehensive, effective,
and efficient for youth as recommended by the World Health
Organization (34).

Pregnancy Testing and Counseling
Providers of family planning services should offer pregnancy
testing and counseling services as part of core family planning
services, in accordance with recommendations of major
professional medical organizations, such as the American
College of Obstetricians and Gynecologists (ACOG) and the
American Academy of Pediatrics (AAP) (95–97).
Pregnancy testing is a common reason for a client to visit a
provider of family planning services. Approximately 65% of
pregnancies result in live births, 18% in induced abortion,
and 17% spontaneous fetal loss (98). Among live births, only
1% of infants are placed for adoption within their first month
of life (99).
The visit should include a discussion about her reproductive
life plan and a medical history that includes asking about
any coexisting conditions (e.g., chronic medical illnesses,
physical disability, psychiatric illness) (95,96). In most cases,

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a qualitative urine pregnancy test will be sufficient; however,
in certain cases, the provider may consider performing a
quantitative serum pregnancy test, if exact hCG levels would
be helpful for diagnosis and management. The test results
should be presented to the client, followed by a discussion of
options and appropriate referrals.
Options counseling should be provided in accordance with
recommendations from professional medical associations, such as
ACOG and AAP (95–97). A female client might wish to include
her partner in the discussion; however, if a client chooses not to
involve her partner, confidentiality must be assured.

Positive Pregnancy Test
If the pregnancy test is positive, the clinical visit should include
an estimation of gestational age so that appropriate counseling
can be provided. If a woman is uncertain about the date of her
last normal menstrual period, a pelvic examination might be
needed to help assess gestational age. In addition, clients should
receive information about the normal signs and symptoms of
early pregnancy, and should be instructed to report any concerns
to a provider for further evaluation. If ectopic pregnancy or
other pregnancy abnormalities or problems are suspected, the
provider should either manage the condition or refer the client
for immediate diagnosis and management.
Referral to appropriate providers of follow-up care should
be made at the request of the client, as needed. Every effort
should be made to expedite and follow through on all referrals.
For example, providers might provide a resource listing or
directory of providers to help the client identify options for
care. Depending upon a client’s needs, the provider may make
an appointment for the client, or call the referral site to let them
know the client was referred. Providers also should assess the
client’s social support and refer her to appropriate counseling
or other supportive services, as needed.
For clients who are considering or choose to continue the
pregnancy, initial prenatal counseling should be provided
in accordance with the recommendations of professional
medical associations, such as ACOG (97). The client should
be informed that some medications might be contraindicated
in pregnancy, and any current medications taken during
pregnancy need to be reviewed by a prenatal care provider
(e.g., an obstetrician or midwife). In addition, the client should
be encouraged to take a daily prenatal vitamin that includes
folic acid; to avoid smoking, alcohol, and other drugs; and
not to eat fish that might have high levels of mercury (97). If
there might be delays in obtaining prenantal care, the client
should be provided or referred for any needed STD screening
(including HIV) and vaccinations (36).

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Negative Pregnancy Test
Women who are not pregnant and who do not want to
become pregnant at this time should be offered contraceptive
services, as described previously. The contraceptive counseling
session should explore why the client thought that she was
pregnant and sought pregnancy testing services, and whether
she has difficulties using her current method of contraception.
A negative pregnancy test also provides an opportunity to discuss
the value of making a reproductive life plan. Ideally, these services
will be offered in the same visit as the pregnancy test because
clients might not return at a later time for contraceptive services.
Women who are not pregnant and who are trying to become
pregnant should be offered services to help achieve pregnancy or
basic infertility services, as appropriate (see “Clients Who Want
to Become Pregnant” and “Basic Infertility Services”). They also
should be offered preconception health and STD services (see
“Preconception Health Services” and “STD services”).

Clients Who Want to
Become Pregnant
Providers should advise clients who wish to become pregnant
in accordance with the recommendations of professional
medical organizations, such as the American Society for
Reproductive Medicine (ASRM) (100).
Providers should ask the client (or couple) how long she or
they have been trying to get pregnant and when she or they
hope to become pregnant. If the client’s situation does not
meet one of the standard definitions of infertility (see “Basic
Infertility Services”), then she or he may be counseled about
how to maximize fertility. Key points are as follows:
t The client should be educated about peak days and signs
of fertility, including the 6-day interval ending on the day
of ovulation that is characterized by slippery, stretchy
cervical mucus and other possible signs of ovulation.
t Women with regular menstrual cycles should be advised
that vaginal intercourse every 1–2 days beginning soon
after the menstrual period ends can increase the likelihood
of becoming pregnant.
t Methods or devices designed to determine or predict the time
of ovulation (e.g., over-the-counter ovulation kits, digital
telephone applications, or cycle beads) should be discussed.
t It should be noted that fertility rates are lower among
women who are very thin or obese, and those who consume
high levels of caffeine (e.g., more than five cups per day).
t Smoking, consuming alcohol, using recreational drugs,
and using most commercially available vaginal lubricants
should be discouraged as these might reduce fertility.

Recommendations and Reports

Basic Infertility Services
Providers should offer basic infertility care as part of
core family planning services in accordance with the
recommendations of professional medical organizations, such
as ACOG, ASRM, and the American Urological Association
(AUA) (96,101,102).
Infertility commonly is defined as the failure of a couple
to achieve pregnancy after 12 months or longer of regular
unprotected intercourse (101). Earlier assessment (such as
6 months of regular unprotected intercourse) is justified
for women aged >35 years, those with a history of oligoamenorrhea (infrequent menstruation), those with known or
suspected uterine or tubal disease or endometriosis, or those
with a partner known to be subfertile (the condition of being
less than normally fertile though still capable of effecting
fertilization) (101). An early evaluation also might be warranted
if risk factors of male infertility are known to be present or
if there are questions regarding the male partner’s fertility
potential (102). Infertility visits to a family planning provider
are focused on determining potential causes of the inability to
achieve pregnancy and making any needed referrals to specialist
care (101,102). ASRM recommends that evaluation of both
partners should begin at the same time (101).

Basic Infertility Care for Women
The clinical visit should focus on understanding the client’s
reproductive life plan (24) and her difficulty in achieving
pregnancy through a medical history, sexual health assessment
and physical exam, in accordance with recommendations
developed by professional medical associations such as
ASRM (101) and ACOG (96). The medical history should
include past surgery, including indications and outcome(s),
previous hospitalizations, serious illnesses or injuries, medical
conditions associated with reproductive failure (e.g., thyroid
disorders, hirsutism, or other endocrine disorders), and
childhood disorders; results of cervical cancer screening and
any follow-up treatment; current medication use and allergies;
and family history of reproductive failure. In addition, a
reproductive history should include how long the client has
been trying to achieve pregnancy; coital frequency and timing,
level of fertility awareness, and results of any previous evaluation
and treatment; gravidity, parity, pregnancy outcome(s), and
associated complications; age at menarche, cycle length and
characteristics, and onset/severity of dysmenorrhea; and
sexual history, including pelvic inflammatory disease, history
of STDs, or exposure to STDs. A review of systems should
emphasize symptoms of thyroid disease, pelvic or abdominal
pain, dyspareunia, galactorrhea, and hirsutism (101).

The physical examination should include: height, weight, and
body mass index (BMI) calculation; thyroid examination to
identify any enlargement, nodule, or tenderness; clinical breast
examination; and assessment for any signs of androgen excess.
A pelvic examination should assess for: pelvic or abdominal
tenderness, organ enlargement or mass; vaginal or cervical
abnormality, secretions, or discharge; uterine size, shape, position,
and mobility; adnexal mass or tenderness; and cul-de-sac mass,
tenderness, or nodularity. If needed, clients should be referred
for further diagnosis and treatment (e.g., serum progesterone
levels, follicle-stimulating hormone/luteinizing hormone levels,
thyroid function tests, prolactin levels, endometrial biopsy,
transvaginal ultrasound, hysterosalpingography, laparoscopy,
and clomiphene citrate).

Basic Infertility Care for Men
Infertility services should be provided for the male partner
of an infertile couple in accordance with recommendations
developed by professional medical associations such as AUA
(102). Providers should discuss the client’s reproductive life
plan, take a medical history, and conduct a sexual health
assessment. AUA recommends that the medical history include
a reproductive history (102). The medical history should
include systemic medical illnesses (e.g., diabetes mellitus),
prior surgeries and past infections; medications (prescription
and nonprescription) and allergies; and lifestyle exposures. The
reproductive history should include methods of contraception,
coital frequency and timing; duration of infertility and prior
fertility; sexual history; and gonadal toxin exposure, including
heat. Patients also should be asked about their female partners’
history of pelvic inflammatory disease, their partners’ histories
of STDs, and problems with sexual dysfunction.
In addition, a physical examination should be conducted with
particular focus given to 1) examination of the penis, including
the location of the urethral meatus; 2) palpation of the testes
and measurement of their size; 3) presence and consistency of
both the vas deferens and epididymis; 4) presence of a varicocele;
5) secondary sex characteristics; and 6) a digital rectal exam
(102). Male clients concerned about their fertility should have
a semen analysis. If this test is abnormal, they should be referred
for further diagnosis (i.e., second semen analysis, endocrine
evaluation, post-ejaculate urinalysis, or others deemed necessary)
and treatment. The semen analysis is the first and most simple
screen for male fertility.

Infertility Counseling
Counseling provided during the clinical visit should be
guided by information elicited from the client during the
medical and reproductive history and the findings of the
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physical exam. If there is no apparent cause of infertility
and the client does not meet the definition above, providers
should educate the client about how to maximize fertility (see
“Clients Who Want to Become Pregnant”). ACOG notes
the importance of addressing the emotional and educational
needs of clients with infertility and recommends that providers
consider referring clients for psychological support, infertility
support groups, or family counseling (96).

Preconception Health Services
Providers of family planning services should offer
preconception health services to female and male clients
in accordance with CDC’s recommendations to improve
preconception health and health care (24).
Preconception health services are beneficial because of
their effect on pregnancy and birth outcomes and their
role in improving the health of women and men. The term
preconception describes any time that a woman of reproductive
potential is not pregnant but at risk of becoming pregnant,
or when a man is at risk for impregnating his female partner.
Preconception health-care services for women aim to identify
and modify biomedical, behavioral, and social risks to a
woman’s health or pregnancy outcomes through prevention and
management. It promotes the health of women of reproductive
age before conception, and thereby helps to reduce pregnancyrelated adverse outcomes, such as low birthweight, premature
birth, and infant mortality (24). Moreover, the preconception
health services recommended here are equally important
because they contribute to the improvement of women’s health
and well-being, regardless of her childbearing intentions. CDC
recommends that preconception health services be integrated
into primary care visits made by women of reproductive age,
such as family planning visits (24).
In the family planning setting, providers may prioritize
screening and counseling about preconception health for
couples that are trying to achieve pregnancy and couples
seeking basic infertility services. Women who are using
contraception to prevent or delay pregnancy might also
benefit from preconception health services, especially those
at high risk of unintended pregnancy. A woman is at high
risk of unintended pregnancy if she is using no method or a
less effective method of contraception (e.g., barrier methods,
rhythm, or withdrawal), or has a history of contraceptive
discontinuation or incorrect use (38,39). A woman is at lower
risk of unintended pregnancy if she is using a highly effective
method, such as an IUD or implant, or has an established
history of using methods of contraception, such as injections,
pills, patch, or ring correctly and consistently (38,39). Clients

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who do not want to become pregnant should also be provided
preconception health services, since they are recommended by
USPSTF for the purpose of improving the health of adults.
Recommendations for improving the preconception health
of men also have been identified, although the evidence base
for many of the recommendations for men is less than that
for women (103). This report includes preconception health
services that address men as partners in family planning (i.e., both
preventing and achieving pregnancy), their direct contributions
to infant health (e.g., genetics), and their role in improving the
health of women (e.g., through reduced STD/HIV transmission).
Moreover, these services are important for improving the health
of men regardless of their pregnancy intention.
In a family planning setting, all women planning or capable
of pregnancy should be counseled about the need to take a daily
supplement containing 0.4 to 0.8 mg of folic acid, in accordance
with the USPSTF recommendation (Grade A) (104).
Other preconception health services for women and men
should include discussion of a reproductive life plan and
sexual health assessment (Boxes 2 and 4), as well as the
screening services described below (24,103,105). Services
should be provided in accordance with the cited clinical
recommendations, and any needed follow up (further
diagnosis, treatment) should be provided either on-site or
through referral.
Medical History
For female clients, the medical history should include
the reproductive history, history of poor birth outcomes
(i.e., preterm, cesarean delivery, miscarriage, and stillbirth),
environmental exposures, hazards and toxins (e.g., smoking,
alcohol, other drugs), medications that are known teratogens,
genetic conditions, and family history (24,105).
For male clients, the medical history should include asking about
the client’s past medical and surgical history that might impair his
reproductive health (e.g., genetic conditions, history of reproductive
failures, or conditions that can reduce sperm quality, such as obesity,
diabetes mellitus, and varicocele) and environmental exposures,
hazards and toxins (e.g., smoking) (103).
Intimate Partner Violence
Providers should screen women of childbearing age for
intimate partner violence and provide or refer women who screen
positive to intervention services, in accordance with USPSTF
(Grade B) recommendations (106).
Alcohol and Other Drug Use
For female and male adult clients, providers should screen for
alcohol use in accordance with the USPSTF recommendation
(Grade B) for how to do so, and provide behavioral counseling

Recommendations and Reports

interventions, as indicated (107). Screening adults for other
drug use and screening adolescents for alcohol and other drug
use has the potential to reduce misuse of alcohol and other
drugs, and can be recommended (105,108,109). However,
the USPSTF recommendation for screening for other drugs
in adults, and for alcohol and other drugs in adolescents, is an
“I,” and patients should be informed that there is insufficient
evidence to assess the balance of benefits and harms of this
screening (107,110).
Tobacco Use
For female and male clients, providers should screen for
tobacco use in accordance with the USPSTF recommendation
(111,112) for how to do so. Adults (Grade A) who use tobacco
products should be provided or referred for tobacco cessation
interventions, including brief behavioral counseling sessions
(<10 minutes) and pharmacotherapy delivered in primary
care settings (111). Adolescents (Grade B) should be provided
intervention to prevent initiation of tobacco use (112).
Immunizations
For female and male clients, providers should screen for
immunization status in accordance with recommendations
of CDC’s Advisory Committee on Immunization Practices
(113) and offer vaccination, as indicated, or provide referrals
to community providers for immunization. Female and male
clients should be screened for age-appropriate vaccinations,
such as influenza and tetanus–diphtheria–pertussis (Tdap),
measles, mumps, and rubella (MMR), varicella, pneumococcal,
and meningococcal. In addition, ACOG recommends that
rubella titer be performed in women who are uncertain about
MMR immunization (108). (For vaccines for reproductive
health-related conditions, i.e., human papillomavirus and
hepatitis B, see “Sexually Transmitted Disease Services.”)
Depression
For all clients, providers should screen for depression
when staff-assisted depression care supports are in place to
ensure accurate diagnosis, effective treatment, and follow-up
(114,115). Staff-assisted care supports are defined as clinical
staff members who assist the primary care clinician by
providing some direct depression care, such as care support or
coordination, case management, or mental health treatment.
The lowest effective staff supports consist of a screening nurse
who advises primary care clinicians of a positive screen and
provides a protocol facilitating referral to behavioral therapy.
Providers also may follow American Psychiatric Association
(116) and American Academy of Child and Adolescent
Psychiatry (117) recommendations to assess risk for suicide
among persons experiencing depression and other risk factors.

Height, Weight, and Body Mass Index
For all clients, providers should screen adult (Grade B) and
adolescent (Grade B) clients for obesity in accordance with
the USPSTF recommendation, and obese adults should be
referred for intensive counseling and behavioral interventions
to promote sustained weight loss (118,119). Clients likely will
need to be referred for this service. These interventions typically
comprise 12 to 26 sessions in a year and include multiple
behavioral management activities, such as group sessions,
individual sessions, setting weight-loss goals, improving diet
or nutrition, physical activity sessions, addressing barriers to
change, active use of self-monitoring, and strategizing how to
maintain lifestyle changes.
Blood Pressure
For female and male clients, providers should screen for
hypertension in accordance with the USPSTF’s recommendation
(Grade A) that blood pressure be measured routinely
among adults (120) and the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure’s recommendation that persons with blood
pressure less than 120/80 be screened every 2 years, and every
year if prehypertensive (i.e., blood pressure 120–139/80–89)
(121). Providers also may follow AAP’s recommendation that
adolescents receive annual blood pressure screening (109).
Diabetes
For female and male clients, providers should follow the
USPSTF recommendation (Grade B) to screen for type 2
diabetes in asymptomatic adults with sustained blood pressure
(either treated or untreated) >135/80 mmHg (122).

Sexually Transmitted
Disease Services
Providers should offer STD services in accordance with CDC’s
STD treatment and HIV testing guidelines (36,123,124). It
is important to test for chlamydia annually among young
sexually active females and for gonorrhea routinely among all
sexually active females at risk for infection because they can
cause tubal infertility in women if left untreated. Testing for
syphilis, HIV/AIDS, and hepatitis C should be conducted
as recommended (36,123,124). Vaccination for human
papillomavirus (HPV) and hepatitis B are also important parts
of STD services and preconception care (113).
STD services should be provided for persons with no signs or
symptoms suggestive of an STD. STD diagnostic management
recommendations are not included in these guidelines, so
providers should refer to CDC’s STD treatment guidelines

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(36) when caring for clients with STD symptoms. STD services
include the following steps, which should be provided at the
initial visit and at least annually thereafter:
Step 1. Assess: The provider should discuss the client’s
reproductive life plan, conduct a standard medical history
and sexual health assessment (see text box above), and check
immunization status. A pelvic exam is not indicated in patients
with no symptoms suggestive of an STD.
Step 2. Screen: A client who is at risk of an STD
(i.e., sexually active and not involved in a mutually
monogamous relationship with an uninfected partner) should
be screened for HIV and the other STDs listed below, in
accordance with CDC’s STD treatment guidelines (36) and
recommendations for HIV testing of adults, adolescents,
and pregnant women in health-care settings (123). Clients
also should follow CDC’s recommendations for testing
for hepatitis C (124), and the Advisory Committee on
Immunization Practice’s recommendations on reproductive
health-related immunizations (113). It is important to follow
these guidelines both to ensure that clients receive needed
services and to avoid unnecessary screening.
Chlamydia

<25 years are at highest risk for gonorrhea infection. Other risk
factors that place women at increased risk include a previous
gonorrhea infection, the presence of other STDs, new or multiple
sex partners, inconsistent condom use, commercial sex work, and
drug use. Females with gonnorrhea infection should be re-screened
for re-infection at 3 months after treatment. Pregnant women
should be screened for gonorrhea at the time of their pregnancy
test if there might be delays in obtaining prenatal care (36).
For male clients, providers should screen MSM for gonorrhea
at anatomic sites of exposure, in accordance with CDC’s STD
treatment guidelines (36). Males with symptoms suggestive of
gonorrhea (urethral discharge or dysuria or whose partner has
gonorrhea) should be tested and empirically treated at the initial
visit. Males with gonorrhea infection should be re-screened for
reinfection at 3 months after treatment (36,126–128).
Syphilis
For female and male clients, providers should screen clients for
syphilis, in accordance with CDC’s STD treatment guidelines
(36). CDC recommends that persons at risk for syphilis infection
should be screened. Populations at risk include MSM, commercial
sex workers, persons who exchange sex for drugs, those in adult
correctional facilities and those living in communities with high
prevalence of syphilis (36). Pregnant women should be screened
for syphilis at the time of their pregnancy test if there might be
delays in obtaining prenatal care (36).

For female clients, providers should screen all sexually active
women aged ≤25 years for chlamydia annually, in addition
to sexually active women aged >25 years with risk factors for
chlamydia infection (36). Women aged >25 years at higher
risk include sexually active women who have a new or more
than one sex partner or who have a partner who has other
concurrent partners. Females with chlamydia infection should
be rescreened for re-infection at 3 months after treatment.
Pregnant women should be screened for chlamydia at the time
of their pregnancy test if there might be delays in obtaining
prenatal care (36).
For male clients, chlamydia screening can be considered for
males seen at sites with a high prevalence of chlamydia, such
as adolescent clinics, correctional facilities, and STD clinics
(36,125,126). Providers should screen men who have sex with
men (MSM) for chlamydia at anatomic sites of exposure, in
accordance with CDC’s STD treatment guidelines (36). Males
with symptoms suggestive of chlamydia (urethral discharge or
dysuria or whose partner has chlamydia) should be tested and
empirically treated at the initial visit. Males with chlamydia
infection should be re-screened for reinfection at 3 months (36).

For female and male clients, providers should screen
clients for HIV/AIDS, in accordance with CDC HIV
testing guidelines (123). Providers should follow CDC
recommendations that all clients aged 13–64 years be screened
routinely for HIV infection and that all persons likely to be at
high risk for HIV be rescreened at least annually (123). Persons
likely to be at high risk include injection-drug users and their
sex partners, persons who exchange sex for money or drugs, sex
partners of HIV-infected persons, and MSM or heterosexual
persons who themselves or whose sex partners have had more
than one sex partner since their most recent HIV test. CDC
further recommends that screening be provided after the
patient is notified that testing will be performed as part of
general medical consent unless the patient declines (opt-out
screening) or otherwise prohibited by state law. The USPSTF
also recommends screening for HIV (Grade A) (129).

Gonorrhea

Hepatitis C

For female clients, providers should screen clients for gonorrhea,
in accordance with CDC’s STD treatment guidelines (36).
Routine screening for N. gonorrhoeae in all sexually active women
at risk for infection is recommended annually (36). Women aged

For female and male clients, CDC recommends one-time
testing for hepatitis C (HCV) without prior ascertainment of
HCV risk for persons born during 1945–1965, a population
with a disproportionately high prevalence of HCV infection

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Recommendations and Reports

and related disease. Persons identified as having HCV
infection should receive a brief screening for alcohol use and
intervention as clinically indicated, followed by referral to
appropriate care for HCV infection and related conditions.
These recommendations do not replace previous guidelines for
HCV testing that are based on known risk factors and clinical
indications. Rather, they define an additional target population
for testing: persons born during 1945–1965 (124). USPSTF
also recommends screening persons at high risk for infection
for hepatitis C and one-time screening for HCV infection
for persons in the 1945–1965 birth cohort (Grade B) (130).
Immunizations Related to Reproductive Health
Female clients aged 11–26 years should be offered either
human papillomavirus (HPV) 2 or HPV4 vaccine for the
prevention of HPV and cervical cancer if not previously
vaccinated, although the series can be started in persons as
young as age 9 years (113); recommendations include starting
at age 11–12 years and catch up vaccine among females aged
13–26 who have not been vaccinated previously or have
not completed the 3-dose series through age 26. Routine
hepatitis B vaccination should be offered to all unvaccinated
children and adolescents aged <19 years and all adults who
are unvaccinated and do not have any documented history of
hepatitis B infection (113).
Male clients aged 11–21 years (minimum age: 9 years)
should be offered HPV4 vaccine, if not vaccinated previously;
recommendations include starting at age 11–12 years and catch
up vaccine among males aged 13–21 years who have not been
vaccinated previously or have not completed the 3-dose series
through age 21 years; vaccination is recommended among
at-risk males, including MSM and immune-compromised
males through age 26 years if not vaccinated previously or
males who have not completed the 3-dose series through age 26
years. Heterosexual males aged 22–26 years may be vaccinated
(131). Routine hepatitis B vaccination should be offered to all
unvaccinated children and adolescents aged <19 years, and all
unvaccinated adults who do not have a documented history
of hepatitis B infection (113).
Step 3. Treat: A client with an STD and her or his
partner(s) should be treated in a timely fashion to prevent
complications, re-infection and further spread of the infection
in the community in accordance with CDC’s STD treatment
guidelines; clients with HIV infection should be linked to
HIV care and treatment (36,123). Clients should be counseled
about the need for partner evaluation and treatment to avoid
reinfection at the time the client receives the positive test
results. For partners of clients with chlamydia or gonorrhea,
one option is to schedule them to come in with the client;
another option for partners who cannot come in with the client

is expedited partner therapy (EPT), as permissible by state laws,
in which medication or a prescription is provided to the patient
to give to the partner to ensure treatment. EPT is a partner
treatment strategy for partners who are unable to access care
and treatment in a timely fashion. Because of concerns related
to resistant gonorrhea, efforts to bring in for treatment partners
of patients with gonorrhea infection are recommended; EPT
for gonorrhea should be reserved for situations in which efforts
to treat partners in a clinical setting are unsuccessful and EPT
is a gonorrhea treatment of last resort.
All clients treated for chlamydia or gonorrhea should be
rescreened 3 months after treatment; HIV-infected females
with Trichomonas vaginalis should be linked to HIV care and
rescreened for T. vaginalis at 3 months. If needed, the client also
should be vaccinated for hepatitis B and HPV (113). Ideally,
STD treatment should be directly observed in the facility
rather than a prescription given or called in to a pharmacy.
If a referral is made to a service site that has the necessary
medication available on-site, such as the recommended
injectable antimicrobials for gonorrhea and syphilis, then the
referring provider must document that treatment was given.
Step 4. Provide risk counseling: If the client is at risk for
or has an STD, high-intensity behavioral counseling for sexual
behavioral risk reduction should be provided in accordance
with the USPSTF recommendation (Grade B) (132). One
high-intensity behavioral counseling model that is similar to
the contraceptive counseling model is Project Respect (133),
which could be implemented in family planning settings. All
sexually active adolescents are at risk, and adults are at increased
risk if they have current STDs, had an STD in the past
year, have multiple sexual partners, are in nonmonogamous
relationships, or are sexually active and live in a community
with a high rate of STDs.
Other key messages to give infected clients before they
leave the service site include the following: a) refrain from
unprotected sexual intercourse during the period of STD
treatment, 2) encourage partner(s) to be screened or to get
treatment as quickly as possible in accordance with CDC’s
STD treatment guidelines (partners in the past 60 days for
chlamydia and gonorrhea, 3 to 6 months plus the duration of
lesions or signs for primary and secondary syphilis, respectively)
if the partner did not accompany the client to the service site
for treatment, and 3) return for retesting in 3 months. If the
partner is unlikely to access treatment quickly, then EPT for
chlamydia or gonorrhea should be considered, if permissible
by state law.
A client using or considering contraceptive methods other
than condoms should be advised that these methods do not
protect against STDs. Providers should encourage a client
who is not in a mutually monogamous relationship with an

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uninfected partner to use condoms. Patients who do not know
their partners’ infection status should be encouraged to get
tested and use condoms or avoid sexual intercourse until their
infection status is known.

Related Preventive Health Services
For many women and men of reproductive age, a family
planning service site is their only source of health care;
therefore, visits should include provision of or referral to other
preventive health services. Providers of family planning services
that do not have the capacity to offer comprehensive primary
care services should have strong links to other community
providers to ensure that clients have access to primary care. If
a client does not have another source of primary care, priority
should be given to providing related reproductive health
services or providing referrals, as needed.
For clients without a primary care provider, the following
screening services should be provided, with appropriate
follow-up, if needed, while linking the client to a primary care
provider. These services should be provided in accordance with
federal and professional medical recommendations cited below
regarding the frequency of screening, the characteristics of the
clients that should be screened, and the screening procedures
to be used.
Medical History
USPSTF recommends that women be asked about family
history that would be suggestive of an increased risk for
deleterious mutations in BRCA1 or BRCA2 genes (e.g.,
receiving a breast cancer diagnosis at an early age, bilateral
breast cancer, history of both breast and ovarian cancer,
presence of breast cancer in one or more female family
members, multiple cases of breast cancer in the family, both
breast and ovarian cancer in the family, one or more family
members with two primary cases of cancer, and Ashkenazi
background). Women with identified risk(s) should be referred
for genetic counseling and evaluation for BRCA testing
(Grade B) (134). The USPSTF also recommends that women
at increased risk for breast cancer should be counseled about
risk-reducing medications (Grade B) (135).
Cervical Cytology
Providers should provide cervical cancer screening to clients
receiving related preventive health services. Providers should
follow USPSTF recommendations to screen women aged
21–65 years with cervical cytology (Pap smear) every 3 years,
or for women aged 30–65 years, screening with a combination
of cytology and HPV testing every 5 years (Grade A) (136).

MMWR / April 25, 2014 / Vol. 63 / No. 4

Cervical cytology no longer is recommended on an annual
basis. Further, it is not recommended (Grade D) for women
aged <21 years (136). Women with abnormal test results should
be treated in accordance with professional standards of care,
which may include colposcopy (96,137). The need for cervical
cytology should not delay initiation or hinder continuation of
a contraceptive method (42).
Providers should also follow ACOG and AAP recommendations
that a genital exam should accompany a cervical cancer screening
to inspect for any suspicious lesions or other signs that might
indicate an undiagnosed STD (96,97,138).
Clinical Breast Examamination
Despite a lack of definitive data for or against, clinical
breast examination has the potential to detect palpable breast
cancer and can be recommended. ACOG recommends
annual examination for all women aged >19 years (108).
ACS recommends screening every 3 years for women aged
20–39 years, and annually for women aged ≥40 years (139).
However, the USPSTF recommendation for clinical breast
exam is an I, and patients should be informed that there is
insufficient evidence to assess the balance of benefits and harms
of the service (140).
Mammography
Providers should follow USPSTF recommendations
(Grade B) to screen women aged 50–74 years on a biennial
basis; they should screen women aged <50 years if other
conditions support providing the service to an individual
patient (140).
Genital Examination
For adolescent males, examination of the genitals should be
conducted. This includes documentation of normal growth and
development and other common genital findings, including
hydrocele, varicocele, and signs of STDs (141). Components
of this examination include inspecting skin and hair, palpating
inguinal nodes, scrotal contents and penis, and inspecting the
perinanal region (as indicated).

Summary of Recommendations for
Providing Family Planning and
Related Preventive Health Services
The screening components for each family planning and
related preventive health service are provided in summary
checklists for women (Table 2) and men (Table 3). When
considering how to provide the services listed in these
recommendations (e.g., the screening components for each

Recommendations and Reports

service, risk groups that should be screened, the periodicity of
screening, what follow-up steps should be taken if screening
reveals the presence of a health condition), providers should
follow CDC and USPSTF recommendations cited above,
or, in the absence of CDC and USPSTF recommendations,
the recommendations of professional medical associations.
Following these recommendations is important both to ensure
clients receive needed care and to avoid unnecessary screening
of clients who do not need the services.
The summary tables describe multiple screening steps, which
refer to the following: 1) the process of asking questions about
a client’s history, including a determination of whether risk
factors for a disease or health condition exist; 2) performing
a physical exam; and 3) performing laboratory tests in
at-risk asymptomatic persons to help detect the presence of
a specific disease, infection, or condition. Many screening
recommendations apply only to certain subpopulations
(e.g., specific age groups, persons who engage in specific risk
behaviors or who have specific health conditions), or some
screening recommendations apply to a particular frequency
(e.g., a cervical cancer screening is generally recommended
every 3 years rather than annually). Providers should be aware
that the USPSTF also has recommended that certain screening
services not be provided because the harm outweighs the
benefit (see Appendix F).
When screening results indicate the potential or actual
presence of a health condition, the provider should either provide
or refer the client for the appropriate further diagnostic testing or
treatment in a manner that is consistent with the relevant federal
or professional medical associations’ clinical recommendations.

Conducting Quality Improvement
Service sites that offer family planning services should
have a system for conducting quality improvement, which is
designed to review and strengthen the quality of services on an
ongoing basis. Quality improvement is the use of a deliberate
and continuous effort to achieve measurable improvements
in the identified indicators of quality of care, which improve
the health of the community (142). By improving the quality
of care, family planning outcomes, such as reduced rates of
unintended pregnancy, improved patient experiences, and
reduced costs, are more likely to be achieved (10,12,143,144).
Several frameworks for conducting quality improvement
have been developed (144–146). This section presents a general
overview of three key steps that providers should take when
conducting quality improvement of family planning services:
1) determine which measures are needed to monitor quality;
2) collect the information needed; and 3) use the findings to

make changes to improve quality (147). Ideally, these steps
will be conducted on a frequent (optimally, quarterly) and
ongoing basis. However, since quality cuts across all aspects
of a program, not all domains of quality can necessarily be
considered at all times. Within a sustainable system of quality
improvement, programs can opt to focus on a subset of quality
dimensions and their respective measures.

Determining Which Measures Are Needed
Performance measures provide information about how
well the service site is meeting pre-established goals (148).
The following questions should be considered when selecting
performance measures (143):
t Is the topic important to measure and report? For example,
does it address a priority aspect of health care, and is there
opportunity for improvement?
t What is the level of evidence for the measure (e.g., that a
change in the measure is likely to represent a true change in
health outcomes)? Does the measure produce consistent
(reliable) and credible (valid) results about the quality of care?
t Are the results meaningful and understandable and useful
for informing quality improvement?
t Is the measure feasible? Can it be implemented without
undue burden (e.g., captured with electronic data or
electronic health records)?
Performance measures should consider the quality of the
structure of services (e.g., the characteristics of the settings in which
providers deliver health care, including material resources, human
resources, and organizational structure), the process by which care
is provided (whether services are provided correctly and completely,
and how clients perceive the care they receive), and the outcomes
of that care (e.g., client behaviors or health conditions that result)
(149). They also may assess each dimension of quality services
(10,13). Examples of measures that can be used for monitoring the
quality of family planning services (150) and suggested measures
that might help providers monitor quality of care have been listed
(Table 6). However, other measures have been developed that also
might be useful (151–153). Service sites that offer family planning
services should select, measure, and assess at least one intermediate
or outcome measure on an ongoing basis, for which the service site
can be accountable. Structure- and process-based measures that
assess the eight dimensions of quality services may be used to better
determine how to improve quality (154).

Collecting Information
Once providers have determined what information is needed,
the next steps are to collect and use that information to improve
the quality of care. Commonly used methods of data collection
include the following:
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Recommendations and Reports

TABLE 2. Checklist of family planning and related preventive health services for women
Family planning services
(provide services in accordance with the appropriate clinical recommendation)
Contraceptive
services*

Screening components
History
Reproductive life plan§
Medical history§,**
Current pregnancy status§
Sexual health assessment§,**
Intimate partner violence §,¶,**
Alcohol and other drug use§,¶,**
Tobacco use§,¶

Screen
Screen
Screen
Screen

Pregnancy testing and
Preconception health
counseling
Basic infertility services
services
Screen
Screen

STD services†

Related preventive
health services

Screen

Screen
Screen

Screen

Screen
Screen
Screen
Screen

Screen

Immunizations§

Screen

Screen for HPV &
HBV§§

Depression§,¶

Screen
Screen

Screen (combined
hormonal methods
for clients aged ≥35
years)

Folic acid§,¶
Physical examamination
Height, weight and BMI§,¶
Blood pressure§,¶
Clinical breast exam**
Pelvic exam§,**

Screen (hormonal
methods)††
Screen (combined
hormonal methods)
Screen (initiating
diaphragm or IUD)

Screen

Screen§§

Screen (if clinically
indicated)

Signs of androgen excess**
Thyroid exam**
Laboratory testing
Pregnancy test **
Chlamydia§, ¶
Gonorrhea§, ¶
Syphilis§,¶
HIV/AIDS§,¶
Hepatitis C§,¶
Diabetes§,¶
Cervical cytology¶
Mammography¶

Screen

Screen§§

Screen
Screen
Screen
Screen

Screen (if clinically
indicated)
Screen¶¶
Screen¶¶

Screen
Screen§§
Screen§§
Screen§§
Screen§§
Screen§§
Screen§§
Screen§§
Screen§§

Abbreviations: BMI = body mass index; HBV = hepatitis B virus; HIV/AIDS = human immunodeficiency virus/acquired immunodeficiency syndrome; HPV = human papillomavirus;
IUD = intrauterine device; STD = sexually transmitted disease.
* This table presents highlights from CDC’s recommendations on contraceptive use. However, providers should consult appropriate guidelines when treating individual patients to obtain
more detailed information about specific medical conditions and characteristics (Source: CDC. U.S. medical eligibility criteria for contraceptive use 2010. MMWR 2010;59(No. RR-4).
† STD services also promote preconception health but are listed separately here to highlight their importance in the context of all types of family planning visits. The services listed in this column
are for women without symptoms suggestive of an STD.
§ CDC recommendation.
¶ U.S. Preventive Services Task Force recommendation.
** Professional medical association recommendation.
†† Weight (BMI) measurement is not needed to determine medical eligibility for any methods of contraception because all methods can be used (U.S. Medical Eligibility Criteria 1) or generally
can be used (U.S. Medical Eligibility Criteria 2) among obese women (Source: CDC. U.S. medical eligibility criteria for contraceptive use 2010. MMWR 2010;59[No. RR-4]). However, measuring
weight and calculating BMI at baseline might be helpful for monitoring any changes and counseling women who might be concerned about weight change perceived to be associated
with their contraceptive method.
§§ Indicates that screening is suggested only for those persons at highest risk or for a specific subpopulation with high prevalence of an infection or condition.
¶¶ Most women do not require additional STD screening at the time of IUD insertion if they have already been screened according to CDC’s STD treatment guidelines (Sources: CDC. STD treatment
guidelines. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cdc.gov/std/treatment. CDC. Sexually transmitted diseases treatment guidelines,
2010. MMWR 2010;59[No. RR-12]). If a woman has not been screened according to guidelines, screening can be performed at the time of IUD insertion and insertion should not be delayed.
Women with purulent cervicitis or current chlamydial infection or gonorrhea should not undergo IUD insertion (U.S. Medical Eligibility Criteria 4) women who have a very high individual
likelihood of STD exposure (e.g. those with a currently infected partner) generally should not undergo IUD insertion (U.S. Medical Eligibility Criteria 3) (Source: CDC. US medical eligibility
criteria for contraceptive use 2010. MMWR 2010;59[No. RR-4]). For these women, IUD insertion should be delayed until appropriate testing and treatment occurs.

t Review of medical records. All records that detail service
delivery activities can be reviewed, including encounters
and claims data, client medical records, facility logbooks,
and others. It is important that records be carefully
designed, sufficiently detailed, provide accurate
information, and have access restricted to protect
confidentiality. The use of electronic health records can
facilitate some types of medical record review.

MMWR / April 25, 2014 / Vol. 63 / No. 4

t Exit interview with the client. A patient is asked (through
either a written or in-person survey) to describe what
happened during the encounter or their assessment of their
satisfaction with the visit. Both quantitative (close-ended
questions) and qualitative (open-ended questions)
methods can be used. Limitations include a bias toward
clients reporting higher degrees of satisfaction, and the

Recommendations and Reports

TABLE 3. Checklist of family planning and related preventive health services for men
Family planning services
(provide services in accordance with the appropriate clinical recommendation)
Screening components and source
of recommendation
History
Reproductive life plan¶
Medical history¶,††
Sexual health assessment¶,††
Alcohol & other drug use ¶,**,††
Tobacco use¶,**
Immunizations¶
Depression¶,**
Physical examination
Height, weight, and BMI¶,**
Blood pressure**,††
Genital exam††

Contraceptive services*

Basic infertility
services

Screen
Screen
Screen

Preconception
health services†
Screen
Screen
Screen
Screen
Screen
Screen
Screen

STD services§

Related preventive
health services

Screen
Screen
Screen
Screen for HPV & HBV§§

Screen
Screen§§
Screen (if clinically
indicated)

Laboratory testing
Chlamydia¶
Gonorrhea¶
Syphilis¶,**
HIV/AIDS¶,**
Hepatitis C¶,**
Diabetes¶,**

Screen (if clinically
indicated)

Screen§§

Screen§§
Screen§§
Screen§§
Screen§§
Screen§§
Screen§§

Abbreviations: HBV = hepatitis B virus; HIV/AIDS = human immunodeficiency virus/acquired immunodeficiency syndrome; HPV = human papillomavirus virus;
STD = sexually transmitted disease.
* No special evaluation needs to be done prior to making condoms available to males. However, when a male client requests advice on pregnancy prevention, he
should be provided contraceptive services as described in the section “Provide Contraceptive Services.”
† The services listed here represent a sub-set of recommended preconception health services for men that were recommended and for which there was a direct link
to fertility or infant health outcomes (Source: Frey K, Navarro S, Kotelchuck M, Lu M. The clinical content of preconception care: preconception care for men. Am J
Obstet Gynecol 2008;199[6 Suppl 2]:S389–95).
§ STD services also promote preconception health, but are listed separately here to highlight their importance in the context of all types of family planning visit. The
services listed in this column are for men without symptoms suggestive of an STD.
¶ CDC recommendation.
** U.S. Preventive Services Task Force recommendation.
†† Professional medical association recommendation.
§§ Indicates that screening is suggested only for those persons at highest risk or for a specific subpopulation with high prevalence of infection or other condition.

provider’s behavior might be influenced if she or he knows
clients are being interviewed.
t Facility audit. Questions about a service site’s structure
(e.g., on-site availability of a broad range of FDA-approved
methods) and processes (e.g., skills and technical
competence of staff, referral mechanisms) can be used to
determine the readiness of the facility to serve clients.
t Direct observation. A provider’s behavior is observed
during an actual encounter with a client. Evaluation of a
full range of competencies, including communication
skills, can be carried out. A main limitation is that the
observer’s presence might influence the provider’s
performance.
t Interview with the health-care provider. Providers are
interviewed about how specific conditions are managed.
Both closed- and open-ended questions can be used,
although it is important to frame the question so that the
‘correct’ answer is not suggested. A limitation is that
providers tend to over-report their performance.

Consideration and Use of the Findings
After data are collected, they should be tabulated, analyzed,
and used to improve care. Staff whose performance was assessed
should be involved in the development of the data collection
tools and analysis of results. Analysis should address the
following questions (155):
t What is the performance level of the facility?
t Is there a consistent pattern of performance among
providers?
t What is the trend in performance?
t What are the causes of poor performance?
t How can performance gaps be minimized?
Given the findings, service site staff should use a systematic
approach to identifying ways to improve the quality of care.
One example of a systematic approach to improving the
quality of care is the “Plan, Do, Study, and Act” (PDSA) model
(147,156), in which staff first develop a plan for improving
quality, then execute the plan on a small scale, evaluate feedback
to confirm or adjust the plan, and finally, make the plan

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

TABLE 4. Suggested measures of the quality of family planning services
Type of measure and dimension of quality

Measure

Source

Health outcome

t
t
t
t

Safe (Structure)

t Proportion of providers that follow the most current CDC recommendations on
contraceptive safety

Effective
(Structure, or the characteristics of the
settings in which providers deliver health
care, including material resources,
human resources, and organizational
structure)

t Site dispenses or provides on-site a full range of FDA-approved contraceptive methods
to meet the diverse reproductive needs and goals of clients; short-term hormonal,
long-acting reversible contraception (LARC), emergency contraception (EC).
t Proportion of female users aged ≥24 years who are screened annually for chlamydial
infection.
t Proportion of female users aged ≥24 years who are screened annually for gonorrhea.
t Proportion of users who were tested for HIV during the past 12 months.
t Proportion of female users aged ≥21 years who have received a Pap smear within
the past 3 years.

PIMS*

Client-centered
(Process, or whether services are provided
correctly and completely, and how
clients perceive the care they receive)

t Proportion of clients who report the provider communicates well, shows respect,
spends enough time with the client, and is informed about the client’s medical
history.
t Proportion of clients who report that
– Staff are helpful and treat clients with courtesy and respect.
– His or her privacy is respected.
– She or he receives contraceptive method that is acceptable to her or him.

CAHPS†
RQIP§

Efficient
(Structure)

t Site uses electronic health information technology or electronic health records to
improve client reproductive health.

PIMS*

Timely
(Structure and process)

t
t
t
t

PIMS*

Accessible
(Structure and process)

t Site offers family planning services during expanded hours of operation.
t Proportion of total family planning encounters that are encounters with ongoing or
continuing users.
t Proportion of clients who report that his or her care provider follows up to give test
results, has up-to-date information about care from specialists, and discusses other
prescriptions.
t Site has written agreements (e.g., MOUs) with the key partner agencies for health
care (especially prenatal care, primary care, HIV/AIDS) and social service (domestic
violence, food stamps) referrals.

PIMS*
CAHPS–PCMH item set
on care coordination†

Equitable
(Structure)

t Site offers language assistance at all points of contact for the most frequently
encountered language(s).

PIMS*

Value

t Average cost per client.

CDC¶

Unintended pregnancy
Teen pregnancy
Birth spacing
Proportion of female users at risk for unintended pregnancy who adopt or
continue use of an FDA-approved contraceptive method (measured for any
method; highly effective methods; or long-acting reversible methods)
[Intermediate outcome]

Average number of days to the next appointment.
Site offers routine contraceptive resupply on a walk-in basis.
Site offers on-site HIV testing (using rapid technology).
Site offers on-site HPV and hepatitis B vaccination.

PIMS*

Abbreviations: CAPHS = Agency for Healthcare Research and Quality’s Consumer Assessment of Health Care Providers and Systems; FDA = Food and Drug Administration;
HPV = human papillomavirus; MOU = memorandum of understanding; PIMS = Performance Information and Monitoring System; RQIP = Regional Quality Indicators Program.
* Source: Fowler C. Title X Family Planning Program Performance Information and Monitoring System (PIMS): Description of Proposed Performance Measures [DRAFT].
Washington, DC: Research Triangle Institute; 2012.
† Source: Agency for Healthcare Research and Quality. Consumer Assessment of Healthcare Providers and Systems (CAHPS). Available at https://www.cahps.ahrq.
gov/default.asp.
§ Source: John Snow International. The Regional Quality Indicators Project (RQIP). Boston, MA: John Snow International; 2014. Available at http://www.jsi.com/
JSIInternet/USHealth/project/display.cfm?ctid=na&cid=na&tid=40&id=2621.
¶ Sources: Haddix A, Corso P, Gorsky R. Costs. In: Haddix A, Teutsch S, Corso P, eds. Prevention effectiveness: a guide to decision analysis and economic evaluation. 2nd
ed. Oxford, UK: Oxford University Press; 2003; Stiefel M, Nolan K. A guide to measuring the triple aim: population health, experience of care, and per capita cost.
Cambridge, MA: Institute for Healthcare Improvements; 2012.

permanent. Examples of steps that may be taken to improve
the quality of care include developing job aids, providing
task-specific training for providers, conducting more patient
education, or strengthening relationships with referral sites
through formal memoranda of understanding (146).

MMWR / April 25, 2014 / Vol. 63 / No. 4

Conclusion
The United States continues to face substantial challenges to
improving the reproductive health of the U.S. population. The
recommendations in this report can contribute to improved
reproductive health by defining a core set of family planning

Recommendations and Reports

services for women and men, describing how to provide
contraceptive and other family planning services to both adult
and adolescent clients, and encouraging the use of the family
planning visit to provide selected preventive health services for
women and men. This guidance is intended to assist primary
care providers to offer the family planning services that will
help persons and couples achieve their desired number and
spacing of children and increase the likelihood that those
children are born healthy.
Recommendations are updated periodically. The most recent
versions are available at http://www.hhs.gov/opa.
References
1. Finer LB, Zolna MR. Unintended pregnancy in the United States:
incidence and disparities, 2006. Contraception 2011;84:478–85.
2. CDC. Adolescent pregnancy and childbirth—United States, 1991–2008.
In: CDC. CDC health disparities and inequalities report—United States,
2011. MMWR 2011;60(Suppl; January 14, 2011):105–8.
3. Martin J, Hamilton B, Osterman J, et al. Births: final data for 2012.
Natl Vital Stat Rep 2013;62(9).
4. Mathews T, Macdorman M. Infant mortality statistics from the 2010
period linked birth/infant data set. Natl Vital Stat Rep 2013:62(8).
5. US Department of Health and Human Services, Office of Population
Affairs. Mission statement for the Office of Family Planning. Washington,
DC: US Department of Health and Human Services; 2013. Available
at http://www.hhs.gov/opa/about-opa-and-initiatives/mission.
6. Institute of medicine. Clinical preventive services for women: closing
the gaps. Washington, DC: The National Academies Press; 2011.
Available at http://www.nap.edu/catalog.php?record_id=13181.
7. US Department of Health and Human Services, Office of Population
Affairs. Title X family planning. Washington, DC: US Department of
Health and Human Services; 2013. Available at http://www.hhs.gov/
opa/title-x-family-planning/index.html.
8. Frost J. U.S. women’s use of sexual and reproductive health services:
trends, sources of care and factors associated with use, 1995–2010.
New York, NY: Guttmacher Institute; 2013.
9. US Department of Health and Human Services Coverage of certain
preventive services under the Affordable Care Act: final rules. 45 CFR
Parts 147 and 156. July 19, 2010. Washington, DC: US Department
of Health and Human Services; 2010.
10. Institute of Medicine. Committee on Quality of Health Care in
America. Crossing the quality chasm: a new health system for the 21st
century. Washington, DC: National Academies of Science; 2001.
11. Bruce J. Fundamental elements of the quality of care: a simple
framework. Stud Fam Plann 1990;21:61–91.
12. Becker D, Koenig MA, Kim YM, Cardona K, Sonenstein FL. The
quality of family planning services in the United States: findings from
a literature review. Perspect Sex Reprod Health 2007;39:206–15.
13. Institute of Medicine. Future directions for the national health care
quality and disparities reports. Ullmer CBM, Burke S, eds. Washington,
DC: The National Academies Press; 2010.
14. Tucker CM. US Department of Health and Human Services, Advisory
Committee on Minority Health. Reducing health disparities by
promoting patient-centered culturally and linguistically sensitive/
competent health care. Rockville, MD: US Department of Health and
Human Services, Public Health Service; 2009.

15. US Department of Health and Human Services, Office of Minority
Health. The national standards for culturally and linguistically
appropriate services in health and health care. Washington, DC: US
Department of Health and Human Services; 2012. Available at https://
www.thinkculturalhealth.hhs.gov/Content/clas.asp#clas_standards.
16. Olavarria M, Beaulac J, Belanger A, Young M, Aubry T. Organizational
cultural competence in community health and social service
organizations: how to conduct a self-assessment. J Cult Divers
2009;16:140–50.
17. Frost J, Finer L, Tapales A. The impact of publicly funded family
planning clinic services on unintended pregnancies and government
cost savings. J Health Care Poor Underserved 2008;19:778–96.
18. Trussell J, Henry N, Hassan F, Prezioso A, Law A, Filonenko A. Burden
of unintended pregnancy in the United States: potential savings with
increased use of long-acting reversible contraception. Contraception
2013;87:154–61.
19. Foster DG, Rostovtseva DP, Brindis CD, Biggs MA, Hulett D, Darney
PD. Cost savings from the provision of specific methods of
contraception in a publicly funded program. Am J Public Health
2009;99:446–51.
20. GRADE Working Group. GRADE: going from evidence to
recommendations. BMJ 2008;336:1049–51.
21. Institute of Medicine. Clinical practice guidelines we can trust.
Washington, DC: The National Academies Press; 2011. Available at
http://www.nap.edu/catalog.php?record_id=13058.
22. US Preventive Services Task Force. USPSTF: methods and processes.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2013. Available at http://www.
uspreventiveservicestaskforce.org/methods.htm.
23. Lu M. Recommendations for preconception care. Am Fam Physician
2007;76:397–400.
24. CDC. Recommendations to improve preconception health and health
care—United States. MMWR 2006;55(No. RR-6).
25. Moos M. Preconceptional health promotion: progress in changing a
prevention paradigm. J Perinat Neonatal Nurs 2004;18:2–13.
26. American College of Obstetricians and Gynecologists. Committee Opinion
#512: health care for transgender individuals. Obstet Gynecol
2011;118:1454–8.
27. American College of Obstetricians and Gynecologists, Committee on
Health Care for Underserved Women. ACOG Committee Opinion
No. 525: health care for lesbians and bisexual women. Obstet Gynecol
2012;119:1077–80.
28. McNair R, Hegarty K. Guidelines for the primary care of lesbian, gay and
bisexual people: a systematic review. Ann Fam Med 2010;8:533–41.
29. World Professional Association for Transgender Health. Standards of
care for the health of transsexual, transgender, and gendernonconforming people. Minneapolis, MN: World Professional
Association for Transgender Health; 2011.
30. The Center of Excellence for Transgender Health. Primary care protocol
for transgender patient care. San Francisco, CA: University of
California–San Francisco; 2011.
31. American Academy of Pediatrics. Office-based care for lesbian, gay,
bisexual, transgender, and questioning youth: Policy statement and
Technical report. Pediatrics 2013;132:198–203.
32. Adelson SL, American Academy of Child and Adolescent Psychiatry
Committee on Quality Issues. Practice parameter on gay, lesbian or
bisexual orientation, gender nonconformity, and gender discordance
in children and adoelscents. J Am Acad Child Adolesc Psychiatry
2012;51:957–74.

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

33. Office on Women’s Health. Illnesses and disabilities: sexual and
reproductive health. Available at http://www.womenshealth.gov/
illnesses-disabilities/your-health/sexuality-reproductive-health.cfm.
34. McIntyre P. Adolescent friendly health services: an agenda for change.
Geneva, Switzerland: World Health Organization; 2002.
35. CDC. U.S. medical eligibility criteria for contraceptive use 2010.
MMWR 2010;59(No. RR-4).
36. CDC. Sexually transmitted diseases treatment guidelines, 2010.
MMWR 2010;59(No. RR-12).
37. Jaccard J. Careful, current, and consistent: tips to improve contraceptive use.
Washington, DC: National Campaign to Prevent Teen Pregnancy; 2010.
38. Trussell J. Contraceptive failure in the United States. Contraception
2011;83:397–404.
39. Winner B, Peipert J, Zhao Q, et al. Effectiveness of long-acting
reversible contraception. N Engl J Med 2012;366:1998–2007.
40. Beerthuizen R. State-of-the-art of non-hormonal methods of
contraception: V. Female sterilisation. Eur J Contracept Reprod Health
Care 2010;15:124–35.
41. Michielsen D, Beerthuizen R. State-of-the art of non-hormonal
methods of contraception: VI. Male sterilisation. Eur J Contracept
Reprod Health Care 2010;15:136–49.
42. CDC. U.S. Selected practice recommendations for contraceptive use
2013. MMWR 2013;62(No. RR-5).
43. Kerns J, Westhoff C, Morroni C, Murphy P. Partner influence on early
discontinuation of the pill in a predominantly Hispanic population.
Perspect Sex Reprod Health 2003;35:256–60.
44. Forste R, Morgan J. How relationships of US men affect contraceptive
use and efforts to prevent STD. Fam Plann Perspect 1998;30:56–62.
45. Severy L, Silver S. Two reasonable people: joint decision-making in
contraceptive choice and use. In: LJ S, ed. Advances in population:
psychosocial perspectives. London, UK: Jessica Kingsley Publishers;
1994:207–27.
46. Grady W, Klepinger D. BIlly J, Cubbins L. The role of relationship
power in couple decisions about contraception in the US. J Biosoc Sci
2010;42:307–25.
47. Jaccard J. Unlocking the contraceptive conundrum. Washington, DC:
The National Campaign to Prevent Teen and Unplanned Pregnancy;
2009.
48. Pallitto CC, Campbell JC, O’Campo P. Is intimate partner violence
associated with unintended pregnancy? A review of the literature.
Trauma Violence Abuse 2005;6:217–35.
49. Paterno MT, Jordan ET. A review of factors associated with unprotected
sex among adult women in the United States. J Obstet Gynecol
Neonatal Nurs 2012;41:258–74.
50. Rehm J, Shield KD, Joharchi N, Shuper PA. Alcohol consumption
and the intention to engage in unprotected sex: systematic review and
meta-analysis of experimental studies. Addiction 2012;107:51–9.
51. Harper C, Balistreri E, Boggess J, Leon K, Darney P. Provision of
hormonal contraceptives without a mandatory pelvic examination: the
first stop demonstration project. Fam Plann Perspect 2001;33:13–8.
52. Stormo A, Hawkins N, Cooper C, Saraiya M. The pelvic examination
as a screening tool: practices of US physicians. Arch Intern Med
2011;171:2053–4.
53. Labbok M, Perez A, Valdez V, et al. The Lactational Amenorrhea
Method (LAM): a postpartum introductory family planning method
with policy and program implications. Adv Contracept Deliv Syst
1994;10:93–109.

MMWR / April 25, 2014 / Vol. 63 / No. 4

54. Huber L, Hogue C, Stein A, et al. Contraceptive use and discontinuation:
findings from the contraceptive history, initiation and choice study. Am
J Obstet Gynecol 2006;194:1290–5.
55. CDC. Guide to community preventive services: prevention of HIV/
AIDS, other STIs and pregnancy, group-based comprehensive risk
reduction interventions for adolescents. Atlanta, GA: US Department
of Health and Human Services, CDC; 2011. Available at www.
thecommunityguide.org/hiv/riskreduction.html.
56. Kirby DB, Laris BA, Rolleri LA. Sex and HIV education programs:
their impact on sexual behaviors of young people throughout the world.
J Adolesc Health 2007;40:206–17.
57. Oringanje C, Meremikwu MM, Eko H, Esu E, Meremikwu A, Ehiri
JE. Interventions for preventing unintended pregnancies among
adolescents. Cochrane Database Syst Rev 2009:CD005215.
58. English A. State minor consent laws: a summary. 3rd ed. Washington,
DC: Center for Adolescent Health and the Law; 2010.
59. US Department of Health and Human Services. State requirements
for reporting child abuse. Washington, DC: US Department of Health
and Human Services; 2013. Available at http://www.childwelfare.gov/
systemwide/laws_policies/state.
60. Guldi M. Fertility effects of abortion and birth control pill access for
minors. Demography 2008;45:817–27.
61. Klein JD, McNulty M, Flatau CN. Adolescents’ access to care: teenagers’
self-reported use of services and perceived access to confidential care.
Arch Pediatr Adolesc Med 1998;152:676–82.
62. Lehrer JA, Pantell R, Tebb K, Shafer MA. Forgone health care among
U.S. adolescents: associations between risk characteristics and
confidentiality concern. J Adolesc Health 2007;40:218–26.
63. Lyren A, Kodish E, Lazebnik R, O’Riordan MA. Understanding
confidentiality: perspectives of African American adolescents and their
parents. J Adolesc Health 2006;39:261–5.
64. Reddy DM, Fleming R, Swain C. Effect of mandatory parental
notification on adolescent girls’ use of sexual health care services. JAMA
2002;288:710–4.
65. Vo DX, Pate OL, Zhao H, Siu P, Ginsburg KR. Voices of Asian
American youth: important characteristics of clinicians and clinical
sites. Pediatrics 2007;120:e1481–93.
66. Zabin LS, Stark HA, Emerson MR. Reasons for delay in contraceptive
clinic utilization. Adolescent clinic and nonclinic populations
compared. J Adolesc Health 1991;12:225–32.
67. Zavodny M. Fertility and parental consent for minors to receive
contraceptives. Am J Public Health 2004;94:1347–51.
68. Klein J. Achieving quality health services for adolescents: policy
statement of the Committee on Adolescence, American Academy of
Pediatrics. Pediatrics 2008;121:1263.
69. Ford C, English A, Sigman G. Confidential health care for adolescents:
position paper for the Society for Adolescent Medicine. J Adolesc Health
2004;35:160–7.
70. American College of Obstetricians and Gynecologists. Confidentiality in
adolescent health care. guidelines for adolescent health care. 2nd ed.
Washington, DC: American College of Obstetricians and Gynecologists; 2011.
71. Anderson NLR, Koniak-Griffin D, Keenan CK, Uman G, Duggal BR,
Casey C. Evaluating the outcomes of parent-child family life education.
Sch Inq Nurs Pract 1999;13:211–38.
72. Guilamo-Ramos V, Bouris A, Jaccard J, Gonzalez B, McCoy W, Aranda
D. A parent-based intervention to reduce sexual risk behavior in early
adolescence: building alliances between physicians, social workers, and
parents. J Adolesc Health 2011;48:159–63.

Recommendations and Reports

73. Blake SM, Simkin L, Ledsky R, Perkins C, Calabrese JM. Effects of a
parent-child communications intervention on young adolescents’ risk for
early onset of sexual intercourse. Fam Plann Perspect 2001;33:52–61.
74. Brody GH, Murry VM, Gerrard M, et al. The Strong African American
Families Program: translating research into prevention programming.
Child Dev 2004;75:900–17.
75. Evans WD, Davis KC, Ashley OS, Blitstein J, Koo H, Zhang Y. Efficacy
of abstinence promotion media messages: findings from an online
randomized trial. J Adolesc Health 2009;45:409–16.
76. Forehand R, Armistead L, Long N, et al. Efficacy of a parent-based sexualrisk prevention program for African American preadolescents: a randomized
controlled trial. Arch Pediatr Adolesc Med 2007;161:1123–9.
77. Haggerty KP, Skinner ML, MacKenzie EP, Catalano RF. A randomized
trial of Parents Who Care: effects on key outcomes at 24-month
follow-up. Prev Sci 2007;8:249–60.
78. Huston RL, Martin LJ, Foulds DM. Effect of a program to facilitate parentchild communication about sex. Clin Pediatr (Phila) 1990;29:626–33.
79. Lederman RP, Chan W, Roberts-Gray C. Sexual risk attitudes and
intentions of youth aged 12–14 years: survey comparisons of parentteen prevention and control groups. Behavioral Medicine (Washington,
DC) 2004;29:155–63.
80. Lederman RP, Chan W, Roberts-Gray C. Parent-adolescent relationship
education (PARE): program delivery to reduce risks for adolescent
pregnancy and STDs. Behav Med 2008;33:137–43.
81. Lefkowitz ES, Sigman M, Au TK. Helping mothers discuss sexuality
and AIDS with adolescents. Child Dev 2000;71:1383–94.
82. Miller BC, Norton MC, Jenson GO. Pregnancy prevention programs:
Impact Evaluation of Facts and Feelings: a home-based video sex
education curriculum. Fam Relat 1993;42:392–400.
83. Murry VM, Berkel C, Brody GH, Gerrard M, Gibbons FX. The Strong
African American Families program: longitudinal pathways to sexual
risk reduction. J Adolesc Health 2007;41:333–42.
84. Schuster MA, Corona R, Elliott MN, et al. Evaluation of Talking
Parents, Healthy Teens, a new worksite based parenting programme to
promote parent-adolescent communication about sexual health:
randomised controlled trial. BMJ 2008;337:a308.
85. Stanton B, Cole M, Galbraith J, et al. Randomized trial of a parent
intervention: parents can make a difference in long-term adolescent
risk behaviors, perceptions, and knowledge. Arch Pediatr Adolesc Med
2004;158:947–55.
86. Stanton BF, Li X, Galbraith J, et al. Parental underestimates of
adolescent risk behavior: a randomized, controlled trial of a parental
monitoring intervention. J Adolesc Health 2000;26:18–26.
87. American Academy of Pediatrics. Parents matter: your children want
to learn about the facts of life from you. Elk Grove Village, IL: American
Academy of Pediatrics; ND. Available at http://www2.aap.org/visit/
ParentsMatterBrochure.pdf.
88. Hamilton B. Births: final Data for 2010. National Vital Statistics
Reports 2012;61(1).
89. Olds DL, Henderson CR Jr, Tatelbaum R, Chamberlin R. Improving
the life-course development of socially disadvantaged mothers: a
randomized trial of nurse home visitation. Am J Public Health
1988;78:1436–45.
90. Olds DL, Kitzman H, Cole R, et al. Effects of nurse home-visiting on
maternal life course and child development: age 6 follow-up results of
a randomized trial. Pediatrics 2004;114:1550–9.
91. Olds DL, Kitzman H, Hanks C, et al. Effects of nurse home visiting
on maternal and child functioning: age-9 follow-up of a randomized
trial. Pediatrics 2007;120:e832–45.

92. Rabin JM, Seltzer V, Pollack S. The long term benefits of a
comprehensive teenage pregnancy program. Clin Pediatr (Phila)
1991;30:305–9.
93. Avellar S, Paulsell D, Sama-Miller E, Del Grosso P. Home visiting
evidence of effectiveness review. Washington, DC: US Department of
Health and Human Services, Office of Planning, Research and
Evaluation, Administration for Children and Families; 2012.
94. Black M, Bentley M, Papas M, et al. Delaying second births among
adolescent mothers: a randomized, controlled trial of a home-based
mentoring program. Pediatrics 2006;118:1087–99.
95. American Academy of Pediatrics. Counseling the adolescent about
pregnancy options. Pediatrics 2006;101:938–40.
96. American College of Obstetricians and Gynecologists. Guidelines for
women’s health care: a resource manual. 3rd ed. Washington, DC:
American College of Obstetricians and Gynecologists; 2007.
97. American College of Obstetricians and Gynecologists. Guidelines for
perinatal care. 6th ed. Washington, DC: American College of
Obstetricians and Gynecologists; 2007.
98. Ventura S, Curtin S, Abma J, Henshaw S. Estimated pregnancy rates
and rates of pregnancy outcomes for the US: 1990–2008. Natl Vital
Stat Rep 2012;60(7).
99. Jones J. Adoption experiences of women and men and demand for
children to adopt by women 18–44 years of age in the United States,
2002. Vital Health Stat 2008;23(7).
100. American Society for Reproductive Medicine in collaboration with the
Society for Reproductive Endocrinology and Infertility. Optimizing
natural fertility. Fertil Steril 2008;90(Suppl):S1–6.
101. American Society for Reproductive Medicine. Optimal evaluation of
the infertile female. Fertil Steril 2006;86.
102. American Urological Association. The optimal evaluation of the infertile
male: AUA best practice statement. Linthicum, MD: American
Urological Association; 2010.
103. Frey K, Navarro S, Kotelchuck M, Lu M. The clinical content of
preconception care: preconception care for men. Am J Obstet Gynecol
2008;6:S389–95.
104. US Preventive Services Task Force. Folic acid to prevent neural tube
defects. Rockville, MD: US Department of Health and Human
Services, Agency for Healthcare Research and Quality; 2009. Available
at http://www.uspreventiveservicestaskforce.org/uspstf/uspsnrfol.htm.
105. Jack B, Atrash H, Coonrod D, Moos M, O’Donnell J, Johnson K. The
clinical content of preconception care: an overview and preparation of
this supplement. Am J Obstet Gynecol 2008;199(Suppl B):S266–79.
106. US Preventive Services Task Force. Screening for intimate partner
violence and abuse of elderly and vulnerable adults. Rockville, MD:
US Department of Health and Human Services, Agency for Healthcare
Research and Quality; 2013. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspsipv.htm.
107. US Preventive Services Task Force. Screening and Behavioral
Counseling Interventions in Primary Care to Reduce Alcohol Misuse.
AHRQ, US Department of Health and Human Services; 2013.
108. American College of Obstetricians and Gynecologists. Committee
Opinion No. 483: primary and preventive care: periodic assessments.
Obstet Gynecol 2011;117:1008–15.
109. Committee on Practice and Ambulatory Medicine, Bright Futures
Periodicity Schedule Workgroup. 2014 recommendations for pediatric
preventive health care. Pediatrics 2014;133;568.
110. US Preventive Services Task Force. Screening for illicit drug use.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2008.

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Recommendations and Reports

111. US Preventive Services Task Force. Counseling and interventions to
prevent tobacco use and tobacco-caused disease in adults and pregnant
women. Rockville, MD: US Department of Health and Human
Services, Agency for Healthcare Research and Quality; 2009. Available
at http://www.uspreventiveservicestaskforce.org/uspstf/uspstbac2.htm.
112. US Preventive Services Task Force. Primary care interventions to prevent
tobacco use in children and adolescents. Rockville, MD: US
Department of Health and Human Services, Agency for Healthcare
Research and Quality; 2013.
113. CDC. Advisory Committee on Immunization Practices (ACIP)
recommended immunization schedules for persons aged 0 through 18
years and adults aged 19 years and older—United States, 2013. MMWR
2013;62(Suppl 1):1–19.
114. US Preventive Services Task Force. Screening for depression in adults.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2009. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspsaddepr.htm.
115. US Preventive Services Task Force. Major depressive disorder in children
and adolescents. Rockville, MD: US Department of Health and Human
Services, Agency for Healthcare Research and Quality; 2009. Available
at http://www.uspreventiveservicestaskforce.org/uspstf/uspschdepr.htm.
116. American Psychiatric Association. Practice guideline for the assessment
and treatment of patients with suicidal behaviors. Am J Psychiatry
2003;160(Suppl):1–60.
117. American Academy of Child and Adolescent Psychiatry. Practice
parameter for the assessment and treatment of children and adolescents
with suicidal behavior. J Am Acad Child Adolesc Psychiatry
2001;40(Suppl):24S–51S.
118. US Preventive Services Task Force. Screening for obesity in children and
adolescents: US Preventive Services Task Force recommendation
statement. Rockville, MD: US Department of Health and Human
Services, Agency for Healthcare Research and Quality; 2010. Available
at http://www.uspreventiveservicestaskforce.org/uspstf/uspschobes.htm.
119. US Preventive Services Task Force. Screening for and management of
obesity in adults. Rockville, MD: US Department of Health and
Human Services, Agency for Healthcare Research and Quality; 2012.
Available at http://www.uspreventiveservicestaskforce.org/uspstf11/
obeseadult/obesers.htm.
120. US Preventive Services Task Force. Screening for high blood pressure
in adults. Rockville, MD: US Department of Health and Human
Services, Agency for Healthcare Research and Quality; 2007. Available
at http://www.uspreventiveservicestaskforce.org/uspstf/uspshype.htm.
121. US Department of Health and Human Services. The seventh report
of the Joint National Committee on the Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure. Washington, DC:
US Department of Health and Human Services; 2004.
122. US Preventive Services Task Force. Screening for type 2 diabetes mellitus
in adults. Rockville, MD: US Department of Health and Human
Services, Agency for Healthcare Research and Quality; 2008. Available
at http://www.uspreventiveservicestaskforce.org/uspstf/uspsdiab.htm.
123. CDC. Revised recommendations for HIV testing of adults, adolescents and
pregnant women in health care settings. MMWR 2006;55(No. RR-14).
124. CDC. Recommendations for the identification of chronic hepatitis C
virus infection among persons born during 1945–1965. MMWR
2012;61(No. RR-4).
125. CDC. Male chlamydia screening consultation. Atlanta, GA: US
Department of Health and Human Services, DCD; 2006. Available at
http://www.cdc.gov/std/chlamydia.

MMWR / April 25, 2014 / Vol. 63 / No. 4

126. Burstein GR, Eliscu A, Ford K, et al. Expedited partner therapy for
adolescents diagnosed with chlamydia or gonorrhea: a position paper
of the Society for Adolescent Medicine. J Adolesc Health
2009;45:303–9.
127. American Academy of Pediatrics. Promoting healthy sexual development
and sexuality. Bright Futures: guidelines for health supervision of
infants, children, and adolescents. Elk Grove, IL: American Academy
of Pediatrics; 2007.
128. US Preventive Services Task Force. Screening for gonorrhea. Rockville,
MD: US Department of Health and Human Services, Agency for
Healthcare Research and Quality; 2005. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspsgono.htm.
129. US Preventive Services Task Force. Screening for HIV. Rockville, MD: US
Department of Health and Human Services, Agency for Healthcare Research
and Quality; 2013. Available at http://www.uspreventiveservicestaskforce.
org/uspstf/uspshivi.htm.
130. US Preventive Services Task Force. Screening for hepatitis C virus
infection in adults. Rockville, MD: US Department of Health and
Human Services, Agency for Healthcare Research and Quality; 2013.
Available at http://www.uspreventiveservicestaskforce.org/uspstf12/
hepc/hepcfinalrs.htm#recommendations.
131. CDC. Recommendations on the use of quadrivalent human
papillomavirus vaccine in males—Advisory Committee on
Immunization Practices (ACIP). MMWR 2011;60:1705–8.
132. US Preventive Services Task Force. Behavioral counseling to prevent
sexually transmitted infections. Rockville, MD: US Department of
Health and Human Services, Agency for Healthcare Research and
Quality; 2008. Available at http://www.uspreventiveservicestaskforce.
org/uspstf/uspsstds.htm.
133. Kamb ML, Fishbein M, Douglas JM Jr, et al. Efficacy of risk-reduction
counseling to prevent human immunodeficiency virus and sexually
transmitted diseases: a randomized controlled trial. Project RESPECT
Study Group. JAMA 1998;280:1161–7.
134. US Preventive Services Task Force. Risk assessment, genetic counseling,
and genetic testing for BRCA-related cancer in women. Rockville, MD:
US Department of Health and Human Services, Agency for Healthcare
Research and Quality; 2013. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspsbrgen.htm.
135. US Preventive Services Task Force. Medications for risk reduction of
primary breast cancer in women. Rockville, MD: US Department of
Health and Human Services, Agency for Healthcare Research and
Quality; 2013. Available at http://www.uspreventiveservicestaskforce.
org/uspstf/uspsbrpv.htm.
136. US Preventive Services Task Force. Screening for cervical cancer.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2012. Available at www.
uspreventiveservicestaskforce.org/uspstf11/cervcancer/cervcancerrs.htm.
137. Massad L, Einstein M, Huh W, et al. 2012 updated consensus guidelines
for the management of abnormal cervical cancer screening tests and
cancer precursors. Obstet Gynecol 2013;121:829–46.
138. Braverman P, Breech L. Gynecologic examination for adolescents in
the pediatric office setting. Pediatrics 2010;126:583–90.
139. Smith RA, Brooks D, Cokkinides V, Saslow D, Brawley OW. Cancer
screening in the United States, 2013: a review of current American
Cancer Society guidelines, current issues in cancer screening, and new
guidance on cervical cancer screening and lung cancer screening. CA
Cancer J Clin 2013;63:88–105.

Recommendations and Reports

140. US Preventive Services Task Force. Screening for breast cancer.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2009. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspsbrca.htm.
141. Marcell A, Bell D, Joffe A. The male genital examination: a position
paper of the Society for Adolescent Health and Medicine: a position
paper of the Society for Adolescent Health and Medicine. J Adolesc
Health 2012;50:424–5.
142. Riley W, Moran J, Corso L, Beitsch L, Bialek R, Cofsky A. Defining
quality improvement in public health. J Public Health Manag Pract
2010;16:5–7.
143. National Quality Forum. ABCs of measurement. Washington, DC:
National Quality Forum; 2011. Available at http://www.qualityforum.
org/Measuring_Performance/ABCs_of_Measurement.aspx.
144. Berwick D, Nolan T, Whittington J. The Trip Aim: care, health and
cost. Health Aff 2008;27:759–69.
145. CDC. National Public Health Performance Standards Program. Atlanta,
GA: US Department of Health and Human Services, CDC; 2012.
Available at www.cdc.gov/od/ocphp/nphpsp.
146. Berwick D. A user’s manual for the IOM’s “Quality Chasm” Report.
Health Affairs 2002;21:80–90.
147. Langley G, Nolan K, Nolan T, Norman C, Provost L. The Improvement
Guide: A practical approach to enhancing organizational performance.
2nd ed. San Francisco, CA: Jossey-Bass Publishers; 2009.
148. Government Accountability Office. Performance measurement and
evaluation: definitions and relationships. Washington, DC:
Government Accountability Office; 2011.

149. Donabedian A. The quality of care. JAMA 1988;260:1743–8.
150. Fowler C. Title X Family Planning Program Performance Information
and Monitoring System (PIMS): description of proposed performance
measures. Washington, DC: Research Triangle Institute; 2012.
151. California Family Health Council. Performance measures: guiding
quality improvement for family planning services. Los Angeles, CA:
California Family Health Council; 2011. Available at http://www.cfhc.
org/TitleX/PerformanceMeasures/default.htm.
152. John Snow International. The Regional Quality Indicators Project
(RQIP). Boston, MA: John Snow International; 2012. Available at
http://www.jsi.com/JSIInternet/USHealth/project/display.cfm?ctid=n
a&cid=na&tid=40&id=2621.
153. Family Planning Councils of America. Performance Measurement
System. Los Angeles, CA: Family Planning Councils of America; ND.
Available at http://www.fpcai.org/pms.html.
154. Palmer R. Process-based measures of quality: the need for detailed
clinical data in large health care databases. Ann Intern Med 1997;
127:733–8.
155. Bouchet B. Health manager’s guide: monitoring the quality of primary
care. Bethesda, MD: Center for Human Services; ND. Available at
http://pdf.usaid.gov/pdf_docs/PNACK584.pdf.
156. Institute for Health Care Improvement. How to improve. Cambridge,
MA: Institute for Health Care Improvement; 2014. Available at http://
www.ihi.org/knowledge/Pages/HowtoImprove/default.aspx.

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Recommendations and Reports

Appendix A
How the Recommendations Were Developed
The recommendations were developed jointly under the
auspices of CDC’s Division of Reproductive Health (DRH)
and the Office of Population Affairs (OPA), in consultation
with a wide range of experts and key stakeholders. A
multistage process that drew on established procedures for
developing clinical guidelines (1,2) was used to develop the
recommendations. In April 2010, an Expert Work Group
(EWG) comprising family planning clinical providers, program
administrators, representatives from relevant federal agencies,
and representatives from professional medical organizations
was created to advise OPA and CDC on the structure and
content of the revised recommendations and to help make the
recommendations more feasible and relevant to the needs of
the field. This group made two key initial recommendations:
1) to examine the scientific evidence for three priority areas of
focus identified as key components of family planning service
delivery, (i.e., counseling and education, serving adolescents,
and quality improvement); and 2) to guide providers of family
planning services in the use of various recommendations for
how to provide clinical care to women and men.

Developing Recommendations on
Counseling, Adolescent Services,
and Quality Improvement
Systematic reviews of the published literature from January 1985
through December 2010 were conducted for each priority topic
to identify evidence-based and evidence-informed approaches to
family planning service delivery. Standard methods for conducting
the reviews were used, including the development of key questions
and analytic frameworks, the identification of the evidence base
through a search of the published as well as “gray literature”
(i.e., studies published somewhere other than in a peer-reviewed
journal), and a synthesis of the evidence in which findings were
summarized and the quality of individual studies was considered,
using the methodology of the U.S. Preventive Services Task Force
(USPSTF) (3). Eight databases were searched (i.e., MEDLINE,
PsychInfo, PubMed, CINAHL, Cochrane, EMBASE, POPLINE,
and the U.K. National Clearinghouse Service Economic
Evaluation Database) and were restricted to literature from the
United States and other developed countries. Summaries of the
evidence used to prepare these recommendations will appear in
background papers that will be published separately.
In May 2011, three technical panels (one for each priority
topic) comprising subject matter experts were convened

MMWR / April 25, 2014 / Vol. 63 / No. 4

to consider the quality of the evidence and suggest what
recommendations might be justified on the basis of the
evidence. CDC and OPA used this feedback to develop core
recommendations for counseling, serving adolescents, and
quality improvement. EWG members subsequently reviewed
these core recommendations; EWG members differed from the
subject matter experts in that they were more familiar with the
family planning service delivery context and could comment
on the feasibility and appropriateness of the recommendations
as well as on their scientific justification. EWG members met
to consider the core recommendations using 1) the quality
of the evidence; 2) the positive and negative consequences of
implementing the recommendations on health outcomes, costs
or cost-savings, and implementation challenges; and 3) the
relative importance of these consequences (e.g., the ability of
the recommendations to have a substantial effect on health
outcomes may be weighed more than the logistical challenges
of implementing them) (1). In certain cases, when the evidence
was inconclusive or incomplete, recommendations were made on
the basis of expert opinion (see Appendix B). Finally, CDC and
OPA staff considered the feedback from EWG members when
finalizing the core recommendations and writing this report.

Developing Recommendations
on Clinical Services
DRH and OPA staff members synthesized recommendations
for clinical care for women and for men that were developed
by >35 federal and professional medical organizations. They
were assisted in this effort by staff from OPA’s Office of Family
Planning Male Training Center and from CDC’s Division of
STD Prevention, Division of Violence Prevention, Division
of Immunization Services, and Division of Cancer Prevention
and Control. The synthesis was needed because clinical
recommendations are sometimes inconsistent with each other
and can vary by the extent to which they are evidence-based.
The clinical recommendations addressed contraceptive services,
achieving pregnancy, basic infertility services, preconception
health services, sexually transmitted disease services, and related
health-care services.
An attempt was made to apply the Institute of Medicine’s
criteria for clinical practice guidelines when deciding which
professional medical organizations to include in the review (2).
However, many organizations did not articulate the process
used to develop the recommendations fully, and many did not

Recommendations and Reports

conduct comprehensive and systematic reviews of the literature.
In the end, to be included in the synthesis, the recommending
organization had to be a federal agency or major professional
medical organization that represents established medical
disciplines. In addition, a recommendation had to be made on
the basis of an independent review of the evidence or expert
opinion and be considered a primary source that was developed
for the United States.
In July 2011, two technical panels comprising subject matter
experts on clinical services for women and men were convened
to review the synthesis of federal and professional medical
recommendations, reconcile inconsistent recommendations,
and provide individual feedback to CDC and OPA about the
implications for family planning service delivery. CDC and OPA
used this individual feedback to develop core recommendations
for clinical services. The core recommendations were subsequently
reviewed by EWG members, and feedback was used to finalize
the core recommendations and write this report.
Members of the technical panels recommended that
contraceptive services, pregnancy testing and counseling,
services to achieve pregnancy, basic infertility care, STD services,
and other preconception health services should be considered
family planning services. This feedback considered federal
statute and regulation, CDC and USPSTF recommendations
for clinical care, and EWG members’ opinion.
Because CDC’s preconception health recommendations
include many services, the panel narrowed the range of
preconception services that were included by using the following
criteria: 1) the Select Panel on Preconception Care (4) had
assigned an A or B recommendation to that service for women,
which means that there was either good or fair evidence to
support the recommendation that the condition be considered
in a preconception care evaluation (Table 1), or 2) the service
was included among recommendations made by experts in
preconception health for males (5). Services for men that
addressed health conditions that affect reproductive capacity
or pregnancy outcomes directly were included as preconception
health; services that addressed men’s health but that were not
related directly to pregnancy outcomes were considered to be
related preventive health services.
The Expert Work Group noted that more preventive services
are recommended than can be offered feasibly in some settings.
However, a primary purpose of this report is to set a broad
framework within which individual clinics will tailor services
to meet the specific needs of the populations that they serve.
In addition, EWG members identified specific subgroups that
should have the greatest priority for preconception health
services (i.e., those trying to achieve pregnancy and those

at high risk of unintended pregnancy). Future operational
research should provide more information about how to deliver
these services most efficiently during multiple visits to clients
with diverse needs.

Determining How Clinical Services
Should Be Provided
Various federal agencies and professional medical associations
have made recommendations for how to provide family
planning services. When considering these recommendations,
the Expert Work Group used the following hierarchy:
t Highest priority was given to CDC guidelines because
they are developed after a rigorous review of scientific
evidence. CDC guidelines tailor recommendations for
higher risk individuals, (whereas USPSTF focuses on
average risk individuals), who are more representative of
the clients seeking family planning services.
t When no CDC guideline existed to guide the
recommendations, the relevant USPSTF A or B
recommendations (which indicate a high or moderate
certainty that the benefit is moderate to substantial) were
used. USPSTF recommendations are made on the basis of
a thorough review of the available evidence.
t If neither a CDC nor a USPSTF A or B recommendation
existed, the recommendations of selected major professional
medical associations were considered as resources. The
American Academy of Pediatrics’ (AAP) Bright Futures
guidelines (6) were used as the primary source of
recommendations for adolescents when no CDC or
USPSTF recommendations existed.
t For a limited number of recommendations, there were no
federal or major professional medical recommendations, but
the service was recommended by EWG members on the basis
of expert opinion for family planning clients.
In some cases, a service was graded as an I recommendation
by USPSTF for the general population (an I recommendation
means that the current evidence is insufficient to assess the balance
of benefits and harms of the service, so if the service is offered,
patients should be informed of this fact), but either CDC, EWG
members, or another organization recommended the service for
women or men seeking family planning services. The situations
in which this occurred and the reasons why the service was
recommended despite its receiving an I recommendation by
USPSTF have been summarized (Table 2). The approach used to
consider the evidence and make recommendations that are used
by USPSTF have been summarized (Tables 3 and 4) (7).

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References
1. GRADE Working Group. GRADE: going from evidence to
recommendations. BMJ 2008;336:1049–51.
2. Institute of Medicine. Clinical practice guidelines we can trust. Washington,
DC: The National Academies Press; 2011. Available at http://www.nap.
edu/catalog.php?record_id=13058.
3. US Preventive Services Task Force. USPSTF: methods and processes.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2013. Available at http://www.
uspreventiveservicestaskforce.org/methods.htm.
4. Jack BW, Atrash H, Coonrod D, Moos M, O’Donnell J, Johnson K. The
clinical content of preconception care: an overview and preparation of this
supplement. Am J Obstet Gynecol 2008;199(Suppl 2):S266–79.

MMWR / April 25, 2014 / Vol. 63 / No. 4

5. Frey KA, Navarro S, Kotelchuck M, Lu M. The clinical content of
preconception care: preconception care for men. Am J Obstet Gynecol
2008;199(Suppl 2):S389–95.
6. Committee on Practice and Ambulatory Medicine, Bright Futures
Periodicity Schedule Workgroup. 2014 recommendations for pediatric
preventive health care. Pediatrics 2014;133;568.
7. US Preventive Services Task Force. Grade definitions. Rockville, MD: US
Department of Health and Human Services, Agency for Healthcare Research
and Quality; 2013. Available at http://www.uspreventiveservicestaskforce.
org/uspstf/grades.htm.

Recommendations and Reports

TABLE 1. Select Panel on Preconception Care grading system
Quality of the evidence*
Evidence was obtained from at least one properly conducted, randomized, controlled trial that was performed with subjects who were not pregnant.
I-a
I-b
Evidence was obtained from at least one properly conducted, randomized, controlled trial that was done not necessarily before pregnancy.
II-1
Evidence was obtained from well-designed, controlled trials without randomization.
II-2
Evidence was obtained from well-designed cohort or case-control analytic studies, preferably conducted by more than one center or research group.
II-3
Evidence was obtained from multiple-time series with or without the intervention, or dramatic results in uncontrolled experiments.
III
Opinions were gathered from respected authorities on the basis of clinical experience, descriptive studies and case reports, or reports of expert
committees.
Strength of the recommendation
A
There is good evidence to support the recommendation that the condition be considered specifically in a preconception care evaluation.
B
There is fair evidence to support the recommendation that the condition be considered specifically in a preconception care evaluation.
C
There is insufficient evidence to recommend for or against the inclusion of the condition in a preconception care evaluation, but recommendation to
include or exclude may be made on other grounds.
D
There is fair evidence to support the recommendation that the condition be excluded in a preconception care evaluation.
E
There is good evidence to support the recommendation that the condition be excluded in a preconception care evaluation.
Source: Jack B, Atrash H, Coonrod D, Moos M, O’Donnell J, Johnson K. The clinical content of preconception care: an overview and preparation of this supplement.
Am J Obstet Gynecol 2008;199(6 Suppl 2):S266–79.

TABLE 2. Services included in these recommendations that received a U.S. Preventive Services Task Force (USPSTF) I recommendation
Service/screen

USPSTF recommendation

Alcohol

I for adolescents

Other drugs

I for adolescents and adults

Clinical breast exam

I for all women

Chlamydia
Gonorrhea

I for all males
I for all males

Why the service is recommended despite a USPSTF I recommendation
The recommendations are consistent with CDC’s recommendations on preconception health and
AAP’s Bright Futures* guidelines.
The recommendations are consistent with CDC’s recommendations on preconception health and
AAP’s Bright Futures guidelines.
No CDC recommendation exists, but ACOG and ACS recommend conducting clinical breast exams,
and the Expert Work Group endorsed the ACOG recommendation.
The recommendations are consistent with CDC’s STD treatment guidelines.
The recommendations are consistent with CDC’s STD treatment guidelines.

Source: US Preventive Services Task Force. USPSTF recommendations. Available at http://www.uspreventiveservicestaskforce.org/recommendations.htm.
Abbreviations: AAP = American Academy of Pediatrics; ACS = American Cancer Society; ACOG = American Congress of Obstetricians and Gynecologists; STD = sexually
transmitted disease.
* Source: Committee on Practice and Ambulatory Medicine, Bright Futures Periodicity Schedule Workgroup. 2014 recommendations for pediatric preventive health
care. Pediatrics 2014;133;568.

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TABLE 3. U.S. Preventive Services Task Force (USPSTF) grades, definitions, and suggestions for practice
Grade
A

Definition

Suggestions for practice

USPSTF recommends the service. There is high certainty that the net
benefit is substantial.
USPSTF recommends the service. There is high certainty that the net
benefit is moderate, or there is moderate certainty that the net
benefit is moderate to substantial.

This service should be offered or provided.

Clinicians may provide this service to selected patients depending on
individual circumstances. However, for a majority of persons without
signs or symptoms there is likely to be only a limited benefit from
this service.

This service should be offered or provided only if other
considerations support the offering or providing the service in an
individual patient.

USPSTF recommends against the service. There is moderate or high
certainty that the service has no net benefit or that the harms
outweigh the benefits.

Use of this service should be discouraged.

I Statement

USPSTF concludes that the current evidence is insufficient to assess
the balance of benefits and harms of the service. Evidence is lacking,
of poor quality, or conflicting, and the balance of benefits and harms
cannot be determined.

The clinical considerations section of USPSTF recommendation
statement should be consulted. If the service is offered, patients
should be educated about the uncertainty of the balance of
benefits and harms.

This service should be offered or provided.

Source: US Preventive Services Task Force. USPSTF: methods and processes. Available at http://www.uspreventiveservicestaskforce.org/methods.htm.

TABLE 4. Levels of certainty regarding net benefit
Level of certainty*

Description

High

The available evidence usually includes consistent results from well-designed, well-conducted studies in representative primary care
populations. These studies assess the effects of the preventive service on health outcomes. This conclusion is therefore unlikely to be
strongly affected by the results of future studies.

Moderate

The available evidence is sufficient to determine the effects of the preventive service on health outcomes, but confidence in the estimate is
constrained by such factors as
t the number, size, or quality of individual studies;
t inconsistency of findings across individual studies;
t limited generalizability of findings to routine primary care practice; and
t lack of coherence in the chain of evidence.
As more information becomes available, the magnitude or direction of the observed effect could change, and this change may be large
enough to alter the conclusion.

Low

The available evidence is insufficient to assess effects on health outcomes is insufficient because of
t the limited number or size of studies,
t important flaws in study design or methods,
t inconsistency of findings across individual studies,
t gaps in the chain of evidence,
t findings not generalizable to routine primary care practice,
t lack of information on important health outcomes, or
t more information required to allow estimation of effects on health outcomes.

Source: US Preventive Services Task Force. USPSTF: methods and processes. Available at http://www.uspreventiveservicestaskforce.org/methods.htm.
* The US Preventive Services Task Force (USPSTF) defines certainty as the likelihood that the USPSTF assessment of the net benefit of a preventive service is correct.
The net benefit is defined as benefit minus harm of the preventive service as implemented in a general, primary care population. USPSTF assigns a certainty level
on the basis of the nature of the overall evidence available to assess the net benefit of a preventive service.

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Appendix B
The Evidence, Potential Consequences, and Rationales for Core Recommendations
Sixteen core recommendations that were considered by
the Expert Work Group (EWG) are presented below. Each
recommendation is accompanied by a summary of the
relevant evidence (full summaries of which will be published
separately), a list of potential consequences of implementing
the recommendation, and its rationale. When considering the
recommendations, the Expert Work Group was divided into
two groups (one comprising seven members and the other five
members), and each group considered separate recommendations.

Definition of Family
Planning Services
Recommendation: Primary care providers should offer the
following family planning services: contraceptive services for
women and men who want to prevent pregnancy and space
births, pregnancy testing and counseling, help for clients who
wish to achieve pregnancy, basic infertility services, sexually
transmitted disease (STD) services and preconception health
services to improve the health of women, men, and infants.
Quality of evidence: A systematic review was not conducted;
the recommendation was made on the basis of federal statute
and regulation (1,2), CDC clinical recommendations (3–5),
and expert opinion.
Potential consequences: Adding preconception health
services means that more women and men will receive
preconception health services. The recommended services
also will promote the health of women and men even if
they do not have children. The human and financial cost of
providing preconception health services might mean that fewer
contraceptive and other services can be offered in some settings.
Rationale: Services to prevent and achieve pregnancy
are core to the federal government’s efforts to promote
reproductive health. Adding preconception health as a family
planning service is consistent with this mission; it emphasizes
achieving a healthy pregnancy and also promotes adult health.
Adding preconception health is also consistent with CDC
recommendations to integrate preconception health services
into primary care platforms (3). All seven EWG members
agreed to this recommendation.

Preconception Health — Women
Recommendation: Preconception health services for
women include the following screening services: reproductive

life plan; medical history; sexual health assessment; intimate
partner violence, alcohol, and other drug use; tobacco use;
immunizations; depression; body mass index (BMI); blood
pressure; chlamydia, gonorrhea, syphilis, and HIV/AIDS; and
diabetes. All female clients also should be counseled about the
need to take a daily supplement of folic acid. When screening
results indicate the presence of a health condition, the provider
should take steps either to provide or to refer the client for
the appropriate further diagnostic testing and or treatment.
Services should be provided in a manner that is consistent
with established federal and professional medical associations’
recommendations to enable clients who need services to receive
them and to avoid over-screening.
Quality of evidence: A systematic review was not conducted;
the recommendation was made on the basis of CDC’s
recommendations to improve preconception health and health
care (3) and a review of preconception health services by an
expert panel on preconception care for women (6).
Potential consequences: More women will receive specified
preconception health services, which will improve the health of
infants and women. The evidence base for preconception health
is not fully established. There is a potential risk that a client with
a positive screen will not be able to afford treatment if the client is
uninsured and not eligible for public programs. The human and
financial cost of providing preconception health services might
mean that fewer contraceptive and other services can be offered.
Rationale: The potential benefits to the health of women and
infants were thought by the panel to be greater than the costs,
potential harms, and opportunity costs of providing these services.
Implementation (e.g., training and monitoring of providers) can
address the issues related to providers over-screening and not
following the federal and professional medical recommendations.
CDC will continue to monitor related research and modify these
recommendations, as needed. Health-care reform might make
follow-up care more available to low-income clients. All seven
EWG members agreed to this recommendation.

Preconception Health — Men
Recommendation: Preconception health services for men
include the following screening services: reproductive life
plan; medical history; sexual health assessment; alcohol and
other drug use; tobacco use; immunizations; depression;
BMI; blood pressure; chlamydia, gonorrhea, syphilis, and
HIV/AIDS; and diabetes. When screening results indicate
the presence of a health condition, the provider should take

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steps either to provide or to refer the client for the appropriate
further diagnostic testing and or treatment. Services should be
provided in a manner that is consistent with established federal
and professional medical associations’ recommendations to
ensure that clients who need services receive them and to avoid
over-screening.
Quality of evidence: A systematic review was not conducted;
the recommendation was made on the basis of CDC’s
recommendations to improve preconception health and
health care (3) and a review of preconception health services
for men (7).
Potential consequences: More men will receive
preconception health services, which might improve infant and
men’s health. The evidence base for preconception health is not
well established and is less than that for women’s preconception
health. There is a risk of over-screening if recommendations
are not followed. There is a potential risk that a client with
a positive screen might not be able to afford treatment if the
client is uninsured and not eligible for public programs. The
human and financial cost of providing preconception health
services might mean that fewer contraceptive and other services
can be offered.
Rationale: The potential benefits to men and infant health
were thought by the panel to be greater than the costs, potential
harms, and opportunity costs of not providing these services.
Implementation (e.g., training and monitoring of providers)
can address the issues related to providers over-screening
and not following the federal and professional medical
recommendations. CDC will continue to monitor related
research and modify these recommendations, as needed.
Health-care reform might make follow-up care more available
to low-income clients. All seven EWG members agreed to this
recommendation.

Contraceptive Services —
Contraceptive Counseling Steps
Recommendation: To help a client who is initiating or
switching to a new method of contraception, providers should
follow these steps, which are in accordance with the key principles
for providing quality counseling: 1) establish and maintain
rapport with the client; 2) obtain clinical and social information
from the client; 3) work with the client interactively to select the
most effective and appropriate contraceptive method for her or
him; 4) provide a physical assessment related to contraceptive
use, when warranted; and 5) provide the contraceptive method
along with instructions about correct and consistent use, help
the client develop a plan for using the selected method and for
follow-up, and confirm understanding.

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Quality of evidence: Twenty-two studies were identified
that examined the impact of contraceptive counseling
in clinical settings and met the inclusion criteria. Of the
16 studies that focused on adults or mixed populations
(adolescents and adults) (8–23), 11 found a statistically
significant positive impact of counseling interventions with low
(11,12,14–16,18–21), moderate (8), or unrated (22) intensity
on at least one outcome of interest; study designs included two
cross-sectional surveys (14,22), one pre-post study (21), one
prospective cohort study (8), one controlled trial (15), and
six randomized controlled trials (RCTs) (11,12,16,18–20).
Six studies examined the impact of contraceptive counseling
among adolescents (24–29), with four finding a statistically
significant positive impact of low-intensity (27) or moderateintensity (24,25,29) counseling interventions on at least one
outcome of interest; study designs included two pre-post
studies (24,30), one controlled trial (29), and one RCT (27). In
addition, five studies were identified that examined the impact
of reminder system interventions in clinical settings on family
planning outcomes and met the inclusion criteria (31–35); of
these, two found a statistically significant positive impact of
reminder systems on perfect oral contraceptive compliance, a
retrospective historical nonrandomized controlled trial that
examined daily reminder email messages (31) and a cohort
study that examined use of a small reminder device that
emitted a daily audible beep (34). In addition, two studies
examined the impact of reminder systems among depot
medroxyprogesterone acetate users (DMPA) (33,35) with one,
a retrospective cohort study, finding a statistically significant
positive impact of receiving a wallet-sized reminder card with
the date of the next DMPA injection and a reminder postcard
shortly before the next injection appointment on timely
DMPA injections. Statements about safety and unnecessary
medical examinations and tests are made on the basis of CDC
guidelines on contraceptive use (36,37).
Potential consequences: Fewer clients will use methods that
are not safe for them, there will be increased contraceptive use,
increased use of more effective methods, increased continuation
of method use, increased use of dual methods, increased
knowledge, increased satisfaction with services, and increased
use of repeat or follow-up services.
Rationale: Making sure that a contraceptive method is
safe for an individual client is a fundamental responsibility of
all providers of family planning services. Removing medical
barriers to contraceptive use is key to increasing access
to contraception and helping clients prevent unintended
pregnancy. Consistent use of contraceptives is needed to prevent
unintended pregnancies, so appropriate counseling is critical
to ensure clients make the best possible choice of methods for
their unique circumstances, and are supported in continued

Recommendations and Reports

use of the chosen method. The principles of quality counseling,
from which the steps listed in the recommendations are based,
are supported by a substantial body of evidence and expert
opinion. Future research to evaluate the five principles will be
monitored and the recommendations modified, as needed. All
seven EWG members agreed to this recommendation.

Contraceptive Services — Tiered
Approach to Counseling
Recommendation: For clients who might want to get
pregnant in the future and prefer reversible methods of
contraception, providers should use a tiered approach to
presenting a broad range of contraceptive methods (including
long-acting reversible contraception such as intrauterine
devices and contraceptive implants), in which the most
effective methods are presented before less effective methods.
Quality of evidence: National surveys have demonstrated
low rates of LARC use overall (38,39). However, Project
CHOICE has demonstrated high uptake of long-acting
reversible contraception (approximately two thirds of clients
when financial barriers are removed) and a very substantial
reduction in rates of unintended pregnancy (40). Further, a
recent study of postpartum contraceptive use shows that 50%
of teen mothers with a recent live birth are using long-acting
reversible contraception postpartum in Colorado, which
demonstrates high levels of acceptance in the context of a
statewide program to remove financial barriers (41).
Potential consequences: Use of long-acting reversible
contraception has the potential to help many more persons
prevent unintended pregnancy because of its ease of use, safety,
and effectiveness. Several questions were raised about ethical
issues in using a tiered approach to counseling. First, is it ethical
to educate about long-acting reversible contraception when
the methods are not all available on-site? Second, conversely,
is it ethical not to inform clients about the most effective
methods? In other health service areas, the standard of care
is to inform the client about the most effective treatment
(e.g., blood pressure medications), so the client can make a
fully informed decision, and this standard should apply in
this instance as well. On the basis of historic experiences,
there is a need to ensure that methods always are offered on
a completely voluntary and noncoercive basis. Health-care
reform might make contraceptive services more available to
the majority of clients.
Rationale: Providers have an obligation to inform clients
about the most effective methods available, even if they cannot
provide them. Further, health-care reform will reduce the

financial barriers to long-acting reversible contraception for
many persons. The potential increase in use of long-acting
reversible contraception and other more effective methods is
likely to help reduce rates of unintended pregnancy. All seven
EWG members agreed to this recommendation.

Contraceptive Services — Broad
Range of Methods
Recommendation: A broad range of methods should be
available on-site or through referral.
Quality of evidence: Three descriptive studies from the review
of quality improvement literature identified contraceptive choice
as an important aspect of quality care (42–44).
Potential consequences: Clients will be more likely to select
a method that they will use consistently and correctly.
Rationale: A central tenet of quality health care is that
it be client-centered. Being able to provide a client with
a method that best fits her or his unique circumstances is
essential for that reason. All seven EWG members agreed to
this recommendation.

Contraceptive Services — Education
Recommendation: The content, format, method, and
medium for delivering education should be evidence-based.
Quality of evidence: Seventeen studies were identified
that met the inclusion criteria for this systematic review. Of
these, 15 studies looked at knowledge of correct method use
or contraceptive risks and benefits, including side effects
and method effectiveness (45–59). All but one study (56)
found a statistically significant positive impact of educational
interventions on increased knowledge. These studies included
six randomized controlled trials with low risk for bias.
Potential consequences: Clients will make more informed
decisions when choosing a contraceptive method. More clients will
be satisfied with the process of selecting a contraceptive method.
Rationale: Knowledge obtained through educational
activities, as integrated into the larger counseling model, is
a critically important precondition for the client’s ability to
make informed decisions. The techniques described in the
recommendations have a well-established evidence base for
increasing knowledge and satisfaction with services. This
knowledge lays the foundation for further counseling steps that
will increase the likelihood of correct and consistent use, and
increased satisfaction will increase return visits to the service
site, as needed. Four of seven EWG members agreed to this
recommendation; three members did not express an opinion.

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Contraceptive Services —
Confirm Understanding
Recommendation: A check box or written statement should
be available in the medical record that can be used to document
that the client expressed understanding of the most important
information about her/his chosen contraceptive method. The
teach-back method may be used to get clients to express the
most important points by repeating back messages about
risks and benefits and appropriate method use and follow-up.
Documentation of understanding using the teach-back method
and a check box or written statement can be used in place of
a written method-specific informed consent.
Quality of evidence: Two studies from outside the family
planning literature (one cohort study and one controlled
trial with unclear randomization) (60,61) and a strong
recommendation by members of the Technical Panel on
Counseling and Education were considered.
Potential consequences: More clients will make informed
decisions, adherence to contraceptive and treatment plans will
improve, and reproductive and other health conditions will be
better controlled.
Rationale: Asking providers to document in the record
that the client is making an informed decision will increase
providers’ attention to this task. This recommendation will
replace a previous requirement that providers obtain methodspecific informed consent from each client (in addition to a
general consent form). Six of seven EWG members agreed to
this recommendation.

Adolescent Services —
Comprehensive Information
Recommendation: Providers should provide comprehensive
information to adolescent clients about how to prevent
pregnancy and STDs. This should include information about
contraception and that avoiding sex (abstinence) is an effective
way to prevent pregnancy and STDs.
Quality of evidence: A systematic review was not conducted
because other recent reviews were available that have shown a
substantial impact of comprehensive sexual health education
on reduced adolescent risk behavior (62–66). The evidence for
abstinence-only education was more limited: CDC’s Community
Guide concluded that there was insufficient evidence (67), but
the Department of Health and Human Services’ Office of
Adolescent Health has identified two abstinence-based programs
as having evidence of effectiveness (68).
Potential consequences: Teens will make more informed
decisions and will delay initiation of sexual intercourse. The

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absence of harmful effects from comprehensive sexual health
education was noted.
Rationale: The benefits of informing adolescents about all ways
to prevent pregnancy are substantial. Ultimately, each adolescent
should make an informed decision that meets her or his unique
circumstances, based on the counseling provided by the provider.
Six of seven EWG members agreed to this recommendation.

Adolescent Services — Use of LongActing Reversible Contraception
Recommendation: Education about contraceptive methods
should include an explanation that long-acting reversible
contraception is safe and effective for nulliparous women
(women who have not been pregnant or given birth), including
adolescents.
Quality of evidence: CDC guidelines on contraceptive use
(37) provide evidence that long-acting reversible contraception
is safe and effective for adolescents and nulliparous women.
Potential consequences: More providers will encourage
adolescents to consider long-acting reversible contraception;
more adolescents will choose long-acting reversible
contraception, resulting in reduced rates of teen pregnancy,
including rapid repeat pregnancy.
Rationale: Long-acting reversible contraception is safe for
adolescents (37). As noted above, providers should inform
clients about the most effective methods available. The
potential increase in use of long-acting reversible contraception
and other more effective methods by adolescents is substantial
and is likely to lead to further reductions in teen pregnancy.
Three EWG members agreed to this recommendation; two
EWG members abstained.

Adolescent Services —
Confidential Services
Recommendation: Confidential family planning services
should be made available to adolescents, while observing state
laws and any legal obligations for reporting.
Quality of evidence: Six descriptive studies documented
one or more of the following: that confidentiality is important
to adolescents; that many adolescents reported they will not
use reproductive health services if confidentiality cannot be
assured; and that adolescents might not be honest in discussing
reproductive health with providers if confidentiality cannot be
assured (69–74). One RCT showed a slight reduction in use of
services after receiving conditional confidentiality, compared
with complete confidentiality (75). One study showed a

Recommendations and Reports

positive association between confidentiality and intention to
use services (73).
Potential consequences: Consequences might include an
increased intention to use services, increased use of services, and
reduced rates of teen pregnancy. However, explaining the need
to report under certain circumstances (rape, child abuse) might
deter some adolescent clients from using services. Further, some
parents/guardians might not agree that adolescents should have
access to confidential services.
Rationale: Minors’ rights to confidential reproductive health
services are consistent with state and federal law. The risks of
not providing confidential services to adolescents are great and
likely to result in an increased rate of teen pregnancies. Finally,
this recommendation is consistent with the recommendations
of three professional medical associations that endorse
provision of confidential services to adolescents (76–78). All
seven EWG members agreed to this recommendation.

Adolescent Services —
Family-Child Communication
Recommendation: Providers should encourage and promote
family-child communication about sexual and reproductive health.
Quality of evidence: From the family planning literature,
16 parental involvement programs (most using an RCT study
design) were found to be positively associated with at least one
short-term (13 of 16 studies) or medium-term (four of seven
studies) outcome (79–94). However, only one of these studies
was linked to clinical services (80); others were implemented
in community settings.
Potential consequences: Consequences might include
increased parental/guardian involvement and communication,
improved knowledge/awareness, increased intentions to use
contraceptives, and the adoption of more pro-social norms
that support parent-child communication about sexual health.
Rationale: The literature provides strong evidence that
increased communication between a child and her/his parent/
guardian will lead to safer sexual behavior among teens,
and numerous community-based programs have created an
evidence base for how to strengthen parents/guardians’ ability
to hold those conversations. Although less is known about
how to do so in a clinical setting, providers can refer their
clients to programs in the community, and principles from the
community-based approaches can be used to help providers
develop appropriate approaches in the clinical setting. Research
in this area will be monitored, and the recommendations will be
revised, as needed. Four of five EWG members who provided
input agreed to this recommendation; one member abstained.

Adolescent Services —
Repeat Teen Pregnancy
Recommendation: Providers should refer pregnant and
parenting adolescents to home visiting and other programs
that have been shown to provide needed support and reduce
rates of repeat teen pregnancy.
Quality of evidence: Three of four studies of clinic-based
programs (using retrospective case-control cohort, ecological
evaluation, and prospective cohort study designs) showed that
comprehensive teen pregnancy prevention programs (programs
with clinical, school, case management, and community
components) were associated with both medium- and longterm outcomes (95–98). In addition, several randomized trials
of community-based home visiting programs, and an existing
systematic review of the home visiting literature, demonstrated
a protective impact of these programs on preventing repeat teen
pregnancy and other relevant outcomes (99–103).
Potential consequences: Consequences might include
decreased rapid repeat pregnancy and abortion rates, and
increased use of contraceptives.
Rationale: There is sufficient evidence to recommend that
providers link pregnant and parenting teens to community and
social services that might reduce rates of rapid repeat pregnancy.
Three of seven EWG members agreed to an earlier version of
this recommendation. Other members wanted to remove a
clause about prioritizing the contraceptive needs of pregnant/
parenting teens because they felt that all clients should be
treated as priority clients. This suggestion was adopted, but
the EWG did not have a chance to vote again on the modified
recommendation.

Contraceptive Method Availability
Recommendation: Family planning programs should stock
and offer a broad a range of FDA-approved contraceptive
methods so that the needs of individual clients can be met.
These methods are optimally available on-site, but strong
referrals can serve to make methods not available on-site real
options for clients.
Quality of evidence: No research was identified that
explicitly addressed the question of whether having a broad
range of methods was associated with short-, medium-, or
long-term reproductive health outcomes. However, as noted
above, three descriptive studies from the review of quality
improvement literature identified contraceptive choice as an
important aspect of quality care (42–44).
Potential consequences: Consequences might include
increased use of contraception and increased use of reproductive

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

health services. It also was noted that there are sometimes high
costs to stocking certain methods (e.g., intrauterine devices
and contraceptive implants).
Rationale: Having a broad range of contraceptive methods is
central to client-centered care, a core aspect of providing quality
services. Individual clients need to have a choice so they can
select a method that best fits their particular circumstances.
This is likely to result in more correct and consistent use of
the chosen methods. The benefits of this recommendation
were weighed more heavily than the negative outcomes
(e.g., additional cost). All five EWG members agreed to this
recommendation.

Youth-Friendly Services
Recommendation: Family planning programs should take
steps to make services “youth-friendly.”
Quality of evidence: Of 20 studies that were identified,
six looked at short-, medium-, or long-term outcomes with
mixed designs (one group time series, one cross-sectional, three
prospective cohort, and one nonrandomized trial); protective
effects were found on long-term (two of three studies),
medium-term (three of three), and short-term (three of three)
outcomes (29,30,104–107). One of these six studies (29), plus
13 other descriptive studies (for a total of 14 studies), presented
adolescents’ or providers’ views on facilitators for adolescent
clients in using youth-friendly family planning services. Key
factors described were confidentiality (13 of 14), accessibility
(11 of 14), peer involvement (three of 14), parental or familial
involvement (four of 14), and quality of provider interaction
(11 of 14) (105–121). Four of these studies (111,112,114,121)
plus one other descriptive study (108) described barriers to
clinics adopting and implementing youth-friendly family
planning services.
Potential consequences: Consequences might include
increased use of reproductive health services by adolescents,
improved contraceptive use, use of more effective methods,
more consistent use of contraception, and reduced rates of teen
pregnancy. It is also likely to lead to improved satisfaction with
services and greater knowledge about pregnancy prevention
among adolescents. It is possible that there will be higher costs,
and some uncertainty regarding the benefits due to a relatively
weak evidence base.
Rationale: Existing evidence has demonstrated the
importance of specific characteristics to adolescents’ attitudes
and use of clinical services. The potential benefits of providing
youth-friendly services outweigh the potential costs and
weak evidence base. All five EWG members agreed to this
recommendation. Some thought that it should be cast as an

MMWR / April 25, 2014 / Vol. 63 / No. 4

example of comprehensively client-centered care, rather than
an end of its own.

Quality Improvement
Recommendation: Family planning programs should have
a system for quality improvement, which is designed to review
and strengthen the quality of services on an ongoing basis.
Family planning programs should select, measure, and assess
at least one outcome measure on an ongoing basis, for which
the service site can be accountable.
Quality of evidence: A recent systematic review (122) was
supplemented with 10 articles that provided information related
to client and/or provider perspectives regarding what constitutes
quality family planning services (42–44,113,123–128). These
studies used a qualitative (k = 4) or cross-sectional (k = 6) study
design. Ten descriptive studies identified client and provider
perspectives on what constitutes quality family planning services,
which include stigma and embarrassment reduction (n = 9), client
access and convenience (n = 8); confidentiality (n = 3); efficiency
and tailoring of services (n = 6); client autonomy and confidence
(n = 5); contraceptive access and choice (n = 4); increased time
of patient-provider interaction (n = 3); communication and
relationship (n = 3); structure and facilities (n = 2); continuity
of care (n = 2). Well-established frameworks for guiding quality
improvement efforts were referenced (122,129–132).
Potential consequences: Consequences might include
increased use by clients of more effective contraceptive methods,
clients might be more likely to return for care, client satisfaction
might improve, and there might be reduced rates of teen and
unintended pregnancy, and improved spacing of births.
Rationale: Research, albeit limited, has demonstrated that
quality services are associated with improved client experience
with care and adoption of more protective contraceptive
behavior. Further, these recommendations on quality
improvement are consistent with those made by national leaders
in the quality improvement field. Research is either under way
or planned to validate a core set of performance measures, and
the recommendations will be updated as new findings emerge.
All five EWG members agreed to these recommendations.
References
1. Family Planning Services and Population Research Act of 1970, Title
X. Population Research and Voluntary Family Planning Programs
Project Grants and Contracts for Family Planning Services Pub. L. No.
Public Law 91-572 (1970).
2. Project Grants for Family Planning Services. 42 CFR Part 59, Subpart A,
(1971).
3. CDC. Recommendations to improve preconception health and health
care—United States. MMWR 2006;55(No. RR-06).

Recommendations and Reports

4. CDC. Sexually transmitted diseases treatment guidelines, 2010.
MMWR 2010;59(No. RR-12).
5. CDC. Revised recommendations for HIV testing of adults, adolescents and
pregnant women in health care settings. MMWR 2006;55(No. RR-14).
6. Jack B, Atrash H, Coonrod D, Moos M, O’Donnell J, Johnson K. The
clinical content of preconception care: an overview and preparation of this
supplement. Am J Obstet Gynecol 2008;199(Supplement B):S266–79.
7. Frey K, Navarro S, Kotelchuck M, Lu M. The clinical content of
preconception care: preconception care for men. Am J Obstet Gynecol
2008;199(6 Suppl 2):S389–95.
8. Adams-Skinner J, Exner T, Pili C, Wallace B, Hoffman S, Leu CS. The
development and validation of a tool to assess nurse performance in
dual protection counseling. Patient Educ Couns 2009;76:265–71.
9. Bender SS, Geirsson RT. Effectiveness of preabortion counseling on
postabortion contraceptive use. Contraception 2004;69:481–7.
10. Boise R, Petersen R, Curtis KM, et al. Reproductive health counseling
at pregnancy testing: a pilot study. Contraception 2003;68:377–83.
11. Custo G, Saitto C, Cerza S, Sertoli G. The adjusted contraceptive score
(ACS) improves the overall performance of behavioural and barrier
contraceptive methods. Adv Contracept Deliv Syst 1987;3:367–73.
12. Gilliam M, Knight S, McCarthy M Jr. Success with oral contraceptives:
a pilot study. Contraception 2004;69:413–8.
13. Langston AM, Rosario L, Westhoff CL. Structured contraceptive
counseling—a randomized controlled trial. Patient Educ Couns
2010;81:362–7.
14. Lee JK, Parisi SM, Akers AY, Borrero S, Schwarz EB. The impact of
contraceptive counseling in primary care on contraceptive use. J Gen
Intern Med 2011;26:731–6.
15. Namerow PB, Weatherby N, Williams-Kaye J. The effectiveness of
contingency-planning counseling. Fam Plann Perspect 1989;21:115–9.
16. Nobili MP, Piergrossi S, Brusati V, Moja EA. The effect of patientcentered contraceptive counseling in women who undergo a voluntary
termination of pregnancy. Patient Educ Couns 2007;65:361–8.
17. Petersen R, Albright J, Garrett JM, Curtis KM. Pregnancy and STD
prevention counseling using an adaptation of motivational interviewing: a
randomized controlled trial. Perspect Sex Reprod Health 2007;39:21–8.
18. Proctor A, Jenkins TR, Loeb T, Elliot M, Ryan A. Patient satisfaction
with 3 methods of postpartum contraceptive counseling: a randomized,
prospective trial. J Reprod Med 2006;51:377–82.
19. Schunmann C, Glasier A. Specialist contraceptive counselling and
provision after termination of pregnancy improves uptake of long-acting
methods but does not prevent repeat abortion: a randomized trial.
Hum Reprod 2006;21:2296–303.
20. Shlay JC, Mayhugh B, Foster M, Maravi ME, Baron AE, Douglas JM
Jr. Initiating contraception in sexually transmitted disease clinic setting:
a randomized trial. Am J Obstet Gynecol 2003;189:473–81.
21. Todres R. Effectiveness of counseling in the transmission of family
planning and sexuality knowledge. J Sex Educ Ther 1990;16:279–85.
22. Weisman CS, Maccannon DS, Henderson JT, Shortridge E, Orso CL.
Contraceptive counseling in managed care: preventing unintended
pregnancy in adults. Womens Health Issues 2002;12:79–95.
23. Yassin AS, Cordwell D. Does dedicated pre-abortion contraception
counselling help to improve post-abortion contraception uptake? J Fam
Plann Reprod Health Care 2005;31:115–6.
24. Berger DK, Perez G, Kyman W, et al. Influence of family planning
counseling in an adolescent clinic on sexual activity and contraceptive
use. J Adolesc Health Care 1987;8:436–40.

25. Brindis CD, Geierstanger SP, Wilcox N, McCarter V, Hubbard A.
Evaluation of a peer provider reproductive health service model for
adolescents. Perspect Sex Reprod Health 2005;37:85–91.
26. Cowley CB, Farley T, Beamis K. ‘Well, maybe I’ll try the pill for just
a few months...’: Brief motivational and narrative-based interventions
to encourage contraceptive use among adolescents at high risk for early
childbearing. Fam Syst Health 2002;20:183–204.
27. Hanna KM. Effect of nurse-client transaction on female adolescents’
oral contraceptive adherence. Image J Nurs Sch 1993;25:285–90.
28. Kirby D, Raine T, Thrush G, Yuen C, Sokoloff A, Potter SC. Impact
of an intervention to improve contraceptive use through follow-up
phone calls to female adolescent clinic patients. Perspect Sex Reprod
Health 2010;42:251–7.
29. Winter L, Breckenmaker LC. Tailoring family planning services to the
special needs of adolescents. Fam Plann Perspect 1991;23:24–30.
30. Brindis CD, Geierstanger SP, Wilcox N, McCarter V, Hubbard A.
Evaluation of a peer provider reproductive health service model for
adolescents. Perspect Sex Reprod Health 2005;37:85–91.
31. Fox MC, Creinin MD, Murthy AS, Harwood B, Reid LM. Feasibility
study of the use of a daily electronic mail reminder to improve oral
contraceptive compliance. Contraception 2003;68:365–71.
32. Hou MY, Hurwitz S, Kavanagh E, Fortin J, Goldberg AB. Using daily
text-message reminders to improve adherence with oral contraceptives:
a randomized controlled trial. Obstet Gynecol 2010;116:633–40.
33. Keder LM, Rulin MC, Gruss J. Compliance with depot
medroxyprogesterone acetate: a randomized, controlled trial of intensive
reminders. Am J Obstet Gynecol 1998;179:583–5.
34. Lachowsky M, Levy-Toledano R. Improving compliance in oral
contraception: ‘the reminder card’. Eur J Contracept Reprod Health
Care 2002;7:210–5.
35. Madlon-Kay DJ. The effectiveness of a mail reminder system for depot
medroxyprogesterone injections. Arch Fam Med 1996;5:234–6.
36. CDC. U.S. selected practice recommendations for contraceptive use
2013. MMWR 2013;62(No. RR-4).
37. CDC. U.S. medical eligibility criteria for contraceptive use 2010.
MMWR 2010;59(No. RR-4).
38. Daniels K, Mosher W, Jones J. Contraceptive methods women have ever
used: United States, 1982–2010. National health statistics reports; 2013;62.
39. Martinez G, Copen C, Abma J. Teenagers in the United States: sexual
activity, contraceptive use, and childbearing, 2006–2010 National
Survey of Family Growth. Vital Health Stat 2011;23(31).
40. Winner B, Peipert J, Zhao Q, et al. Effectiveness of long-acting
reversible contraception. N Engl J Med 2012;366:1998–2007.
41. CDC. Vital signs: repeat births among teens—United States, 2007–2010.
MMWR 2013;62:249–55.
42. Becker D, Klassen AC, Koenig MA, LaVeist TA, Sonenstein FL, Tsui
AO. Women’s perspectives on family planning service quality: an
exploration of differences by race, ethnicity and language. Perspect Sex
Reprod Health 2009;41:158–65.
43. Gilliam ML, Hernandez M. Providing contraceptive care to lowincome, African American teens: the experience of urban community
health centers. J Community Health 2007;32:231–44.
44. Landry DJ, Wei J, Frost JJ. Public and private providers’ involvement
in improving their patients’ contraceptive use. Contraception
2008;78:42–51.
45. Deijen JB, Kornaat H. The influence of type of information,
somatization, and locus of control on attitude, knowledge, and
compliance with respect to the triphasic oral contraceptive Tri-Minulet.
Contraception 1997;56:31–41.

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

46. Kirby D, Harvey PD, Claussenius D, Novar M. A direct mailing to
teenage males about condom use: its impact on knowledge, attitudes
and sexual behavior. Fam Plann Perspect 1989;21:12–8.
47. Little P, Griffin S, Kelly J, Dickson N, Sadler C. Effect of educational
leaflets and questions on knowledge of contraception in women taking
the combined contraceptive pill: randomised controlled trial. BMJ
1998;316:1948–52.
48. Smith LF, Whitfield MJ. Women’s knowledge of taking oral contraceptive
pills correctly and of emergency contraception: effect of providing
information leaflets in general practice. Br J Gen Pract 1995;45:409–14.
49. Steiner MJ, Dalebout S, Condon S, Dominik R, Trussell J.
Understanding risk: a randomized controlled trial of communicating
contraceptive effectiveness. Obstet Gynecol 2003;102:709–17.
50. DeLamater J, Wagstaff DA, Havens KK. The impact of a culturally
appropriate STD/AIDS education intervention on black male
adolescents’ sexual and condom use behavior. Health Educ Behav
2000;27:454–70.
51. Mason V, McEwan A, Walker D, Barrett S, James D. The use of video
information in obtaining consent for female sterilisation: a randomised
study. BJOG 2003;110:1062–71.
52. Schwarz EB, Gerbert B, Gonzales R. Computer-assisted provision of
emergency contraception a randomized controlled trial. J Gen Intern
Med 2008;23:794–9.
53. Paperny DM, Starn JR. Adolescent pregnancy prevention by health
education computer games: computer-assisted instruction of knowledge
and attitudes. Pediatrics 1989;83:742–52.
54. Reis J, Tymchyshyn P. A longitudinal evaluation of computer-assisted
instruction on contraception for college students. Adolescence
1992;27:803–11.
55. Roberto AJ, Zimmerman RS, Carlyle KE, Abner EL, Cupp PK, Hansen
GL. The effects of a computer-based pregnancy, STD, and HIV
prevention intervention: a nine-school trial. Health Commun
2007;21:115–24.
56. Lindenberg CS, Solorzano RM, Bear D, Strickland O, Galvis C,
Pittman K. Reducing substance use and risky sexual behavior among
young, low-income, Mexican-American women: comparison of two
interventions. Appl Nurs Res 2002;15:137–48.
57. Chewning B, Mosena P, Wilson D, et al. Evaluation of a computerized
contraceptive decision aid for adolescent patients. Patient Educ Couns
1999;38:227–39.
58. O’Donnell L, San Doval A, Duran R, O’Donnell CR. The effectiveness
of video-based interventions in promoting condom acquisition among
STD clinic patients. Sex Transm Dis 1995;22:97–103.
59. Pedrazzini AE, McGowan H, Lucking L, Johanson RJ. ‘The trouble
with sex–it always gets in the way’: an evaluation of a peer-produced
teenage pregnancy video. Br J Fam Plann 2000;26:131–5.
60. McMahon SR, Rimsza ME, Bay RC. Parents can dose liquid medication
accurately. Pediatrics 1997;100:330–3.
61. Schillinger D, Piette J, Grumbach K, et al. Closing the loop: physician
communication with diabetic patients who have low health literacy.
Arch Intern Med 2003;163:83–90.
62. Kirby D. Comprehensive sex education: strong public support and
persuasive evidence of impact, but little funding. Arch Pediatr Adolesc
Med 2006;160:1182–4.
63. Guide to Community Preventive Services. Preventing HIV/AIDS,
other STIs, and teen pregnancy: group-based comprehensive risk
reduction interventions for adolescents. Atlanta, GA: US Department
of Health and Human Services, CDC; 2009. Available at http://www.
thecommunityguide.org/hiv/riskreduction.html.

MMWR / April 25, 2014 / Vol. 63 / No. 4

64. Kirby D, Obasi A, Laris BA. The effectiveness of sex education and
HIV education interventions in schools in developing countries. World
Health Organ Tech Rep Ser 2006;938:103–50, discussion 317–41.
65. Kirby DB, Laris BA, Rolleri LA. Sex and HIV education programs:
their impact on sexual behaviors of young people throughout the world.
J Adolesc Health 2007;40:206–17.
66. Oringanje C, Meremikwu MM, Eko H, Esu E, Meremikwu A, Ehiri
JE. Interventions for preventing unintended pregnancies among
adolescents. Cochrane Database Syst Rev 2009;(4):CD005215.
67. Guide to Community Preventive Services. Preventing HIV/AIDS,
other STIs, and teen pregnancy: group-based abstinence education
interventions for adolescents. Atlanta, GA: US Department of Health
and Human Services, CDC; 2009; Available at http://www.
thecommunityguide.org/hiv/abstinence_ed.html.
68. Office of Adolescent Health. Information about effective programs for
preventing teen pregnancy. Washington, DC: US Department of Health
and Human Services; 2011. Available at www.hhs.gov/ash/oah/oahinitiatives/tpp/programs.html.
69. Ford CA, Thomsen SL, Compton B. Adolescents’ interpretations of
conditional confidentiality assurances. J Adolesc Health 2001;29:156–9.
70. Garside R, Ayres R, Owen M, Pearson VA, Roizen J. Anonymity and
confidentiality: rural teenagers’ concerns when accessing sexual health
services. J Fam Plann Reprod Health Care 2002;28:23–6.
71. Rainey DY, Brandon DP, Krowchuk DP. Confidential billing accounts
for adolescents in private practice. J Adolesc Health 2000;26:389–91.
72. Schuster MA, Bell RM, Petersen LP, Kanouse DE. Communication
between adolescents and physicians about sexual behavior and risk
prevention. Arch Pediatr Adolesc Med 1996;150:906–13.
73. Thomas N, Murray E, Rogstad KE. Confidentiality is essential if young
people are to access sexual health services. Int J STD AIDS
2006;17:525–9.
74. Thrall JS, McCloskey L, Ettner SL, Rothman E, Tighe JE, Emans SJ.
Confidentiality and adolescents’ use of providers for health information and
for pelvic examinations. Arch Pediatr Adolesc Med 2000;154:885–92.
75. Ford CAMS, Halpern-Felsher BL, Irwin CE Jr. Influence of physician
confidentiality assurances on adolescents’ willingness to disclose
information and seek future health care. A randomized controlled trial.
JAMA 1997;278:1029–34.
76. American College of Obstetricians and Gynecologists. Confidentiality
in adolescent health care: guidelines for adolescent health care. 2nd
ed. Washington, DC: American College of Obstetricians and
Gynecologists; 2011.
77. American Academy of Pediatrics. Achieving quality health services for
adolescents: policy statement of the Committee on Adolescence,
American Academy of Pediatrics. Pediatrics 2008;121:1263.
78. Ford C, English A, Sigman G. Confidential health care for adolescents:
position paper for the society for adolescent medicine. J Adolesc Health
2004;35:160–7.
79. Anderson NLR, Koniak-Griffin D, Keenan CK, Uman G, Duggal BR,
Casey C. Evaluating the outcomes of parent-child family life education
[including commentary by Hayman LL]. Sch Inq Nurs Pract
1999;13:211–38.
80. Guilamo-Ramos V, Bouris A, Jaccard J, Gonzalez B, McCoy W, Aranda
D. A parent-based intervention to reduce sexual risk behavior in early
adolescence: building alliances between physicians, social workers, and
parents. J Adolesc Health;48:159–63.
81. Blake SM, Simkin L, Ledsky R, Perkins C, Calabrese JM. Effects of a
parent-child communications intervention on young adolescents’ risk for
early onset of sexual intercourse. Fam Plann Perspect 2001;33:52–61.

Recommendations and Reports

82. Brody GH, Murry VM, Gerrard M, et al. The Strong African American
Families Program: translating research into prevention programming.
Child Dev 2004;75:900–17.
83. Evans WD, Davis KC, Ashley OS, Blitstein J, Koo H, Zhang Y. Efficacy
of abstinence promotion media messages: findings from an online
randomized trial. J Adolesc Health 2009;45:409–16.
84. Forehand R, Armistead L, Long N, et al. Efficacy of a parent-based sexualrisk prevention program for African American preadolescents: a randomized
controlled trial. Arch Pediatr Adolesc Med 2007;161:1123–9.
85. Haggerty KP, Skinner ML, MacKenzie EP, Catalano RF. A randomized
trial of Parents Who Care: effects on key outcomes at 24-month
follow-up. Prev Sci 2007;8:249–60.
86. Huston RL, Martin LJ, Foulds DM. Effect of a program to facilitate
parent-child communication about sex. Clin Pediatr (Phila)
1990;29:626–33.
87. Lederman RP, Chan W, Roberts-Gray C. Sexual risk attitudes and
intentions of youth aged 12–14 years: survey comparisons of parentteen prevention and control groups. Behavioral Medicine (Washington,
DC) 2004;29:155–63.
88. Lederman RP, Chan W, Roberts-Gray C. Parent-adolescent relationship
education (PARE): program delivery to reduce risks for adolescent
pregnancy and STDs. Behav Med 2008;33:137–43.
89. Lefkowitz ES, Sigman M, Au TK. Helping mothers discuss sexuality
and AIDS with adolescents. Child Dev 2000;71:1383–94.
90. Miller BC, Norton MC, Jenson GO. Impact Evaluation of Facts and
Feelings: a home-based video sex education curriculum. Fam Relat
1993;42:392–400.
91. Murry VM, Berkel C, Brody GH, Gerrard M, Gibbons FX. The Strong
African American Families program: longitudinal pathways to sexual
risk reduction. J Adolesc Health 2007;41:333–42.
92. Schuster MA, Corona R, Elliott MN, et al. Evaluation of Talking
Parents, Healthy Teens, a new worksite based parenting programme to
promote parent-adolescent communication about sexual health:
randomised controlled trial. BMJ 2008;337:a308.
93. Stanton B, Cole M, Galbraith J, et al. Randomized trial of a parent
intervention: parents can make a difference in long-term adolescent
risk behaviors, perceptions, and knowledge. Arch Pediatr Adolesc Med
2004;158:947–55.
94. Stanton BF, Li X, Galbraith J, et al. Parental underestimates of
adolescent risk behavior: a randomized, controlled trial of a parental
monitoring intervention. J Adolesc Health 2000;26:18–26.
95. Elster AB, Lamb ME, Tavare J, Ralston CW. The medical and
psychosocial impact of comprehensive care on adolescent pregnancy
and parenthood. JAMA 1987;258:1187–92.
96. Omar HA, Fowler A, McClanahan KK. Significant reduction of repeat
teen pregnancy in a comprehensive young parent program. J Pediatr
Adolesc Gynecol 2008;21:283–7.
97. Rabin JM, Seltzer V, Pollack S. The long term benefits of a
comprehensive teenage pregnancy program. Clin Pediatr (Phila)
1991;30:305–9.
98. Stevens-Simon C, Kelly L, Kulick R. A village would be nice but...it
takes a long-acting contraceptive to prevent repeat adolescent
pregnancies. Am J Prev Med 2001;21:60–5.
99. Eckenrode J, Campa M, Luckey DW, et al. Long-term effects of prenatal
and infancy nurse home visitation on the life course of youths: 19-year
follow-up of a randomized trial. Arch Pediatr Adolesc Med
2010;164:9–15.

100. Olds D, Henderson CR Jr, Cole R, et al. Long-term effects of nurse
home visitation on children’s criminal and antisocial behavior: 15-year
follow-up of a randomized controlled trial. JAMA 1998;280:1238–44.
101. Olds DL, Eckenrode J, Henderson CR Jr, et al. Long-term effects of home
visitation on maternal life course and child abuse and neglect. Fifteen-year
follow-up of a randomized trial. JAMA 1997;278:637–43.
102. Black M, Bentley M, Papas M, et al. Delaying second births among
adolescent mothers: a randomized, controlled trial of a home-based
mentoring program. Pediatrics 2006;118:1087–99.
103. Avellar S, Paulsell D, Sama-Miller E, Del Grosso P. Home visiting
evidence of effectiveness review. Washington, DC: US Department of
Health and Human Services, Office of Planning, Research and
Evaluation, Administration for Children and Families; 2012.
104. Wilson S, Daniel S, Pearson J, Hopton C, Madeley R. An evaluation
of a new teenage clinic and its impact on teenage conceptions in
Nottingham from 1986 to 1992. Contraception 1994;50:77–86.
105. Gupta S, Hogan R, Kirkman RJ. Experience of the first pelvic
examination. Eur J Contracept Reprod Health Care 2001;6:34–8.
106. Morrison A, Mackie CM, Elliott L, Elliott LM, Gruer L, Bigrigg A.
The Sexual Health Help Centre: a service for young people. J Public
Health Med 1997;19:457–63.
107. Herz EJ, Olson LM, Reis JS. Family planning for teens: strategies for
improving outreach and service delivery in public health settings. Public
Health Rep 1988;103:422–30.
108. Bethea J, Hippisley-Cox J, Coupland C, Pringle M. General practitioners’
attitudes towards the provision of services to young people aged under
16: a cross-sectional survey. Qual Prim Care 2007;15:11–9.
109. Kapphahn CJ, Wilson KM, Klein JD. Adolescent girls’ and boys’
preferences for provider gender and confidentiality in their health care.
J Adolesc Health 1999;25:131–42.
110. Wilson A, Williams R. Sexual health services: what do teenagers want?
Ambul Child Health 2000;6:253–60.
111. Alberti PM, Steinberg AB, Hadi EK, Abdullah RB, Bedell JF. Barriers
at the frontline: assessing and improving the teen friendliness of South
Bronx medical practices. Public Health Rep 2010;125:611–4.
112. Brindis CD, Loo VS, Adler NE, Bolan GA, Wasserheit JN. Service
integration and teen friendliness in practice: a program assessment of
sexual and reproductive health services for adolescents. J Adolesc Health
2005;37:155–62.
113. Chambers R, Boath E, Chambers S. Young people’s and professionals’
views about ways to reduce teenage pregnancy rates: to agree or not
agree. J Fam Plann Reprod Health Care 2002;28:85–90.
114. Cromer BA, McCarthy M. Family planning services in adolescent
pregnancy prevention: the views of key informants in four countries.
Fam Plann Perspect 1999;31:287–93.
115. Donovan C, Mellanby AR, Jacobson LD, Taylor B, Tripp JH; The
Adolescent Working Group. Teenagers’ views on the general practice
consultation and provision of contraception. Br J Gen Pract
1997;47:715–8.
116. French RS. The experience of young people with contraceptive
consultations and health care workers. Int J Adolesc Med Health
2002;14:131–8.
117. Hayter M. Reaching marginalized young people through sexual health
nursing outreach clinics: evaluating service use and the views of service
users. Public Health Nurs 2005;22:339–46.
118. Ingram J, Salmon D. ‘No worries!’ Young people’s experiences of nurseled drop-in sexual health services in South West England. J Res Nurs
2007;12:305–16.

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Recommendations and Reports

119. Peremans L, Hermann I, Avonts D, Van Royen P, Denekens J.
Contraceptive knowledge and expectations by adolescents: an
explanation by focus groups. Patient Educ Couns 2000;40:133–41.
120. Perry C, Thurston M. Meeting the sexual health care needs of young
people: a model that works? Child Care Health Dev 2008;34:98–103.
121. Russell ST, Lee FCH. Practitioners’ perspectives on effective practices
for Hispanic teenage pregnancy prevention. Perspect Sex Reprod Health
2004;36:142–9.
122. Becker D, Koenig MA, Kim YM, Cardona K, Sonenstein FL. The
quality of family planning services in the United States: findings from
a literature review. Perspect Sex Reprod Health 2007;39:206–15.
123. Becker D, Tsui AO. Reproductive health service preferences and perceptions
of quality among low-income women: racial, ethnic and language group
differences. Perspect Sex Reprod Health 2008;40:202–11.
124. Becker H, Stuifbergen A, Tinkle M. Reproductive health care
experiences of women with physical disabilities: a qualitative study.
Arch Phys Med Rehabil 1997;78:S26–33.
125. Bender SS. Attitudes of Icelandic young people toward sexual and
reproductive health services. Fam Plann Perspect 1999;31:294–301.

MMWR / April 25, 2014 / Vol. 63 / No. 4

126. Dixon-Woods M, Stokes T, Young B, Phelps K, Windridge K, Shukla
R. Choosing and using services for sexual health: a qualitative study of
women’s views. Sex Transm Infect 2001;77:335–9.
127. Khan NS, Kirkman R. Intimate examinations: use of chaperones in
community-based family planning clinics. BJOG 2000;107:130–2.
128. Fiddes P, Scott A, Fletcher J, Glasier A. Attitudes towards pelvic
examination and chaperones: a questionnaire survey of patients and
providers. Contraception 2003;67:313–7.
129. Bruce J. Fundamental elements of the quality of care: a simple
framework. Stud Fam Plann 1990;21:61–91.
130. Donabedian A. The quality of care. JAMA 1988;260:1743–8.
131. Institute of Medicine. Crossing the quality chasm: a new health system for
the 21st century. Washington, DC: National Academies of Science; 2001.
132. National Quality Forum. ABCs of measurement. Washington, DC:
National Quality Forum; 2011. Available at http://www.qualityforum.
org/Measuring_Performance/ABCs_of_Measurement.aspx.

Recommendations and Reports

Appendix C
Principles for Providing Quality Counseling
Counseling is a process that enables clients to make
and follow through on decisions. Education is an integral
component of the counseling process that helps clients to
make informed decisions. Providing quality counseling is an
essential component of client-centered care.
Key principles of providing quality counseling are listed below
and may be used when providing family planning services. The
model was developed in consultation with the Technical Panel
on Contraceptive Counseling and Education and reviewed by
the Expert Work Group. Although developed specifically for
providing contraceptive counseling, the principles are broad and
can be applied to health counseling on other topics. Although
the principles are listed here in a particular sequence, counseling
is an iterative process, and at every point in the client encounter
it is necessary to determine whether it is important to readdress
and emphasize a given principle.

Principles of Quality Counseling
Principle 1. Establish and Maintain
Rapport with the Client
Establishing and maintaining rapport with a client is vital
to the encounter and achieving positive outcomes (1). This
can begin by creating a welcoming environment and should
continue through every stage of the client encounter, including
follow-up. The contraceptive counseling literature indicates
that counseling models that emphasized the quality of the
interaction between client and provider have been associated
with decreased teen pregnancy, increased contraceptive use,
increased use of more effective methods, increased use of repeat
or follow-up services, increased knowledge, and enhanced
psychosocial determinants of contraceptive use (2–5) .

Principle 2. Assess the Client’s Needs and
Personalize Discussions Accordingly
Each visit should be tailored to the client’s individual
circumstances and needs. Clients come to family planning
providers for various services and with varying needs.
Standardized questions and assessment tools can help providers
determine what services are most appropriate for a given visit
(6). Contraceptive counseling studies that have incorporated
standardized assessment tools during the counseling process
have resulted in increased contraceptive use, increased correct

use of contraceptives, and increased use of more effective
methods (2,7,8). Contraceptive counseling studies that have
personalized discussions to meet the individual needs of
clients have been associated with increased contraceptive use,
increased correct use of contraceptives, increased use of more
effective methods, increased use of dual-method contraceptives
to prevent both sexually transmitted diseases (STDs) and
pregnancy, increased quality and satisfaction with services,
increased knowledge, and enhanced psychosocial determinants
of contraceptive use (4,7,9–12).

Principle 3. Work with the Client
Interactively to Establish a Plan
Working with a client interactively to establish a plan,
including a plan for follow-up, is important. Establishing a
plan should include setting goals, discussing possible difficulties
with achieving goals, and developing action plans to deal with
potential difficulties. The amount of time spent establishing a
plan will differ depending on the client’s purpose for the visit
and health-care needs. A client plan that requires behavioral
change should be made on the basis of the client’s own goals,
interests, and readiness for change (13–15). Use of computerized
decision aids before the appointment can facilitate this process
by providing a structured yet interactive framework for
clients to analyze their available options systematically and to
consider the personal importance of perceived advantages and
disadvantages (16,17). The contraceptive counseling literature
indicates that counseling models that incorporated goal
setting and development of action plans have been associated
with increased contraceptive use, increased correct use of
contraceptives, increased use of more effective methods, and
increased knowledge (2,9,18–20). Furthermore, contraceptive
counseling models that incorporated follow-up contacts
resulted in decreased teen pregnancy, increased contraceptive
use, increased correct use of contraceptives, increased use of
more effective methods, increased continuation of method
use, increased use of dual-method contraceptives to prevent
both STDs and pregnancy, increased use of repeat or follow-up
services, increased knowledge, and enhanced psychosocial
determinants of contraceptive use (2,3,7,11,21,22) . From the
family planning education literature, computerized decision
aids have helped clients formulate questions and have been
associated with increased knowledge, selection of more effective
methods, and increased continuation and compliance (23–25).

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

Principle 4. Provide Information That Can
Be Understood and Retained by the Client
Clients need information that is medically accurate,
balanced, and nonjudgmental to make informed decisions and
follow through on developed plans. When speaking with clients
or providing educational materials through any medium (e.g.,
written, audio/visual, or computer/web-based), the provider
must present information in a manner that can be readily
understood and retained by the client. Strategies for making
information accessible to clients are provided (see Appendix D).

Principle 5. Confirm Client Understanding
It is important to ensure that clients have processed the
information provided and discussed. One technique for
confirming understanding is to have the client restate the most
important messages in her or his own words. This teach-back
method can increase the likelihood of the client and provider
reaching a shared understanding, and has improved compliance
with treatment plans and health outcomes (26,27). Using the
teach-back method early in the decision-making process will
help ensure that a client has the opportunity to understand her
or his options and is making informed choices (28).
References
1. Lambert M. Implications of outcome research for psychotherapy
integration. In: Norcross J, Goldfind M, eds. Handbook of psychotherapy
integration. New York, NY: Basic Books; 1992:94–129.
2. Adams-Skinner J, Exner T, Pili C, Wallace B, Hoffman S, Leu CS. The
development and validation of a tool to assess nurse performance in dual
protection counseling. Patient Educ Couns 2009;76:265–71.
3. Brindis CD, Geierstanger SP, Wilcox N, McCarter V, Hubbard A.
Evaluation of a peer provider reproductive health service model for
adolescents. Perspect Sex Reprod Health 2005;37:85–91.
4. Nobili MP, Piergrossi S, Brusati V, Moja EA. The effect of patientcentered contraceptive counseling in women who undergo a voluntary
termination of pregnancy. Patient Educ Couns 2007;65:361–8.
5. Proctor A, Jenkins TR, Loeb T, Elliot M, Ryan A. Patient satisfaction
with 3 methods of postpartum contraceptive counseling: a randomized,
prospective trial. J Reprod Med 2006;51:377–82.
6. Fiore M, Jaén C, Baker T, Bailey W, Benowitz N, Curry S. Treating
tobacco use and dependence: 2008 update. Clinical practice guideline.
Rockville, MD: US Department of Health and Human Services; 2008.
Available at http://www.ncbi.nlm.nih.gov/books/NBK63952.
7. Boise R, Petersen R, Curtis KM, et al. Reproductive health counseling
at pregnancy testing: a pilot study. Contraception 2003;68:377–83.
8. Custo G, Saitto C, Cerza S, Sertoli G. The adjusted contraceptive score
(ACS) improves the overall performance of behavioural and barrier
contraceptive methods. Adv Contracept Deliv Syst 1987;3:367–73.

MMWR / April 25, 2014 / Vol. 63 / No. 4

9. Hanna KM. Effect of nurse-client transaction on female adolescents’
oral contraceptive adherence. Image J Nurs Sch 1993;25:285–90.
10. Schunmann C, Glasier A. Specialist contraceptive counselling and
provision after termination of pregnancy improves uptake of long-acting
methods but does not prevent repeat abortion: a randomized trial. Hum
Reprod 2006;21:2296–303.
11. Shlay JC, Mayhugh B, Foster M, Maravi ME, Baron AE, Douglas JM
Jr. Initiating contraception in sexually transmitted disease clinic setting:
a randomized trial. Am J Obstet Gynecol 2003;189:473–81.
12. Weisman CS, Maccannon DS, Henderson JT, Shortridge E, Orso CL.
Contraceptive counseling in managed care: preventing unintended
pregnancy in adults. Womens Health Issues 2002;12:79–95.
13. Kaplan D. Family Counseling for all counselors. Greensboro, NC: CAPS
Publications; 2003.
14. Nupponen R. What is counseling all about—basics in the counseling
of health-related physical activity. Patient Educ Couns 1998;
33(Suppl):S61–7.
15. Whitlock EP, Orleans CT, Pender N, Allan J. Evaluating primary care
behavioral counseling interventions: an evidence-based approach. Am
J Prev Med 2002;22:267–84.
16. French RS, Wellings K, Cowan F. How can we help people to choose a
method of contraception? The case for contraceptive decision aids. J Fam
Plann Reprod Health Care 2009;35:219–20.
17. O’Connor AM, Bennett CL, Stacey D, et al. Decision aids for people
facing health treatment or screening decisions. Cochrane Database Syst
Rev 2009;CD001431.
18. Cowley CB, Farley T, Beamis K. “Well, maybe I’ll try the pill for just a
few months...”: brief motivational and narrative-based interventions to
encourage contraceptive use among adolescents at high risk for early
childbearing. Fam Syst Health 2002;20:183–204.
19. Gilliam M, Knight S, McCarthy M Jr. Success with oral contraceptives:
a pilot study. Contraception 2004;69:413–8.
20. Namerow PB, Weatherby N, Williams-Kaye J. The effectiveness of
contingency-planning counseling. Fam Plann Perspect 1989;21:115–9.
21. Berger DK, Perez G, Kyman W, et al. Influence of family planning
counseling in an adolescent clinic on sexual activity and contraceptive
use. J Adolesc Health Care 1987;8:436–40.
22. Winter L, Breckenmaker LC. Tailoring family planning services to the
special needs of adolescents. Fam Plann Perspect 1991;23:24–30.
23. Chewning B, Mosena P, Wilson D, et al. Evaluation of a computerized
contraceptive decision aid for adolescent patients. Patient Educ Couns
1999;38:227–39.
24. Garbers S, Meserve A, Kottke M, Hatcher R, Chiasson MA. Tailored health
messaging improves contraceptive continuation and adherence: results from
a randomized controlled trial. Contraception 2012;86:536–42.
25. Garbers S, Meserve A, Kottke M, Hatcher R, Ventura A, Chiasson MA.
Randomized controlled trial of a computer-based module to improve
contraceptive method choice. Contraception 2012;86:383–90.
26. McMahon SR, Rimsza ME, Bay RC. Parents can dose liquid medication
accurately. Pediatrics 1997;100:330–3.
27. Schillinger D, Piette J, Grumbach K, et al. Closing the loop: physician
communication with diabetic patients who have low health literacy. Arch
Intern Med 2003;163:83–90.
28. National Quality Forum. Health literacy: a linchpin in achieving national
goals for health and healthcare, Issue Brief #13 2009. Available at http://www.
qualityforum.org/Publications/2009/03/Health_Literacy__A_Linchpin_in_
Achieving_National_Goals_for_Health_and_Healthcare.aspx.

Recommendations and Reports

Appendix D
Contraceptive Effectiveness
Providers should counsel clients about the effectiveness
of different contraceptive methods. Method effectiveness
is measured as the percentage of women experiencing an

unintended pregnancy during the first year of use, and is
estimated for both typical and perfect use (Table).

TABLE. Percentage of women experiencing an unintended pregnancy during the first year of typical use* and the first year of perfect use† of
contraception and the percentage continuing use at the end of the first year — United States
% of women experiencing an unintended pregnancy
within the first year of use
Method
No method¶
Spermicides**
Fertility awareness-based methods
Standard days method††
2-day method††
Ovulation method††
Symptothermal method
Withdrawal
Sponge
Parous women
Nulliparous women
Condom§§
Female
Male
Diaphragm¶¶
Combined pill and progestin-only pill
Evra patch
NuvaRing
Depo-Provera
Intrauterine contraceptives
ParaGard (copper T)
Mirena (LNG)
Implanon
Female sterilization
Male sterilization

Typical use

Perfect use

85.0
28.0
24.0

85.0
18.0

% of women continuing use at 1 year§
42.0
47.0

22.0

5.0
4.0
3.0
0.4
4.0

24.0
12.0

20.0
9.0

21.0
18.0
12.0
9.0
9.0
9.0
6.0

5.0
2.0
6.0
0.3
0.3
0.3
0.2

41.0
43.0
57.0
67.0
67.0
67.0
56.0

0.6
0.2
0.05
0.5
0.1

78.0
80.0
84.0
100.0
100.0

0.8
0.2
0.05
0.5
0.15

46.0
36.0

Emergency Contraceptives: Emergency contraceptive pills or insertion of a copper intrauterine contraceptive after unprotected intercourse substantially reduces the risk of pregnancy.***
Lactational Amenorrhea Method: LAM is a highly effective, temporary method of contraception.†††
Source: Adapted from Trussell J. Contraceptive efficacy. In: Hatcher RA, Trussell J, Nelson AL, Cates W, Kowal D, Policar M, eds. Contraceptive technology: 20th revised ed. New York, NY: Ardent
Media; 2011.
* Among typical couples who initiate use of a method (not necessarily for the first time), the percentage of couples who experience an accidental pregnancy during the first year if they
do not stop use for any other reason. Estimates of the probability of pregnancy during the first year of typical use for spermicides and the diaphragm are taken from the 1995 National
Survey of Family Growth corrected for underreporting of abortion; estimates for fertility awareness-based methods, withdrawal, the male condom, the pill, and Depo-Provera are taken
from the 1995 and 2002 National Survey of Family Growth corrected for underreporting of abortion. See the text for the derivation of estimates for the other methods.
† Among couples who initiate use of a method (not necessarily for the first time) and who use it perfectly (both consistently and correctly), the percentage of couples who experience an
accidental pregnancy during the first year if they do not stop use for any other reason. See the text for the derivation of the estimate for each method.
§ Among couples attempting to avoid pregnancy, the percentage of couples who continue to use a method for 1 year.
¶ The percentages becoming pregnant in columns labeled “typical use” and “perfect use” are based on data from populations in which contraception is not used and from women who
cease using contraception to become pregnant. Among such populations, approximately 89% become pregnant within 1 year. This estimate was lowered slightly (to 85%) to represent
the percentage of women who would become pregnant within 1 year among women now relying on reversible methods of contraception if they abandoned contraception altogether.
** Foams, creams, gels, vaginal suppositories, and vaginal film.
†† The Ovulation and 2-day methods are based on evaluation of cervical mucus. The Standard Days method avoids intercourse on cycle days 8 through 19. The Symptothermal method is
a double-check method based on evaluation of cervical mucus to determine the first fertile day and evaluation of cervical mucus and temperature to determine the last fertile day.
§§ Without spermicides.
¶¶ With spermicidal cream or jelly.
*** Ella, Plan B One-Step, and Next Choice are the only dedicated products specifically marketed for emergency contraception. The label for Plan B One-Step (1 dose is 1 white pill) says to
take the pill within 72 hours after unprotected intercourse. Research has indicated that all of the brands listed here are effective when used within 120 hours after unprotected intercourse.
The label for Next Choice (1 dose is 1 peach pill) says to take one pill within 72 hours after unprotected intercourse and another pill 12 hours later. Research has indicated that that both
pills can be taken at the same time with no decrease in efficacy or increase in side effects and that they are effective when used within 120 hours after unprotected intercourse. The Food
and Drug Administration has in addition declared the following 19 brands of oral contraceptives to be safe and effective for emergency contraception: Ogestrel (1 dose is 2 white pills),
Nordette (1 dose is 4 light-orange pills), Cryselle, Levora, Low-Ogestrel, Lo/Ovral, or Quasence (1 dose is 4 white pills), Jolessa, Portia, Seasonale or Trivora (1 dose is 4 pink pills), Seasonique
(1 dose is 4 light-blue-green pills), Enpresse (1 dose is 4 orange pills), Lessina (1 dose is 5 pink pills), Aviane or LoSeasonique (one dose is 5 orange pills), Lutera or Sronyx (1 dose is 5 white
pills), and Lybrel (1 dose is 6 yellow pills).
††† However, for effective protection against pregnancy to be maintained, another method of contraception must be used as soon as menstruation resumes, the frequency or duration of
breastfeeds is reduced, bottle feeds are introduced, or the baby reaches age 6 months.

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

Appendix E
Strategies for Providing Information to Clients
The client should receive and understand the information
she or he needs to make informed decisions and follow
treatment plans. This requires careful attention to how
information is communicated. The following strategies can
make information more readily comprehensible to clients:

Strategies for Providing Information to Clients
Educational materials should be provided that are clear and
easy to understand. Educational materials delivered through
any one of a variety of media (for example, written, audio/
visual, computer/web-based) need to be presented in a format
that is clear and easy to interpret by clients with a 4th to 6th
grade reading level (1–3). Many adults have only a basic
ability to obtain, process, and understand health information
necessary to make decisions about their health (4). Making
easy-to-access materials enhances informed decision-making
(1–3). Test all educational materials with the intended
audiences for clarity and comprehension before wide-scale use.
The following evidence-based tools provide recommendations
for increasing the accessibility of materials through careful
consideration of content, organization, formatting, and
writing style:
t Health Literacy Universal Precautions Toolkit, provided
by the Agency for Healthcare Research and Quality
(available at http://www.ahrq.gov/qual/literacy),
t Toolkit for Making Written Material Clear and Effective,
provided by the Centers for Medicare and Medicaid Services
(available at http://www.cms.gov/WrittenMaterialsToolkit),
and
t Health Literacy Online, provided by the Office of Disease
Prevention and Health Promotion (available at http://
www.health.gov/healthliteracyonline).
Information should be delivered in a manner that is
culturally and linguistically appropriate. In presenting
information it is important to be sensitive to the client’s
cultural and linguistic preferences (5,6). Ideally information
should be presented in the client’s primary language, but
translations and interpretation services should be available
when necessary. Information presented must also be culturally
appropriate, reflecting the client’s beliefs, ethnic background,
and cultural practices. Tools for addressing cultural and
linguistic differences and preferences include
t Health Literacy Universal Precautions Toolkit, provided
by the Agency for Healthcare Research and Quality
(available at http://www.ahrq.gov/qual/literacy), and

MMWR / April 25, 2014 / Vol. 63 / No. 4

t Toolkit for Making Written Material Clear and Effective,
Part 11; Understanding and using the “Toolkit Guidelines
for Culturally Appropriate Translation,” provided by the
Centers for Medicare and Medicaid Services (available at
http://www.cms.gov/outreach-and-education/outreach/
writtenmaterialstoolkit/downloads/toolkitpart11.pdf ).
The amount of information presented should be limited and
emphasize essential points. Providers should focus on needs
and knowledge gaps identified during the assessment. Many
clients immediately forget or remember incorrectly much of
the information provided. This problem is exacerbated as
more information is presented (7–9). Limiting the amount
of information presented and highlighting important facts
by presenting them first improves comprehension (10–14).
Numeric quantities should be communicated in a way that
is easily understood. Whenever possible, providers should use
natural frequencies and common denominators (for example,
85 of 100 sexually active women are likely to get pregnant
within 1 year using no contraceptive, as compared with 1
in 100 using an IUD or implant), and display quantities in
graphs and visuals. Providers also should avoid using verbal
descriptors without numeric quantities (for example, sexually
active women using an IUD or implant almost never become
pregnant). Finally, they should quantify risk in absolute rather
than relative terms (for example, “the chance of unintended
pregnancy is reduced from 8 in 100 to 1 in 100 by switching
from oral contraceptives to an IUD” versus the chance of
unintended pregnancy is reduced by 87%). Numeracy is more
highly correlated with health outcomes than the ability to read
or listen effectively (15). The strategies listed above can help
clients interpret numeric quantities correctly (16–28).
Balanced information on risks and benefits should be
presented and messages framed positively. In addition to
discussing risks, contraindications, and warnings, providers
should discuss the advantages and benefits of contraception.
In presenting this information, providers should express risks
and benefits in a common format (for example, do not present
risks in relative terms and benefits in absolute terms), and frame
messages in positive terms (for example “99 out of 100 women
find this a safe method with no side effects,” versus “1 out of
100 women experience noticeable side effects”). Many clients
prefer to receive a balance of information on risks and benefits
(29), and using a common format avoids bias in presentation
of information (18,22,26,30). Framing messages positively
increases acceptance and comprehension (18,22,31,32).

Recommendations and Reports

Active client engagement should be encouraged. Providers
should use educational materials that encourage active
information processing (e.g., questions, quizzes, fill-in-theblank, web-based games, and activities). In addition, they
should be sure the client has an opportunity to discuss the
information provided, and when speaking with a client,
providers should engage her or him actively. Research has
indicated that interactive materials improve knowledge
of contraceptive risks, benefits, and correct method use
(33–35). Clients also value spoken information (29,36); and
educational materials, when delivered by a provider, more
effectively increase knowledge (10,37). In particular, presenting
information in a question and answer format is more effective
than simply presenting the information (10,15,37–41).
References
1. Centers for Medicare and Medicaid Services. Toolkit for making written
material clear and effective. Baltimore, MD: Centers for Medicare and
Medicaid Services; 2011.
2. US Department of Health and Human Services, Office of Disease
Prevention and Health Promotion. Health literacy online: A guide to
writing and designing easy-to-use health Web sites. Washington, DC:
US Department of Health and Human Services; 2010.
3. DeWalt D, Callahan L, Hawk V, et al. Health literacy universal
precautions toolkit. AHRQ Publication No. 10–0046-EF. Rockville,
MD: Agency for Healthcare Research and Quality; 2010.
4. Kutner M, Greenberg E, Jin Y, Paulsen C. The health literacy of America’s
adults: results from the 2003 National Assessment of Adult Literacy
(NCES 2006–483). Washington, DC: U.S. Department of Education:
National Center for Education Statistics; 2006.
5. Olavarria M, Beaulac J, Belanger A, Young M, Aubry T. Organizational
cultural competence in community health and social service organizations:
how to conduct a self-assessment. J Cult Divers 2009;16:140–50.
6. Tucker C. Reducing health disparities by promoting patient-centered
culturally and linguistically sensitive/competent health care. U.S.
Department of Health and Human Services Advisory Committee on
Minority Health, US Public Health Service; 2009.
7. Anderson JL, Dodman S, Kopelman M, Fleming A. Patient information
recall in a rheumatology clinic. Rheumatol Rehabil 1979;18:18–22.
8. Crane JA. Patient comprehension of doctor-patient communication on
discharge from the emergency department. J Emerg Med 1997;15:1–7.
9. McGuire LC. Remembering what the doctor said: organization and adults’
memory for medical information. Exp Aging Res 1996;22:403–28.
10. Little P, Griffin S, Kelly J, Dickson N, Sadler C. Effect of educational
leaflets and questions on knowledge of contraception in women taking
the combined contraceptive pill: randomised controlled trial. BMJ
1998;316:1948–52.
11. McGee J. Toolkit for making written material clear and effective:
Baltimore, MD: Centers for Medicare and Medicaid Services; 2010.
Available at http://www.cms.gov/WrittenMaterialsToolkit.
12. Peters E, Dieckmann N, Dixon A, Hibbard JH, Mertz CK. Less is more
in presenting quality information to consumers. Med Care Res Rev
2007;64:169–90.
13. Steiner MJ, Dalebout S, Condon S, Dominik R, Trussell J. Understanding
risk: a randomized controlled trial of communicating contraceptive
effectiveness. Obstet Gynecol 2003;102:709–17.
14. Berry DC, Michas IC. Rosis F. Evaluating explanations about drug
prescriptions: Effects of varying the nature of information about side
effects and its relative position in explanations. Psychol Health
1998;13:767–84.

15. Berkman N, Sheridan S, Donahue K, et al. Health literacy interventions
and outcomes: an updated systematic review. Evidence Report/
Technology Assesment No. 199. Rockville, MD: Agency for Healthcare
Research and Quality; 2011.
16. Berry DC. Informing people about the risks and benefits of medicines:
implications for the safe and effective use of medicinal products. Curr
Drug Saf 2006;1:121–6.
17. Berry DC, Raynor DK, Knapp P, Bersellini E. Patients’ understanding
of risk associated with medication use: impact of European Commission
guidelines and other risk scales. Drug Saf 2003;26:1–11.
18. Edwards A, Elwyn G, Mulley A. Explaining risks: turning numerical
data into meaningful pictures. BMJ 2002;324:827–30.
19. Galesic M, Gigerenzer G, Straubinger N. Natural frequencies help older
adults and people with low numeracy to evaluate medical screening tests.
Med Decis Making 2009;29:368–71.
20. Garcia-Retamero R, Galesic M. Communicating treatment risk reduction
to people with low numeracy skills: a cross-cultural comparison. Am J
Public Health 2009;99:2196–202.
21. Garcia-Retamero R, Galesic M, Gigerenzer G. Do icon arrays help reduce
denominator neglect? Med Decis Making 2010;30:672–84.
22. Gigerenzer G, Edwards A. Simple tools for understanding risks: from
innumeracy to insight. BMJ 2003;327:741–4.
23. Knapp P, Gardner PH, Raynor DK, Woolf E, McMillan B. Perceived
risk of tamoxifen side effects: a study of the use of absolute frequencies
or frequency bands, with or without verbal descriptors. Patient Educ
Couns 2010;79:267–71.
24. Kurz-Milcke E, Gigerenzer G, Martignon L. Transparency in risk
communication: graphical and analog tools. Ann N Y Acad Sci
2008;1128:18–28.
25. Lipkus IM. Numeric, verbal, and visual formats of conveying health
risks: suggested best practices and future recommendations. Med Decis
Making 2007;27:696–713.
26. Paling J. Strategies to help patients understand risks. BMJ 2003;
327:745–8.
27. Skolbekken JA. Communicating the risk reduction achieved by
cholesterol reducing drugs. BMJ 1998;316:1956–8.
28. Visschers VH, Meertens RM, Passchier WW, de Vries NN. Probability
information in risk communication: a review of the research literature.
Risk Anal 2009;29:267–87.
29. Raynor DK, Blenkinsopp A, Knapp P, et al. A systematic review of
quantitative and qualitative research on the role and effectiveness of
written information available to patients about individual medicines.
Health Technol Assess 2007;11:iii, 1–160.
30. Fahey T, Griffiths S, Peters TJ. Evidence based purchasing: understanding
results of clinical trials and systematic reviews. BMJ 1995;311:1056–9,
discussion 9–60.
31. Armstrong K, Schwartz JS, Fitzgerald G, Putt M, Ubel PA. Effect of framing
as gain versus loss on understanding and hypothetical treatment choices:
survival and mortality curves. Med Decis Making 2002;22:76–83.
32. Gurm HS, Litaker DG. Framing procedural risks to patients: is 99%
safe the same as a risk of 1 in 100? Acad Med 2000;75:840–2.
33. Paperny DM, Starn JR. Adolescent pregnancy prevention by health
education computer games: computer-assisted instruction of knowledge
and attitudes. Pediatrics 1989;83:742–52.
34. Reis J, Tymchyshyn P. A longitudinal evaluation of computer-assisted
instruction on contraception for college students. Adolescence
1992;27:803–11.
35. Roberto AJ, Zimmerman RS, Carlyle KE, Abner EL, Cupp PK, Hansen
GL. The effects of a computer-based pregnancy, STD, and HIV
prevention intervention: a nine-school trial. Health Commun
2007;21:115–24.
36. Grime J, Blenkinsopp A, Raynor DK, Pollock K, Knapp P. The role and
value of written information for patients about individual medicines: a
systematic review. Health Expect 2007;10:286–98.

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

37. DeLamater J, Wagstaff DA, Havens KK. The impact of a culturally
appropriate STD/AIDS education intervention on black male
adolescents’ sexual and condom use behavior. Health Educ Behav
2000;27:454–70.
38. McMahon SR, Rimsza ME, Bay RC. Parents can dose liquid medication
accurately. Pediatrics 1997;100:330–3.
39. Belcher L, Kalichman S, Topping M, et al. A randomized trial of a brief
HIV risk reduction counseling intervention for women. J Consult Clin
Psychol 1998;66:856–61.

MMWR / April 25, 2014 / Vol. 63 / No. 4

40. Eldridge GD, St Lawrence JS, Little CE, et al. Evaluation of the HIV
risk reduction intervention for women entering inpatient substance
abuse treatment. AIDS Educ Prev 1997;9(Suppl):62–76.
41. Jaccard J. Unlocking the contraceptive conundrum. Washington, DC:
The National Campaign to Prevent Teen and Unplanned Pregnancy;
2009. Available at http://thenationalcampaign.org/resource/
unlocking-contraception-conundrum.

Recommendations and Reports

Appendix F
Screening Services For Which Evidence Does Not Support Screening
The following services have been given a D recommendation
from the U.S. Preventive Services Task Force (USPSTF), which
indicates that the potential harms of routine screening outweigh
the benefits. Providers should not perform these screening services.
The USPSTF has recommended against offering the
following services to women and men:
t Asymptomatic bacteriuria: USPSTF recommends
against screening for asymptomatic bacteriuria in men
and nonpregnant women (1).
t Gonorrhea: USPSTF recommends against routine
screening for gonorrhea infection in men and women who
are at low risk of infection (2).
t Hepatitis B: USPSTF recommends against routinely
screening the general asymptomatic population for
chronic hepatitis B virus infection (3).
t Herpes simplex virus (HSV): USPSTF recommends
against routine serological screening for HSV in
asymptomatic adolescents and adults (4).
t Syphilis: USPSTF recommends against screening of
asymptomatic persons who are not at increased risk of
syphilis infection (5).
The USPSTF has recommended against offering the
following services to women:
t BRCA mutation testing for breast and ovarian cancer
susceptibility: USPSTF recommends against routine
referral for genetic counseling or routine breast cancer
susceptibility gene (BRCA) testing for women whose family
history is not associated with an increased risk of deleterious
mutations in breast cancer susceptibility gene 1 (BRCA1) or
breast cancer susceptibility gene 2 (BRCA2) (6). However,
USPSTF continues to recommend that women whose family
history is associated with an increased risk of deleterious
mutations in BRCA1 or BRCA2 genes be referred for genetic
counseling and evaluation for BRCA testing.
t Breast self-examination: USPSTF recommends against
teaching breast self-examination (7).
t Cervical cytology: USPSTF recommends against routine
screening for cervical cancer with cytology (Pap smear) in
the following groups: women aged <21 years, women aged
>65 years who have had adequate prior screening and are
not otherwise at high risk for cervical cancer, women who
have had a hysterectomy with removal of the cervix and
who do not have a history of a high-grade precancerous
lesion (i.e., cervical intraepithelial neoplasia grade 2 or 3)
or cervical cancer. USPSTF recommends against screening
for cervical cancer with HPV testing, alone or in
combination with cytology, in women aged <30 years (8).

t Ovarian cancer: USPSTF recommends against routine
screening for ovarian cancer (9).
The USPSTF has recommended against offering the
following services to men:
t Prostate cancer: USPSTF recommends against prostatespecific antigen (PSA)-based screening for prostate cancer (10).
t Testicular cancer: USPSTF recommends against screening
for testicular cancer in adolescent or adult males (11).
References
1. US Preventive Services Task Force. Screening for asymptomatic bacteriuria
in adults. Rockville, MD: US Department of Health and Human Services,
Agency for Healthcare Research and Quality; 2008. Available at http://
www.uspreventiveservicestaskforce.org/uspstf/uspsbact.htm.
2. US Preventive Services Task Force. Screening for gonorrhea. Rockville,
MD: US Department of Health and Human Services, Agency for
Healthcare Research and Quality; 2005. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspsgono.htm.
3. US Preventive Services Task Force. Screening for hepatitis B infection.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2004. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspshepb.htm.
4. US Preventive Services Task Force. Screening for genital herpes:
recommendation statement. Rockville, MD: US Department of Health
and Human Services, Agency for Healthcare Research and Quality;
2005. Available at http://www.uspreventiveservicestaskforce.org/
uspstf05/herpes/herpesrs.htm.
5. US Preventive Services Task Force. Screening for syphilis infection.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2004. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspssyph.htm.
6. US Preventive Services Task Force. Risk assessment, genetic counseling, and
genetic testing for BRCA-related cancer in women. Rockville, MD: US
Department of Health and Human Services, Agency for Healthcare Research
and Quality; 2013. Available at http://www.uspreventiveservicestaskforce.
org/uspstf/uspsbrgen.htm.
7. US Preventive Services Task Force. Screening for breast cancer. Rockville,
MD: US Department of Health and Human Services, Agency for
Healthcare Research and Quality; 2009. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspsbrca.htm.
8. US Preventive Services Task Force. Screening for cervical cancer.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2012. Available at www.
uspreventiveservicestaskforce.org/uspstf11/cervcancer/cervcancerrs.htm.
9. US Preventive Services Task Force. Screening for ovarian cancer: U.S.
Preventive Services Task Force reaffirmation recommendation statement.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2012. Available at http://www.
uspreventiveservicestaskforce.org/uspstf12/ovarian/ovarcancerrs.htm.
10. US Preventive Services Task Force. Screening for prostate cancer.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2012. Available at http://www.
uspreventiveservicestaskforce.org/prostatecancerscreening.htm.
11. US Preventive Services Task Force. Screening for testicular cancer.
Rockville, MD: US Department of Health and Human Services, Agency
for Healthcare Research and Quality; 2011. Available at http://www.
uspreventiveservicestaskforce.org/uspstf/uspstest.htm.

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

Lead Authors
Loretta Gavin, PhD, Division of Reproductive Health, CDC
Susan Moskosky, MS, Office of Population Affairs, CDC

Systematic Review Authors and Presenters
Anna Brittain, MHS, Division of Reproductive Health, CDC
Marion Carter, PhD, Division of Reproductive Health, CDC
Kathryn Curtis, PhD, Division of Reproductive Health, CDC
Emily Godfrey, MD, Division of Reproductive Health, CDC
Arik V. Marcell, MD, The Johns Hopkins University and the Male Training Center
Cassondra Marshall, MPH, Division of Reproductive Health, CDC
Karen Pazol, PhD, Division of Reproductive Health, CDC
Naomi Tepper, MD, Division of Reproductive Health, CDC
Marie Tiller, PhD, MANILA Consulting Group, Inc.
Stephen Tregear, DPhil, MANILA Consulting Group, Inc.
Michelle Tregear, PhD, MANILA Consulting Group, Inc.
Jessica Williams, MPH, MANILA Consulting Group, Inc.
Lauren Zapata, PhD, Division of Reproductive Health, CDC

Expert Work Group
Courtney Benedict, MSN, Marin Community Clinics
Jan Chapin, MPH, American College of Obstetricians and Gynecologists
Clare Coleman, President and CEO, National Family Planning and Reproductive Health Association
Vanessa Cullins, MD, Planned Parenthood Federation of America
Daryn Eikner, MS, Family Planning Council
Jule Hallerdin, MN, Advisor to the Office of Population Affairs
Mark Hathaway, MD, Unity Health Care and Washington Hospital Center
Seiji Hayashi, MD, Bureau of Primary Health Care, Health Resources and Services Administration
Beth Jordan, MD, Association of Reproductive Health Professionals
Ann Loeffler, MSPH, John Snow Research and Training Institute
Arik V. Marcell, MD, The Johns Hopkins University and the Male Training Center
Tom Miller, MD, Alabama Department of Health
Deborah Nucatola, MD, Planned Parenthood Federation of America
Michael Policar, MD, State of California and UCSF Bixby Center
Adrienne Stith-Butler, PhD, Keck Center of the National Academies
Denise Wheeler, ARNP, Iowa Department of Public Health
Gayla Winston, MPH, Indiana Family Health Council
Jacki Witt, MSN, Clinical Training Center for Family Planning, University of Missouri—Kansas City
Jamal Gwathney, MD, Bureau of Primary Health Care, Health Resources and Services Administration

Technical Panel on Women’s Clinical Services
Courtney Benedict, MSN, Marin Community Clinics
Janet Chapin, MPH, American College of Obstetricians and Gynecologists
Elizabeth DeSantis, MSN, South Carolina Department of Health and Environmental Control
Linda Dominguez, CNP, Southwest Women’s Health
Eileen Dunne, MD, Division of STD Prevention, CDC
Jamal K. Gwathney, MD, Bureau of Primary Health Care, Health Resources and Services Administration
Jule Hallerdin, Consultant Advisor
Mark Hathaway, MD, Washington Hospital Center
Arik V. Marcell, MD, Johns Hopkins University and the Male Training Center
Cheri Moran, University of Illinois Medical Center at Chicago
Deborah Nucatola, MD, Planned Parenthood Federation of America
Michael Policar, MD, Family PACT Program - California State Office of Family Planning
Pablo Rodriguez, MD, Women’s Care Inc., Providence Office
Denise Wheeler, ARNP, Iowa Department of Public Health
Jacki Witt, MSN, Clinical Training Center for Family Planning, University of Missouri—Kansas City

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

Technical on Men’s Clinical Services
Linda Creegan, FNP, California STD/HIV Prevention Training Center
Dennis Fortenberry, MD, Indiana University School of Medicine
Emily Godfrey, MD, University of Illinois at Chicago
Wendy Grube, PhD, University of Pennsylvania School of Nursing
Arik V. Marcell, MD, The Johns Hopkins University and the Male Training Center
Elissa Meites, MD, Division of STD Prevention, CDC
Anne Rompalo, MD, Johns Hopkins University
Thomas Walsh, MD, University of Washington Medical Center
Jacki Witt, MSN, Clinical Training Center for Family Planning, University of Missouri—Kansas City
Sandra Wolf, MD, Women’s Care Center, Philadelphia

Technical Panel on Adolescents
Claire Brindis, DrPH, University of California, San Francisco
Gale Burstein, MD, SUNY at Buffalo School of Medicine and Biomedical Sciences, Department of Pediatrics
Laura Davis, MA, Advocates for Youth
Patricia J. Dittus, PhD, Division of STD Prevention, CDC
Paula Duncan, MD, University of Vermont College of Medicine
Carol Ford, MD, The Children’s Hospital of Philadelphia
Melissa Gilliam, MD, The University of Chicago
Mark Hathaway, MD, Unity Health Care & Washington Hospital Center
Deborah Kaplan, PhD, New York City Department of Health and Mental Hygiene
Arik V. Marcell, MD, The Johns Hopkins University and the Male Training Center
Brent C. Miller, PhD, Utah State University
Elizabeth M. Ozer, PhD, Division of Adolescent Medicine, University of California, San Francisco
John Santelli, MD, Columbia University, Mailman School of Public Health

Technical Panel on Counseling and Education
Beth Barnet, MD, University of Maryland
Betty Chewning, PhD, University of Wisconsin School of Pharmacy
Christine Dehlendorf, MD, University of California, San Francisco
Linda Dominguez, CNP, Southwest Women’s Health
Jillian Henderson, PhD, University of California, San Francisco
James Jaccard, PhD, New York University
Beth Jordan, MD, Association of Reproductive Health Professionals—East
David Kaplan, PhD, American Counseling Association
Alicia Luchowski, American Congress of Obstetricians and Gynecologists
Merry-K Moos, FNP, University of North Carolina at Chapel Hill
Patricia Murphy, DrPH, University of Utah College of Nursing
Elizabeth O’Connor, PhD, Kaiser Permanente Center for Health Research
Jeff Peipert, MD, Washington University in St. Louis

Technical Panel on Quality Improvement
Davida Becker, PhD, Bixby Center for Global Reproductive Health University of California, San Francisco
Peter Briss, MD, National Center for Chronic Disease Prevention and Health Promotion, CDC
Denise Dougherty, PhD, Agency for Healthcare Research and Quality
Daryn Eikner, MS, Family Planning Council
Christina I. Fowler, PhD, RTI International
Evelyn Glass, MSPH, Consultant Advisor
Yvonne Hamby, MPH, Regional Quality Improvement and Infertility Prevention Programs
A. Seiji Hayashi, MD, Bureau of Primary Health Care, Health Resources and Services Administration
Michael D. Kogan, PhD, Health Resources and Services Administration /Maternal and Child Health Bureau
Tom Miller, MD, Alabama Department of Health
Sam Posner, PhD, National Center for Chronic Disease Prevention and Health Promotion, CDC
Donna Strobino, PhD, Johns Hopkins University
Amy Tsui, PhD, Johns Hopkins Bloomberg School of Public Health
Reva Winkler, MD, National Quality Forum

MMWR / April 25, 2014 / Vol. 63 / No. 4

Recommendations and Reports

Adivsors on Community Outreach and Participation*
Paula Baraitser, MBBS, Kings College Hospital NHS Foundation Trust/Health Protection Agency
Joy Baynes, MPH, Advocates for Youth
Diane Chamberlain, California Family Health Council
Clare Coleman, National Family Planning & Reproductive Health Association
Emily Godfrey, MD, University of North Carolina and Division of Reproductive Health, CDC
Rachel Gold, MPA, Guttmacher Institute
Rachel Kachur, MPH, Division of STD Prevention, CDC
Michelle Kegler, PhD, Rollins School of Public Health, Emory
Eleanor McLellan-Lemal, PhD, Division of HIV/AIDS Prevention, CDC
Paula Parker-Sawyers, National Campaign to Prevent Teen and Unplanned Pregnancy
Denise Wheeler, MS, Iowa Department of Public Health
Gayla Winston, MPH, Indiana Family Health Council, Inc.

CDC and Office of Population Affairs Reviewers
Wanda Barfield, MD, Division of Reproductive Health, CDC
Gail Bolan, MD, Division of STD Prevention, CDC
Linda Dahlberg, PhD, Division of Violence Prevention, CDC
Patricia Dietz, PhD, Division of Reproductive Health, CDC
Sherry Farr, PhD, Division of Reproductive Health, CDC
Evelyn Glass, MSPH, Office of Population Affairs
Tamara Haegerich, PhD, Division of Violence Prevention, CDC
David Johnson, MPH, Office of Population Affairs
Pamela Kania, MS, Office of Population Affairs
Marilyn Keefe, MPH, Deputy Assistant Secretary for Population Affairs
Dmitry Kissin, MD, Division of Reproductive Health, CDC
Nancy Mautone-Smith, MSW, Office of Population Affairs
Jacqueline Miller, MD, Division of Cancer Prevention and Control, CDC
Sam Posner, PhD, National Center for Chronic Disease and Health Promotion, CDC
Cheryl Robbins, PhD, Division of Reproductive Health, CDC
Lance Rodewald, MD, Division of Immunization Services, CDC
Mona Saraiya, MD, Division of Cancer Prevention and Control, CDC
Van Tong, MPH, Division of Reproductive Health, CDC
Lee Warner, PhD, Division of Reproductive Health, CDC
Kim Workowski, MD, Division of STD Prevention, CDC

External Reviewers
Paula Braverman, MD, Department of Pediatrics at the University of Cincinnati
Claire Brindis, DrPH, University of California–San Francisco
Sarah Brown, MPH, National Campaign to Prevent Teen and Unplanned Pregnancy
Marji Gold, MD, Albert Einstein School of Medicine
Milton Kotelchuck, PhD, Massachusetts General Hospital for Children and Harvard Medical School
David Levine, MD, Morehouse School of Medicine
Pamela Murray, MD, West Virginia University School of Medicine
Competing interests for the development of these guidelines were not assessed.
* These persons made important contributions to a discussion about community outreach and participation. A decision was made to narrow the focus of this report
to clinical services, so recommendations informed by the input of these persons will be published separately.

MMWR / April 25, 2014 / Vol. 63 / No. 4

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ISSN: 1057-5987

Methodologies for
Improving Response Rates
in Surveys of Physicians

Evaluation &
the Health Professions
Volume 30 Number 4
December 2007 303-321
© 2007 Sage Publications
10.1177/0163278707307899
http://ehp.sagepub.com
hosted at
http://online.sagepub.com

A Systematic Review
Jonathan B. VanGeest
Kennesaw State University, Georgia

Timothy P. Johnson
University of Illinois at Chicago

Verna L. Welch
Morehouse School of Medicine, Atlanta

Although physician surveys are an important tool in health services and policy
research, they are often characterized by low response rates. The authors
conducted a systematic review of 66 published reports of efforts to improve
response rates to physician surveys. Two general strategies were explored in
this literature: incentive and design-based approaches. Even small financial
incentives were found to be effective in improving physician response. Token
nonmonetary incentives were much less effective. In terms of design strategies,
postal and telephone strategies have generally been more successful than
have fax or Web-based approaches, with evidence also supporting use of
mixed-mode surveys in this population. In addition, use of first-class stamps
on return envelopes and questionnaires designed to be brief, personalized,
and endorsed by legitimizing professional associations were also more likely
to be successful. Researchers should continue to implement design strategies
that have been documented to improve the survey response of physicians.
Keywords: physicians; surveys; research methods; response rates

hysician surveys are an important tool in health services and policy
research, providing cost-effective sources of information on physicians’
attitudes, knowledge, and practices related to care delivery. Surveys have
been used to assess a range of issues, from more routine subjects like knowledge of and/or compliance with evidence-based practice recommendations
(Mosca et al., 2005; Schroy et al., 2001; Webster, Courtney, Huang, Matz, &
Christiani, 2005) to highly sensitive topics such as substance abuse among
303

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Evaluation & the Health Professions

physicians (Hughes et al., 1999; McAuliffe et al., 1986), physician attitudes
toward euthanasia (Emanuel et al., 2000; Farber et al., 2006; Meier et al.,
1998), and physician manipulation of reimbursement rules for patients (Wynia,
Cummins, VanGeest, & Wilson, 2000). Despite their importance, however,
physician surveys are characterized by low response rates, raising concerns
about the validity and generalizability of their findings (Asch, Connor,
Hamilton, & Fox, 2000; Asch, Jedrziewski, & Christakis, 1997; Berk, 1985;
Cartwright, 1978; Cull, O’Connor, Sharp, & Tang, 2005; Cummings, Savitz, &
Konrad, 2001; Kellerman & Herold, 2001). Specifically, low response rates
raise concerns about nonresponse bias or the likelihood that nonresponding
physicians will be systematically different from the population under study.
This concern is supported by research showing modest differences between
responders and nonresponders and between early and late respondents
on demographic and/or practice-related characteristics (Cartwright, 1978;
Cockburn, Campbell, Gordon, & Sanson-Fisher, 1988; Cull et al., 2005;
Goodman & Jensen, 1981; McFarlane, Olmsted, Murphy, & Hill, 2006;
Myerson, 1993; Parsons, Warnecke, Czaja, Barnsley, & Kaluzny, 1994; Stocks
& Gunnell, 2000; Tambor et al., 1993; Templeton, Deehan, Taylor, Drummond,
& Strang, 1997; Thran and Gonzalez, 1999). As a result, researchers have
investigated why physicians are less likely to respond to surveys and implemented strategies for improving physician participation.

Why Physicians Do Not Respond
In a seminal article, Seymour Sudman (1985) identified a number of
reasons why professionals (e.g., physicians) might refuse to participate in
surveys. Arguably the most important reason for nonresponse is lack of time.
Physicians are busy and time spent completing a survey is time that could
be spent seeing patients or used to attend to other—more important—tasks.
A second and related issue involves the perceived salience of the study. Like
other professionals, physicians will not take the time to complete a survey
if the value of the study is not clear or is clear but perceived to be low. Third,
physicians will generally not complete a survey when they have concerns
about the confidentiality of the results. Finally, the likelihood of nonresponse
is greater in cases where individual questions may appear biased or not
allow the respondent a full range of choices on the subject. Lack of time is
compounded by the increasing volume and length of surveys physicians are
asked to respond to (Kaner, Haighton, & McAvoy, 1998; MacPherson &
Bisset, 1995; McAvoy & Kaner, 1996). Researchers have also identified the

VanGeest et al. / Improving Response Rates

305

private practice office setting (with its various gatekeepers) as an additional
barrier to physician participation (Berry & Kanouse, 1987; Heywood, Mudge,
Ring, & Sanson-Fisher, 1995; Moore & An, 2001; Parsons et al., 1994).

Strategies to Encourage Physician Participation
Numerous strategies have been devised to increase physician response to
surveys (Field et al., 2002; Kellerman & Herold, 2001; Sudman, 1985). These
strategies generally fall into two categories: incentive-based interventions
(both monetary and nonmonetary) and design-based approaches (e.g., personalized mailings, design-friendly questionnaires, sponsorship, etc.). Previous
reviews have found token monetary incentives to be effective at improving
physician participation (Field et al., 2002; Kellerman & Herold, 2001).
However, questions remain regarding how much of an incentive is most costeffective (Field et al., 2002; Halpern, Ubel, Berlin, & Asch, 2002; VanGeest,
Wynia, Cummins, & Wilson, 2001). Less is know about the efficacy of nonmonetary incentives, although a review of the literature suggests mixed results
in surveys of physicians (Thran & Berk, 1993). Design-based approaches
have also been shown to increase physician cooperation (Cummings et al.,
2001). Again, however, there is little consensus on the efficacy of the full
range of techniques purported to increase response rates of physicians. In this
article, we conducted a systematic review to determine the extent to which
incentive- and designed-based strategies have been found to be effective in
improving physician response to surveys.

Method
Experimental studies examining methods to improve physician response
to mail surveys were identified through keyword searches of the MEDLINE, Scopus, Sociological Abstracts, and PsychINFO databases from 1975 to
2006. Searches by author using the same databases were also conducted for
investigators with identified relevant articles. Finally, several seed sources
(e.g., Medical Care, Public Opinion Quarterly, Evaluation and the Health
Professions) were also referenced manually in an effort to establish a comprehensive set of studies to be included in the analyses. Further relevant articles
and books were selected from the reference listings of the primary journal
articles. Where appropriate, odds ratios (ORs) were calculated for individual
studies as a measure of effect size for the different interventions identified

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Evaluation & the Health Professions

(Tu, 2003). In addition, weighted overall ORs were calculated for groups of
studies analyzing like interventions.

Results
Impact of Incentives on Response
Rates Among Physicians
Monetary incentives. A total of 21 articles (1981 to 2006) were identified
that examined the effects of token monetary incentives on physician response
to surveys. Incentive amounts ranged $1 to $50 and included both cash
payments and charitable donations. Incentives also included opportunities to
win cash lottery prizes. Selected studies comparing incentives to no-incentive
controls are presented in Table 1. Taken as a whole, the weighted overall
effect size reflected an association between monetary incentives and physician
response (OR 2.13; 95% confidence interval [CI] 1.7–2.6). Unweighted
average effect sizes for different incentive levels (minimum of 2 studies
per level) are presented in Figure 1. Generally, even modest $1 incentives
were associated with higher response rates among physicians (average OR
across the relevant studies was 2.11) when compared with physicians
receiving no incentive (Berk, Edwards, & Gay, 1993; Deehan, Templeton,
Taylor, Drummond, & Strang, 1997; Donaldson et al., 1999, Easton, Price,
Telljohann, & Boehm, 1997; Everett, Price, Bedell, & Telljohann, 1997; Gunn &
Rhodes, 1981; Kasprzyk, Montano, St. Lawrence, & Phillips, 2001; Leung,
Ho, Chan, Johnston, & Wong, 2002; Mizes, Fleece, & Roos, 1984; Moore &
An, 2001; Robertson, Walkom, & McGettigan, 2005). The only exception
was a small $1 donation to charity (Olson, Schneiderman, & Armstrong,
1993). With regard to larger incentives, results are mixed. As illustrated in
Figure 1, there are little differences in serial increments over $1. This is supported by studies (not shown) which tested for and found no or nonsignificant
differences between incentive levels (Gunn & Rhodes, 1981; Kasprzyk et al.,
2001; Mizes et al., 1984; VanGeest et al., 2001). The only exceptions were
studies by Asch, Christakis, & Ubel (1998) and Halpern et al. (2002), although
their results may be compromised by the uniqueness of the $2 bill option
employed. Comparative studies indicate that cash payments are more effective
compared with charity inducements (Deehan et al., 1997), monetary donations
to their alma mater (Gattellari & Ward, 2001), nonmonetary incentives (Easton
et al., 1997; Tambor et al., 1993), or opportunities to win a cash lottery prize
(Leung et al. 2002; Tamayo-Sarver & Baker, 2004). Prepaid monetary incentives are also superior to promised incentives (Berry & Kanouse, 1987;

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Table 1
Selected Studies Examining Monetary and Nonmonetary
Incentives on Physician Response Rates
Monetary Incentives

Intervention

95% CI

Delveno et al. (2004)
Leung et al. (2004)
Burt & Woodwell (2005)
Robertson et al. (2005)

$25 vs. no incentive
$50 vs. no incentive
$1 vs. no incentive
$5 vs. no incentive
Prepayment vs. postpayment
$10 vs. no incentive
$1 vs. no incentive
£5 vs. no incentive
£10 vs. no incentive
$1 vs. booklet
$5 vs. no incentive
$10 vs. no incentive
$15 vs. no incentive
$25 vs. no incentive
HKD$10
HKD$20
HKD$40
Prepayment vs. postpayment
Prepayment vs. postpayment
$50 vs. no incentive
AU$2 lottery

1.59
2.46
2.66
2.66
1.83
2.01
2.07
2.07
3.03
2.12
1.62
1.98
6.38
6.06
1.07
2.09
2.52
1.81
1.81
1.00
1.48

0.98–2.59
1.47–4.12
1.03–6.86
1.03–6.86
1.50–2.23
1.15–3.50
1.46–2.93
1.55–2.76
2.30–3.99
1.47–3.04
1.09–2.41
1.37–2.87
3.36–12.12
3.20–11.47
0.52–2.23
1.13–3.88
1.38–4.58
1.42–2.30
1.32–2.48
0.74–1.35
1.00–2.18

Nonmonetary Incentives

Intervention

95% CI

2.30
0.91
1.11
1.05
0.96
1.29
0.96
0.62
1.09
0.79

0.81–6.54
0.41–2.03
0.75–1.66
0.80–1.36
0.72–1.28
1.00–1.67
0.77–1.19
0.49–0.79
0.88–1.35
0.58–1.06

Gunn & Rhodes (1981)
Mizes et al. (1984)
Berry & Kanouse (1987)
Berk et al. (1993)
Everett et al. (1997)
Deehan et al. (1997)
Easton et al. (1997)
Donaldson et al. (1999)
Moore & An (2001)
Kasprzyk et al. (2001)
Leung et al. (2002)

Sallis et al. (1984)
2nd mailing
3rd mailing
Mullen et al. (1987)
Bonito et al. (1997)
Ward et al. (1998)
Baron et al. (2001)
Clark et al. (2001a)
Halpern et al. (2002)
Moses & Clark (2004)
Burt & Woodwell (2005)

Pencil
Pencil
Sticker
Risk disk
Pen
Prize draw
Pen
Candy
Prize draw
Candy

Note: OR = odds ratio; CI = confidence interval. Table includes only those studies where
sufficient information was available to calculate odds ratio measures of effect size.

Delnevo, Abatemarco, & Steinberg, 2004; Leung et al., 2004). Collectively,
when compared to promised incentives, prepaid incentives have a weighted
overall effect size reflecting an association with improved physician response
(OR 1.82; 95% CI 1.6–2.1).

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Figure 1
Average Effect Size (OR) by Monetary Incentive Level
3
2.8
2.6

2.4
2.2
2
1.8
1.6
1.4
1.2
1
$0

$5
Incentive

$10

$20

Nonmonetary incentives. Several studies also assessed the effectiveness
of token nonmonetary incentives on physician participation, including
stickers (Mullen, Easling, Nixon, Koester, & Biddle, 1987), pencils (Sallis,
Fortmann, Solomon, & Farquhar, 1984), pens (Clark, Khan, & Gupta, 2001a;
Ward, Bruce, Holt, D’Este, & Sladden, 1998), informational brochures (Easton
et al., 1997), risk-assessment computer programs (Bonito, Samsa, Akin, &
Matchar, 1997), and candy (Burt & Woodwell, 2005; Halpern et al., 2002;
see Table 1). The effects of more substantial incentives (e.g., prize draws
for a weekend trip or a personal digital assistant [PDA]) were also explored
(Baron et al., 2001; Moses & Clark, 2004). Generally, when compared to
physicians receiving no incentive, token nonmonetary incentives appear
to have little or no impact on response rates (Bonito et al., 1997; Burt &
Woodwell, 2005; Clark et al., 2001a; Easton et al., 1997; Halpern et al.,
2002; Mullen et al., 1987; Ward et al., 1998). This is supported in the
present analyses in which nonmonetary incentives had a weighted overall
effect size (OR 0.97; 95% CI 0.82–1.14) reflecting a nonsignificant impact
on physician response. There are, however, a couple of exceptions. In one
study, the opportunity to receive continuing medical education (CME) credits
was deemed to be an effective motivation for physician participation in a
mailed questionnaire (McDermott et al., 2003). However, the CME credits
were offered in conjunction with a small ($5) monetary incentive, making

VanGeest et al. / Improving Response Rates

309

it impossible to determine the independent effects of the CME credit on
physician participation. The impact of CME credit is also not consistent, with
a similar study concluding that CME credit was not as effective as a monetary
incentive for inducing physician response (Tambor et al., 1993). In the other
exception, the inclusion of a pencil in a second mailing resulted in an increased
response (Sallis et al., 1984). However, when the same questionnaire was sent
to another sample, inclusion of a pencil in the third mailing had no impact.
Studies examining more substantial nonfinancial inducements also had mixed
results, with only the opportunity to win a weekend trip for two resulting
in a small but significant increase in physician response (OR 1.29; 95%
CI 1.00–1.67; Baron et al., 2001). One study also explored the effect of
magnitude of the prize draw—one big prize versus many small prizes—
on physician response, finding the larger prize to be more effective despite
lower odds of winning (Thomson, Paterson-Brown, Russell, McCaldin, &
Russell, 2004).

Impact of Design-Based Strategies
Questionnaire design. Nine studies examined the impact of questionnaire
design (e.g., length of questionnaire, paper size/quality, questionnaire format)
on physician response. Intuitively, length of questionnaire would be of particular interest given that time constraints so prominently figure in physician
participation. Only four studies, however, were identified that examined the
effect of questionnaire length on physician response. One relatively small
study found nonsignificant differences in response rates related to length of
the survey (Marin & Howe, 1984). Other studies, however, suggest that shorter
questionnaires result in higher cooperation rates (Cartwright & Ward, 1968;
Hing, Schappert, Burt, & Shimizu, 2005; Jepson, Asch, Hershey, & Ubel,
2005). A simple average of individual ORs across the latter three studies was
2.33 (Table 2), with the weighted overall effect size reflecting an association
between shorter questionnaire length and physician response (OR 2.0; 95%
CI 1.1–3.7). Evidence from Jepson et al. (2005) even suggests that under
certain conditions, physician participation will be sensitive to relatively small
(under 1,000 vs. more than 1,000 word) differences in questionnaire length
(OR 2.348; 95% CI 1.20–4.61). Studies have also examined print format,
paper size, and paper quality on physician cooperation rates, with mixed
results. For example, a recent study comparing single- versus double-sided
printing found no differences in physician cooperation rates (Brehaut, Graham,
Visentin, & Stiell, 2006). Other studies found the use of an attractive business
letter format (Gullen & Garrison, 1973) and standard-sized (8.5 in. × 11 in.)

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Evaluation & the Health Professions

Table 2
Selected Studies Examining Design-Based Interventions
on Physician Cooperation
Questionnaire Design
Cartwright & Ward (1968)
Hing et al. (2005)
Jepson et al.(2005)

Intervention

95% CI

Short form
Short form
Short form

3.33
1.30
3.35

1.70–6.54
0.89–1.90
1.20–4.61

Handwritten letter
Personalized mailout
Physician contact
Sponsorship
Telephone prompt
Physician contact
Advance contact
Advance contact
Physician contact
Sponsorship
Handwritten signature
Personalized letter

1.90
1.52
5.92
1.35
2.36
3.27
1.88
1.35
1.46
0.62
1.06
2.07

1.27–2.83
1.05–2.19
3.54–9.91
1.03–1.77
1.25–4.44
1.17–9.15
1.19–2.98
0.80–2.27
1.04–2.03
0.41–0.92
0.91–1.24
1.19–3.60

First-class mail
First-class stamps
First-class stamps
Certified mail
FedEx
First-class stamps

2.02
1.15
2.04
2.09
1.44
1.30

1.69–2.42
1.06–1.25
1.22–3.43
1.35–3.22
0.90–2.33
1.12–1.51

Personalization and Sponsorship
Maheux et al. (1989)
Bostic et al. (1992)
Asch & Christakis (1994)
Ward & Wain (1994)
Heywood et al. (1995)
Osborn et al. (1996)
Temple-Smith et al. (1998)
Ward et al. (1998)
Bhandari et al. (2003)
McKenzie-McHarg et al. (2005)
Leece et al. (2006)
Type of Mailing
Gullen & Garrison (1973)
Shiono & Klebanoff (1991)
Urban et al. (1993)
Del Valle et al. (1997)
Kasprzyk et al. (2001)
Streiff et al. (2001)

Note: OR = odds ratio; CI = confidence interval. Table includes only those studies where sufficient information was available to calculate odds ratio measures of effect size.

questionnaire booklets (Johnson, Parsons, Warnecke, & Kaluzny, 1993) to be
associated with higher response rates. Paper quality, on the other hand, was
not associated with increased physician cooperation (Clark, Khan, & Gupta,
2001b). Finally, one study was identified that examined open- versus closedended questionnaire formats on physician response (Griffith, Cook, Guyatt, &
Charles, 1999). The closed-ended questionnaire format resulted in a 22%
higher cooperation rate compared with the open-ended format.
Personalization and sponsorship. Several studies assessed the impact of
a personalized cover letter on physician participation (Table 2). Three studies

VanGeest et al. / Improving Response Rates

311

found that a personalized cover letter and/or the inclusion of a handwritten
note resulted in significantly higher response rates (Leece et al., 2006; Maheux,
Legault, & Lambert, 1989; Olson et al., 1993). Another, however, found no
difference in response rate between those sent a hand-signed letter and those
sent a letter with a scanned signature (McKenzie-McHarg, Tully, Gates,
Ayers, & Brocklehurst, 2005). Collectively, personalized cover letters and/or
mailout packages had a weighted overall effect size (OR 1.51; 95% CI 1.1–2.2)
reflecting an association with higher physician response. Direct contact
(e.g., prenotification calls and/or letters in advance of a survey and follow-up
contact) is another mechanism to personalize a survey that often results in
improved physician response (Bostick, Pirie, Luepker, & Kofron, 1992;
Heywood et al., 1995; Osborn, Ward, & Boyle, 1996; Ward et al., 1998;
Ward & Wain, 1994). This includes contact by a medical peer, which has been
found in some studies to increase physician participation (Bostick et al., 1992;
Haywood et al., 1995). Exceptions include a study by Temple-Smith, Mulvey, &
Doyle (1998) in which a medical researcher was able to contact a higher
proportion of cases (80% vs. 69%), without increasing overall response. Taken
as a whole, direct contact had a weighted overall effect size denoting a relationship with increased physician response (OR 2.3; 95% CI 1.42–3.64).
Finally, attempts have been made to personalize surveys using endorsements
by opinion leaders and/or professional associations, with mixed results (Asch &
Christakis, 1994; Bhandari et al., 2003; Olson et al., 1993). Although organizational sponsorship generally improved participation, a study supported by
expert surgeons actually resulted in a lower response rate, suggesting possible
“limits of leadership” related to collegial sponsorship (Bhandari et al., 2003).
Type of mailing. Six studies were identified that compared physician
response by type of mail and/or return mail employed (Table 2). Two studies
were identified that examined the impact of the initial mailing on physician
participation. In one study, certified mail resulted in a 16.5% increase in
participation (OR 2.085; 95% CI 1.35–3.22) compared with first-class mail
(Del Valle, Morgenstern, Rogstad, Albright, & Vickrey, 1997). In the other,
FedEx resulted in an 8% increase over first-class mail (OR 1.444; 95% CI
0.90–2.33; Kasprzyk et al., 2001). With regard to the return mailing, studies
have consistently found that return envelopes with first-class stamps result
in higher physician response compared with franked or business reply return
envelopes (Shiono & Klebanoff, 1991; Streiff, Dundes, & Spivak, 2001;
Urban, Anderson, & Tseng, 1993). The weighted overall effect size across
these three studies reflected an association between the use of first-class
stamps and physician response (OR 1.3; 95% CI 1.1–1.5). Additionally, one

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Evaluation & the Health Professions

study compared the influence of multiple return mailing strategies on physician response to mailed questionnaires (Gullen & Garrison, 1973). Although
this study identified a postcard reply as having the lowest participation rate
compared to bulk and first-class mail, the different strategies were assessed
in conjunction with other changes in the mail out package (e.g., different
cover letters), making it impossible to determine the independent effects of
the return mailing on physician cooperation. With regard to follow-up mailings,
research suggests that the inclusion of a replacement questionnaire with the
follow-up contact will improve participation (Ogborne, Rush, & Fondacaro,
1986; Vogel, Nowacek, Harlan, Tribble, & Thorup, 1983). One study was
also identified that examined envelope size (initial mailing) on physician
cooperation (Halpern et al., 2002). This study found no differences in
the response rates of general internists and family practitioners to a study
received in either a large or small envelope. Although the interventions
differ, collectively the weighted overall effect size across studies examining
postage/mailing strategies reflected an association between use of these
strategies and physician response (OR 1.4; 95% CI 1.11–1.69).
Survey mode. Finally, several studies have examined survey mode as one
potential mechanism to improve physician participation. For example, studies have examined response rates for telephone versus mailed surveys, with
mixed results. Although some studies found mail surveys to have higher
response rates compared with telephone surveys (Hocking, Lim, Read, &
Hellard, 2006; Ogborne et al., 1986), others suggest that telephone interviews
result in higher response rates (Parsons et al., 1994; Sibbald, Addington-Hall,
Brenneman, & Freeling, 1994; Thran & Hixson, 2000). Parsons et al. (1994)
also found evidence of mode preference across different medical specialties,
with family practitioners more likely to select the mail option than surgeons.
Use of e-mail and fax technologies has also been explored. In direct comparisons with mailed questionnaires, e-mail resulted in significantly lower physician response rates (Akl, Maroun, Klocke, Montori, & Schunemann, 2005;
Raziano, Jayadevappa, Valenzula, Weiner, & Lavizzo-Mourey, 2001; Seguin,
MacDonald, Godwin, & McCall, 2004; VanDenKerkhof, Parlow, Goldstein, &
Milne, 2004). With regard to fax technology, there is evidence suggesting
that, when incorporated within a mixed-method design, it may be a costeffective method of increasing physician participation. In one study where
pediatricians were offered a choice of three response modes, 26% responded
by e-mail, 47% by fax, and 41% by mail (McMahon et al., 2003). In another,
a larger percentage of respondents requested to be surveyed by fax compared
with telephone or mail (Lensing et al., 2000). Finally, researchers have also

VanGeest et al. / Improving Response Rates

313

begun to explore the utility of the Internet in surveying physicians (see
Braithwaite, Emery, de Lusignan, & Sutton, 2003). In one controlled comparison, an Internet-based survey resulted in a significantly lower response rate
compared with a traditional mail survey (Leece et al., 2004). Other mixed
mode (Internet vs. mail) studies of American urologists identified similar
problems (Hollowell, Patel, Bales, & Gerber, 2000; Kim et al., 2000). There
is also evidence that Internet surveys may present methodological issues
related to sample representativeness (Braithwaite et al., 2003).

Discussion
Despite the importance of physician surveys in health services and policy
research, and the ongoing concern over potential biases associated with low
response rates to these surveys, there are relatively few randomized trials
examining potential strategies to improve physician cooperation. Our review
of available studies, however, does suggest a number of promising strategies
for enhancing physician cooperation. Financial incentives, in particular, were
shown to be effective in improving physician response to surveys. Surprisingly,
even a small $1 incentive significantly improved participation by 18% to
21% (Everett et al., 1997; Mizes et al. 1984). In fact, the combined evidence
regarding appropriate levels of incentive suggests that the steepest part of
the incentive/response curve may be between $0 and $1, with diminishing
returns to serial increments above that amount (Halpern et al., 2002; VanGeest &
Johnson, 2001). These results mirror general population studies in which
the use of token financial incentives averaged nearly a 20% increase in
survey participation (Church, 1993; Fox, Clark, & Kim, 1988; Heberlein &
Baumgartner, 1978; Yammarino, Skinner, & Childress, 1991). They are also
consistent with studies examining the use of monetary incentives in surveys
of nurses and allied health professionals (Paul, Walsh, & Tzelepis, 2005; Ulrich
et al., 2005). In contrast, token nonmonetary incentives were much less effective in improving physician cooperation, with the cumulative evidence suggesting that nonmonetary inducements work only if physicians value them.
A number of design-based strategies were also identified as being potentially effective in improving physician response rates. For example, survey
mode clearly had an impact on response, with postal and telephone surveys
resulting in higher average return rates across the studies reviewed. Existing
evidence also supports the use of mixed-mode formats that include fax and
possibly e-mail options, as these give physicians more alternatives by which
to respond to a survey in their busy schedules (Lensing et al., 2000; Parsons

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Evaluation & the Health Professions

et al., 1994). Choice of survey mode, however, often entails significant cost
considerations and more studies are needed to identify the most cost-effective
methodologies in surveys of physicians.
Although only a limited number of studies examined the impact of questionnaire design on physician cooperation, existing evidence does suggest
that researchers should be succinct when designing physician questionnaires.
Again, this is no surprise, given previous research on the association between
questionnaire length and survey response (Dillman, Sinclair, & Clark, 1993;
Heberlein & Baumgartner, 1978; Nakash, Hutton, Jorstad-Stein, Gates, &
Lamb, 2006; Olmsted, Murphy, McFarlane, & Hill, 2005). Previous qualitative
research with physicians also identified questionnaire length as a major factor
in their willingness to participate (Kasprzyk et al., 2001). With regard to
item response format, caution is necessary when drawing conclusions from
the single study supporting the use of closed- versus open-item formats, as
previous reviews have identified professionals as being more resistant to
closed-ended questions compared with the general public (Deutscher, 1956;
Sudman, 1985).
Findings related to personalization, sponsorship, and even mailing strategies are consistent with Sudman’s (1985) recommendation concerning the
need to establish relevance as a means of improving response. In a metaanalysis of population-based studies, use of prenotification letters and sponsorship had the largest effect sizes for increasing response rates (Fox et al.,
1988). Similarly, endorsements by local, state, or national organizations also
typically result in improved physician participation (Asch & Christakis, 1994).
Use of certified mail and/or courier companies such as FedEx also enhances
the importance of the mail out package, increasing the likelihood of physician
receipt and cooperation. Finally, a note with regard to the use of replacement
questionnaires in follow-up mailings: decisions must be carefully balanced
against cost considerations, as previous reviews have found little evidence
supporting the use of replacement questionnaires in promoting participation
generally (Heberlein & Baumgartner, 1981).
Although not addressed explicitly in this review, number of contacts/length
of field periods may be one of the most important determinants of physician
response. Research suggests that number of contacts may explain up to 40%
of the variance in response rates in surveys of the general public (Heberlein &
Baumgartner, 1978). Similarly, there is growing consensus in the literature
that lengthy field periods may be necessary in maximizing physician
participation (Goodman & Jensen, 1981; Parsons et al., 1994; Sudman, 1985;
Thran, Olson, & Strouse, 1987). For example, in one study, more than 30% of
the completed surveys were obtained after 1 contact, but another 20% required

VanGeest et al. / Improving Response Rates

315

11 or more contact attempts (Parsons et al., 1994). This same study highlighted
differences in number of contact attempts by mode of data collection, with only
6% of telephone interviews completed after 1 contact attempt compared with
60% finalized mail surveys in one mailing of the questionnaire.
Ultimately, a decision regarding what methodologies to employ to improve
physician cooperation are embedded within cost-quality trade offs (Olmsted
et al., 2005). The good news for those working in limited resource environments is that previous reviews identified smaller-than-anticipated differences
between physician respondents and nonrespondents and between early and
late responders (Field et al., 2002; Kellerman & Herold, 2001; McFarlane
et al., 2006), suggesting low rates of nonresponse bias. This is often because
of the homogeneity of physicians with regard to knowledge, training, attitudes,
and behavior. Although changing, physicians remain a relatively homogeneous population compared to the general population. This suggests that
researchers can still be strategic in employing any of the strategies identified
in this review, especially when conducting a survey on a tight budget. That
said, researchers should still make every effort to improve access to their
target population by implementing design strategies demonstrated to improve
physician participation rates, thereby increasing the legitimacy and credibility
of their results.

References
Akl, E. A., Maroun, N., Klocke, R. A., Montori, V., & Schunemann, H. J. (2005). Electronic
mail was not better than postal mail for surveying residents and faculty. Journal of Clinical
Epidemiology, 58, 425-429.
Asch, D. A., & Christakis, N. A. (1994). Different response rates in a trial of two envelop
styles in mail survey research. Epidemiology, 5, 364-365.
Asch, D. A., Christakis, N. A., & Ubel, P. A. (1998). Conducting physician mail surveys on a
limited budget: A randomized trial comparing $2 bill versus $5 bill incentives. Medical
Care, 36, 95-99.
Asch, D. A., Connor, S. E., Hamilton, E. G., & Fox, S. A. (2000). Problems in recruiting
community-based physicians for health services research. Journal of General Internal
Medicine, 15, 591-599.
Asch, D. A., Jedrziewski, M. K., & Christakis, N. A. (1997). Response rates to mail surveys
published in medical journals. Journal of Clinical Epidemiology, 50, 1129-1136.
Baron, G., De Wals, P., & Milord, F. (2001). Cost effectiveness of a lottery for increasing
physicians’ responses to a mail survey. Evaluation and the Health Professions, 24, 47-52.
Berk, M. L. (1985). Interviewing physicians: The effect of improved response rate. American
Journal of Public Health, 75, 1338-1340.
Berk, M. L., Edwards, W. S., & Gay, N. L. (1993). The use of a prepaid incentive to convert
nonresponders on a survey of physicians. Evaluation and the Health Professions,
16, 239-245.

316

Evaluation & the Health Professions

Berry, S. H., & Kanouse, D. E. (1987). Physician response to a mailed survey: An experiment
in timing of payment. Public Opinion Quarterly, 51, 102-114.
Bhandari, M., Devereaux, P. J., Swiontkowski, M. F., Schemitsch, E. H., Shankardass, K.,
Sprague, S., et al. (2003). A randomized trial of opinion leader endorsement in a survey of
orthopaedic surgeons: Effect on primary response rate. International Journal of Epidemiology,
32, 634-636.
Bonito, A. J., Samsa, G. P., Akin, D. R., & Matchar, D. B. (1997). Use of a non-monetary
incentive to improve physician responses to a mail survey. Academic Medicine, 72, 73.
Bostick, R. M., Pirie, P., Luepker, R. V., & Kofron, P. M. (1992). Using physician caller followups to improve the response rate to a physician telephone survey: Its impact and implications.
Evaluation and the Health Professions, 15, 420-433.
Braithwaite, D., Emery, J., de Lusignan, S., & Sutton, S. (2003). Using the Internet to conduct
surveys of health professionals: A valid alternative? Family Practice, 20, 545-551.
Brehaut J. C., Graham, I. D., Visentin, L., & Stiell, I. G. (2006). Print format and sender recognition
were related to survey completion rate. Journal of Clinical Epidemiology, 59, 635-641.
Burt, C. W., & Woodwell, D. (2005, November). Tests of methods to improve response to physician surveys. Paper presented at the 2005 Federal Committee on Statistical Methodology,
Arlington, VA.
Cartwright, A. (1978). Professionals as responders: Variations in and effects of response rates
to questionnaires, 1961-77. British Medical Journal, 2, 1419-1421.
Cartwright A., & Ward, A. W. (1968). Variations in general practitioners’ response to postal
questionnaires. British Journal of Preventive and Social Medicine, 22, 199-205.
Church, A. H. (1993). Estimating the effect of incentives on mail survey response rates:
A metal-analysis. Public Opinion Quarterly, 57, 62-79.
Clark, T. J., Khan, K. S., & Gupta, J. K. (2001a). Provision of pen along with questionnaire
does not increase the response rate to a postal survey: A randomized controlled trial.
Journal of Epidemiology and Community Health, 55, 595-596.
Clark, T. J., Khan, K. S., & Gupta, J. K. (2001b). Effect of paper quality on the response rate to
a postal survey: A randomized controlled trial. BMC Medical Research Methodology, 1, 12.
Cockburn, J., Campbell, E., Gordon, J. J., & Sanson-Fisher, R. W. (1988). Response bias in a
study of general practice. Family Practice, 5, 18-23.
Cull, W. L., O’Connor, K. G., Sharp, S., & Tang, S. S. (2005). Response rates and response
bias for 50 surveys of pediatricians. Health Services Research, 40, 213-226.
Cummings, S. M., Savitz, L. A., & Konrad, T. R. (2001). Reported response rates to mailed
physician questionnaires. Health Services Research, 35, 1347-1355.
Deehan, A., Templeton, L., Taylor, C., Drummond, C., & Strang, J. (1997). The effect of cash
and other financial inducements on the response rate of general practitioners in a national
postal survey. British Journal of General Practice, 47, 87-90.
Delnevo, C. D., Abatemarco, D. J., & Steinberg, M. B. (2004). Physician response rates to a
mail survey by specialty and timing of incentive. American Journal of Preventive Medicine,
26, 234-236.
Del Valle, M., Morgenstern, H., Rogstad, T. L., Albright, C., & Vickrey, B. G. (1997). A randomized trial of the impact of certified mail on response rate to a physician survey, and a costeffectiveness analysis. Evaluation and the Health Professions, 20, 389-406.
Deutscher, I. (1956). Physician reactions to a mailed questionnaire: A study in “resistentialism.”
Public Opinion Quarterly, 20, 599-604.
Dillman, D. A., Sinclair, M. D., & Clark, J. R. (1993). Effects of questionnaire length, respondentfriendly design, and a difficult question on response rates for occupant-addressed census
mail surveys. Public Opinion Quarterly, 57, 289-304.

VanGeest et al. / Improving Response Rates

317

Donaldson, G. W., Moinpour, C. M., Bush, N. E., Chapko, M., Jocom, J., Siadak, M., et al.
(1999). Physician participation in research surveys: A randomized study of inducements to
return mailed research questionnaires. Evaluation and the Health Professions, 22, 427-441.
Easton, A. N., Price, J. H., Telljohann, S. K., & Boehm, K. (1997). An informational versus
monetary incentive in increasing physicians’ response rates. Psychological Reports,
81, 968-970.
Emanuel, E. J., Fairclough, D., Clarridge, B. C., Blum, D., Bruera, E., Penley, W.C., et al. (2000).
Attitudes and practices of U.S. oncologists regarding euthanasia and physician-assisted
suicide. Annals of Internal Medicine, 133, 527-532.
Everett, S. A., Price, J. H., Bedell, A. W., & Telljohann, S. K. (1997). The effect of a monetary
incentive in increasing the return rate of a survey to family physicians. Evaluation and the
Health Professions, 20, 207-214.
Farber N. J., Simpson, P., Salam, T., Collier, V. U., Weiner, J., & Boyer, E. G. (2006). Physicians’
decisions to withhold and withdraw life-sustaining treatment. Archives of Internal Medicine,
166, 560-564.
Field, T. S., Cadoret, C. A., Brown, M. L., Ford, M., Greene, S. M., Hill, D., et al. (2002).
Surveying physicians: Do components of the “Total Design Approach” to optimizing survey
response rates apply to physicians? Medical Care, 40, 596-606.
Fox, R. J., Clark, M. R., & Kim, J. (1988). Mail survey response rate: A meta-analysis of
selected techniques for inducing response. Public Opinion Quarterly, 52, 467-491.
Gattellari, M., & Ward, J. E. (2001). Will donations to their learned college increase surgeons’
participation in surveys? A randomized trial. Journal of Clinical Epidemiology, 54, 645-650.
Goodman, L., & Jensen, L. (1981). Economic surveys of medical practice: AMA’s periodic
survey of physicians, 1966-1978. In Sudman S (Ed.), Proceedings of the Third Biennial
Conference on Health Services Research (pp. 56-65). Rockville, MD: National Center for
Health Services Research.
Griffith, L. E., Cook, D. J., Guyatt, G. H., & Charles C. A. (1999). Comparison of open and closed
questionnaire formats in obtaining demographic information from Canadian general internists.
Journal of Clinical Epidemiology, 52, 977-1005.
Gullen, W. H., & Garrison, G. E. (1973). Factors influencing physicians’ response to mailed
questionnaires. Health Services Reports, 88, 510-514.
Gunn, W. J., & Rhodes, I. N. (1981). Physician response rates to a telephone survey: Effects
of monetary incentive level. Public Opinion Quarterly, 45, 109-115.
Halpern, S. D., Ubel, P. A., Berlin, J. A., & Asch, D. A. (2002). Randomized trail of $5 versus
$10 monetary incentives, envelope size, and candy to increase physician response rates to
mailed questionnaires. Medical Care, 40, 834-839.
Heberlein, T. A., & Baumgartner, R. (1978). Factors affecting response rates to mailed questionnaires: A quantitative analysis of the published literature. American Sociological Review,
43, 447-462.
Heberlein, T. A., & Baumgartner, R. (1981). Is a questionnaire necessary in a second mailing?
Public Opinion Quarterly, 45, 102-108.
Heywood, A., Mudge, P., Ring, I., & Sanson-Fisher, R. (1995). Reducing systematic bias in
studies of general practitioners: The use of a medical peer in the recruitment of general
practitioners in research. Family Practice, 12, 227-231.
Hing, E., Schappert, S. M., Burt, C. W., & Shimizu, I. M. (2005). Effects of form length and
item format on response patterns and estimates of physician office and hospital outpatient
department visits. National Ambulatory Medical Care Survey and National Hospital
Ambulatory Medical Care Survey. Vital Health Statistics, 2, 139, 1-32.

318

Evaluation & the Health Professions

Hocking, J. S., Lim, M. S., Read, T., & Hellard, M. (2006). Postal surveys of physicians gave
superior response rates over telephone interviews in a randomized trial. Journal of Clinical
Epidemiology, 59, 521-524.
Hollowell, C. M. P., Patel, R. V., Bales, G. T., & Gerber, G. S. (2000). Internet and postal survey
of endourologic practice patterns among American urologists. The Journal of Urology,
163, 1779-1782.
Hughes, P. H., Storr, C. L., Brandenburg, N. A., Baldwin, D.C., Jr., Anthony, J. C., & Sheehan, D. V.
(1999). Physician substance use by medical specialty. Journal of Addictive Diseases,
18, 23-37.
Jepson, C., Asch, D. A., Hershey, J. C., & Ubel, P. A. (2005). In a mailed physician survey,
questionnaire length had a threshold effect on response rate. Journal of Clinical Epidemiology,
58, 103-105.
Johnson T. P., Parsons, J. A., Warnecke, R. B., & Kaluzny, A. D. (1993). Dimensions of mail
questionnaires and response quality. Sociological Focus, 26, 271-274.
Kaner, E. F., Haighton, C. A., & McAvoy, B. R. (1998). “So much post, so busy with practice—
so, no time!”: A telephone survey of general practitioners’ reasons for not participating in
postal questionnaire surveys. British Journal of General Practice, 48, 1067-1069.
Kasprzyk, D., Montano, D. E., St. Lawrence, J. S., & Phillips, W. R. (2001). The effects of
variations in mode of delivery and monetary incentive on physicians’ responses to a mailed
survey assessing STD practice patterns. Evaluation and the Health Professions, 24, 3-17.
Kellerman, S. E., & Herold, J. (2001). Physician response to surveys: A review of the literature.
American Journal of Preventive Medicine, 20, 61-67.
Kim, H. L., Hollowell, C. M. P., Patel, R. V., Bales, G. T., Clayman, R. V., & Gerber, G. S. (2000).
Use of new technology in endourology and laparoscopy by American urologists: Internet
and postal survey. Urology, 56, 760-765.
Leece, P., Bhandari, M., Sprague, S., Swiontkowski, M. F., Schemitsch, E. H., & Tornetta, P.
(2006). Does flattery work? A comparison of 2 different cover letters for an international
survey of orthopedic surgeons. Canadian Journal of Surgery, 49, 90-95.
Leece, P., Bhandari, M., Sprague, S., Swiontkowski, M. F., Schemitsch, E. H., Tornetta, P., et al.
(2004). Internet versus mailed questionnaires: A controlled comparison. Journal of Medical
Internet Research, 6, e39.
Lensing, S. Y., Gillaspy, S. R., Simpson, P. M., Jones, S. M., James, J. M., & Smith, J. M.
(2000). Encouraging physicians to respond to surveys through the use of fax technology.
Evaluation and the Health Professions, 23, 348-359.
Leung, G. M., Ho, L. M., Chan, M. F., Johnston, J. M., & Wong, F. K. (2002). The effects of
cash and lottery incentives on mailed surveys to physicians: A randomized trial. Journal
of Clinical Epidemiology, 55, 801-807.
Leung, G. M., Johnston, J. M., Saing, H., Tin, K. Y. K., Wong, I. O. L., & Ho, L. (2004).
Prepayment was superior to postpayment cash incentives in a randomized postal survey
among physicians. Journal of Clinical Epidemiology, 57, 777-784.
MacPherson, I., & Bisset, A. (1995). Not another questionnaire!: Eliciting the views of general
practitioners. Family Practice, 12, 335-338.
Maheux, B., Legault, C., & Lambert, J. (1989). Increasing response rates in physicians’ mail
surveys: An experimental study. American Journal of Public Health, 79, 638-639.
Marin, J., & Howe, H. L. (1984). Physicians’ attitudes toward breast self-examination: A pilot
study. Evaluation and the Health Professions, 7, 193.
McAuliffe, W. E., Rohman, M., Santangelo, S., Fieldman, B., Magnuson, E., Sobol, A., et al. (1986).
Psychoactive drug use among practicing physicians and medical students. New England Journal
of Medicine, 315, 805-810.

VanGeest et al. / Improving Response Rates

319

McAvoy, B. R., & Kaner, E. F. S. (1996). General practice postal surveys: A questionnaire too
far? British Medical Journal, 313, 732-733.
McDermott, M. M., Greenland, P., Hahn, E.A., Brogan, D., Cella, D., Ockene, J., et al. (2003).
The effects of continuing medical education credits on physician response rates to a mailed
questionnaire. Health Marketing Quarterly, 20, 27-42.
McFarlane, E., Olmsted, M. G., Murphy, J., & Hill, C. A. (2006, May). Nonresponse bias in
a mail survey of physicians. Paper presented at the annual conference of the American
Association for Public Opinion Research, Montreal, Quebec.
McKenzie-McHarg, K., Tully, L., Gates, S., Ayers, S., & Brocklehurst, P. (2005). Effect on survey
response rate of hand written versus printed signature on a covering letter: Randomised
controlled trial. BMC Health Services Research, 5, 52.
McMahon, S. R., Iwamoto, M., Massoudi, M. S., Yusuf, H. R., Stevenson, J. M., David, F.,
et al. (2003). Comparison of e-mail, fax and postal surveys of pediatricians. Pediatrics,
111, e299-e303.
Meier, D. E., Emmons, C. A., Wallenstein, S., Quill, T., Morrison, R. S., & Cassel, C. K.
(1998). A national survey of physician-assisted suicide and euthanasia in the United States.
New England Journal of Medicine, 338, 1193-1201.
Mizes, S., Fleece, L., & Roos, C. (1984). Incentives for increasing return rates: Magnitude levels,
response bias, and format. Public Opinion Quarterly, 48, 794-800.
Moore, D., & An, L. (2001, August). The effect of repetitive token incentives and priority mail
on response to physician surveys. Proceedings of the annual meeting of the American
Statistical Association, Atlanta, GA.
Mosca, L., Linfante, A. H., Benjamin, E. J., Berra, K., Hayes, S. N., Walsh, B. W., et al. (2005).
National study of physician awareness and adherence to cardiovascular disease prevention
guidelines. Circulation, 111, 499-510.
Moses, S. H., & Clark, T. J. (2004). Effect of prize draw incentive on the response rate to a
postal survey of obstetricians and gynecologists: A randomized controlled trial. BMC Health
Services Research, 4, 14.
Mullen, P. D., Easling, I., Nixon, S. A., Koester, D. R., & Biddle, A. K. (1987). The costeffectiveness of randomized incentive and follow-up contacts in a national mail survey of
family physicians. Evaluation and the Health Professions, 10, 232-245.
Myerson, S. (1993). Improving the response rates in primary care research. Some methods
used in a survey on stress in general practice since the new contract (1990). Family Practice,
10, 342-346.
Nakash, R. A., Hutton, J. L., Jorstad-Stein, E. C., Gates, S., & Lamb, S. E. (2006). Maximising
response to postal questionnaires: A systematic review of randomized trials in health
research. BMC Medical Research Methodology, 6, 5.
Ogborne, A. C., Rush, R., & Fondacaro, R. (1986). Dealing the nonrespondents in a mail survey
of professionals. Evaluation and the Health Professions, 9, 121-128.
Olmsted, M. G., Murphy, J., McFarlane, E., & Hill, C. (2005, May). Evaluating methods for
increasing physician survey cooperation. Paper presented at the annual conference of the
American Association for Public Opinion Research, Miami Beach, FL.
Olson, L., Schneiderman, M., & Armstrong, R. V. (1993). Increasing physician survey
response rates without biasing survey results. In Proceedings of the section on survey
research methods of the American Statistical Association (pp. 1036-1041) Alexandria, VA:
American Statistical Association.
Osborn, M., Ward, J., & Boyle, C. (1996). Effectiveness of telephone prompts when surveying
general practitioners: A randomized trial. Australian Family Physician, 25, S41-S43.

320

Evaluation & the Health Professions

Parsons, J. A., Warnecke, R. B., Czaja, R. F., Barnsley, J., & Kaluzny, A. (1994). Factors
associated with response rates in a national survey of primary care physicians. Evaluation
Review, 18, 756-766.
Paul, C. L., Walsh, R. A., & Tzelepis, F. (2005). A monetary incentive increases postal
survey response rates for pharmacists. Journal of Epidemiology and Community Health,
59, 1099-1101.
Raziano, D. B., Jayadevappa, R., Valenzula, D., Weiner, M., & Lavizzo-Mourey, R. (2001). E-mail
versus conventional postal mail survey of geriatric chiefs. Gerontologist, 41, 799-804.
Robertson, J, Walkom, E. J., & McGettigan, P. (2005). Response rates and representativeness:
A lottery incentive improves physician survey return rates. Pharmacoepidemiology and
Drug Safety, 14, 571-577.
Sallis, J. F., Fortmann, S. P., Solomon, D. S., & Farquhar, J. F. (1984). Increasing returns of
physician surveys. American Journal of Public Health, 74, 1043.
Schroy, P. C., 3rd, Geller, A. C., Crosier Wood, M., Page, M., Sutherland, L., Holm, L.J., et al.
(2001). Utilization of colorectal cancer screening tests: A 1997 survey of Massachusetts
internists. Preventive Medicine, 33, 381-391.
Seguin, R., MacDonald, S., Godwin, M., & McCall, M. (2004). E-mail or snail mail? Randomized
controlled trial on which works better for surveys. Canadian Family Physician, 50, 414-419.
Shiono, P. H., & Klebanoff, M. A. (1991). The effect of two mailing strategies on the response
to a survey of physicians. American Journal of Epidemiology, 134, 539-542.
Sibbald, B., Addington-Hall, J., Brenneman, D., & Freeling, P. (1994). Telephone versus
postal surveys of general practitioners: Methodological considerations. British Journal of
General Practice, 44, 297-300.
Stocks N., & Gunnell, D. (2000). What are the characteristics of GPs who routinely do not return
postal questionnaires: A cross sectional study. Journal of Epidemiology and Community
Health, 54, 940-941.
Streiff, M. B., Dundes, L., & Spivak, J. L. (2001). A mail survey of United States hematologists
and oncologists: A comparison of business reply versus stamped return envelopes. Journal
of Clinical Epidemiology, 54, 430-432.
Sudman, S. (1985). Mail surveys of reluctant professionals. Evaluation Review, 9, 349-360.
Tamayo-Sarver, J. H., & Baker, D. W. (2004). Comparison of responses to a $2 bill versus a
chance to win $250 in a mail survey of emergency physicians. Academic Emergency
Medicine, 11, 888-892.
Tambor, E. S., Chase, G. A., Faden, R. R., Geller, G., Hofman, K. J., & Holtzman, N. A.
(1993). Improving response rates through incentive and follow-up: The effect on a survey
of physicians’ knowledge of genetics. American Journal of Public Health, 83, 1599-1603.
Temple-Smith, M., Mulvey, G., & Doyle, W. (1998). Maximizing response rates in a survey
of general practitioners: Lessons from a Victorian survey on sexually transmissible diseases.
Australian Family Physician, 27(Suppl. 1), S15-S18.
Templeton, L., Deehan, A., Taylor, C., Drummond, C., & Strang, J. (1997). Surveying general
practitioners: Does a low response rate matter? British Journal of General Practice,
47, 91-94.
Thomson C. E., Paterson-Brown, S., Russell, D., McCaldin, D., & Russell, I. T. (2004). Short
report: Encouraging GPs to complete postal questionnaires—one big prize or many small
prizes? A randomized controlled trial. Family Practice, 21, 697-698.
Thran, S. L., & Berk M. L. (1993). Survey of physicians: An overview. In Proceedings of the
International Conference on Establishment Surveys (pp. 83-92). Alexandria, VA: American
Statistical Association.

VanGeest et al. / Improving Response Rates

321

Thran, S. L., & Gonzalez, M. L. (1999). Characteristics of unlocatable physicians. In Proceedings
of the section on survey research methods of the American Statistical Association (pp. 529-532).
Alexandria, VA: American Statistical Association.
Thran, S. L., & Hixson, J. S. (2000). Physician surveys: Recent difficulties and proposed solutions. In Proceedings of the section on survey research methods of the American Statistical
Association (pp. 233-237). Alexandria, VA: American Statistical Association.
Thran, S. L., Olson, L., & Strouse, R. (1987). The effectiveness and costs of special data
collection efforts in a telephone survey of physicians. In Proceedings of the survey research
section of the American Statistical Association (pp. 761-766). Alexandria, VA: American
Statistical Association.
Tu, S. (2003). Developmental epidemiology: A review of three key measures of effect. Journal
of Clinical Child & Adolescent Psychology, 32(2), 187-192.
Ulrich, C. M., Danis, M., Koziol, D., Garrett-Mayer, E., Hubbard, R., & Grady, C. (2005).
Does it pay to play? A randomized trial of prepaid financial incentives and lottery incentives
in surveys of nonphysician healthcare professionals. Nursing Research, 54, 178-183.
Urban, N., Anderson, G. L., & Tseng, A. (1993). Effects on response rates and cost of stamps
vs. business reply in a mail survey of physicians. Journal of Clinical Epidemiology,
46, 455-459.
VanDenKerkhof, E. G., Parlow, J. L., Goldstein, D. H., & Milne, B. (2004). In Canada, anesthesiologists are less likely to respond to an electronic, compared to a paper questionnaire.
Canadian Journal of Anesthesia, 51, 449-454.
VanGeest, J. B., & Johnson, T. P. (2001, October). Methodologies for improving response rates
in surveys of physicians. Paper presented at the annual meeting of the American Public
Health Association, Atlanta, GA.
VanGeest, J. B., Wynia, M. K., Cummins, D. S., & Wilson, I. B. (2001). Effects of different
monetary incentives on the return rate of a national survey of physicians. Medical Care,
39, 197-201.
Vogel, L. L., Nowacek, G., Harlan, J. F., Tribble, A., & Thorup, O. A. (1983). Impact of
replacement questionnaire on the response rate of practicing physicians to mail questionnaire.
Journal of Medical Education, 58, 905.
Ward, J., Bruce, T., Holt, P., D’Este, K., & Sladden, M. (1998). Labour-saving strategies to
maintain survey response rates: A randomized trial. Australian New Zealand Journal of
Public Health, 22(Suppl.), 394-396.
Ward, J., & Wain, G. (1994). Increasing response rates of gynecologists to a survey: A randomized trial of telephone prompts. Australian Journal of Public Health, 18, 332-334.
Webster, B. S., Courtney, T. K., Huang, Y. H., Matz, S., & Christiani, D. C. (2005). Physicians’
initial management of acute low back pain versus evidence-based guidelines. Influence of
Sciatica. Journal of General Internal Medicine, 20, 1132-1135.
Wynia, M. K., Cummins, D. S., VanGeest, J. B., & Wilson, I. B. (2000). Physician manipulation
of reimbursement rules for patients: Between a rock and a hard place. Journal of the
American Medical Association, 283, 1858-1865.
Yammarino, F. J., Skinner, S. J., & Childress, T. L. (1991). Understanding mail survey response
behavior: A meta-analysis. Public Opinion Quarterly, 55, 613-639.

Contraception 75 (2007) 177 – 184

Original research article

Intrauterine contraception: evaluation of clinician practice patterns in
Kaiser Permanente Northern California
Debbie Postlethwaitea,4, Ruth Shabera, Victoria Mancusoa, Jean Floresb, Mary Anne Armstrongc
a

Kaiser Permanente Women’s Health Research Institute, Oakland, CA 94612, USA
b
Kaiser Permanente Quality and Operations Support, Oakland, CA 94612, USA
c
Kaiser Permanente Division of Research, Oakland, CA 94612, USA
Received 28 July 2006; revised 23 October 2006; accepted 24 October 2006

Abstract
Background: Despite the medical evidence, few women of reproductive age in the United States use intrauterine contraception (IUC) in
comparison with women worldwide. To reduce cost as a barrier, Kaiser Permanente removed the cost to the patient for IUC throughout
California in 2002. The goal of this study was to evaluate whether providing evidence-based information about IUC would result in changes
in the knowledge, attitudes and practice patterns of clinicians and in greater IUC utilization as compared with removing cost alone.
Study Design: A comprehensive education intervention was conducted in half of Kaiser Permanente Northern California ob-gyn
departments. To make comparisons between the intervention and comparison sites, we surveyed clinicians in both groups before and after the
intervention about their IUC knowledge, attitudes as well as practice patterns and collected utilization data for 27 months.
Results: Statistically significant changes in attitudes and practice patterns were reported by the intervention group as compared with the usual
care comparison group. By the end of the study, change in IUC utilization was significantly greater in the intervention group (utilization
rate = 9.57/1000) as compared with the comparison group (utilization rate = 7.35/1000) (p = .02).
Conclusion: A multifaceted approach to providing evidence-based clinician and patient education resulted in statistically significant reported
changes in attitudes and practice patterns and in greater IUC utilization as compared with usual practice.
D 2007 Elsevier Inc. All rights reserved.
Keywords: IUC; LNG-20 IUC; Cu-T 380A; Academic detailing

1. Introduction
Much concern has been voiced in recent years about the
lag time from research to the integration of the medical
evidence into clinical practice toward improved patient
outcomes. It was recently stated in Harvard Business
Review that it takes on average 17 years for emerging
research to be translated into standard practice [1]. In recent
years, there has been much research devoted to studying the
gap that exists between research and evidence-based
practice [2–6].
The story about intrauterine contraception (IUC) use in
the United States is a perfect example of the delay from
acquiring clinical evidence to changing clinician practice.
Worldwide, IUC is used by approximately 15% of women
of reproductive age overall, 9% of those in developed
4 Corresponding author. Tel.: +1 510 987 3257; fax: +1 510 873 5089.
E-mail address: [email protected] (D. Postlethwaite).
0010-7824/$ – see front matter D 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.contraception.2006.10.010

countries and 15% of those in underdeveloped countries
[7,8]. Although there has been more than a decade of
evidence presented about the effectiveness and cost-effectiveness of IUC [9,10], its safety [11–18] and the high
reported satisfaction [19] among women who use it, IUC is
still used by fewer than 2% of women of reproductive age in
the United States [7,8]. Experts in the reproductive field
continue to pose the following questions: (1) What will it
take to change clinician practice and consumer attitudes
regarding intrauterine contraception? and (2) What will it
take to shift couples toward use of more cost-effective
contraception? There have been numerous efforts over the
last decade to share the medical evidence about IUC
regarding its safety and efficacy among health care
professionals and consumers. However, it is remarkable
how little has changed in attitudes toward IUC and in its
utilization across the United States.
In January 2002, Kaiser Permanente Northern California
(KPNC) removed copayment (cost to the patient) for the

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D. Postlethwaite et al. / Contraception 75 (2007) 177–184

most cost-effective contraceptives (intrauterine, injectable,
implantable and emergency). This change was made
throughout the region, affecting all KPNC health plan
members regardless of the plan they purchased. Additional
operational changes were made throughout the region, which
made it easier for patients to obtain IUC directly from their
medical providers, such as stocking devices in the medical
offices instead of the pharmacies. The investigators hypothesized that offering current and consistent evidence-based
information about IUC to clinicians and patients after
removal of cost as a barrier would result in changes in
knowledge and attitudes and would have a more rapid impact
on changing practice patterns and IUC device insertion rates.
2. Materials and methods
The KPNC Women’s Health Research Institute conducted
a study approved by the KPNC Institutional Review Board to
evaluate ob-gyn clinician IUC knowledge, attitudes and
practice patterns, to provide a multifaceted educational
intervention and to track IUC utilization over a 27-month
period. The findings were based on changes in IUC device
insertion rates in the medical offices that participated in the
educational intervention as compared with usual practice
sites. Before the study began, KPNC was divided into six
medical service areas that comprised 17 large medical
centers and multiple satellite medical offices. Each service
area was assigned to either the intervention group or the
comparison group based on matching preintervention IUC
device insertion rates between the six medical service areas.
IUC device insertion rates were obtained for each medical
center in all six medical service areas from outpatient service
clinical records (OSCRs) for calendar quarters 3 and 4 of
2001. There was a wide variation in IUC device insertion
rates in some of the medical centers within and across
medical service areas. To control for these outliers, we
matched service areas that had high and low insertion rates
for them to be equally divided between the intervention
group and the control group. It was necessary to keep
medical centers within the same service area in the same
research group to control for contamination due to greater
interaction between clinicians in the same medical service
area. Across the KPNC region, the female member population is widely varied. Overall, female members between
20 and 44 years old are primarily employed (89%), have a
middle income and are educated (38% with some college
education or higher); their approximate distribution by race
and ethnicity is as follows: 55% White, 7% African
American, 16% Latina, 19% Asian, 1.3% Native American
and less than 1% Pacific Islander [19]. Specific demographics by medical center are more difficult to determine. For
this study, it was not practical to randomly assign clinicians
or facilities within each service area to strict experimental or
control grouping because of the existing interaction between
clinicians across medical centers within the same geographic service area.

The evidence-based education with academic detailing
started in the second quarter of 2002 and ended in
December 2002. The study team recruited four enthusiastic
physicians who had their clinical practice at one of the
intervention sites to be IUC champions. The IUC champions and study investigators developed the evidence-based
clinician education program. The study team, the Regional
Health Education and the IUC champions developed new
or revised existing patient education materials about IUC
use that paralleled the evidence-based clinician education
component. The patient education materials were proactively placed in the intervention sites but were also made
available for purchase to the comparison sites in their usual
manner. A KPNC quarterly newsletter mailed to all health
plan members in the intervention sites included an article
about IUC and featured comments by the local IUC
champion. The article clarified common concerns about
safety, alerted women that IUC was available at no cost
and invited appropriate candidates to discuss IUC use with
their clinician. Peer-to-peer clinician education and academic detailing activities were conducted by the IUC
champions at the intervention sites, including continuing
medical education (CME)-approved grand rounds and
IUC device insertion training sessions. The comparison
sites were exposed to the usual offsite clinician educational opportunities.
2.1. Preintervention survey
The preintervention survey aimed at measuring baseline
knowledge, attitudes and practice patterns regarding IUC
use and was administered to all KPNC ob-gyn clinicians
(306 physicians and 180 nurse practitioners). The survey
developed was based on some of the questions from two
published surveys reviewed in the literature [20,21] and
additional questions that address experience with use of the
levonorgestrel 20-containing (LNG-20) IUC device. The
survey was pretested on clinician investigators and the IUC
champions who developed and conducted the evidencebased peer-to-peer education. The voluntary survey was sent
through interoffice mail in early March 2002 to eligible
clinicians in a sealed envelope containing an informed
consent cover letter. A second mailing was done, in the
same manner, to all nonrespondents 2 weeks later to
increase the response rate. Of the 486 eligible providers
surveyed, 304 responded, giving a 63% response rate.
2.2. Intervention
A multifaceted intervention was delivered to the three
intervention service areas over a 9-month period. The
intervention included evidence-based CME-approved education, patient education as well as outreach and peer-topeer academic detailing (Table 1).
2.3. Postintervention survey
The postintervention survey compared changes in the
intervention group and usual care comparison group from

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D. Postlethwaite et al. / Contraception 75 (2007) 177–184
Table 1
Peer-to-peer education and academic detailing activities
Type

Activity

Exposure

Peer-to-peer clinician education

CME-approved grand rounds

10 sessions; 17 facilities; more than
350 clinicians from all departments
30 IUC device insertion training sessions

Patient outreach
Reinforcement: Clinicians and staff

IUC champion consultation service
IUC device insertion training sessions
Member News features about IUC,
featuring IUC champions
Case presentations; question-and-answer
fora; barrier reduction
Proactive distribution of IUC tip sheets
IUC champion consultation service
Clinician/staff incentives: post-it note
pads and coffee mugs with slogan

1.5 million KPNC members in three service
areas exposed to the intervention
17 facilities; ob-gyn department meetings
1500 pads of 50 tip sheets in English,
Spanish and Chinese
Four IUD champions for nine intervention sites
1500 mugs and 3000 post-it note pads
(bGive Her the Choice To Change Her Mind,
Intrauterine ContraceptionQ)

Final distribution of IUC tip sheet,
December 2002

preintervention to postintervention. The survey was distributed 1 year after the CME-approved education and 7 months
after the end of the full intervention to 533 clinicians using
the same inclusion and exclusion criteria as those observed
for the baseline survey. Questions in the postintervention
survey were added or modified from the baseline survey to
reflect possible exposure to the intervention. All modifications were approved by the KPNC Institutional Review
Board. Of the 533 eligible providers surveyed, 334 responded, giving a 63% response rate.
2.4. Survey analysis
Survey data were analyzed using SAS version 8 software
(SAS Institute, Cary, NC). Unless otherwise noted, Pearson
m2 tests were used to detect statistically significant differences in demographic characteristics among survey respondents and nonrespondents and among the intervention and
comparison groups. Pearson m2 tests were also used to detect
statistically significant differences between the intervention
and control groups’ responses to selected postsurvey
questions. In cases in which the number of observations in
survey response categories was very low (i.e., b5), Fisher’s
exact test was used.
Several questions in the baseline and postintervention
surveys used a four-point Likert scale to capture an ordinal
range of responses to assess the providers’ comfort level
with various scenarios around recommending and inserting
an IUC device (e.g., 1= strongly disagree; 2 =somewhat
disagree; 3 =agree; 4 = strongly agree). To compare the
changes in the intervention and comparison groups’
comfort level over the intervention period with the different
scenarios, we calculated the number and percentage of
respondents indicating a higher degree of agreement on the
postsurvey as compared with the presurvey. Pearson m2
tests were used to determine if the number of providers
indicating a higher level of comfort in the intervention
group was significantly different from that in the comparison group.

2.5. IUC utilization
There were nine medical centers in the intervention
group and eight medical centers in the comparison group.
Documentation of IUC device insertion data was collected
from the third quarter of 2001 through the third quarter of
2003 for each medical center using KPNC OSCRs. Each of
the three study periods consisted of three calendar quarters
of data: preintervention (third quarter of 2001 to first quarter
of 2002); intervention (second quarter of 2002 to fourth
quarter of 2002); and postintervention (first quarter of 2003
to third quarter of 2003). For the analysis, the 9-month rate
was used because full-year data were not available for each
study period.
Rates were determined based on the number of IUC
device insertions for each calendar quarter per 1000 women
between 15 and 44 years old. The denominator for the rate
was based on all female KPNC members between 15 and
44 years old who had been an active member (paid medical
coverage) anytime during the quarter for each quarter
that data were collected. Assignment of a member to a
service area was determined using an algorithm based on
medical center utilization, location of the primary care
provider and the home zip code, known as the PARFU
(population at risk for utilization). The OSCR IUC device
insertion code did not distinguish which type of device
was inserted.
2.6. IUC utilization rate analysis
To calculate the 9-month rate, we first summed the
number of IUC device insertions during the 9-month period
and then divided the result by the average number of female
health plan members (PARFU) aged between 15 and
44 years during the 9-month period for each medical center.
The 9-month rates by study period and by group were then
calculated. Independent-samples t tests were calculated to
see if the IUC device insertion rates (number of IUC device
insertions per 1000 women aged between 15 and 44 years)

180

D. Postlethwaite et al. / Contraception 75 (2007) 177–184

Table 2
Demographic data on the intervention versus comparison groups and respondents versus nonrespondents
Variable

Intervention
[n = 114; n (%)]

Comparison
[n = 98; n (%)]

Respondents
[n = 212; n (%)]

Nonrespondents
[n = 208; n (%)]

Age V 47 yearsa
Femalea
Racea
White
Asian
Hispanic
Black
Native American
Physicians (vs. nurse practitioners)
Years as licensed practitioner b 15

53/110 (48)
89/113 (79)

42/91 (46)
73/92 (79)

.77
.92

95/201 (47)
162/205 (79)

82/198 (41)
115/202 (57)

.24
b .001

83/111 (75)
18/111 (16)
7/111 (6)
3/111 (3)
0/111 (0)
70 (61)
60 (53)

68/91
12/91
8/91
2/91
1/91
56
52

.70b

151/202
30/202
15/202
5/202
1/202
126
–

142/198
35/198
8/198
13/198
0/198
144
–

a
b
c

(75)
(13)
(9)
(2)
(1)
(57)
(53)

.53
.95

(75)
(15)
(7)
(2)
( b 1)
(59)

.10c

(72)
(18)
(4)
(7)
(0)
(69)

.04
–

Some observations are missing; the number of providers in each group for whom data are available is cited.
The Black and Native American subjects were not included in the m2 analysis due to their low cell counts.
The Native American subjects were not included in the m2 analysis due to their low cell counts.

were different in the two study groups. Changes over time
were evaluated using paired t tests to see if changes were
statistically significant.

3. Results
3.1. Demographics of respondents
There were 420 presurvey and postsurvey questionnaire
recipients. Fifty percent (n = 212) of the preintervention and
postintervention survey questionnaire recipients responded
to both surveys. Respondents and nonrespondents were

similar in demographic characteristics, except that females
were more likely than males to respond (pb .001) and nurse
practitioners were more likely than physicians to respond
(p = .04) (Table 2). Among the survey respondents, demographic comparisons between the intervention and comparison groups showed no statistically significant difference in
age, sex, race, provider type and years licensed.
3.2. Knowledge changes
Both groups reported attendance at IUC-related conferences, departmental meetings about IUC and device
insertion training sessions. However, respondents from the

Table 3
Postintervention IUC knowledge and attitude clinician survey responses
Intervention group
[n (%) indicating yes]
Knowledge
Attended KPNC-sponsored CME grand rounds about IUCa
Increased familiarity with LNG-20 IUC deviceb
Attitudes
Positive attitude about Cu-T 380A IUC device currentlya
Positive attitude about LNG-20 IUC device currentlya
Improved attitude about Cu-T 380A IUC device from 1 year agoa
Improved attitude about LNG-20 IUC device from 1 year agoa
I am more likely to recommend IUC to women who are
considering permanent sterilization as compared with 1 year agoa
Greater comfort in recommending IUC for women with diabetesb
Greater comfort in recommending an LNG-20 IUC device to a
woman with a history of menorrhagia instead of endometrial ablationb
Greater comfort in offering an LNG-20 IUC device to a
woman with dysmenorrheab
Greater comfort in inserting an IUC device when a woman is not on
her menses as long as pregnancy can be ruled outb
Greater comfort in inserting an LNG IUC device as progesterone
replacement or supplementation for perimenopausal or menopausal womenb
Greater comfort in inserting an LNG-20 IUC device in a patient
with a history of ectopic pregnancyb
a

Comparison group
[n (%) indicating yes]

7/98 (7)
44/98 (45)

b .001
.02

84/98
71/98
9/98
32/98
46/98

(88)
(75)
(9)
(34)
(49)

.20
b .001
.59
.02
.03

36/107 (34)
25/102 (25)

20/95 (21)
9/92 (10)

.05
.007

29/105 (28)

12/91 (13)

.01

27/107 (25)

8/92 (9)

.002

35/101 (35)

13/88 (15)

.002

39/103 (38)

14/85 (16)

.001

33/114 (29)
32/108 (30)
91/114
102/114
13/114
57/114
70/114

(82)
(92)
(12)
(51)
(64)

Provider responses to questions in the postintervention survey.
Providers indicating higher degree of agreement/comfort in their response to a question at postintervention as compared with their response to the same
question at preintervention.
b

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D. Postlethwaite et al. / Contraception 75 (2007) 177–184
Table 4
Postintervention practice pattern clinician survey responses
Practice pattern

Intervention group
[n (%) indicating yes]

Comparison group
[n (%) indicating yes]

Likely to recommend IUC for birth control at
Tubal sterilization consultation
88/106 (83)
62/91 (68)
Routine visit
100/110 (91)
76/95 (80)
Postabortion visit
70/104 (67)
49/95 (52)
I am more likely to recommend IUC to a woman who desires
54/112 (48)
33/96 (34)
long-term birth control compared with 1 year ago
I am more likely to do the insertion of an IUC device
42/107 (39)
25/95 (26)
myself compared with 1 year ago
Information about the safety and efficacy of IUC I received from KPNC education has affected my frequency of recommending this method
Not at all
22/112 (20)
37/95 (39)
Somewhat
28/112 (25)
25/95 (26)
Moderately
23/112 (21)
14/95 (15)
A great deal
32/112 (29)
13/95 (14)
No additional information
7/112 (6)
6/95 (6)
18/98 (18)
8/93 (9)
I require a woman to be on her menses for IUC device insertiona
IUC device insertion training I received from KPNC affected the frequency of IUC device insertions I perform
Not at all
36/109 (33)
45/94 (48)
Somewhat
23/109 (21)
17/94 (18)
Moderately
29/109 (27)
15/94 (16)
A great deal
13/109 (12)
5/94 (5)
No additional training
8/109 (7)
12/94 (13)
Compared with 1 year ago I have
More experience inserting the LNG-20 IUC device
85/104 (82)
61/90 (68)
The same amount of experience inserting the LNG-20 IUC device
19/104 (18)
29/90 (32)
The fact that IUC is now a covered benefit (reduced cost to patient) has affected my frequency of recommending this method
Not at all
38/112 (34)
46/95 (48)
Somewhat
31/112 (28)
26/95 (27)
Moderately
24/112 (21)
13/95 (14)
A great deal
19/112 (17)
10/95 (11)

.01
.03
.02
.04
.05

.01

.05
.047

.02

.12

Data presented are providers’ responses to questions in the postintervention survey unless otherwise indicated.
a
Providers who changed their response from yes in the preintervention survey to no in the postintervention survey.

intervention group reported a higher frequency of attending
KPNC-developed IUC CME-approved grand rounds as
compared with respondents from the comparison group
(pb .001) (Table 3). Familiarity with the copper T (Cu-T
380A) IUC device was reported as bvery highQ in both
groups at baseline and postintervention. Reported familiarity with the LNG-20 IUC device was higher in the
intervention group as compared with the comparison group
at baseline (bvery familiarQ: intervention = 56% vs. comparison =35%) and remained higher at postintervention (bvery
familiarQ: intervention =74% vs. comparison = 59%), but the
comparison group actually reported greater gains in
familiarity with the LNG-20 IUC device as compared with
the intervention group (p= .02) (Table 3).

IUC to women considering permanent sterilization. The
comfort level reported by the intervention group improved
significantly more as compared with that reported by the
comparison group over the course of the intervention period
with respect to recommending IUC to women with diabetes,
menorrhagia, dysmenorrhea or a history of ectopic pregnancy or to perimenopausal/menopausal women as progestin replacement/supplement. Neither group reported
reluctance in recommending IUC due to a history of pelvic
inflammatory disease. Only a small percentage of survey
respondents in both groups reported reluctance to recommend IUC to women desiring a future pregnancy or because
of medical liability concerns or beliefs that IUC acts as an
abortifacient (Table 3).

3.3. Attitude changes
At baseline, survey respondents from both groups
reported a positive attitude toward the Cu-T 380A, which
remained positive after the intervention. After the intervention, respondents from the intervention group reported a
more positive attitude toward the LNG-20 IUC device as
compared with those from the comparison group (Table 3).
At postintervention, the intervention group reported a
greater likelihood than the comparison group to recommend

Table 5
IUC device insertion rates by group and by period
Period

Intervention group
(IUC device insertions
per 1000 women
aged 15–44 years)

Comparison group
(IUC device insertions
per 1000 women
aged 15–44 years)

Preintervention
Intervention
Postintervention

6.31
8.04
9.57

5.46
6.30
7.35

.30
.08
.02

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D. Postlethwaite et al. / Contraception 75 (2007) 177–184

Table 6
IUC device insertion rate changes by study group
Group

Preintervention rate
per 1000 women
aged 15–44 years

Intervention rate
per 1000 women
aged 15–44 years

Postintervention rate
per 1000 women
aged 15–44 years

Preintervention
to intervention
rate change

Intervention
to postintervention
rate change

Preintervention
to postintervention
rate change

Intervention
Comparison

6.31
5.46

8.04
6.30

9.57
7.35

1.73 (p = .0005)
0.84 (p = .04)

1.53 (p = .002)
1.05 (p = .005)

3.26 (p b .0001)
1.89 (p = .003)

3.4. Practice pattern changes
The intervention group was more likely than the
comparison group to report that the information they had
received in 2002 about the safety and effectiveness of IUC
had affected their frequency of recommending it and that the
IUC device insertion training they received had affected the
number of insertions they performed themselves, especially
with experience in inserting the LNG-20 IUC device. The
intervention group also reported a greater likelihood to
recommend IUC for patients who desire a long-term method
of birth control at sterilization consults, routine visits and at
postabortion visits and to allow IUC device insertion when
women were not on their menses (Table 4).
3.5. IUC utilization results
IUC device insertion rates were determined for the
intervention and comparison groups for each 9-month study
period (Table 5). The preintervention insertion rate was
6.31 per 1000 women for the intervention group and was
5.46 per 1000 women for the comparison group. The
differences in preintervention rates are not statistically
significant (p= .30) between the two groups. During the
intervention period, the IUC device insertion rate increased
to 8.04 per 1000 for the intervention group and to 6.30 per
1000 for the comparison group. The difference in rates
during the intervention period is not statistically significant
between the two groups (p= .08). Finally, the postintervention insertion rate was 9.57 per 1000 for the intervention
group and was 7.35 per 1000 for the comparison group. The
difference in these two rates is statistically significant
(p =.02) (Table 5).
Overall, the IUC device insertion rate increased from
5.91 to 8.53 per 1000 women aged between 15 and 44 years.
The intervention and comparison groups showed an upward
trend. The increases from preintervention to intervention,
intervention to postintervention and preintervention to
postintervention were statistically significant for both
groups (Table 6).
Rate increases were not significantly different between
the intervention and comparison groups from preintervention to intervention (p = .07) and from intervention to
postintervention (p = .28); however, the rate increase
was significantly different between the two groups
from preintervention to postintervention (p = .02). The
intervention group demonstrated a rate increase of 3.3 per
1000 women aged between 15 and 44 years, as compared

with an increase of 1.9 per 1000 women aged between
15 and 44 years for the comparison group (Table 7).
4. Discussion
4.1. Clinician knowledge, attitudes and practice pattern
changes
It was evident from the results of the preintervention
survey that general IUC familiarity and knowledge levels
were high among the KPNC respondents and that attitudes
toward IUC were generally positive. This presented additional challenge to demonstrate an increase in knowledge and
more positive attitudes toward IUC. For example, at
preintervention, 86% of the intervention group and 90% of
the comparison group reported being bvery familiarQ with the
Cu-T 380A IUC device and 93% of the intervention group
and 89% of the comparison group indicated that they would
be comfortable recommending IUC to a woman younger
than 25 years if she were parous and monogamous. Similarly,
at preintervention, 81% of the intervention group and 80% of
the comparison group agreed with a statement about feeling
comfortable with recommending IUC to a woman who had a
sexually transmitted infection 2 years before her current
monogamous relationship and the birth of her children.
At postintervention, when asked about the frequency of
their IUC device insertion, 20% of the comparison group
versus 25% of the intervention group reported IUC device
insertions being performed more than once per week. This
reflects increases of 11% and 12% from the preintervention
levels of 9% and 13%, respectively. This change may be a
reflection of the removal of copayment, however.
Reported changes in attitudes and practice patterns in the
intervention group that were significantly greater in magnitude than those in the comparison group from preintervention to postintervention included an increased frequency of
recommending IUC due to information received about the
safety and efficacy of IUC, greater likelihood to insert IUC

Table 7
Comparisons of 9-month IUC device insertion rate changes by study group
Nine-month rate changes

Intervention
group

Comparison
group

Preintervention to intervention
Intervention to postintervention
Preintervention to postintervention

1.73
1.53
3.26

0.84
1.05
1.89

.07
.28
.02

D. Postlethwaite et al. / Contraception 75 (2007) 177–184

devices themselves and greater likelihood to recommend
IUC for birth control at routine medical office visits (e.g.,
annual examination and postabortion), especially for women
who desire long-term contraception or permanent sterilization (tubal sterilization consults). The intervention group also
demonstrated an increased likelihood over the course of the
intervention to insert an IUC device without requiring a
woman to be menstruating, to recommend IUC to women
with chronic diseases such as diabetes and to use IUC for
some of the noncontraceptive benefits of the LNG-20 IUC
device. Based on the medical evidence, the intervention
group was also less likely to avoid recommending an LNG20 IUC device to women with a history of ectopic pregnancy
as compared with control subjects.
4.2. Did reported changes in attitudes and practice patterns
lead to changes in IUC utilization?
IUC utilization increased over the 27-month period in all
KPNC sites. This overall trend may be attributed to the
removal of cost as a barrier for IUC. The IUC utilization
trends in the sites exposed to the peer-to-peer education
and academic detailing showed a more consistent upward
trend, reaching statistical significance by the postintervention period.
4.3. Peer-to-peer education
The concept of an IUC champion participating in formal
clinician education, onsite consultation and academic
detailing reinforcement activities in the intervention sites
added value to the intervention. The IUC champions
reported that they were tapped to assist with difficult
insertions and consultations about the use of IUC in
nontraditional candidates (e.g., nulliparity, history of pelvic
inflammatory disease and previous ectopic pregnancy) and
in the use of progestin IUC for noncontraceptive benefits.
Although the usual practice comparison sites possibly
received the very same evidence about IUC from offsite
conferences and meetings sponsored by professional affiliations, academic institutions or industry, the peer-to-peer
educational approach employed in this study may have been
more effective in changing clinician practice.
4.4. Transitioning research into practice
Despite more than a decade of medical evidence showing
the safety and cost-effectiveness of IUC, we hypothesized
that a comprehensive approach was needed to supplement
the removal of cost as a barrier to promote change in
clinician practice. The literature shows that CME alone
(passive dissemination) is relatively ineffective in promoting
evidence-based changes in practice [5,6]. Strategies that
have been shown to facilitate the transition from research to
practice include common themes, such as the following:
!

strong evidence of the need for change (although safe
and cost-effective, IUC is used by b 2% of American
women of reproductive age);

183

! appropriate identification of the problem (safety
myths prevail about IUC);
! stakeholders and strong opinion leaders (IUC champions and academic detailing);
! comprehensive and multidisciplinary strategies to
effect the change and diffusion of information
(multifaceted approach to clinician and patient education); and
! strong organizational commitment (removal of cost
for IUC as a barrier).
This study employed these strategies and demonstrated
an impact on IUC utilization. Multifaceted interventions
have demonstrated a higher probability for positive changes
in health care outcomes as compared with single or double
interventions [5,6].
Removing the cost of IUC for the patient occurred before
the onset of the study, affecting the intervention and
comparison sites equally. Further studies might investigate
the difference in rates of all methods of contraception use
between sites with education alone and those with removal of
cost alone. Additional studies could also look into whether
health plan providers, such as KPNC, that assume the costs
for IUC and other cost-effective reversible methods of
contraception have reduced unintended pregnancies, improved patient outcomes and led to greater cost savings.
4.5. Study limitations
One limitation of this study was its inability to identify
what method of contraception was used by each woman
before the insertion of an IUC device during the study
period. A second limitation was the use of a 9-month
utilization rate rather than an annual rate. A 9-month
intervention was feasible, and full-year rate information
was not available for the preintervention period. Another
limitation of the study was its inability to accurately
document the types of IUC devices inserted for comparisons
between the Cu-T 380A and the LNG-20. This limitation
was due to the documentation of insertion through ICD-9
procedure codes, which do not account for product type. A
fourth limitation of this study was its inability to randomize
all medical centers to the intervention or usual care
comparison group. There was a wide variation in IUC
device insertion rates within each medical service area, but
clinicians within a service area would have a greater chance
for interaction. This increased the risk for contamination if
facilities within each service area were randomized. There is
a potential for bias in the results because the sites were not
chosen randomly. It was also not in the scope of the study to
include follow-up data to track patient satisfaction, complication rates or IUC device removals after insertion.
5. Conclusion
This study demonstrated a comprehensive effort that
resulted in a change in reported attitudes and practice

184

D. Postlethwaite et al. / Contraception 75 (2007) 177–184

patterns and in a statistically significant increase in
IUC utilization in the intervention group within a large
health plan organization. It is an example of how a
multifaceted approach can rapidly effect change in practice
based on medical evidence. Several components of the
intervention (IUC champion, IUC clinician education,
academic detailing of health education materials and
reminder incentives for clinicians and staff) are being
replicated in the comparison sites. All materials created in
conjunction with this project can be shared with the health
care community. (Contact Debbie Postlethwaite through
[email protected].)
Acknowledgments
We thank Berlex Lab for providing an unrestricted
research grant to conduct the study; Kaiser Permanente
Women’s Health Research Institute, Quality and Operations
Support and Division of Research for data collection and
analysis; and Felicia Stewart, MD (posthumously), for her
critical manuscript review.
References
[1] Porter M, Teisberg EO. Redefining competition in health care. Harv
Bus Rev 2004;82:64–76,136.
[2] Berwick DM. Disseminating innovations in health care. JAMA 2003;
289:1969 – 75.
[3] Dopson S, Fitzgerald L, Ferlie E, et al. No magic targets! Changing
clinical practice to become more evidence based. Health Care Manage
Rev 2002;27:35 – 47.
[4] Gruman J, Follock M. Putting evidence into practice. Office of
Behavioral and Social Science Research, NIH 1997. Available from:
www.obssr.od.nih.gov [accessed 3/6/06].
[5] Davis DA, Thompson MA, Oxman AD, et al. Changing physician
performance: a systematic review of the effect of continuing medical
education strategies. JAMA 1995;274:700 – 5.

[6] Bero LA, Grilli R, Grimshaw JM, et al. Getting research findings into
practice: closing the gap between research and practice: an overview
of systematic reviews of interventions to promote the implementation
of research findings. BMJ 1998;317:465 – 8.
[7] Family Planning Worldwide Data Sheet, 2002. Population Reference
Bureau. Available at: www.prb.org [accessed 3/6/06].
[8] Mosher WD, Martinez GM, Chandra A. et al. Use of contraception
and use of family planning services in the United States: 1982–2002.
Available at: http://www.cdc.gov/nchs/nsfg.htm [accsessed 6/18/06].
Advance data from Vital and Health Statistics, USDHHS, CDC,
350;2004:1–35.
[9] Trussell J, Leveque JA, Koenig JD, et al. The economic value of
contraception; a comparison of 15 methods. Am J Public Health 1995;
85:494 – 503.
[10] Hatcher RA, Trussell J, Stewart F, et al. Contraceptive technology.
18th ed. New York7 NY Ardent Media Inc; 2004.
[11] Summary of changes from the first edition of WHO medical eligibility
criteria for contraceptive use. Contracep Rept 2001;12:12 – 4.
[12] Hicks D. What risk of infection with IUD use? Lancet 1998;351:
1222 – 3.
[13] Darney P. Time to pardon the IUD? N Engl J Med 2001;345:608.
[14] Duenas JL, Albert A, Carrasco F. Intrauterine contraception in
nulligravid vs parous women. Contraception 1996;53:23 – 4.
[15] Farley T, Rosenberg M, Rowe PJ, et al. Intrauterine devices and pelvic
inflammatory disease: an international perspective. Lancet 1992;339:
785 – 8.
[16] Sivin I, Stern J. Health during prolonged use of levonorgestrel 20 Ag/d
and the copper TCu 380Ag intrauterine contraceptive devices:
a multicenter study. Fertil Steril 1994;61:70 – 7.
[17] Toivonen J, Luukkainen T, Allonen H. Protective effect of intrauterine
release of levonorgestrel on pelvic infection: three years’ comparative
experience of levonorgestrel- and copper-releasing intrauterine devices. Obstet Gynecol 1991;77:261 – 4.
[18] Forrest JD. U.S. women’s perception of and attitudes about the IUD.
Obstet Gynecol Surv 1996;51:S30 – 4.
[19] Gordon NP. Kaiser Permanente Member Health Survey, 2002. http://
dor-ent1.kaiser.org/dor/mhsnet/pdf_02/mhs02reg_e.pdf [accessed 6/01/06].
[20] Kooiker CH, Scutchfield FD. Barriers to prescribing the copper T 380A
intrauterine device by physicians. West J Med 1990;153:279 – 82.
[21] Stanwood N, Garrett J, Konrad T. Obstetrician-gynecologists and the
intrauterine device: a survey of attitudes and practice. Obstet Gynecol
2002;99:275 – 80.

Challenges in Translating Evidence to
Practice
The Provision of Intrauterine Contraception
Cynthia C. Harper, PhD, Maya Blum, MPH, Heike Thiel de Bocanegra, PhD, MPH,
Philip D. Darney, MD, MSc, J. Joseph Speidel, MD, MPH, Michael Policar, MD,
and Eleanor A. Drey, MD, EdM
OBJECTIVE: Intrauterine contraception is used by many
women worldwide, however, it is rarely used in the
United States. Although available at no cost from the
state family planning program for low-income women in
California, only 1.3% of female patients obtain intrauterine contraceptives annually. This study assessed knowledge and practice patterns of practitioners regarding
intrauterine contraception.

insertions. Fewer than half of clinicians considered nulliparous women (46%) and postabortion women (39%) to
be appropriate candidates. Evidence-based views of the
types of patients who could be safely provided with
intrauterine contraception were associated with more
counseling and method provision, as well as with knowledge of bleeding patterns for the levonorgestrel-releasing intrauterine system and copper devices.

METHODS: We conducted a survey among physicians,
nurse practitioners, and physician assistants (n51,246)
serving more than 100 contraceptive patients per year in
the California State family planning program. The response rate was 65% (N5816). We used multiple logistic
regression to measure the association of knowledge with
clinical practice among different provider types.

CONCLUSION: Prescribing practices reflected the erroneous belief that intrauterine contraceptives are appropriate
only for a restricted set of women. The scientific literature
shows intrauterine contraceptives can be used safely by
many women, including postabortion patients. Results revealed a need for training on updated insertion guidelines
and method-specific side effects, including differences between hormonal and nonhormonal devices.

RESULTS: Forty percent of providers did not offer intrauterine contraception to contraceptive patients, and 36%
infrequently provided counseling, although 92% thought
their patients were receptive to learning about the
method. Regression analyses showed younger physicians
and those trained in residency were more likely to offer
From the Bixby Center for Reproductive Health Research & Policy, Department
of Obstetrics, Gynecology and Reproductive Sciences, University of California,
San Francisco, California.
Supported by funds from the State of California, Department of Health Services,
contract 05-45122, and the William and Flora Hewlett Foundation. All analyses,
interpretations, or conclusions are those of the authors and not of the funders.
The authors thank Debbie Postlethwaite, RNP, MPH, for her detailed review of
the survey and Debbie Weiss, MPH, for her contributions to the survey and
provider interviews.
Corresponding author: Cynthia C. Harper, PhD, Assistant Professor, Department of Obstetrics, Gynecology and Reproductive Sciences, Box 0744 UCSF,
3333 California St., Ste. 335, San Francisco, CA 94118; e-mail:
[email protected].
Financial Disclosure
The authors have no potential conflicts of interest to disclose.
© 2008 by The American College of Obstetricians and Gynecologists. Published
by Lippincott Williams & Wilkins.
ISSN: 0029-7844/08

VOL. 111, NO. 6, JUNE 2008

(Obstet Gynecol 2008;111:1359–69)

LEVEL OF EVIDENCE: III

f the 6 million pregnancies among U.S. women
each year, nearly half are unintended, and the rate
is increasing among low-income women.1 Intrauterine
contraception is safe and highly effective, with a failure
rate of less than 1%.2,3 However, it is infrequently
prescribed by health care providers in the United States.
Intrauterine contraception does not depend on individual compliance to be highly effective, but it does depend
on health care providers for insertion and removal, and
provider practices vary widely. In Europe, intrauterine
contraception use ranges from 20 –26% in certain countries (France 20%, Norway 24%, Finland 26%). In other
parts of the world, use is even higher, for example, Israel
(30%), China (34%), Egypt (37%), Korea (49%), and
Uzbekistan (52%). In the United States, by contrast,
intrauterine contraception use is negligible at about 1%.4
Specific—and unfounded— concerns related to intrauterine contraception safety include a correlation

OBSTETRICS & GYNECOLOGY

1359

between intrauterine contraception and ectopic pregnancy,3 which was disproved in the 1980s,5 and a
heightened risk of pelvic inflammatory disease (PID)
and future infertility.6,7 The Dalkon Shield, a poorly
designed and tested device, was associated with an
eightfold increase in PID risk and was removed from
the market in the 1970s.7,8 Although these events
occurred three decades ago, they continue to influence providers’ perceptions of intrauterine contraception, and the fear of litigation has been found to be
associated with low intrauterine contraception provision in practice.9 However, the forms of intrauterine
contraception currently on the market do not pose
similar risks.6,8,10,11 In addition, concern that copper
intrauterine contraceptives increase the risk of infertility in nulliparous women also has been refuted.12
Newly improved devices have been developed and
widely used throughout the world; two methods currently on the market in the United States are the
levonorgestrel-releasing intrauterine system (Mirena,
Bayer HealthCare Pharmaceuticals, Wayne, NJ) and the
Copper T 380A (ParaGard, Barr Pharmaceuticals,
Montvale, NJ). A limited number of studies have examined barriers that health care providers face in the
United States in offering newer devices to women.
Barriers to provision generally are related to lack of
clinical training and limited knowledge. A national
survey of fellows of the American College of Obstetricians and Gynecologists (ACOG) found that 95% of
respondents considered the Copper T 380A to be safe.
However, nearly one third felt that there was a causal
relationship between intrauterine contraception use and
PID, and having this belief was significantly associated
with lower provision. Although only 16% agreed that
intrauterine contraception use leads to litigation, there
was also an association with fewer insertions.9 This study
was not able to collect specific data on the levonorgestrel-releasing system, as it had just become available.
A more recent training and educational intervention in
a Northern California HMO including physicians and
nurse practitioners (N5212) showed an increase in
positive attitudes about the newer levonorgestrel-releasing intrauterine contraceptive and a greater comfort in
recommending it to patients.13 This intervention is
promising and leads to the research question of what
knowledge and content is most important for providers
to gain to be proficient in intrauterine contraception
provision.
This study builds on the new and growing literature in this area by examining the specific method
characteristics of each of the available devices, includ-

1360

Harper et al

ing benefits and side effects. We used multivariable
modeling to assess knowledge and practice patterns of
physicians and advance practice clinicians.

MATERIALS AND METHODS
As part of an evaluation program of the California
State family planning program for low-income populations, Family PACT, we conducted a study on
intrauterine contraception practices among health
care providers. In this program, 2,834 clinician providers served more than 1.5 million clients in 2003–
2004.14 Women eligible for Family PACT can obtain
contraception at no cost, but only 1.3% of female
patients received an intrauterine contraceptive in
2003, a level that has not varied since program
inception. Claims data showed that fewer than half of
providers received reimbursement for any intrauterine contraception-related procedure in 2003.
We collected data in 2006 through a small set of
in-depth interviews and then a large-scale self-administered written survey of 1,246 clinicians, including
physicians, nurse practitioners and physician assistants.
Responses to the in-depth interviews generated questions for the survey, and we also included survey items
from published provider surveys on intrauterine contraception.9,13 The survey was pretested among clinician
researchers. Two weeks before the initial survey mailing, a letter was sent to prospective participants to
inform them of the survey. The survey was mailed with
a cover letter and instructions that the survey was to be
completed by a physician, nurse practitioner, or physician assistant who offers contraceptive services. Providers
then were mailed a reminder postcard later that week,
and a second survey was mailed to nonrespondents 4
weeks later. Providers were telephoned a maximum of
four times, and data collection ended 12 weeks after the
initial mailing. The survey was conducted on the entire
population of Family PACT providers, serving more than
100 female contraceptive patients per year. A Family
PACT provider refers to a public or private health care
facility where contraceptive services are provided by
clinicians.
The survey had 816 respondents, including 399
physicians and 402 nonphysicians, for a response rate
of 65%. The number of respondents was more than
sufficient to show a difference in proportion of physician and nonphysician intrauterine contraception
insertions of .65 and .55, respectively, with alpha
equal to 0.05 and power of 80% with a two-tailed test.
The regression models adjusting for covariates require a slightly larger size to account for correlation
between covariates, although we still have 80% power

Provider Practices With Intrauterine Contraception

OBSTETRICS & GYNECOLOGY

for a one-tailed test with a squared multiple correlation coefficient of the predictor provider type compared with other covariates to be up to 0.2. The study
was approved by the University of California, San
Francisco Committee on Human Research.
The survey included items on demographic (age,
gender, race/ethnicity), professional (physician, nurse
practitioner, or physician assistant, specialty), and practice characteristics (number of female contraceptive
patients per year, urban or rural location, public or
private practice). Claims data were used for the practice
characteristic variables. For items directly related to
intrauterine contraception, the survey included training
during residency or core training (number of insertions),
counseling (frequency of counseling and content), provider views of the safety and risks of the intrauterine
contraceptive, provider perceptions about which women
make suitable intrauterine contraception candidates, requirements and protocols for insertions, knowledge of
appropriate practices for intrauterine contraception in
general and specifically by intrauterine contraceptive
type—the Copper T 380A or the levonorgestrel-releasing
system—and availability of intrauterine contraception in
each clinician’s practice.
To assess providers’ knowledge of correct practices
and basic method characteristics, including benefits and
side effects, we used a series of scale variables. These
variables measure knowledge of bleeding patterns,
knowledge of hormonal side effects, and general knowledge. All scales were created using Cronbach’s alpha to
assess scale reliability and with tests for validity with
associations with professional and practice variables as
well as outcome variables. The knowledge of bleeding
patterns scale was created from 10 survey items that asked
about the levonorgestrel-releasing intrauterine system
and the Copper T 380A separately. The items in the
bleeding scale on the levonorgestrel-releasing intrauterine
system included appropriate counseling about the system
for patients with dysmenorrhea, patients with menorrhagia, and patients with iron-deficiency anemia, with an
emphasis in counseling on spotting, amenorrhea, and
irregular bleeding. The items for Copper T 380A were
emphasis in counseling for copper intrauterine contraception on menorrhagia, dysmenorrhea, irregular
bleeding, and anemia. The scale reliability coefficient for
the provider practices for bleeding was 0.80.
The scale of hormonal implications included nine
items on the accuracy of the counseling providers give
to their patients on the effect of the levonorgestrelreleasing intrauterine system on breast tenderness,
headaches, mood changes, acne, and smoking. The
scale also captures the accuracy of what providers tell

VOL. 111, NO. 6, JUNE 2008

Harper et al

their patients about Copper T 380A for headaches,
mood changes, acne, and breast tenderness. Cronbach’s alpha gave a scale reliability coefficient of 0.87.
For the general knowledge variable, we included 12
items that contributed to a cohesive scale: accurate
counseling information on the levonorgestrel-releasing intrauterine system on spotting, amenorrhea, irregular bleeding, pain with intercourse, headaches,
mood changes, and acne; and accurate Copper T
380A counseling on menorrhagia, dysmenorrhea, irregular bleeding, anemia, and pain with intercourse.
The scale reliability coefficient is 0.86.
For provider views on which women are suitable
intrauterine contraception candidates, we asked about
consideration of the following nine items: nulliparity,
immediate postpartum usage, immediate postabortion usage, teenager, history of ectopic pregnancy,
STD in the past 2 years, PID in the past 5 years,
current bacterial vaginosis, and human immunodeficiency virus (HIV) positivity. The scale reliability
coefficient, measured by Cronbach’s alpha, for potential intrauterine contraception candidates was 0.77.
We created a scale variable with provider concerns
about risks that affect their willingness to recommend
intrauterine contraception with these seven items: sexually transmitted diseases, PID, infertility, ectopic pregnancy, expulsion, uterine perforation at insertions, and
other risks Cronbach’s alpha gave a scale reliability
coefficient of 0.88 for provider concern of risks.
The two outcome variables we assessed on intrauterine contraception provision were counseling contraceptive patients and availability of method at the provider’s practice (n5812). Of the 816 survey respondents,
we limited analyses to the 812 respondents with data on
whether intrauterine contraception was provided at
their practices. For analysis, the counseling variable was
coded dichotomously to measure a general practice of
usually counseling (always/mostly) or not (sometimes/
rarely). We performed multiple logistic regression analysis to measure the association of demographic, professional, and practice factors with the outcome variables of
provision of counseling and insertions. The models
included demographic (age, gender), professional (clinician type, specialty, level of intrauterine contraception
training), and practice (private/public, patient volume,
urban/rural) characteristics. Additional models included
provider perceptions of safety and risk, perceptions
about which women make suitable intrauterine contraception candidates, and provider knowledge of the
method. The variables that were significant in univariable analyses for either the counseling or provision
outcome were included in the multivariable models, as

Provider Practices With Intrauterine Contraception

1361

well as variables shown in the literature to be associated
with intrauterine contraception counseling and provision. Data were analyzed with Stata 8.2 (StataCorp LP,
College Station, TX) and significance levels reported at
P#.05.

RESULTS
Table 1 presents demographic, professional, and practice characteristics of respondents. Almost half of respondents were physicians (49%), 36% were nurse practitioners, and 15% were physician assistants. By
specialty, they were largely family practice (37%) and
ob-gyn (35%), although there were also women’s health
specialists (12%) and general practice (8%). Within the
ob-gyn specialty, 54% were physicians and 46% advance practice clinicians. Within the family practice
specialty, 46% were physicians and 54% advance practice clinicians. However, in the women’s health specialty, almost all (98%) were advance practice clinicians.
More than half of providers were in private practice
(56%), and the rest were in public/nonprofit. Patient
volume for practice ranged from 100 to more than
10,000 female contraceptive patients per year, with a
mean number of female contraceptive patients of 1,113
per year. The mean age of the providers was 49 years
(standard deviation 10.5), and the sample was diverse,
with 47% white, 21% Asian, 20% Latino, 6% African
American. In comparing claims data on the respondents
and nonrespondents, we found no differences between
respondents and nonrespondents by provider type, urban area, contraceptive patients, or intrauterine contraception patients served. The respondents are similar to
the full population surveyed: 56% of respondents were
in private practice compared with 57% in the population
surveyed; 80% in urban areas compared with 82%; 1.5%
intrauterine contraception clients compared with 1.5%
intrauterine contraception clients; 1,113 mean female
contraceptive clients per year compared with 1,027
mean clients.
Sixty-nine percent of these contraceptive providers
had received training in intrauterine contraceptive insertions during residency or their core training, although
44% reported inserting fewer than 20 intrauterine contraceptives in training. Among ob-gyn physicians, only
4% were not trained; but among other physicians, 32%
were not trained, and among the mid-level practitioners,
41% were not trained. Younger age is significantly
associated with a higher level of training (t test; P5.006).
Although most ob-gyn physicians had received training,
only 74% of them provided intrauterine contraception at
their practices, as did 43% of other physicians. Clinicians
reported substantial intrauterine contraception provi-

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Harper et al

Table 1. Respondent Characteristics and
Intrauterine Contraception Practices
Demographic
Age, mean y (SD)
Race/ethnicity, n (%)
White
Latino
Asian/Pacific Islander
African American
Multi-racial/other
Professional
Professional title, n (%)
Physician
Nurse practitioner
Physician assistant
Specialty, n (%)
Obstetrician-gynecologist
Family practice
Internal medicine, pediatrics, adolescent
medicine
Women’s health
General practice/other
Trained in IUC insertions n (%)
Practice
Private practice (vs public), n (%)
Urban, n (%)
Number female contraceptive patients per
year, n (%)
100–500 patients
501–1,000 patients
More than 1,000 patients
IUC counseling
Frequently discuss IUC with patients
seeking contraception
Sufficient time to counsel patients on
contraceptive options
Patients receptive to learning about IUC
Enough experience to counsel patients on
Copper T 380A
Enough experience to counsel patients on
LNG system
IUC provision
IUCs available at practice
Practitioners inserting IUC at your practice
Physicians
Nurse-practitioners
Physician assistants
Very comfortable in inserting Copper T
380A
Very comfortable in inserting LNG system
Offered IUC in past 5 years but stopped
(n5305)

48.6 10.5
373
161
166
48
49

46.8
20.2
20.8
6.0
6.1

389
118
281

49.4
15.0
35.7

285
302
47

35.1
37.2
5.8

101
77
548

12.4
9.5
69.0

450
644

55.6
79.6

389
185
239

47.8
22.8
29.4

515

64.1

680

85.3

730
657

91.9
82.0

590

74.0

495

61.0

342
291
158
476

67
59
32
59.8

310
106

39.5
34.7

SD, standard deviation; IUC, intrauterine contraception; LNG,
levonorgestrel-releasing intrauterine system.
Not all numbers add up to 812 due to missing data on individual items.

sion by mid-level practitioners in practices where the
method was available (nurse practitioner 59%, physician
assistant 32%), although the greatest proportion was by
physicians (81%). Thirty-six percent of contraceptive

Provider Practices With Intrauterine Contraception

OBSTETRICS & GYNECOLOGY

providers counseled their patients infrequently on the
method, although 85% reported that they had sufficient
time to counsel patients on contraceptive options, and a
full 92% considered their patients to be receptive to
learning about intrauterine contraception. The majority
of providers (55%) considered fewer than one quarter of
their contraceptive patients to be intrauterine contraception candidates.
Of the providers offering intrauterine contraception at their practices, most (72%) had both the
Copper T 380A and the levonorgestrel-releasing system available. Twenty-three percent of providers with
intrauterine contraception offered just the Copper T
380, and 5% offered just the levonorgestrel system. Of
the practices not offering intrauterine contraception to
contraceptive patients, the main reasons cited included
inadequate reimbursement (47%), lack of training (40%),
low patient interest (32%), and concerns about procedure risks (28%). Twenty-three percent cited litigation
concerns, and only 10% of providers cited few intrauterine contraception candidates as a reason for ceasing to
offer services. Thirty-five percent of practices not offering intrauterine contraception had offered it in the
previous 5 years but then stopped.
Provider knowledge as well as providers’ perceptions of the safety and specific risks involved in intrauterine contraception are presented in Table 2. Almost
all clinicians agreed that intrauterine contraception is
safe (94%). However, they had many concerns that kept
them from recommending intrauterine contraception to
their patients. Sexually transmitted diseases and PID
were top concerns affecting the willingness of providers
to recommend intrauterine contraception, followed by
ectopic pregnancy. Providers also showed extremely
restrictive views of the women they were willing to
consider intrauterine contraception candidates. Fewer
than half of providers considered nulliparous, postpartum
(immediate), postabortion (immediate), teenagers, history
of ectopic pregnancy, PID, or HIV-positive women as
candidates for intrauterine contraception, contrary to the
World Health Organization Medical Eligibility Criteria.15
Basic knowledge about intrauterine contraception was inadequate. Roughly 20% of providers emphasized hormonal side effects, such as mood change,
headache, acne, and breast tenderness, when counseling patients about ParaGard®—a copper T device that
contains no hormones. Providers also were confused
about the hormone content in the levonorgestrelreleasing system; the proportion who would insert a
levonorgestrel-releasing intrauterine system for a patient who smoked was only 34%, but levonorgestrel is
not contraindicated for smokers.15 Contraceptive pro-

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Harper et al

Table 2. Provider Attitudes and Knowledge
n
Provider perceptions of IUC safety
Agrees IUC is safe
Concerns affecting IUC recommendation scale
(scale reliability coefficient 0.88)
Sexually transmitted diseases
Pelvic inflammatory disease
Ectopic pregnancy
Infertility
Expulsion
Uterine perforation at insertion
IUC candidate scale (scale reliability coefficient
0.76)
Nulliparous
Immediately postpartum
Immediately postabortion
Teenager
History of ectopic pregnancy
Sexually transmitted disease in past 2 years
PID in past 5 years
Current bacterial vaginosis
HIV positive
Knowledge of hormonal side effects scale
(scale reliability coefficient 0.87)
LNG system
Willing to insert for menorrhagic patients
who smoke
Breast tenderness
Headache
Mood changes
Acne
Copper T 380A
Headaches
Mood changes
Acne
Breast tenderness
General IUC knowledge scale (scale reliability
coefficient 0.86)
LNG system
Appropriate emphasis in counseling on
Spotting
Amenorrhea
Irregular bleeding
Pain with intercourse
Headache
Mood change
Acne
Copper T 380A
Appropriate emphasis in counseling on
Anemia
Irregular bleeding
Dysmenorrhea
Menorrhagia
Pain with intercourse

759 94.2
219
227
144
75
86
81

27.8
28.7
18.2
9.5
10.9
10.3

362
263
313
311
247
486
383
337
340

45.9
33.1
39.4
39.1
31.1
61.1
48.4
42.2
42.9

264 33.7
362
381
396
324

48.5
50.8
53.0
43.4

561
599
639
604

72.0
77.1
82.1
77.6

533
595
629
407
381
396
324

70.4
79.2
83.4
54.3
50.8
53.0
43.4

555
400
551
612
461

71.0
51.5
70.6
78.5
59.3

IUC, intrauterine contraception; PID, pelvic inflammatory disease;
HIV, human immunodeficiency virus; LNG, levonorgestrelreleasing intrauterine system.

Provider Practices With Intrauterine Contraception

1363

viders in general are not yet fully informed about the
benefits of the levonorgestrel-releasing system, nor of
all of the important implications on bleeding patterns
of both devices. Only 33% of providers had ever
recommended the levonorgestrel-releasing intrauterine system for noncontraceptive benefits. Only 39%
reported they would insert a levonorgestrel-releasing
intrauterine system for a patient with dysmenorrhea if
she were interested, and half (51%) for a woman with
menorrhagia. Only 45% of providers responded they
would insert a levonorgestrel-releasing intrauterine system in an iron-deficient anemic patient if she were
interested. Just as bleeding patterns were often forgotten
as a potential benefit of the levonorgestrel-releasing
intrauterine system, they were also omitted in counseling on the Copper T 380, but in this case as a possible
drawback: when discussing the Copper T 380 with
patients, more than 25% of providers did not emphasize
dysmenorrhea or menorrhagia, which can occur.

In other areas of general knowledge, 25% of the
contraceptive providers responded erroneously that antibiotics should be given routinely at the time of intrauterine contraceptive insertion to prevent infection. A
similar proportion (24%) responded that a woman with
diabetes should not have an intrauterine contraceptive,
although it is an appropriate method for this population.15
Providers were unlikely to mention the Copper T 380A
for use as emergency contraception; 85% had never
mentioned it to patients.
Multivariable analyses of the factors associated
with counseling contraceptive patients about intrauterine contraception are presented in Table 3 . The
first model, with socio-demographic, professional,
and practice characteristics, shows that there is no
difference between physicians and advance practice
clinicians (ie, nurse practitioners and physicians assistants) in the frequency of intrauterine contraception
counseling. However, practitioners in ob-gyn prac-

Table 3. Counseling on Intrauterine Contraceptives to Female Contraceptive Patients: Multivariable
Logistic Regression Results
Model 1
Frequently Counsel Patients on IUC
Demographic
Age (y)
Gender
Male (reference)
Female
Professional and practice
Title
Mid-level NP/PA (reference)
Physician
Specialty
Family practice (reference)
Ob-gyn
Women’s health
Other (pediatrics/adolescent, GP,
internist)
Trained in IUC insertions
Female contraceptive patients (#/y)
Provider type
Public (reference)
Private
Urban location
Perceptions and knowledge of IUC
Consider IUC to be safe
Low perception of risks
Expansive view of IUC candidates
High-level knowledge
Knowledge of bleeding patterns
Knowledge of hormonal side effects
Number of observations
Likelihood ratio x2 (degrees of freedom)

Odds Ratio

Model 2

Model 3

95% CI

Odds Ratio

95% CI

Odds Ratio

95% CI

0.96

0.98–1.01

1.00

0.98–1.02

1.00

0.98–1.02

1.50*

1.01–2.21

1.28

0.84–1.95

1.26

0.83–1.92

1.15

0.76–1.72

1.22

0.79–1.89

1.18

0.76–1.81

1.66†
0.96

1.13–2.46
0.56–1.63

1.51*
0.83

1.00–2.28
0.48–1.44

1.45
0.81

0.95–2.21
0.46–1.41

0.64
1.60†
0.98*

0.40–1.01
1.13–2.25
0.97–1.00

0.83
1.52*
0.98‡

0.50–1.39
1.05–2.20
0.96–0.99

0.84
1.51*
0.98‡

0.50–1.39
1.05–2.17
0.96–0.99

0.70
1.24

0.47–1.04
0.82–1.87

0.84
1.05

0.55–1.29
0.67–1.65

0.87*
1.08

0.56–1.33
0.69–1.69

—
—
—
—
—
—

6.19‡
1.21
1.89‡
1.59†
—
—
783
112 (19)

2.68–14.3
0.96–1.54
1.36–2.64
1.21–2.08
—
—

5.68‡
1.17
1.85‡
—
1.45*
0.84
792
111 (20)

2.56–12.6
0.93–1.48
1.32–2.59
—
1.06–1.98
0.66–1.08

—
—
—
—
—
—
801
46.5 (14)

IUC, intrauterine contraception; CI, confidence interval; NP, nurse practitioner; PA, physician assistant; GP, general practitioner.
* P#.050.
†
P#.010.
‡
P#.001.

1364

Harper et al

Provider Practices With Intrauterine Contraception

OBSTETRICS & GYNECOLOGY

tices, whether physicians or advance practice clinicians, are significantly more likely to counsel contraceptive patients on the intrauterine contraception
than clinicians in other specialties (odds ratio
[OR]51.7). Likewise, healthcare providers who have
received training in intrauterine contraception insertion are 1.6 times as likely to counsel patients, but as
the number of female contraceptive patients increases, the frequency of intrauterine contraception
counseling declines, perhaps due to time constraints.
We assessed the contribution of providers’ perceptions and knowledge of intrauterine contraception to
their likelihood of counseling in Model 2, and we
found that those who consider intrauterine contraception to be a safe method have far higher odds
(OR56.2) of counseling their patients frequently
about the method than those who do not consider it to
be safe. Providers who consider many different types

of women eligible for intrauterine contraception and
those with high knowledge levels of basic method
characteristics and contraindications are also more
likely to counsel frequently on the method. However,
providers’ reports of how concerned they are about
the potential risks of insertion (eg, expulsions, perforation) were not associated with counseling. In the final
model tested (Model 3), we included specific knowledge
scales for whether providers were familiar with bleeding
patterns of each device and with the hormonal side
effects, and we found better knowledge of bleeding
patterns to be associated with frequent counseling.
The multivariable logistic results of provision of the
method in the practice showed associations with somewhat different factors than with counseling (Table 4).
Model 1, with the socio-demographic, professional, and
practice characteristics, showed that younger providers
are significantly more likely to offer the method than

Table 4. Provision of Intrauterine Contraceptives to Female Contraceptive Patients: Multivariable
Logistic Regression Results
Model 1
Provide IUC in Practice
Demographic
Age (y)
Gender
Male (reference)
Female
Professional and practice
Title
Mid-level NP/PA (reference)
Physician
Specialty
Family practice (reference)
Ob-gyn
Women’s health
Other (pediatrics/adolescent, GP,
internist)
Trained in IUC insertions
Female contraceptive patients (#/y)
Provider type
Public (reference)
Private
Urban location
Perceptions and knowledge of IUC
Consider IUC to be safe
Low perception of risks
Expansive view of IUC candidates
High-level knowledge
Knowledge of bleeding patterns
Knowledge of hormonal side effects
Number of observations
Likelihood ratio x2 (degree of freedom)

Odds Ratio

Model 2
95% CI

Odds Ratio

Model 3
95% CI

Odds Ratio

95% CI

0.96*

0.94–0.98

0.97†

0.95–0.99

0.97†

0.95–0.99

1.29

0.82–2.03

1.09

0.68–1.76

0.90

0.55–1.47

2.26*

1.40–3.64

2.45*

1.48–4.05

2.53*

1.51–4.23

4.67*
3.85*

2.98–7.32
1.90–7.82

4.52*
3.79*

2.82–7.24
1.81–7.97

3.31
2.64‡

2.03–5.39
1.25–5.56

0.36*
1.82†
1.05*

0.20–0.62
1.21–2.74
1.02–1.07

0.45†
1.66‡
1.03†

0.25–0.83
1.08–2.56
1.01–1.06

0.45‡
1.44
1.04*

0.24–0.83
0.93–2.25
1.01–1.05

0.18*
1.43

0.11–0.28
0.43–1.13

0.16*
0.58

0.10–0.27
0.34–0.99

0.20*
0.56

0.12–0.33
0.32–0.97

2.10–14.8
0.82–1.41
1.13–2.35
1.23–2.31
—
—

3.36‡
0.96
1.40

1.29–8.74
0.73–1.27
0.96–2.05

—
—
—
—
—
—
809
298.2 (14)

—
—
—
—
—
—

5.57*
1.08
1.63†
1.68†
—
—
785
324 (19)

3.24*
1.53†
794
360 (20)

2.23–4.70
1.15–2.03

IUC, intrauterine contraception; CI, confidence interval; NP, nurse practitioner; PA, physician assistant; GP, general practitioner.
* P#.001.
†
P#.010.
‡
P#.050.

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Provider Practices With Intrauterine Contraception

1365

older providers and that physicians have elevated odds
(OR52.3) of offering intrauterine contraception compared with advance practice clinicians. Ob-gyn specialists, whether physicians or advance practice clinicians,
are 4.6 times as likely as family practice clinicians to
offer intrauterine contraception, and women’s health
specialists are 3.8 times as likely. Because these multivariable models are additive, the elevated odds for both
physicians and ob-gyn specialists show that ob-gyn
physicians have the greatest odds of providing intrauterine contraception. Providers in private practice had
greatly reduced odds for offering intrauterine contraception to their patients (OR50.18). Whereas clinicians in
practices with greater numbers of contraceptive patients
were less likely to counsel on intrauterine contraception,
they were significantly more likely to offer the method to
their patients at their practices. As with counseling, training is also significantly associated with increased odds of
intrauterine contraception provision (OR51.8).
In Model 2, we assessed how much of the elevated
odds of ob-gyns and other physicians providing intrauterine contraception resulted from their more favorable perceptions or more informed practices. Results
showed that the differences in age as well as the differences in professional and practice characteristics remain
important, as do intrauterine contraception-specific attitudes and knowledge. As with the counseling results, the
intrauterine contraception provision results show
that considering the method to be safe was a key
factor in its availability at the practice (OR55.6),
and that expansive views of who might be considered as an intrauterine contraception candidate as
well as knowledge about each method were also significantly associated with method provision. We assessed
the different aspects of knowledge in Model 3 and found
that knowledge of bleeding patterns, as well as of
hormonal side effects, were strongly associated with
provision of the method. We also found that the impact
of training was reduced, showing that much of the
significant effect of training (seen in Models 1 and 2) lies
in the ability to provide patients with accurate information and care about the bleeding they might experience
with each method.
Because the physicians differed significantly from
the nonphysicians in provision of intrauterine contraception, we also estimated the models separately for
both groups and found that the results for physicians
were the same as the results for all respondents. For the
mid-level practitioners, the estimated coefficients were
in the same direction, but a few variables lost strength
and did not reach significance level, namely age and
training. The specialty of the practice for mid-level prac-

1366

Harper et al

titioners retained a robust association with intrauterine
contraception provision and is perhaps more important
than core training for nurse practitioners and physician
assistants.

DISCUSSION
Prescribing practices of providers in the United States
reflect erroneous beliefs that intrauterine contraception
is appropriate for an extremely limited segment of
women seeking contraception. Our results showed that
contraceptive providers who are open to the possibility
that the method can be used by many different types of
women are more likely to counsel their patients on
intrauterine contraception and to have it available in
their practices. Recent research has shown that the
levonorgestrel-releasing intrauterine system can be used
for nulliparous women, although clinicians do not generally provide it and the patient information on the
product recommends that the woman have a child.9,16,17
This study showed that fewer than half of providers
would offer intrauterine contraception to nulliparous
women, although ACOG has concluded that the
method is appropriate for this population as long as the
patient is at low risk for sexually transmitted diseases.3
Likewise, nearly 70% believed that women with previous ectopic pregnancies were not eligible for intrauterine contraception, also contrary to ACOG and WHO
recommendations.3,15
Only one third viewed immediate postpartum patients as potential intrauterine contraception candidates.
Immediate postpartum insertions are done within 48
hours of delivery but usually directly after the placenta is
out. Providers have been reluctant to insert intrauterine
contraception in postpartum women for fears of increased risk of perforation or expulsion. However,
women are often highly motivated for contraception at
the time of birth, and the discomfort of insertion is
diminished postpartum. Research has documented unintended pregnancies during the waiting period for
interim insertions, showing that up to 40% of women
requesting intrauterine contraception are lost in this
period, sometimes because providers discourage them
from intrauterine contraceptive use.18,19 Postplacental
insertion, that is within 10 minutes of placental expulsion, has been shown to be safe and acceptable to
women and is a promising area for future research and
practice.20 In this study, only 39% of providers considered postabortion patients to be intrauterine contraception candidates, although the demonstrated need for
contraception at that time is clear; half of the women in
the United States having abortions are having repeat
abortions.21 A large World Health Organization study of

Provider Practices With Intrauterine Contraception

OBSTETRICS & GYNECOLOGY

immediate post first trimester abortion intrauterine contraception insertions showed no increased risk of infection and low expulsion rates, and a Cochrane review of
postabortion insertions found them to be safe and
practical.22,23
Research also has indicated that even women at risk
of infections and those who are already HIV positive
may be able to benefit from intrauterine contraception,
although most providers would not consider them as
candidates. A small body of research has begun to
inquire about the use of intrauterine contraception in
HIV-positive women, even in developing country settings, and has found promising results.24 –27 One study
found that providers in Africa (Zimbabwe) might be
open to the use of intrauterine contraception for women
at high risk of HIV,28 although training efforts and other
interventions to increase insertions have not yet been
launched. Further intrauterine contraception research is
needed to better understand client eligibility, particularly
among immediate postcesarean or vaginal delivery and
post second trimester abortion patients, and use by HIVinfected women.
A limitation with these results is that they may not
apply to all contraceptive clinicians in the publicly
funded program, because survey respondents could
have different approaches to intrauterine contraception
provision than nonrespondents (although they did have
similar numbers of intrauterine contraception clients).
Another limitation of this study is that the data were
collected from a survey administered at one point in
time, so that we cannot measure causality, only association. It is likely that causality does not only go in one
direction; that is, the providers who are able to offer
accurate counseling and evidence-based services are
those who have more experience. However, the one
survey item that does point to a temporal effect is
training in insertions during residency and subsequently
increased provision in practice. Whereas this study
showed ob-gyn physicians were likely to be trained,
family practice physicians and advance practice clinicians had far less training. A promising note was that
younger physicians were more likely to be trained and
to offer intrauterine contraception at their practices.
Training, not only in insertions but in basic method
characteristics, is necessary to improve intrauterine contraception services. Incorrect knowledge about method
benefits, contraindications, side effects, and appropriate
candidates may deter providers from recommending
the method to patients or may cause them to give faulty
information. Although more than 90% of these providers thought their patients were receptive to learning

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about intrauterine contraception, far fewer had integrated it into their contraceptive services. As with providers, misconceptions about intrauterine contraception
limit acceptance by patients.29,30 Results show that even
among these high-volume contraceptive providers,
many were not familiar with the overall decrease in
blood loss and improved dysmenorrhea associated with
the levonorgestrel-releasing intrauterine system. Similarly, a significant minority did not emphasize the
increased bleeding that can occur with the Copper T
380A. Among U.S. women who do choose intrauterine contraception, a main reason for discontinuation
is increased menstrual bleeding.29 Accurate information about the bleeding patterns associated with the
different intrauterine contraceptives would help providers improve their recommendations and would
also help women in their selections.
Improved intrauterine contraception provision
requires medical education as well as training.13,31
Specifically, provider education should involve evidence-based guidelines that emphasize safety and
insertion techniques and should include not only
ob-gyns and women’s health care providers, but all
providers offering family planning counseling and
services.32–34 In addition, less restrictive, evidencebased criteria for intrauterine contraception candidate selection should be developed and promoted.9
Patient counseling should ensure proper knowledge
and expectations of the method to increase adherence.35 Clinical training is also necessary, especially
to alleviate concerns about perforations from postpartum insertions or expulsions from incorrect
placement in postabortion insertions.19,22 Results
from an intervention to use a checklist with the new
medical eligibility criteria of the World Health
Organization showed that a checklist was not sufficient to change providers’ reliance on outdated
knowledge about the intrauterine contraception.36
A randomized trial likewise showed that provider
education, without hands-on training, was insufficient to change practice.37
Finally, the issue of insurance coverage and reimbursements is a large obstacle for those health care
providers who were actually trained and had experience offering intrauterine contraception but then
stopped. Coverage of all contraceptive methods is a
health policy need in the United States, but particularly for those methods that are expensive to pay
out-of-pocket but confer many years of protection.
The abortion rate in the United States is approximately three times higher than that of Western European countries. To prevent unintended pregnancy,

Provider Practices With Intrauterine Contraception

1367

improved use of effective contraception is needed.
Intrauterine contraception is an extremely effective
and safe method that is far underutilized. It is also the
most cost-effective method of reversible contraception.38 Unfortunately, our study showed health care
provider knowledge and practices continue to reflect
erroneous views and unrealistic risk perceptions; current practice does not reflect the body of scientific
evidence. By addressing these deficiencies in provider
perceptions and practices, we can offer women in the
United States greater protection against unintended
pregnancy, similar to that of women in other industrialized countries where intrauterine contraception
use is more frequent.
REFERENCES
1. Finer LB, Henshaw SK. Disparities in rates of unintended
pregnancy in the United States, 1994 and 2001. Perspect Sex
Reprod Health 2006;38:90–6.
2. Trussell J. The essentials of contraception: efficacy, safety, and
personal considerations. In: Hatcher RA, Trussell J, Nelson
AL, Cates C, Guest F, Kowal D, eds. Contraceptive Technology. 18 ed. New York (NY): Ardent Media; 2004:221–52.
3. Clinical management guidelines for obstetrician-gynecologists.
Intrauterine device. ACOG practice bulletin No. 59. American
College of Obstetricians and Gynecologists. Obstet Gynecol
2005;105:223–32.
4. United Nations Department of Economic and Social Affairs
Population Division. World contraceptive use 2005. Available at:
http://www.un.org/esa/population/publications/contraceptive
2005/2005_World_Contraceptive_files/WallChart_WCU2005.
pdf. Retrieved June 19, 2007.
5. Sivin I. IUDs and ectopic pregnancy [French]. Contracept
Fertil Sex (Paris) 1983 Dec;11:1287–94.
6. Grimes D. Intrauterine device and upper-genital-tract infection. Lancet 2000;356:1013–9.
7. Kimble-Haas SL. The intrauterine device: dispelling the
myths. Nurse Pract 1998;23:58, 63–9, 73.

Francisco, CA, 2005. Available at http://www.familypract.org/
_resources/documents/0203.pdf. Retrieved April 8, 2008.
15. World Health Organization. Medical eligibility criteria. Geneva:
WHO; 2004.
16. Prager S, Darney PD. The levonorgestrel intrauterine system
in nulliparous women. Contraception 2007;75:S12–5.
17. Suhonen S, Haukkamaa M, Jakobsson T, Rauramo I. Clinical
performance of a levonorgestrel-releasing intrauterine system
and oral contraceptives in young nulliparous women: a comparative study. Contraception 2004;69:407–12.
18. Ogburn J, Espey E, Stonehocker J. Barriers to intrauterine
device insertion in postpartum women. Contraception 72;
2005:426–9.
19. Grimes D, Schulz K, Van Vliet H, Stanwood N, Lopez L.
Immediate post-partum insertion if intrauterine devices.
Cochrane Database of Systematic Reviews 2001; Art. No.:
CD003036. DOI: 10.1002/14651858.CD003036.
20. Celen S, Möröy P, Sucak A, Aktulay A, Danisman N. Clinical
outcomes of early postplacental insertion of intrauterine contraceptive devices. Contraception 2004;69:279–82.
21. Jones R, Singh S, Finer L, Forhwirth L. Repeat abortion in the
United States: Guttmacher Institute; 2006. Available at http://
www.guttmacher.org/pubs/2006/11/21/or29.pdf. Retrieved April
4, 2008.
22. Grimes D, Lopez L, Schulz K, Stanwood N. Immediate
postabortal insertion of intrauterine devices. Cochrane Database of Systematic Reviews 2004; Art. No.: CD001777. DOI:
10.1002/14651858.CD01777.pub2.
23. Li CF, Lee SS, Pun TC. A pilot study on the acceptability of
levonorgestrel-releasing intrauterine device by young, single,
nulliparous Chinese females following surgical abortion. Contraception 2004;69:247–50.
24. Richardson BA, Morrison CS, Sekadde-Kigondu C, Sinei SK,
Overbaugh J, Panteleeff DD, et al. Effect of intrauterine device use
on cervical shedding in HIV-1 DNA. AIDS 1999;13:2091–7.
25. Morrison CS, Sekadde-Kigondu C, Sinei SK, Weiner DH,
Kwok C, Dokonya D. Is the intrauterine device appropriate
contraception for HIV-1-infected women? Br J Obstet Gynecol
2001;108:784–90.

8. Darney PD. Time to pardon the IUD? N Engl J Med 2001;
345:608–10.

26. Heikinheimo O, Lehtovirta P, Suni J, Paavonen J. The levonorgestrel-releasing intrauterine system (LNG-IUS) in HIV-infected
women-effects on bleeding patterns, ovarian function and genital
shedding of HIV. Hum Reprod 2006;21:2857–61.

9. Stanwood NL, Garrett JM, Konrad TR. Obstetrician-gynecologists and the intrauterine device: a survey of attitudes and
practice. Obstet Gynecol 2002;99:275–80.

27. Lehtovirta P, Paavonen J, Heikinheimo O. Experience with the
levonorgestrel-releasing intrauterine system among HIV-infected women. Contraception 2007;75:37–9.

10. Lee NC, Rubin GL, Ory HW, Burkman RT. Type of intrauterine device and the risk of pelvic inflammatory disease.
Obstet Gynecol 1983;62:1–6.

28. Gaffikin L, Phiri A, McGrath J, Zinanga A, Blumenthal PD.
Provider attitudes toward IUC provision in Zimbabwe: perception of HIV risk and training implications. Adv Contracept
1998;14:27–39.

11. Shelton JD. Risk of clinical pelvic inflammatory disease attributable to an intrauterine device. Lancet 2001;357:443.
12. Hubacher D, Lara-Ricalde R, Taylor DJ, Guerra-Infante F,
Guzman-Rodriguez R. Use of copper intrauterine devices and
the risk of tubal infertility among nulligravid women. N Engl
J Med 2001; 345:561–7.
13. Postlethwaite D, Shaber R, Mancuso V, Flores J, Armstrong
MA. Intrauterine contraception: evaluation of clinician practice patterns in Kaiser Permanente Northern California. Contraception 2007;75:177–84.
14. UCSF Bixby Center for Reproductive Health Research &
Policy. Family PACT Program Report Fiscal Year 03/04. San

1368

Harper et al

29. Mishell DR Sulak PJ. The IUD: dispelling the myths and
assessing the potential. Dialogues Contracept 1997;5:1–4.
30. Cheng D. The intrauterine device: still misunderstood after all
these years. South Med J 2000;93:859–64.
31. Kooiker CH, Scutchfield FD. Barriers to prescribing the Copper T 380A intrauterine device by physicians. West J Med
1990;153:279–82.
32. Espey E, Ogburn T, Espey D, Etsitty V. IUD-related knowledge, attitudes and practices among Navajo Area Indian
Health Service providers. Perspect Sex Reprod Health 2003;
35:169–73.

Provider Practices With Intrauterine Contraception

OBSTETRICS & GYNECOLOGY

33. Rivera R, Best K. Current opinion: consensus statement
on intrauterine contraception. Contraception 2002;65:
385–8.
34. Farr G, Rivera R, Amatya R. Non-physician insertion of
IUDs: clinical outcomes among TCu380A insertions in
three developing-country clinics. Adv Contracept 1998;14:
45–57.

36. Wesson J, Gmach R, Gazi R, Ashraf A, Me´ndez JF, Olenja J,
et al. Provider views on the acceptability of an IUD checklist
screening tool. Contraception 2006;74:382–8.
37. Hubacher D, Vilchez R, Gmach R, Jarquin C, Medrano J,
Gadea A, et al. The impact of clinician education on IUD
uptake, knowledge and attitudes: results of a randomized trial.
Contraception 2006;73:628–33.

35. Freeman S. Nondaily hormonal contraception: considerations
in contraceptive choice and patient counseling. J Am Acad
Nurse Pract 2004;16:226–38.

38. Chiou CF, Trussell J, Reyes E, Knight K, Wallace J, Udani J, et
al. Economic analysis of contraceptives for women. Contraception 2003;68:3–10.

VOL. 111, NO. 6, JUNE 2008

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NIH Public Access
Author Manuscript
Contraception. Author manuscript; available in PMC 2011 February 1.

NIH-PA Author Manuscript

Published in final edited form as:
Contraception. 2010 February ; 81(2): 112. doi:10.1016/j.contraception.2009.08.002.

Intrauterine contraception in Saint Louis: A Survey of Obstetrician
and Gynecologists’ knowledge and attitudes
Tessa Madden*, Jenifer E. Allsworth, Katherine J. Hladky, Gina M. Secura, and Jeffrey F.
Peipert
1Washington University in Saint Louis School of Medicine, Department of Obstetrics and
Gynecology, Saint Louis, MO 63110

Abstract

NIH-PA Author Manuscript

Background—Many obstacles to intrauterine contraception use exist, including provider and
patient misinformation, high upfront cost, and clinician practice patterns. The aim of our study was
to investigate knowledge and attitudes about intrauterine contraception among obstetricians and
gynecologists in the area of Saint Louis.
Study Design—We mailed a self-administered, anonymous survey to 250 clinicians who provide
obstetric and gynecologic care in Saint Louis City and County which included questions about
demographics, training, family planning visits, and intrauterine contraceptive knowledge and use.
Results—The overall survey response rate among eligible clinicians was 73.7%. Clinicians who
had recently finished training or saw higher numbers of contraceptive patients per week were more
likely to insert intrauterine contraception than clinicians who completed training prior to 1989 or saw
fewer contraceptive patients. Several misconceptions among clinicians were identified, including an
association between intrauterine contraceptives and an elevated risk of pelvic inflammatory disease.
Conclusions—Physician misconceptions about the risks of intrauterine contraception continue to
occur. Improved clinician education is greatly needed to facilitate the use of these highly effective,
long-acting, reversible methods of contraception.
Keywords
Intrauterine contraception; intrauterine device; clinician knowledge; obstacles; survey

NIH-PA Author Manuscript

1. Introduction
Unintended pregnancy continues to be a substantial public health problem in the United States;
over 3 million unintended pregnancies occur annually with poor and minority women
disproportionately affected. Inconsistent and incorrect use of contraception is associated with
unintended pregnancy [1]. Intrauterine contraception (IUC) is safe, highly effective with failure
rates of less than 1%, [2] and does not require regular compliance from the user. Two types of
IUC are available in the United States, the levonorgestrel intrauterine system (Mirena®, Bayer

© 2009 Elsevier Inc. All rights reserved.
*Corresponding Author: Tessa Madden, MD, MPH Washington University in Saint Louis School of Medicine, Department of Obstetrics
and Gynecology, 4533 Clayton Ave, Box 8219, Saint Louis, MO 63110, Tel: 314 747 6495, Fax: 314 747 4019, [email protected].
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers
we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting
proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could
affect the content, and all legal disclaimers that apply to the journal pertain.

Madden et al.

Page 2

NIH-PA Author Manuscript

HealthCare Pharmaceuticals, Wayne, NJ) and the copper T380A (Paragard®, Barr
Pharmaceuticals, Montvale, NJ). These methods are associated with minimal side effects [3,
4], and have been shown to be safe when inserted immediately post-abortion [5,6]. Despite the
many advantages of this “forgettable” contraception, only 1.3% of women aged 15 to 44 years
currently use IUC [7]. In fact, use in the United States is substantially lower than many
European and Asian countries with reported rates as high as 27% in Norway [8] and 30% in
China [9]. Factors that contribute to the low uptake of IUC in the United States include
knowledge and attitudes among clinicians and women, practice patterns among providers, and
high initial cost.
A 2002 survey of Fellows of the American College of Obstetricians and Gynecologists
regarding knowledge, attitudes, and practices about IUC found that while 95% of respondents
agreed IUC was safe, the majority stated that nulliparous patients, and patients with a history
of sexually transmitted infections (STIs) and pelvic inflammatory disease (PID) were not
candidates for IUC [10]. Another study of over 800 California family planning providers found
that fewer than 50% of respondents considered nulliparous women, teenagers, women who
were immediate postpartum or postabortion, or women with a history of PID within the past
5 years to be candidates for IUC [11].

NIH-PA Author Manuscript

Increased use of highly effective methods of contraception such as IUC has been shown to
decrease the rate of unintended pregnancies [12]. However, to increase uptake, physicians must
be willing to provide these most effective methods of contraception to a wide range of patients.
The purpose of this cross-sectional survey was to describe local clinician attitudes, knowledge
and practice patterns about IUC; factors greatly influencing access to these contraceptive
methods.

2. Materials and methods
We created a written, self-administered questionnaire to assess knowledge and attitudes about
IUC among practicing providers of obstetrics and gynecology in the Saint Louis area. The
questionnaire included demographics items such as age, race, and ethnicity, as well as questions
about graduate medical training, contraceptive patients seen, and willingness to insert IUC.
The survey was pretested among three clinician researchers.

NIH-PA Author Manuscript

Our goal was to obtain 100 completed surveys which would represent approximately 30% of
practicing obstetrician-gynecologist clinicians in the area. Prior response rates for surveys
mailed to physicians have been reported to be 34 to 51% [13,14]; we estimated a 40% response
rate, requiring [250] mailed surveys We compiled a list of providers of obstetrics and
gynecology in the Saint Louis area using publically available data sources such as faculty
listings, the yellow pages of the telephone book, and Internet listing of obstetriciangynecologist offices. We then performed a simple random sample using computer-generated
numbers and mailed 250 questionnaires to the randomly selected clinicians between April and
June of 2008. Surveys were mailed a second time to non-responders. All mailings contained a
$20 gift card as an incentive.
All respondents were practicing in Saint Louis City or County, English-speaking, and willing
to complete the survey. Written consent was waived, and completion and return of the survey
implied consent to participate. This study was approved by the Washington University in Saint
Louis Human Research Protections Office.
2.1. Statistical methods
Clinician characteristics were compared using the Ȥ2 test statistic. Unfortunately, we had no
information regarding the characteristics of the clinicians who did not respond to the survey.

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Low IUC rate was defined as having both inserted IUC and referred for IUC insertion zero to
10 times in the past year. We created this variable to capture clinicians who were both inserting
none or few IUCs and referring none or few patients to another provider. Fisher exact tests
were used for contingency tables with small cell size (N 5). Since the outcomes of interest
were common (> 10%), odd ratios are computed using Poisson regression as logistic regression
would overestimate the odd ratios [15,16]. Univariable and multivariable odd ratios were
estimated for the outcomes of interest. Statistically significant covariates in the univariable
model were included in the final model. All statistical analyses were conducted using SAS
version 9.1 (SAS Institute Inc., Cary, NC).

3. Results
3.1. Clinician characteristics
A total of 137 (54.8%) surveys were competed and returned. Fig. 1 shows the outcome of the
250 mailed surveys. Our final response rate among eligible clinicians with a valid mailing
address was 73.7%. Table 1 shows the characteristics of the clinician respondents. The mean
age of respondents was 49 years and they were mostly physicians (98.5%), predominantly
white, and non-Hispanic.
3.2. IUC training and use

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Thirty-six percent of clinicians were not trained in IUC insertion during their residency or
advanced practice nurse core clinical training. Clinicians who trained at a Catholic institution
were less likely to have received training in insertion during residency than clinicians who
trained at secular institutions (OR 0.49 95% CI 0.36-0.68). Table 2 shows factors associated
with low IUC rate; clinicians who finished training after 1999 (OR 0.13, 95% CI 0.02-0.85)
or who saw a greater number of contraceptive patients per week (OR 0.36, 95% CI 0.19-0.69)
were less likely to have low rates of IUC insertion and referral than clinicians who finished
training before 1989 or saw fewer contraceptive patients.

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Eighteen percent of respondents reported that they “always” discussed IUC with their patients,
76% reported that they discussed IUC most or some of the time. The majority of providers
(67.9%) reported they had counseled more than 50 patients about IUC in the past year, and
almost 66% reported that they had inserted greater than 10 IUCs in the past year. Less than 2%
reported not counseling patients about intrauterine contraception within the past year and
12.4% reported not inserting IUC. Most respondents (79.6%) reported that they did not refer
patients for IUC insertion; while 17.6% reported that they had referred 1 or more patients for
IUC insertion. Only 2.9% of providers had neither inserted nor referred for IUC insertion in
the past year. Forty percent of clinicians reported “always” and 52% reported “sometimes”
testing for gonorrhea and chlamydia prior to insertion of IUC.
3.3. Clinician knowledge
Most respondents “strongly agreed” or “agreed” that IUC was safe (98.5%); however, 29% of
clinicians reported that IUC causes an increased risk of PID other than at the time of insertion.
The majority of clinicians correctly stated that antibiotics should not be given prophylactically
at the time of insertion (78.1%), and that IUC does not cause abortion (86.1%). Seventy-eight
percent of clinicians routinely recommended a follow-up visit after insertion. Table 3 shows
the typical side effects emphasized by the clinician for each IUC type.
When asked about patient characteristics and the appropriateness of IUC, 62.0% agreed IUC
was appropriate for a nulliparous patient; 30.7% for a teenaged patient, 45.3% for a patient
with a STI in the past 2 years, 36.5% for a patient with PID in the past 5 years, and 36.5% for
a patient in a non-monogamous relationship. The vast majority of clinicians (97.8%) reported

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Madden et al.

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that they would offer IUC to a 35-year-old patient, who was married, monogamous and had 3
children; 67.1% reported they would offer intrauterine contraception to a 30 year old who was
unmarried, had 2 children, and had a boyfriend; 49.6% said they would offer IUC to a 17-yearold who was unmarried, monogamous and had 1 child. Only 19% would be willing to offer
IUC to an unmarried 17-year-old who had never been pregnant.

4. Discussion

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This survey was designed to collect information about providers’ attitudes and knowledge
about IUC. Our results suggest that physicians who completed training after 1999 are more
likely to insert IUC than physicians who completed training prior to 1989. The overwhelming
majority of clinicians (98%) believed IUC is safe, however, almost one third reported
incorrectly that IUC is associated with an increased risk of PID other than the increased periinsertional risk. Table 3 also suggests some providers may not appropriately emphasize the
most common side effects encountered with IUC; 75.9% reported counseling patients about
an increase in spotting and breakthrough bleeding with both levonorgestrel IUC (LNG-IUC)
and copper IUC (copper-IUC); this side effect can be seen with both types of IUC; however,
is more commonly associated with LNG-IUC and is typically limited to the first 3 to 6 months
of use. Eleven percent reported counseling patients about cessation of menstruation with both
LNG-IUC and copper-IUC; however, copper-IUC should not cause amenorrhea. Thirty-three
percent reported that both LNG-IUC and copper-IUC can be associated with painful
menstruation; however, the use of LNG-IUC has been shown to decrease the incidence of
menorrhagia and dysmenorrheal [17].
Most of the clinicians surveyed were willing to offer IUC to a 35-year-old multiparous patient
who is married. However, we find it worrisome that the number of clinicians who will offer
IUC declines dramatically with patients of decreasing age, parity, and non married status. For
example, only 19% would offer IUC to a 17 year old who is not married and has never been
pregnant. This suggests the misconceptions about associations between IUC, PID, and
infertility continue to persist. The World Health Organization states only current cervicitis and
recent PID within 3 months are contraindications to IUC. They do not consider age less than
20 years or nulliparity to be contraindications [18]. A recent editorial identified limited
education and outdated beliefs as one of the main provider-based barriers to contraception
among teens and young adults and called for the increased education and training of healthcare providers [19]. Since young women are at high risk for unintended pregnancy, it is
imperative that we increase this population’s access to the most effective methods of
contraception.

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Our study has similarities to the study by Stanwood et al. [10] However, there are several
important differences: 1) The prior study was administered before the introduction of LNGIUC in the United States; in comparison, our survey obtains knowledge and attitudes about
both types of IUC available, 2) In 2005, the copper-IUC FDA labeling was liberalized to not
restrict insertion in nulliparous women, and in the immediate postabortion and postpartum time
period. In addition, having more than one sexual partner was removed as a contraindication.
Since we surveyed physicians after the new labeling was introduced, our survey adds new
information about clinician knowledge about and attitudes towards IUC.
This study is limited by its relatively small sample size and has limited power to detect
statistically significant differences. Additionally, because our findings are from a single
geographical area, they may not be generalizable to clinicians in other geographical regions.
Strengths of our study include a random sample of practicing obstetrician-gynecologists rather
than a convenience sample, and a high response rate, which strengthens the generalizability of
our findings.

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Page 5

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Despite the introduction of LNG-IUC and liberalization of the current package labeling of
copper-IUC, our survey has identified several potential barriers that remain to increasing the
use of IUC: 1) inadequate training of clinicians (more than one-third of physicians were not
trained in residency); 2) misperceptions regarding appropriate candidates for IUC; and 3)
inaccurate knowledge of IUC and possible side effects. These barriers may influence
contraceptive counseling and subsequent method choice. Targeted education and training
programs to clinicians should dispel these pervasive myths and inaccuracies and encourage the
use of these highly effective and safe contraceptive methods.

Acknowledgments
This research was supported by a grant from an anonymous foundation. Individual investigators (JP and JA) were
supported, in part, by a Mid-career Investigator Award in Women’s Health Research (K24 HD01298) and by the
Clinical and Translational Science Awards (UL1RR024992) and Grant Number KL2RR024994 from the National
Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) and NIH Roadmap
for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the
official view of NCRR or NIH. Information on NCRR is available at http://www.ncrr.nih.gov/. Information on Reengineering the Clinical Research Enterprise can be obtained from
http://nihroadmap.nih.gov/clinicalresearch/overview-translational.asp.
We would like to thank Cynthia Harper for sharing her previously developed survey questions and Younathan Abdia
for his assistance with statistical analysis.

NIH-PA Author Manuscript

References

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1. Finer LB, Henshaw SK. Disparities in rates of unintended pregnancy in the United States, 1994 and
2001. Perspect Sex Reprod Health 2006;38:90–96. [PubMed: 16772190]
2. Trussell, J. Contraceptive Efficacy. In: Hatcher, RATJ.; Nelson, AL.; Cates, W.; Stewart, FH.; Kowal,
D., editors. Contraceptive Technology. New York (NY): Ardent Media; 2007. p. 747-760.
3. Suhonen S, Haukkamaa M, Jakobsson T, Rauramo I. Clinical performance of a levonorgestrel-releasing
intrauterine system and oral contraceptives in young nulliparous women: a comparative study.
Contraception 2004;69:407–412. [PubMed: 15105064]
4. Baldaszti E, Wimmer B, Loschke K. Acceptability of the long-term contraceptive levonorgestrelreleasing intrauterine system (Mirena): a 3-year follow-up study. Contraception 2003;67:87–91.
[PubMed: 12586318]
5. Ortayli N, Bulut A, Sahin T, Sivin I. Immediate postabortal contraception with the levonorgestrel
intrauterine device, Norplant, and traditional methods. Contraception 2001;63:309–314. [PubMed:
11672552]
6. Pakarinen P, Toivonen J, Luukkainen T. Randomized comparison of levonorgestrel- and copperreleasing intrauterine systems immediately after abortion, with 5 years' follow-up. Contraception
2003;68:31–34. [PubMed: 12878284]
7. Chandra A, Martinez GM, Mosher WD, Abma JC, Jones J. Fertility, family planning, and reproductive
health of U.S. women: data from the 2002 National Survey of Family Growth. Vital Health Stat
2005;23:1–60.
8. Sonfield A. Popularity Disparity: Attitudes about the IUD in Europe and the United States. Guttmacher
Policy Review 2007;10:19–24.
9. Wang D. Contraceptive failure in China. Contraception 2002;66:173–178. [PubMed: 12384206]
10. Stanwood NL, Garrett JM, Konrad TR. Obstetrician-gynecologists and the intrauterine device: a
survey of attitudes and practice. Obstet Gynecol 2002;99:275–280. [PubMed: 11814509]
11. Harper CC, Blum M, de Bocanegra HT, et al. Challenges in translating evidence to practice: the
provision of intrauterine contraception. Obstet Gynecol 2008;111:1359–1369. [PubMed: 18515520]
12. Goodman S, Hendlish SK, Benedict C, Reeves MF, Pera-Floyd M, Foster-Rosales A. Increasing
intrauterine contraception use by reducing barriers to post-abortal and interval insertion.
Contraception 2008;78:136–142. [PubMed: 18672115]

Contraception. Author manuscript; available in PMC 2011 February 1.

Madden et al.

Page 6

NIH-PA Author Manuscript

13. Hogben M, Wimberly YH, Moore S. Estimating dissemination of Centers for Disease Control and
Prevention Sexually Transmitted Disease Treatment Guidelines from a survey of physicians. Int J
STD AIDS 2007;18:318–320. [PubMed: 17524191]
14. McCormick D, Woolhandler S, Bose-Kolanu A, Germann A, Bor DH, Himmelstein DU. U.S.
Physicians' Views on Financing Options to Expand Health Insurance Coverage: A National Survey.
J Gen Intern Med 2009;29
15. Zhang J, Yu KF. What's the relative risk? A method of correcting the odds ratio in cohort studies of
common outcomes. JAMA 1998;280:1690–1691. [PubMed: 9832001]
16. McNutt LA, Wu C, Xue X, Hafner JP. Estimating the relative risk in cohort studies and clinical trials
of common outcomes. Am J Epidemiol 2003;157:940–943. [PubMed: 12746247]
17. Varma R, Sinha D, Gupta JK. Non-contraceptive uses of levonorgestrel-releasing hormone system
(LNG-IUS)--a systematic enquiry and overview. Eur J Obstet Gynecol Reprod Biol 2006;125:9–28.
[PubMed: 16325993] WHO. Medical eligibility criteria for contraceptive use. Third edition2008
[Accessed 10/31/08]. http://www.who.int/reproductive-health/publications/mec/iuds.htmlBrown
SS, Burdette L, Rodriguez P. Looking inward: provider-based barriers to contraception among teens
and young adults. Contraception 2008;78:355–357. [PubMed: 18929730]

NIH-PA Author Manuscript
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Page 7

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Figure 1.

Schematic of mailed and returned questionnaires.

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Page 8

Table 1

Characteristics of the 137 Clinician Respondents

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Characteristic

N (%)

Job Title
ᒚPhysician

135 (98.8)

ᒚAdvanced Practice Nurse

2 (1.5)

Race
ᒚWhite

117 (85.4)

ᒚBlack

6 (4.4)

ᒚOther

14 (10.2)

Ethnicity
ᒚHispanic

6 (4.4)

Year Completed Residency
ᒚBefore 1989

59 (43.7)

ᒚ1989 – 1999

55 (40.7)

ᒚAfter 1999

21 (15.6)

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Catholic Institution for Residency
ᒚYes

61 (55.5)

ᒚNo

76 (44.5)

IUC Insertion Included During Residency
ᒚYes

88 (64.2)

ᒚNo

49 (35.8)

Avg. Number of Contraceptive Patients/Week
ᒚ0 – 25

45 (35.43)

ᒚ26 – 50

63(49.61)

ᒚ51 +

19(14.96)

ᒚNot Ascertained

10 (7.30)

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Table 2

Univariable and Multivariable Models of Provider Characteristics Associated with Low IUC Rate

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Characteristic

Univariable
OR (95%CI)

Multivariable
OR (95% CI)*

Reference

ᒚ1989 – 1999

0.66 (0.3 –1.17)

0.62 (0.36–1.07)

ᒚAfter 1999

0.13 (0.02–0.92)

0.13 (0.02–0.85)

ᒚYes

0.68 (0.37–1.26)

1.23 (0.71–2.13)

ᒚNo

Reference

ᒚYes

1.53 (0.78–3.01)

1.16 (0.62–2.15)

ᒚNo

Reference

ᒚ0 – 25

Reference

ᒚ26 – 50

0.36 (0.19–0.69)

0.34 (0.19–0.65)

ᒚ51 +

0.24 (0.06–0.93)

0.20 (0.05–0.77)

Year residency completed
ᒚBefore 1989

Catholic institution

Trained to insert IUC in residency

Average Contraceptive Patients
Seen per Week

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Adjusted for year residency completed, training at a Catholic institution, training in IUC insertion during residency, and average number of
contraceptives seen per week
IUC – Intrauterine contraception

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Table 3

Clinician Report of Side Effects Commonly Associated with Levonorgestrel IUC and Copper IUC

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Side Effect

Spotting or breakthrough
bleeding

LNG-IUC Only

%
Copper-IUC
Only

Both

Neither

15.3

4.4

75.9

8.7

Heavy or prolonged menstruation

0.7

63.5

24.8

8.8

No menstruation

83.2

11.0

3.7

Painful menstruation

0.7

46.0

33.6

17.5

LNG-IUC – levonorgestrel intrauterine contraception; Copper-IUC – copper intrauterine contraception

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Contraception 74 (2006) 389 – 393

Original research article

Conformity with current guidelines on oral contraceptive prescribing
for breastfeeding women: a New Mexico survey
Eve Espeya,4, Tony Ogburna, Larry Leemanb, Shilpa Reddyc, Carisa Leea, Clifford Quallsd
a
Department of Obstetrics and Gynecology, University of New Mexico, Albuquerque, NM 87131, USA
Department of Family and Community Medicine, University of New Mexico, Albuquerque, NM 87131, USA
c
University of New Mexico, School of Medicine, Albuquerque, NM 87131, USA
d
Clinical Research Center, University of New Mexico, Albuquerque, NM 87131, USA
Received 18 April 2006; revised 13 June 2006; accepted 20 June 2006

Abstract
Background: National and international contraceptive guidelines reflect expert opinion that recommends against the use of estrogencontaining hormonal contraception in the early postpartum period. This study was undertaken to estimate providers’ practices in prescribing
hormonal contraception to breastfeeding women.
Methods: A 19-item survey was mailed to 397 obstetrician gynecologists, midwives and family physicians in the state of New Mexico. The
survey included items covering attitudes about the impact of hormonal contraception on breastfeeding and prescribing practices. One hundred
ninety-nine (50%) providers completed the survey.
Results: The majority (70%) of providers prescribe progestin-only contraceptive methods to breastfeeding women within the first 6 weeks. Despite
these recommendations, a sizable minority of providers prescribe combined pills in the early postpartum period: 27% of providers have prescribed
combined pills and 13% of providers, mostly those in a university setting, routinely recommend them within the first 6 weeks postpartum.
Conclusion: Most providers follow expert recommendations regarding the initiation of hormonal contraception for breastfeeding women.
D 2006 Elsevier Inc. All rights reserved.
Keywords: Hormonal contraceptives; Breastfeeding; Prescribing

1. Introduction
A long-standing convention cautions breastfeeding
women against using combined oral contraceptives (OCs).
A number of organizations involved in women’s health care
support this guideline, including the American College of
Obstetricians and Gynecologists (ACOG), the World Health
Organization (WHO) and the International Planned Parenthood Federation (IPPF). The ACOG’s practice bulletin on
the use of contraception in women with coexisting medical
conditions states that, bCombination OCs are not recommended as the first choice for breastfeeding mothers
because of the negative effect of contraceptive doses of
estrogen on lactation. The estrogenic component of combination OCs can reduce the volume of milk production and
the caloric and mineral content of breast milk in lactating
womenQ [1]. In contrast, progestin-only OCs are considered
first line for lactating women.
4 Corresponding author. Tel.: +1 505 272 6309; fax: +1 505 272 6385.
E-mail address: [email protected] (E. Espey).
0010-7824/$ – see front matter D 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.contraception.2006.06.007

The WHO, in its 2004 medical eligibility criteria for
contraceptives, states that combined OCs are contraindicated
in the first 6 weeks of lactation, citing a btheoretical concern
that the neonate may be at risk due to exposure to steroid
hormones during the first 6 weeks postpartum.Q The WHO
states that the use of combined OCs in breastfeeding women
from 6 weeks to 6 months postpartum is a practice for which
harm probably outweighs the benefits, as the buse of
combined oral contraceptives during breastfeeding diminishes the quantity of breast milk, decreases the duration of
lactation and may thereby adversely affect the growth of the
infantQ [2]. The IPPF’s opinion is similar to that of the WHO,
but extends the caution even further, viewing combined OC
use prior to 6 months postpartum in breastfeeding women as
contraindicated, citing diminished quantity of breast milk
and decreased duration of lactation [3].
These recommendations are based on scanty and
flawed research. A recent Cochrane collaboration review
concludes that evidence is insufficient to reach conclusions about the impact of hormonal contraception on

390

E. Espey et al. / Contraception 74 (2006) 389 – 393

Table 1
Demographic characteristics of the three groups of survey respondents (OB-GYNs, CNMs and FPs)
Gender [n (%)]
Male
Female
Deliveries per year [n (%)]
1–50
N 50
Type of practice [n (%)]
Solo–group
Health maintenance organization
University
Other
Age in years [mean (range)]
Years in practice [mean (range)]
a
b

OB-GYN (n = 63)

CNM (n = 65)

FP (n = 71)

30
33 (52)

0
65 (100)

41
28 (41)

b .001a

9 (14)
55 (86)

11 (17)
52 (83)

54 (79)
14 (21)

b .001a

42
9
15
2
47
15

38 (59)
8 (13)
11 (17)
7 (11)
48 (28, N 60)
11 (6 –18)

33
0
16
17
43
10

b .001a

(65)
(9)
(23)
(3)
(33, N 60)
(9–20)

(50)
(0)
(24)
(26)
(28, 58)
(5 –17)

.006b
.01b

Fisher’s Exact Test was used for gender, deliveries per year and type of practice.
Kruskal–Wallis test was used for mean age and years in practice.

breastfeeding [4]. As many women worldwide breastfeed
and use OCs, these recommendations have a major public
health impact. Overall, the combined pill has advantages
over the progestin-only pill: it has fewer side effects (such
as irregular bleeding), better efficacy and higher continuation rates [5]. If, however, the combined pill truly
diminishes the quantity of breast milk, then a progestinonly pill might be preferable, taking into consideration the
needs of a particular patient. As a result of the need to
balance the importance of breastfeeding with the need for
optimal contraception, some providers offer combination
pills to breastfeeding mothers. The extent of this practice
is unknown.
The purpose of this study was to estimate what types of
OCs are prescribed for postpartum breastfeeding women by
New Mexico obstetrician gynecologists (OB-GYNs), family
physicians (FPs) and certified nurse midwives (CNMs), and
to estimate differences between provider types in prescribing practices.
2. Materials and methods
A 19-item survey was designed by the authors to assess
prescribing practices for postpartum OCs. The survey was
mailed to all FPs who performed deliveries and to all OBGYNs and CNMs in the state of New Mexico in January
2005. Contact information was obtained through the
American Medical Association physician list, the CNM
state midwifery society list and a University of New Mexico
Family Practice maternity care database. Reminder postcards were sent at 2 weeks, and telephone follow-up was
used for nonresponders. All survey data remained confidential, available only to the investigators.
The survey was pretested and modified to clarify
questions based on responses from 20 OB-GYN residents.
Survey questions included demographic characteristics such
as age, years in practice, type of medical practice and
number of deliveries per year. Several questions explored
whether providers prescribe hormonal contraception to

breastfeeding women, the timing of initiation of hormonal
contraception relative to delivery and whether providers
routinely prescribe progestin-only methods, combined
methods or both. bTrue–falseQ knowledge and opinion
questions about their understanding of the impact of
hormonal contraception on milk quantity, milk quality and
infant growth were posed.
Two breastfeeding scenarios were presented as part of the
survey to determine whether providers altered their recommendations about hormonal contraception based on patient
factors that could influence the success of breastfeeding. In
the favorable scenario, the patient successfully breastfed her
other children and is breastfeeding without problems in the
hospital. In the unfavorable scenario, the patient is
primiparous and is having difficulty breastfeeding in the
hospital. Responses were categorized into four categories:
bProgestin-only methods to begin after 6 weeksQ (the
most cautious)
bProgestin-only methods to begin within 6 weeksQ
bCombined pills to begin after 6 weeksQ
bCombined pills to begin within 6 weeksQ (the least
cautious).
Additional questions included opinions about the merits of
progestin-only versus combined OCs and whether providers
who recommended progestin-only pills for breastfeeding
women switched their patients to combined pills when they
had stopped breastfeeding.
The study was approved by the Human Research Review
Committee of the University of New Mexico. All data were
analyzed using SAS package. Because data for age and
years in practice were skewed, Kruskal–Wallis tests were
used for comparisons. Fisher’s Exact Test for two-way
frequency tables was used for overall analysis, and post hoc
testing was used to determine differences between providers. For providers’ opinion questions, estimated proportions were reported with 95% confidence intervals (95%
CIs). The Generalized McNemar test was used to compare
differences in providers’ prescribing responses to two

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E. Espey et al. / Contraception 74 (2006) 389 – 393
Table 2
Providers’ opinions on the impact of combined OC pills on breastfeeding
Survey item

OB-GYN

CNM

55/58 (95) [86 – 99]
11/34 (32) [17– 51]
26/29 (90) [73 – 98]
20/33 (61) [42 –77]
45/59 (76) [63 – 86]

45/55
5/49
43/45
23/50
41/64

n yes/total n (%) [95% CI]
Combined OCs decrease milk quantity
Combined OCs decrease milk quality
Breastfeeding infants show appropriate growth
Combined OCs decrease breastfeeding duration
Combined OCs are superior to progestin-only pills

48/61
6/43
40/41
20/42
50/61

(79)
(14)
(98)
(48)
(82)

[66 –88]
[5 –28]
[87 –100]
[32 – 64]
[70 – 91]

(82)
(10)
(96)
(46)
(64)

[69 –81]
[3– 22]
[85 – 96]
[32 – 61]
[51–76]

.02a
.03a
.38
.41
.07

The proportions reported reflect those persons answering either yes or no. Each estimated proportion is followed by its 95% CI. Those answering bdid not
knowQ were excluded from the analysis.
a
CNMs were more likely than FPs or OB-GYNs to answer byesQ in post hoc testing.

different breastfeeding scenarios — one more favorable and
one less favorable.
3. Results
The survey was mailed to 397 providers in total: 160 OBGYNs, 130 CNMs and 107 FPs. We received a total of
205 surveys; 199 answered affirmatively to the first
question, bDo you perform deliveries?Q The six who did
not perform deliveries were excluded from the analysis. The
overall response rate of usable surveys was 51% (63 from
OB-GYNs, 65 from CNMs and 71 from FPs). The
demographic characteristics of the three groups of providers
appear in Table 1. The midwives were all female, creating a
difference in gender from the other two groups. OB-GYNs
and CNMs were older and have performed more deliveries
than FPs. Eighty percent of all practitioners responding to
the questionnaire were either in solo–group practice or in
university practice. OB-GYNs have been in practice longer
than the CNMs and FPs surveyed.
Providers differed in some beliefs about the impact of
combined OC pills on breastfeeding (Table 2). A majority of
providers, but significantly more CNMs, believed that
combined OCs diminished milk supply, and about half of
all providers believed that breastfeeding duration was
decreased in combined OC users. The minority of providers,
but more CNMs, believed that combined OCs affected milk
quality. Most providers believed that infants of breastfeeding mothers using combined OCs grow appropriately and
that combined pills are superior to progestin-only pills.
Only four providers, two OB-GYNs and two CNMs,
reported that they never recommend hormonal contraception
within 6 weeks or after 6 weeks postpartum. Of the
remaining providers, prescribing practices changed as a
function of time postpartum (Table 3). Within the first

6 weeks postpartum, 70% of all providers exclusively
prescribed progestin-only methods of hormonal contraception to breastfeeding women, and the majority reported that
they routinely discouraged combination pills because they
may decrease milk production. Thirty percent of providers
reported they had prescribed both progestin and combined
methods. After 6 weeks postpartum, the percentage of
providers who had ever prescribed both rose to 56%.
Although 30% had ever prescribed combined pills within
the first 6 weeks, 13% routinely recommended them in that
time frame. The majority of those who routinely recommended combined pills within the first 6 weeks were
university providers, and the major reasons they cited for the
recommendation of combination pills over progestin-only
pills were greater effectiveness and better compliance.
Ninety-six percent of OB-GYNs and CNMs versus 79%
of FPs responded that they switched women from progestinonly to combined pills when they stopped breastfeeding
(Fisher’s Exact Test, p =.003).
Providers who prescribe hormonal contraception to
breastfeeding women are more likely to prescribe in a cautious manner when faced with a less favorable breastfeeding
scenario than when faced with a more favorable scenario
(Generalized McNemar test, p= .01). Of 171 respondents,
27 prescribed more cautiously in an unfavorable scenario
versus 7 who prescribed less cautiously and 134 who remained neutral.
4. Discussion
The major finding of this survey is that most providers
prescribe progestin-only methods for hormonal contraception in breastfeeding women. A minority prescribe combined pills prior to 6 weeks postpartum, and more providers
prescribe combined pills after 6 weeks postpartum.

Table 3
Types and timing of methods prescribed by providers who indicated that they beverQ prescribed hormonal contraception to breastfeeding women
Timing

Type prescribed

OB-GYN

CNM

Within 6 weeks postpartum

Progestin methods only
Combined and progestin methods
n
Progestin methods only
Combined and progestin methods
n

34
21
55
27
29
56

53
11
64
35
28
63

37
20
57
16
44
60

After 6 weeks postpartum

(62%)
(38%)
(48%)
(52%)

(83%)
(17%)
(56%)
(44%)

Post hoc test

(65%)
(35% )

.02

OB-GYNs and FPs more likely than
CNMs to prescribe combined pills

(27%)
(73%)

.003

FPs more likely than CNMs and
OB-GYNs to prescribe combined pills

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E. Espey et al. / Contraception 74 (2006) 389 – 393

OB-GYNs were more likely than midwives or FPs to
prescribe combined pills. University providers were more
likely than nonuniversity providers to prescribe combined
pills. The majority of all providers consider combined pills
to be superior to progestin-only pills.
The fact that providers used more caution in prescribing
combined pills to women in an unfavorable breastfeeding
scenario indicates that providers do take into account the
potential negative impact of hormonal contraceptives on
breastfeeding and factor individual patients’ circumstances
into their recommendations for the type and the timing of
hormonal contraceptives.
A limitation of our study is the 49% nonresponse rate.
The main demographic data available in our database for
nonresponders were on type of practice: university versus
nonuniversity. We did find a difference in response rates
between university (88%) and nonuniversity providers
(45%; p b .001). Since university providers were more likely
to routinely recommend combined pills within 6 weeks
postpartum, we probably overestimated the total percentage
of providers who routinely recommend combined pills
within 6 weeks postpartum.
One other report in the literature examines prescribing
practices. A 1981 survey of 754 doctors in 65 countries
found that 45% had ever prescribed a combination pill to
breastfeeding women [6]. The investigators found that
women’s preference, previous breastfeeding history and
the use of feeding supplements influenced their decision to
prescribe an estrogen-containing OC.
Recommendations from maternal–child health authorities, such as the ACOG and the WHO, against the use of
combined OCs in breastfeeding women are unambiguous.
The rationale for the ACOG’s conservative guidance is
that 6 weeks of breastfeeding may give women time to
overcome initial difficulties in establishing milk supply and
that estrogen-containing pills would be less likely to
diminish milk production [7]. Although concerns have been
raised about the passage of hormones in breast milk,
estrogen-containing contraceptives are generally considered
compatible with breastfeeding [8]. An additional rationale
for waiting at least 2–3 weeks before beginning combined
OCs is the hypercoagulable postpartum state. Although
hypercoagulability and increased risk of thrombotic events
have been documented during the puerperium [9], no
studies have shown a higher incidence in women who
breastfeed and use OCs.
Despite strong recommendations against the initiation of
combined hormonal contraceptives prior to 6 weeks, a
sizable minority of providers prescribe combined pills in the
early postpartum period. Ironically, university providers —
those who have a particular responsibility to educate the
next generation of providers — were more likely not to
follow expert guidelines.
One explanation for not following the guidelines may be
the near-universality of providers’ opinions about the
superior contraceptive efficacy of combined pills over

progestin-only pills. In weighing the two important public
health issues of promoting breastfeeding and supporting the
prevention of unintended pregnancy, some providers may
believe that the superior nature of combined pills as a
contraceptive method outweighs the potential negative
impact on breastfeeding. Additionally, patients seen in our
university setting are often poor and may be uninsured or
may have lost their insurance shortly after delivery. Access
to return appointments for switching from one pill type to
another poses a greater difficulty for this population.
Another answer may lie in the scanty and imprecise
evidence linking the use of combined pills to a decline in
milk volume and a reduction in the duration of breastfeeding. Although several reports in the literature address
hormonal contraception and lactation, most studies are
nonrandomized or simply reflect expert opinion [10 –12].
Results are conflicting regarding the impact of estrogencontaining contraceptives on milk volume and, more
importantly, breastfeeding duration and infant growth. A
Cochrane collaborative review cites only three randomized
controlled trials of sufficient quality to be included in their
review of the impact of estrogen-containing OCs on
breastfeeding [4]. All three trials suffered from major
methodologic flaws such as a large loss to follow-up, which
may invalidate the main conclusions. Additionally, the
reports failed to describe adequately a number of elements
of the study design, including randomization allocation,
allocation concealment, blinding of treatments and/or use of
intention-to-treat analysis. The Cochrane review concludes
that existing data are insufficient to make recommendations
about lactation and the use of hormonal contraception.
The study most often cited as the reason for expert
recommendations against prescribing combined OCs in
breastfeeding women is a WHO trial in which 343 women
were randomized to low-dose combined OCs or to progestinonly pills, both initiated at 6 weeks postpartum [13]. The
major outcomes of the study were mean milk volume in a
given feeding, measured using a complicated methodology,
and infant growth. At 12 and 24 weeks postpartum, mean milk
volume was found to be significantly lower in the combined
OC group than in the progestin-only pill group (51 and 41 ml,
respectively, in the combined pill group versus 72 and 65 ml,
respectively, in the progestin-only pill group). No differences
in infant growth were noted between the two groups, and the
investigators concluded that their method of measuring milk
output bmay have little relationship to the amount actually
ingested by the baby during that or any 24-hour period.Q
Despite these limitations, the authors concluded that combination pills should not be used in breastfeeding women.
In a detailed review of the evidence, recommendations
and controversies surrounding estrogen-containing contraceptives for breastfeeding women, Erwin [14] eloquently
describes the importance of choosing the correct contraceptive. He affirms the superior efficacy and side-effect
profile of estrogen-containing pills over progestin-only pills
and alludes to the concern that women may discontinue

E. Espey et al. / Contraception 74 (2006) 389 – 393

breastfeeding in order to initiate combined pills. He acknowledges the risk of rapid repeat pregnancy in a woman who
foregoes her preferred contraceptive in order to breastfeed.
He concludes, in agreement with experts, that combined pills
should not be used in the first 2 months postpartum, although
bno consistent findings show deleterious effects of combined
pill use on infant growth and development when pill use has
begun after lactation is established.Q The Cochrane review
concludes by calling for appropriately designed randomized
controlled trials examining the impact of hormonal contraception on breastfeeding. This study was undertaken to
delineate practice patterns of clinicians in New Mexico and
not to promote changes in prescribing practices. Until welldesigned randomized trials have been completed, providers
may reasonably continue to prescribe according to their
preference or to counsel patients about nonhormonal contraceptive methods such as the intrauterine device, an ideal
method of contraception for breastfeeding women. A welldesigned study is urgently needed to determine the impact of
hormonal contraception on breastfeeding and infant growth
to help guide clinicians’ practice.
References
[1] Kaunitz A. ACOG practice bulletin no. 18. Clinical management
guidelines for obstetrician-gynecologists. The use of hormonal contraception in women with coexisting medical conditions 2000. www.
acog.org/publications/educational_bulletins/pb018.cfm.
[2] WHO medical eligibility criteria. 3rd ed. 2004. Available at: http://
www.who.int/reproductive-health/publications/MEC_3/mec.pdf [Retrieved on 5/15/2005].

393

[3] International Planned Parenthood Federation: directory of hormonal
contraceptives medical and service delivery guidelines. 3rd ed. 2004.
Available at: http://content.ippf.org/output/ORG/files/5950.pdf, [Retrieved on 5/15/2005].
[4] Truitt ST, Fraser AB, Grimes DA, Gallo MF, Schulz KF. Combined
hormonal vs. non-hormonal versus progestin-only contraception in
lactation. Cochrane Database Syst Rev 2003;(2):1 – 14 [art. no.
CD003988, DOI: 10.1002/14651858.CD003988].
[5] Hatcher RA, Rinehart W, Blackburn R, Geller JS, Shelton JD.
Essentials of contractive technology. Baltimore (MD)7 Population
Information Program, Johns Hopkins Bloomberg School of Public
Health; 1997.
[6] Strauss LT, Speckhard M, Rochat RW, Senanayake P. Oral contraception during lactation — a global survey of physician practice. Int
J Gynaecol Obstet 1981;169 – 75.
[7] Queenan J. ACOG educational bulletin no. 258. Breastfeeding:
maternal and infant aspects 2000. http://www.acog.org/publications/
educational_bulletins/btb258.cfm.
[8] American Academy of Pediatrics. The transfer of drugs and other
chemicals into human milk. Pediatrics 2001;108(3):776 – 89.
[9] James AH, Tapson VF, Goldhaber SZ. Thrombosis during pregnancy
and the postpartum period. Am J Obstet Gynecol 2005;193:216 – 9.
[10] Nilsson S, Mellbin T, Hofvander Y, Sundelin C, Valentin J, Nygren
KG. Long-term follow-up of children breast-fed by mothers using oral
contraceptives. Contraception 1986;34:443 – 57.
[11] Halderman LD, Nelson AL. Impact of early postpartum administration
of progestin-only hormonal contraceptives compared with nonhormonal contraceptives on short-term breast-feeding patterns. Am J
Obstet Gynecol 2002;186:1250 – 8.
[12] Visness CM, Rivera R. Progestin-only pill use and pill switching
during breastfeeding. Contraception 1995;51:279 – 81.
[13] Tankeyoon M, Dusitsin N, Chalapati S, Koetsawang S, Saibiang S,
Sas M. Effects of hormonal contraceptives on milk volume and infant
growth. Contraception 1984;30:505 – 22.
[14] Erwin PC. To use or not use combined hormonal oral contraceptives
during lactation. Fam Plann Perspect 1994;26:26 – 31.

Obstetrician-Gynecologists and the Intrauterine
Device: A Survey of Attitudes and Practice
Nancy L. Stanwood, MD, MPH, Joanne M. Garrett, PhD, and Thomas R. Konrad, PhD
OBJECTIVE: To assess obstetrician-gynecologists’ clinical
use of the intrauterine device (IUD), their attitudes toward
the IUD and how they select IUD candidates, and to test the
hypotheses that limited residency training in IUDs, fear of
litigation, and a belief that IUDs cause pelvic inflammatory disease decrease IUD use.
METHODS: We performed a national mailed survey of 811
practicing obstetrician-gynecologists obtained from systematic sampling of ACOG membership listings to assess
use of and attitudes toward the IUD.
RESULTS: The survey response rate was 50%. Most respondents agreed that the copper IUD is safe (95%) and effective
(98%). However, 20% of respondents had not inserted an
IUD in the past year, and of those who had, most (79%)
reported inserting 10 or fewer. Fear of litigation and a belief
that IUDs cause pelvic inflammatory disease were associated with lower IUD use; the number of IUDs inserted
during residency was not. In selecting IUD candidates,
respondents were most restrictive about patient monogamy. Having less conservative criteria for selecting IUD
candidates was associated with greater IUD use. Respondents with liberal criteria inserted a mean of nine IUDs in
the past year, whereas those with conservative criteria
inserted four.
CONCLUSIONS: Because most obstetrician-gynecologists are
inserting few IUDs, educational programs should target
these physicians to expand their IUD use. Such programs
should highlight modern IUD safety and the rarity of
litigation. The number of IUDs inserted in residency may
be less important than the development of less restrictive,
more evidence-based criteria for selecting IUD candidates.
(Obstet Gynecol 2002;99:275– 80. © 2002 by the American College of Obstetricians and Gynecologists.)

The intrauterine device (IUD) provides safe1 and effective2 contraception, and 12% of married women of
reproductive age worldwide use it.1 In the United States,
From the Department of Obstetrics and Gynecology, the Robert Wood Johnson
Clinical Scholars Program, the Division of General Medicine, and the Department
of Social Medicine, Cecil G. Sheps Center for Health Services Research, University
of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
This study was supported by the Robert Wood Johnson Clinical Scholars Program.

however, only 0.8% of women using contraception
use the IUD.3 Before the debacle involving the Dalkon
shield, 9.5% of married, white US women using contraception used the IUD.4 After the Dalkon Shield, manufacturers withdrew most devices from the US market,
and IUD use decreased.5 Physicians and the public
developed a persistent fear that all IUDs cause pelvic
inflammatory disease (PID) despite evidence that PID
after modern copper IUD insertion occurs rarely, at a
rate of 1.6 per 1000 woman-years of use.6 Reanalysis
of the early studies linking IUDs and PID question
their methodology and generalizability.7,8 The relative
underuse of the IUD in the United States reflects these
public and professional concerns. The reluctance of
US physicians to recommend IUDs except in narrowly
selected patients9 contributes to this underuse. Many
factors contribute to this reluctance, including a lack of
training in use of IUDs during residency, a fear of
litigation, and a belief that the IUD creates a high risk for
PID.10 –12
Little is known about how obstetrician-gynecologists
use the IUD in clinical practice, what their attitudes
toward the IUD are, or how they select IUD candidates
in their practices. In 1989, Kooiker and Scutchfield11
surveyed obstetrician-gynecologists and family and general internal medicine physicians in San Diego County,
CA, shortly after the 1988 release of the Paragard
T380A Intrauterine Copper Contraceptive device (Ortho Pharmaceutical Corporation, Raritan, NJ) in the
United States. They asked the physicians whether they
recommended this new IUD to patients and whether
they planned to use it in their practices. In their sample,
40% were not recommending this IUD to any patients.
Respondents with a low knowledge score about this
IUD, limited experience with IUD insertion, and non–
obstetrician-gynecologist specialty had a more negative
attitude toward this IUD and a lower willingness to
recommend it. The top two reasons given for not recommending this IUD were fear of legal liability and a belief
that the IUD was not medically safe.
No surveys of IUD use by US physicians have been

VOL. 99, NO. 2, FEBRUARY 2002
© 2002 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.

0029-7844/02/$22.00
PII S0029-7844(01)01726-4

275

published in the peer-reviewed literature since the study
by Kooiker and Scutchfield. Recent advances in IUD
technology, exemplified by the entry of a new type of
IUD into the US market—the Mirena levonorgestrelreleasing intrauterine system (Berlex Laboratories,
Montville, NJ)—make our study particularly timely. Understanding how physicians feel about and use the IUD
in practice is important in designing targeted educational
programs for the current generation of physicians. We
aimed to assess obstetrician-gynecologists’ current use of
the IUD in practice, their attitudes toward the IUD, and
the factors they consider when selecting patients as IUD
candidates. Further, we aimed to test the hypotheses that
limited IUD training in residency, fear of litigation, and a
belief in a strong causal link between IUDs and PID are
associated with lower IUD use in practice.
MATERIALS AND METHODS
We designed a self-administered written survey to ascertain knowledge, attitudes, and practices among obstetrician-gynecologists with regard to the IUD, as well as
demographic, training, and practice information. We
constructed the sampling frame from the geographic
listing of the membership directory of the ACOG, including all members in active practice (Fellow or Junior
Fellow in Practice) who had a mailing address in the 50
United States or the District of Columbia and were not
listed in the military. Starting at a random number, we
selected a systematic sample of every 30th name, yielding a list of 811 names. We mailed the questionnaire to
each of these obstetrician-gynecologists with a cover
letter signed by the primary investigator and a postpaid
return envelope. We conducted two mailings between
July and September of 2000.
We tested for nonresponse bias by comparing respondents and nonrespondents on county-level demographic
information linked by ZIP code to data in the Area
Resource File (http://www.arfsys.com). Specifically, we
looked at urban or rural practice location, county per
capita income, several physician workforce variables,
and variables reflecting the demographic structure of the
communities served by the physicians (eg, total births
and the percentage of women in the population). We had
no demographic information on nonresponders from
our original sampling frame, the ACOG Membership
Directory. To address this issue, we compared a random
sample of 100 responders and 100 nonresponders. We
obtained information on sex and year of graduation
from medical school in nonresponders by using the
American Medical Association’s Web-based physician
directory (http://www.ama-assn.org). We added four to
the year of medical school graduation to estimate the

276

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Intrauterine Device Survey

year of residency graduation. In analyses comparing
responders with nonresponders, we used a two-sample
Student t test for normally distributed continuous variables, the Wilcoxon rank-sum test for non-normal variables, and the Pearson x2 test for categorical variables.
We performed descriptive analyses of the main outcome of interest—the reported number of IUDs inserted
in the past year—and demographic and attitudinal variables. We tested for associations between the reported
number of IUDs inserted in the past year and demographic and attitudinal variables. Because the main outcome had a non-normal distribution, we performed both
parametric and nonparametric tests; data are reported as
means when results were similar. We used a two-sample
Student t test and Spearman correlation for continuous
independent variables and one-way analysis of variance
and the Kruskal–Wallis test for nominal independent
variables. We also created a scale of conservative-toliberal IUD candidate selection by summing responses to
five variables, measured on a Likert scale, that queried
respondents’ attitude toward parity, history of sexually
transmitted disease (STD) and PID, marital status, and
monogamy. We analyzed this scale in three categories:
most conservative, moderate, and most liberal. This
scale had an acceptable Cronbach a value of .70. We
performed all analyses using Stata 6.0 (Stata Corporation, College Station, TX).
RESULTS
Of the 811 ACOG fellows to whom we mailed our
survey, 400 returned complete responses, 17 had their
mailing returned as undeliverable, and 26 returned invalid or incomplete responses, for a final response rate of
50%. This response rate is only slightly lower than the
52% response typical of large national physician surveys13 and is higher than that reported in previous
random surveys of general ACOG members, which
averaged 40%.14 –22 Respondents and nonrespondents
did not differ in county-level demographic information
on income; rural or urban mix; or physician workforce,
including obstetrician-gynecologist workforce. Respondents completed residency training more recently than
nonrespondents did (mean year of graduation 1984 versus 1981, P 5 .04) and were more likely to be female
(37% versus 26%, P 5 .07). The difference in sex distribution was not significant after adjustment for year of
graduation, and the 3-year difference in the mean year of
residency graduation was small.
Among respondents, 37% were female, the mean age
was 47 years, and the mean year of residency completion
was 1984 (Table 1). Seventy percent were in private
practice and 14% were in academic departments, and

OBSTETRICS & GYNECOLOGY

Table 1. Respondent Characteristics
Characteristic
Female (%)
Male (%)
Age (y)
Year graduated from residency
Generalists (%)
Practice type (%)
Private practice
Academic
Multispecialty
HMO
Other
Patients seen per week

Percentage or
mean (range)
37
63
47 (31–73)
1984 (1957–98)
83
70
14
8
2
6
88 (5–300)

HMO 5 health maintenance organization.

83% were generalists. They reported seeing an average
of 88 patients in the office during a normal week. These
characteristics are similar to those observed in recent
surveys of ACOG members.14 –16,18,19,23
Most respondents (80%) reported inserting IUDs in
the last year, although 79% reported inserting 10 or
fewer. The mean number of IUDs inserted in the past
year was seven. Almost one third (32%) of respondents
inserted 1 to 4 IUDs, 31% inserted 5 to 10 IUDs, and
17% inserted more than 10 IUDs. Respondents reported
that they discussed a new or different contraceptive
method with an average of 15% of their patients seen in
the office. When asked to estimate the proportion of
their patients using contraception whom they consider to
be IUD candidates, half of respondents said 15% or less.
During residency, most respondents reported inserting
some IUDs; 13% inserted none, 38% inserted 1 to 20,
22% inserted 21 to 50, and 27% inserted more than 50.
Respondents had a remarkably positive attitude toward the IUD in general as a contraceptive method.
Ninety-eight percent agreed that the Copper T380A
IUD is effective, and 95% agreed that it is safe. Most
(79%) agreed that they had enough time to counsel their
patients on contraceptive options, and 64% believed that
their patients were receptive to learning about the IUD.
However, 20% percent agreed that the IUD was an
abortifacient, and 16% agreed that it would lead to
lawsuits against them.
Respondents restricted IUD candidates most tightly
on the basis of monogamy and PID history. When
presented with hypothetical characteristics of patients,
84% agreed that a woman in a nonmonogamous relationship should not have an IUD, and 81% agreed that a
woman with a history of PID should not have an IUD.
About two thirds of respondents did not recommend
IUDs to nulliparous women or those with a history of
STDs. Respondents were least restrictive about marital

VOL. 99, NO. 2, FEBRUARY 2002

status; 31% agreed that a woman who is not married
should not have an IUD. We then asked them how
strongly different characteristics affect their selection of
IUD candidates. Most (81%) were strongly affected by
monogamy status. About two thirds (68%) responded
that parity status had a strong effect on their decision,
and a minority felt that marital status and the patient’s
education level affected their decision (40% and 30%,
respectively).
We asked, “By what percent do you believe that a
Copper T380A IUD increases the risk of PID over 10
years?” Twenty percent responded “zero,” indicating
that this minority does not believe in a causal relationship between IUDs and PID. Nearly 40% responded that
the increased risk is 1% to 9%, 17% that the risk is
increased 10%, and 12% that the increase in risk is
greater than 10%. Thus, nearly one third of physicians
responded that IUDs increase the risk of PID by 10% or
more, indicating a strong belief in a long-term causal
relationship.
We tested for associations between the reported number of IUDs inserted in the last year and demographic
characteristics of respondents. Sex and geographic region were not associated with the reported number of
IUDs inserted. Age and year of graduation of residency
were highly correlated, and both were associated with
IUD insertion. Younger and more recent graduates inserted more IUDs. Respondents aged 31 to 45 inserted a
median of 5 IUDs, those aged 46 to 55 inserted a median
of 4, and those aged 56 to 73 inserted a median of 3 (P 5
.04). Each practice type had similar reported median
numbers of IUDs inserted, ranging from 2 to 5, except
for one: Physicians in health maintenance organizations
reported inserting a median of 10 IUDs, but only 8
respondents were in this group.
To test our main hypotheses about underuse of the
IUD in the United States, we tested for associations
between the reported number of IUDs inserted in the
past year and residency training in IUDs, fear of litigation, and a belief in a causal link between IUDs and PID
(Table 2). We found no association between the number
of IUDs inserted during residency and the reported
number inserted in the last year. We found a significant
association between fear of litigation and reported number of IUDs inserted in the last year. Sixteen percent of
respondents agreed that using the IUD in practice puts
them at risk for litigation. These respondents reported
inserting a mean of 4 IUDs, whereas those who disagreed inserted 10 (P , .001).
We found a significant overall association (P 5 .004)
between a belief in a causal link between IUDs and PID

Stanwood et al

Intrauterine Device Survey

277

Table 2. Factors Associated With Reported Intrauterine Device Use in Clinical Practice

Factor
Number of IUDs inserted during residency
None
1–20
21–50
51–100
.100
IUD use leads to litigation
Agreed
Neutral
Disagreed
Percentage increased risk of PID due to IUDs
0%
1–5%
.5%
Unsure/missing
IUD candidate selection criteria
Conservative
Moderate
Liberal

Respondents
(%)

Mean IUDs
inserted
last year (n)

13
38
22
13
14

7
6
8
6
8

.49

16
23
61

4
6
10

,.001

20
36
32
12

9
7
7
3

.004

35
27
38

4
7
9

,.001

IUD 5 intrauterine device; PID 5 pelvic inflammatory disease.
* Overall significance from one-way analysis of variance.

and reported IUD use in practice when we asked the
question, “By what percent do you believe that a Copper
T380A IUD increases the risk of PID over 10 years of
use?” Physicians who responded “zero” had a higher
mean number of IUDs inserted in the past year than did
those who responded “.1%” (nine versus seven, twosample Student t test P 5 .008).
We developed a score of conservative-to-liberal IUD
candidate selection behavior using five questions on
patient characteristics (nulliparity, STD and PID history,
marital status, and monogamy). On the basis of score,
we categorized respondents as conservative, moderate,
or liberal. Reported use of the IUD in practice was
associated with this score. The conservative group reported inserting fewer IUDs in the past year than the
liberal group (four versus nine, P , .001).
DISCUSSION
Most obstetrician-gynecologists insert IUDs in clinical
practice, but they report inserting few per year. Although
attitudes toward the safety and effectiveness of the IUD
are very positive, most respondents believe that a longterm causal relationship exists between the modern copper IUD and PID. Twenty-nine percent of respondents
considered this increased risk to be 10% or greater.
The evidence argues against such a conclusion. A
transient sixfold increased risk exists for 21 days after
insertion, after which the rate of PID decreases to 0.059

278

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Intrauterine Device Survey

per 100 woman-years of use with the Copper T380A
device.6 The evidence does not demonstrate a long-term
risk of PID definitively attributable to the IUD.6 Instead,
sexual behavior and resultant exposure to chlamydia
and gonorrhea produce the largest attributable risk for
PID24 (Shelton JD. Risk of clinical pelvic inflammatory
disease attributable to an intrauterine device [Research
Letter]. Lancet 2001;357:443). No study has answered
the question of whether the risk of progression to PID is
greater or lesser in a woman with cervicitis and a modern
copper IUD than in a woman with cervicitis but no
IUD.8 Nor does evidence indicate that having an IUD in
place will worsen a case of PID. In contrast to current
evidence that the IUD does not cause PID in the long
term, manufacturer recommendations (Paragardt
T380A Copper Contraceptive. Prescribing information.
Raritan, NJ: Ortho Pharmaceutical Corporation, 1997)
list any lifetime history of PID as a contraindication to
use of a copper IUD. Similarly, the ACOG Technical
Bulletin on IUDs9 describes the ideal IUD candidate as
having no history of PID.
Our survey supports the hypothesis that a fear of
litigation limits use of the IUD in practice among obstetrician-gynecologists. Fortunately, a majority of respondents believed that IUDs do not lead to lawsuits, an
opinion supported by reviews of physician litigation
experience.12 Our results do not support the hypothesis
that the number of IUDs inserted in residency is associ-

OBSTETRICS & GYNECOLOGY

ated with current reported use of the IUD in clinical
practice. Rather, the association of a respondent’s conservative-to-liberal score in patient selection with IUD
use may indicate that the teaching of candidate selection
drives physicians’ future use of the IUD.
Our survey has several limitations. Because it is crosssectional, we can find associations but not cause-andeffect relationships. Thus, respondents may have developed more liberal criteria for IUD candidate selection
after inserting many IUDs and becoming comfortable
with the low rate of complications rather than by developing more liberal criteria that then cause them to insert
higher numbers. We also relied on respondents’ recall of
the number of IUDs inserted in the past year and during
residency. Our results may not be generalizable to all
obstetrician-gynecologists in the United States. Because
respondents graduated slightly more recently from residency than did nonrespondents, our survey may overestimate the use of IUDs by practicing obstetriciangynecologists. Finally, our survey addresses neither the
decision to use an IUD from the woman’s perspective
nor issues of insurance coverage for contraceptives.
Our findings nevertheless have important implications for physician training and education. Because most
obstetrician-gynecologists are inserting few IUDs, educational programs should target these physicians to expand their IUD use. Such programs should highlight the
evidence for IUD safety and the rarity of litigation. The
number of IUDs inserted in residency may be less important than the development of less conservative, more
evidence-based criteria for selecting IUD candidates.
The IUD is a safe and effective method of contraception. Its broader use in the United States is limited, not
because obstetrician-gynecologists believe that the IUD
is ineffective, or that they lack skill or knowledge in its
use, but because of a persistent belief that IUDs cause
PID, which results in lawsuits. The evidence does not
support these fears about modern devices, and such tight
restrictions fail to weigh the competing risk of unintended pregnancy from use of less effective methods.
Failure to weigh this risk has profound public health
implications in a country in which 49% of pregnancies
are unintended and 53% of unintended pregnancies happen after contraceptive failure or misuse.25
Many women could safely use the IUD but are not
offered this contraceptive method because physicians’
selection of IUD candidates is unduly restrictive. Educating physicians about the safety of IUDs may expand
their use of IUDs. More women would then be offered a
method of convenient, safe, and highly effective longterm contraception.

VOL. 99, NO. 2, FEBRUARY 2002

REFERENCES
1. Rinehart W. IUDs—An update. Popul Rep B 1995:1–35.
2. Trussell J, Vaughan B. Contraceptive failure, methodrelated discontinuation and resumption of use: Results
from the 1995 National Survey of Family Growth. Fam
Plann Perspect 1999;31:64 –72, 93.
3. Piccinino LJ, Mosher WD. Trends in contraceptive use in
the United States: 1982-1995. Fam Plann Perspect 1998;
30:4 –10, 46.
4. Westoff CF, Jones EF. Contraception and sterilization in
the United States, 1965-1975. Fam Plann Perspect 1977;9:
153–7.
5. Forrest JD. The end of IUD marketing in the United
States: What does it mean for American women? Fam
Plann Perspect 1986;18:52–7.
6. Farley TM, Rosenberg MJ, Rowe PJ, Chen JH, Meirik O.
Intrauterine devices and pelvic inflammatory disease: An
international perspective. Lancet 1992;339:785– 8.
7. Kessel E. Pelvic inflammatory disease with intrauterine
device use: A reassessment. Fertil Steril 1989;51:1–11.
8. Grimes DA. Intrauterine device and upper-genital-tract
infection. Lancet 2000;356:1013–9.
9. American College of Obstetricians and Gynecologists.
The intrauterine device. ACOG technical bulletin no. 164.
Washington, DC: American College of Obstetricians and
Gynecologists, 1992.
10. Westhoff C. The IUD in evolution. Obstet Gynecol Surv
1996;51:S20 – 4.
11. Kooiker CH, Scutchfield FD. Barriers to prescribing the
Copper T 380A intrauterine device by physicians. West
J Med 1990;153:279 – 82.
12. Westhoff C, Marks F, Rosenfield A, Roig A, Nicholas A.
Clinical and legal factors influencing IUD use in the
United States. In: Bardin C, Mishell D, eds. Proceedings
from the Fourth International Conference on IUDs. Boston: Butterworth-Heinemann, 1994:100 – 8.
13. Cummings SM, Savitz LA, Konrad T. Reported response
rates to mailed physician questionnaires. Health Serv Res
2001;36:1347–55.
14. Erickson K, Schmidt L, Santesso DL, Schulkin J, Gregory
K, Hobel C. Obstetrician-gynecologists’ knowledge and
training about antenatal corticosteroids. Obstet Gynecol
2001;97:140 – 6.
15. Power ML, Holzman GB, Schulkin J. Knowledge and
clinical practice regarding folic acid among obstetriciangynecologists. Obstet Gynecol 2000;95:895– 8.
16. Diekman ST, Floyd RL, Decoufle P, Schulkin J, Ebrahim
SH, Sokol RJ. A survey of obstetrician-gynecologists on
their patients’ alcohol use during pregnancy. Obstet
Gynecol 2000;95:756 – 63.
17. Wilkins-Haug L, Hill LD, Power ML, Holzman GB,
Schulkin J. Gynecologists’ training, knowledge, and experiences in genetics: A survey. Obstet Gynecol 2000;95:
421– 4.

Stanwood et al

Intrauterine Device Survey

279

18. Power ML, Holzman GB, Schulkin J. Knowledge and
clinical practice regarding calcium nutrition among obstetrician-gynecologists. Obstet Gynecol 1999;94:421– 6.
19. Wilkins-Haug L, Hill L, Schmidt L, Holzman GB, Schulkin J. Genetics in obstetricians’ offices: A survey study.
Obstet Gynecol 1999;93:642–7.
20. Horan DL, Chapin J, Klein L, Schmidt LA, Schulkin J.
Domestic violence screening practices of obstetrician-gynecologists. Obstet Gynecol 1998;92:785–9.
21. Scroggs JA, Griffin LP, Bayerl M, Schulkin J. Obstetriciangynecologists as primary care physicians: The perspectives
of health maintenance organization medical directors and
obstetrician-gynecologists. Obstet Gynecol 1997;90:
291–5.
22. Schmidt LA, Greenberg BD, Holzman GB, Schulkin J.
Treatment of depression by obstetrician-gynecologists: A
survey study. Obstet Gynecol 1997;90:296 –300.
23. American College of Obstetricians and Gynecologists.

280

Stanwood et al

Intrauterine Device Survey

Profile of Ob-gyn Practice, 1991-1998. Washington, DC:
American College of Obstetricians and Gynecologists,
2000.
24. Lee NC, Rubin GL, Borucki R. The intrauterine device
and pelvic inflammatory disease revisited: New results
from the Women’s Health Study. Obstet Gynecol 1988;
72:1– 6.
25. Henshaw SK. Unintended pregnancy in the United States.
Fam Plann Perspect 1998;30:24 –9.
Address reprint requests to: Nancy L. Stanwood, MD, MPH,
Department of Obstetrics and Gynecology, University of
Rochester Medical Center, Box 668, Room 2-4446, 601 Elmwood Avenue, Rochester, NY 14642-8668; E-mail:
[email protected].
Received May 31, 2001. Received in revised form October 22, 2001.
Accepted October 25, 2001.

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OES OVERVIEW

29-1062 Family and General Practitioners

OES NEWS RELEASES

Physicians who diagnose, treat, and help prevent diseases and injuries that commonly occur in the general population. May refer patients

OES DATA

to specialists when needed for further diagnosis or treatment.

OES CHARTS

National estimates for this occupation
Industry profile for this occupation
Geographic profile for this occupation

OES MAPS
OES PUBLICATIONS
OES DATABASES

National estimates for this occupation: Top

OES FAQS

Employment estimate and mean wage estimates for this occupation:

CONTACT OES

Employment (1)
SEARCH OES
Go

OES TOPICS

126,440

Employment Mean hourly Mean annual
Wage RSE (3)
RSE (3)
wage
wage (2)
2.0 %

$100.27

$208,560

1.0 %

Percentile wage estimates for this occupation:

RESPONDENTS
DOCUMENTATION

Percentile

10%

25%

Hourly Wage

$35.21

$66.39

SPECIAL NOTICES
RELATED LINKS

50%
75% 90%
(Median)
$95.55

Annual Wage (2) $73,240 $138,100 $198,740

(5)

Industry profile for this occupation: Top

Subscribe
to the OES
Update

Industries with the highest published employment and wages for this occupation are provided. For a list of all industries with
employment in this occupation, see the Create Customized Tables function.
Industries with the highest levels of employment in this occupation:

Email Address

Industry

Employment
(1)

Percent of
industry
employment

Hourly mean
wage

Annual mean
wage (2)

Offices of Physicians

83,320

3.27

$102.73

$213,670

General Medical and Surgical Hospitals

22,620

0.41

$97.66

$203,140

Outpatient Care Centers

9,440

1.07

$102.84

$213,900

Colleges, Universities, and Professional Schools

3,820

0.13

$57.35

$119,280

Local Government, excluding schools and hospitals
(OES Designation)

1,510

0.03

$98.21

$204,280

Industries with the highest concentration of employment in this occupation:

Industry

Employment
(1)

Percent of
industry
employment

Hourly mean
wage

Annual mean
wage (2)
$213,670

Offices of Physicians

83,320

3.27

$102.73

Outpatient Care Centers

9,440

1.07

$102.84

$213,900

General Medical and Surgical Hospitals

22,620

0.41

$97.66

$203,140

Psychiatric and Substance Abuse Hospitals

560

0.24

$95.97

$199,620

Colleges, Universities, and Professional Schools

3,820

0.13

$57.35

$119,280

Industry

Employment
(1)

Percent of
industry
employment

Hourly mean
wage

Annual mean
wage (2)

Specialty (except Psychiatric and Substance Abuse)
Hospitals

190

0.07

$112.63

$234,270

Medical and Diagnostic Laboratories

0.03

$112.48

$233,950

Top paying industries for this occupation:

https://www.bls.gov/oes/current/oes291062.htm

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Family and General Practitioners

Page 2 of 9

Residential Intellectual and Developmental
Disability, Mental Health, and Substance Abuse
Facilities

0.01

$112.11

$233,200

Management of Companies and Enterprises

150

0.01

$111.78

$232,510

Management, Scientific, and Technical Consulting
Services

0.01

$106.36

$221,220

Geographic profile for this occupation: Top
States and areas with the highest published employment, location quotients, and wages for this occupation are provided. For a list of all
areas with employment in this occupation, see the Create Customized Tables function.

States with the highest employment level in this occupation:

State

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

California

13,950

0.84

Florida

12,710

1.51

Illinois

9,160

Texas
Missouri

Hourly mean
wage

Annual mean
wage (2)

0.94

$94.32

$196,180

1.70

$103.51

$215,300

1.54

1.74

$105.91

$220,290

7,910

0.67

0.75

$98.39

$204,660

5,280

1.89

2.14

$83.14

$172,940

https://www.bls.gov/oes/current/oes291062.htm

4/21/2018

Family and General Practitioners

Page 3 of 9

States with the highest concentration of jobs and location quotients in this occupation:

State

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Missouri

5,280

1.89

2.14

$83.14

$172,940

Nebraska

1,680

1.73

1.95

$109.15

$227,020

Illinois

9,160

1.54

1.74

$105.91

$220,290

Idaho

1,060

1.54

1.73

$106.03

$220,550

Florida

12,710

1.51

1.70

$103.51

$215,300

https://www.bls.gov/oes/current/oes291062.htm

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Family and General Practitioners

Page 4 of 9

Top paying States for this occupation:
Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

New Hampshire

910

1.41

1.58

$124.36

$258,670

Wisconsin

2,420

0.86

0.96

$116.51

$242,340

Iowa

1,840

1.20

1.35

$116.23

$241,760

South Carolina

2,670

1.33

1.50

$112.70

$234,420

Washington

1,200

0.38

0.42

$110.73

$230,330

State

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Family and General Practitioners

Page 5 of 9

<
Metropolitan areas with the highest employment level in this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Chicago-Naperville-Arlington
Heights, IL Metropolitan Division

6,200

1.69

1.91

$101.36

$210,820

Los Angeles-Long Beach-Glendale,
CA Metropolitan Division

4,440

1.00

1.13

$86.25

$179,400

Houston-The Woodlands-Sugar
Land, TX

2,760

0.94

1.06

$102.55

$213,300

St. Louis, MO-IL

2,570

1.89

2.13

$68.11

$141,670

Boston-Cambridge-Newton, MA
NECTA Division

2,500

1.36

1.53

$104.78

$217,940

Phoenix-Mesa-Scottsdale, AZ

2,330

1.18

1.33

$96.32

$200,340

Atlanta-Sandy Springs-Roswell, GA

1,880

0.72

0.81

$97.17

$202,100

Tampa-St. Petersburg-Clearwater,
FL

1,850

1.44

1.63

$108.25

$225,160

Washington-Arlington-Alexandria,
DC-VA-MD-WV Metropolitan
Division

1,750

0.69

0.78

$82.65

$171,900

Minneapolis-St. Paul-Bloomington,
MN-WI

1,740

0.90

1.01

$103.07

$214,390

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Family and General Practitioners

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<
Metropolitan areas with the highest concentration of jobs and location quotients in this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Columbia, MO

480

5.19

5.85

$115.06

$239,320

Punta Gorda, FL

170

3.60

4.06

$93.56

$194,600

Coeur d'Alene, ID

190

3.20

3.60

$128.54

$267,370

Staunton-Waynesboro, VA

150

3.17

3.57

$114.01

$237,130

New Bedford, MA

200

3.05

3.44

$130.36

$271,140

Sumter, SC

110

3.01

3.39

$124.85

$259,690

Augusta-Richmond County, GA-SC

630

2.87

3.23

$60.19

$125,190

Florence, SC

240

2.85

3.21

$118.12

$245,680

Ames, IA

130

2.85

3.22

$132.48

$275,550

Palm Bay-Melbourne-Titusville, FL

560

2.72

3.06

$108.50

$225,690

https://www.bls.gov/oes/current/oes291062.htm

4/21/2018

Family and General Practitioners

Page 7 of 9

<
Top paying metropolitan areas for this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)
(5)

The Villages, FL

1.28

1.45

(5)

St. Joseph, MO-KS

100

1.90

2.15

(5)

Enid, OK

(8)

$137.07

$285,110

Longview, TX

(8)

$134.69

$280,150

Hilton Head Island-BlufftonBeaufort, SC

120

1.67

1.88

$133.82

$278,350

Sebring, FL

(8)

$133.66

$278,020

Appleton, WI

(8)

$133.59

$277,870

Kankakee, IL

110

2.55

2.87

$133.24

$277,140

Portsmouth, NH-ME

130

1.40

1.58

$133.02

$276,680

Knoxville, TN

140

0.37

0.42

$132.54

$275,680

Nonmetropolitan areas with the highest employment in this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

North Northeastern Ohio nonmetropolitan area (noncontiguous)

330

0.99

1.12

$103.05

$214,350

Northwest Lower Peninsula of
Michigan nonmetropolitan area

270

2.23

2.51

$107.10

$222,770

Southeast Missouri
nonmetropolitan area

260

1.60

1.80

$115.81

$240,880

Central Missouri nonmetropolitan
area

260

1.61

1.82

$115.81

$240,880

Central Nebraska nonmetropolitan
area

250

2.35

2.65

$127.51

$265,220

Nonmetropolitan areas with the highest concentration of jobs and location quotients in this occupation:

https://www.bls.gov/oes/current/oes291062.htm

4/21/2018

Family and General Practitioners

Nonmetropolitan area

Page 8 of 9

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

West Central New Hampshire
nonmetropolitan area

200

3.06

3.45

$127.98

$266,210

Northern New Hampshire
nonmetropolitan area

2.54

2.87

$132.12

$274,810

Southwest Colorado
nonmetropolitan area

240

2.50

2.82

$93.24

$193,940

Central Nebraska nonmetropolitan
area

250

2.35

2.65

$127.51

$265,220

Northwest Lower Peninsula of
Michigan nonmetropolitan area

270

2.23

2.51

$107.10

$222,770

Top paying nonmetropolitan areas for this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

West Texas Region of Texas
nonmetropolitan area

0.39

0.44

$134.51

$279,780

South Georgia nonmetropolitan
area

150

0.83

0.93

$133.62

$277,930

Balance of Alaska nonmetropolitan
area

120

1.66

1.87

$133.23

$277,110

Northeast Nebraska
nonmetropolitan area

(8)

$132.66

$275,930

Northern New Hampshire
nonmetropolitan area

2.54

2.87

$132.12

$274,810

About May 2017 National, State, Metropolitan, and Nonmetropolitan Area Occupational Employment and Wage Estimates
These estimates are calculated with data collected from employers in all industry sectors, all metropolitan and nonmetropolitan areas,
and all states and the District of Columbia. The top employment and wage figures are provided above. The complete list is available in
the downloadable XLS files.
The percentile wage estimate is the value of a wage below which a certain percent of workers fall. The median wage is the 50th
percentile wage estimate--50 percent of workers earn less than the median and 50 percent of workers earn more than the median. More
about percentile wages.

(1) Estimates for detailed occupations do not sum to the totals because the totals include occupations not shown separately. Estimates
do not include self-employed workers.
(2) Annual wages have been calculated by multiplying the hourly mean wage by a "year-round, full-time" hours figure of 2,080 hours; for
those occupations where there is not an hourly wage published, the annual wage has been directly calculated from the reported survey
data.
(3) The relative standard error (RSE) is a measure of the reliability of a survey statistic. The smaller the relative standard error, the more
precise the estimate.
(5) This wage is equal to or greater than $100.00 per hour or $208,000 per year.
(8) Estimate not released.
(9) The location quotient is the ratio of the area concentration of occupational employment to the national average concentration. A
location quotient greater than one indicates the occupation has a higher share of employment than average, and a location quotient less
than one indicates the occupation is less prevalent in the area than average.
Other OES estimates and related information:
May 2017 National Occupational Employment and Wage Estimates
May 2017 State Occupational Employment and Wage Estimates
May 2017 Metropolitan and Nonmetropolitan Area Occupational Employment and Wage Estimates
May 2017 National Industry-Specific Occupational Employment and Wage Estimates
May 2017 Occupation Profiles
Technical Notes

https://www.bls.gov/oes/current/oes291062.htm

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Occupational Employment and Wages, May 2017

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29-1141 Registered Nurses

OES NEWS RELEASES

Assess patient health problems and needs, develop and implement nursing care plans, and maintain medical records. Administer nursing

OES DATA

care to ill, injured, convalescent, or disabled patients. May advise patients on health maintenance and disease prevention or provide case

OES CHARTS

management. Licensing or registration required. Includes Clinical Nurse Specialists. Excludes "Nurse Anesthetists" (29-1151), "Nurse

OES MAPS

Midwives" (29-1161), and "Nurse Practitioners" (29-1171).

OES PUBLICATIONS

National estimates for this occupation
Industry profile for this occupation
Geographic profile for this occupation

OES DATABASES
OES FAQS

National estimates for this occupation: Top

CONTACT OES

Employment estimate and mean wage estimates for this occupation:
SEARCH OES
Go

Employment (1)
OES TOPICS

2,906,840

RESPONDENTS
DOCUMENTATION

Employment Mean hourly Mean annual
Wage RSE (3)
RSE (3)
wage
wage (2)
0.5 %

$35.36

$73,550

0.2 %

Percentile wage estimates for this occupation:

SPECIAL NOTICES
RELATED LINKS

Percentile

10%

25%

50%
(Median)

Hourly Wage

$23.41

$27.57

$33.65

Annual Wage (2) $48,690 $57,340 $70,000

Subscribe
to the OES
Update

75%

90%

$41.33

$50.05

$85,960 $104,100

Industry profile for this occupation: Top
Industries with the highest published employment and wages for this occupation are provided. For a list of all industries with
employment in this occupation, see the Create Customized Tables function.
Industries with the highest levels of employment in this occupation:

Email Address

Industry

Employment
(1)

Percent of
industry
employment

General Medical and Surgical Hospitals

1,685,820

30.64

$36.45

$75,820

Offices of Physicians

196,040

7.69

$32.16

$66,890

Hourly mean
wage

Annual mean
wage (2)

Home Health Care Services

179,310

12.84

$33.77

$70,230

Nursing Care Facilities (Skilled Nursing Facilities)

155,450

9.59

$31.59

$65,710

Outpatient Care Centers

132,070

15.00

$36.39

$75,680

Industries with the highest concentration of employment in this occupation:

Industry

Employment
(1)

Percent of
industry
employment

Hourly mean
wage

Annual mean
wage (2)

General Medical and Surgical Hospitals

1,685,820

30.64

$36.45

$75,820

Specialty (except Psychiatric and Substance Abuse)
Hospitals

62,310

23.98

$37.16

$77,290

Psychiatric and Substance Abuse Hospitals

39,100

16.33

$34.27

$71,290

Outpatient Care Centers

132,070

15.00

$36.39

$75,680

Home Health Care Services

179,310

12.84

$33.77

$70,230

Employment
(1)

Percent of
industry
employment

Hourly mean
wage

Annual mean
wage (2)

Top paying industries for this occupation:

Industry

https://www.bls.gov/oes/current/oes291141.htm

4/21/2018

Registered Nurses

Page 2 of 9

Pharmaceutical and Medicine Manufacturing

210

0.07

$43.51

$90,510

Accounting, Tax Preparation, Bookkeeping, and
Payroll Services

940

0.10

$42.81

$89,050

Federal Executive Branch (OES Designation)

79,220

3.91

$41.84

$87,030

Business Schools and Computer and Management
Training

0.10

$41.82

$86,990

Wholesale Electronic Markets and Agents and
Brokers

240

0.03

$39.99

$83,190

States with the highest employment level in this occupation:

State

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

California

282,290

16.91

0.83

$49.37

$102,700

Texas

212,230

17.85

0.88

$34.65

$72,070

New York

180,170

19.57

0.96

$40.12

$83,450

Florida

178,330

21.18

1.04

$31.20

$64,890

Pennsylvania

143,130

24.76

1.21

$33.57

$69,820

https://www.bls.gov/oes/current/oes291141.htm

4/21/2018

Registered Nurses

Page 3 of 9

States with the highest concentration of jobs and location quotients in this occupation:

State

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

South Dakota

12,530

29.87

1.47

$27.41

$57,010

West Virginia

20,410

29.65

1.45

$29.03

$60,380

Delaware

11,620

26.25

1.29

$35.18

$73,180

Missouri

72,090

25.85

1.27

$30.43

$63,300

Mississippi

28,760

25.69

1.26

$27.74

$57,700

https://www.bls.gov/oes/current/oes291141.htm

4/21/2018

Registered Nurses

Page 4 of 9

Top paying States for this occupation:
Employment
per thousand
jobs

State

Employment
(1)

California

282,290

16.91

Hawaii

10,800

17.07

District of Columbia

11,000

15.54

Massachusetts

82,870

Oregon

35,140

https://www.bls.gov/oes/current/oes291141.htm

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

0.83

$49.37

$102,700

0.84

$46.63

$96,990

0.76

$43.32

$90,110

23.49

1.15

$42.95

$89,330

19.19

0.94

$42.68

$88,770

4/21/2018

Registered Nurses

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<
Metropolitan areas with the highest employment level in this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

New York-Jersey City-White
Plains, NY-NJ Metropolitan Division

122,780

18.34

0.90

$43.67

$90,840

Los Angeles-Long Beach-Glendale,
CA Metropolitan Division

79,420

17.92

0.88

$45.99

$95,650

Chicago-Naperville-Arlington
Heights, IL Metropolitan Division

75,320

20.57

1.01

$36.84

$76,640

Houston-The Woodlands-Sugar
Land, TX

51,610

17.62

0.86

$38.01

$79,060

Boston-Cambridge-Newton, MA
NECTA Division

43,150

23.45

1.15

$46.70

$97,130

Dallas-Plano-Irving, TX
Metropolitan Division

41,140

16.51

0.81

$35.81

$74,480

Atlanta-Sandy Springs-Roswell, GA

40,400

15.42

0.76

$33.92

$70,540

Minneapolis-St. Paul-Bloomington,
MN-WI

39,290

20.34

1.00

$39.19

$81,510

Phoenix-Mesa-Scottsdale, AZ

38,670

19.53

0.96

$36.61

$76,140

St. Louis, MO-IL

36,670

27.03

1.33

$31.69

$65,910

https://www.bls.gov/oes/current/oes291141.htm

4/21/2018

Registered Nurses

Page 6 of 9

<
Metropolitan areas with the highest concentration of jobs and location quotients in this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Bloomsburg-Berwick, PA

3,090

72.52

3.56

$28.26

$58,780

Rochester, MN

7,640

66.54

3.26

$37.46

$77,920

Greenville, NC

4,150

55.65

2.73

$29.36

$61,060

Morgantown, WV

3,050

47.29

2.32

$31.12

$64,730

Gainesville, FL

5,470

41.51

2.04

$32.42

$67,430

Sherman-Denison, TX

1,860

41.34

2.03

$30.83

$64,130

Sioux Falls, SD

6,050

39.93

1.96

$27.77

$57,750

Durham-Chapel Hill, NC

11,700

39.18

1.92

$32.39

$67,360

Rome, GA

1,440

38.92

1.91

$30.65

$63,740

Huntington-Ashland, WV-KY-OH

5,060

38.70

1.90

$29.47

$61,290

https://www.bls.gov/oes/current/oes291141.htm

4/21/2018

Registered Nurses

Page 7 of 9

<
Top paying metropolitan areas for this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

San Francisco-Redwood City-South
San Francisco, CA Metropolitan
Division

14,170

12.69

0.62

$67.16

$139,700

Salinas, CA

2,470

14.36

0.70

$62.47

$129,940

San Jose-Sunnyvale-Santa Clara,
CA

15,990

14.69

0.72

$62.09

$129,140

Santa Cruz-Watsonville, CA

1,520

15.65

0.77

$59.84

$124,470

Vallejo-Fairfield, CA

3,170

23.32

1.14

$57.61

$119,830

Oakland-Hayward-Berkeley, CA
Metropolitan Division

19,550

17.18

0.84

$56.09

$116,660

Sacramento--Roseville--ArdenArcade, CA

18,240

18.99

0.93

$55.85

$116,170

Napa, CA

1,430

19.66

0.96

$54.68

$113,740

Santa Rosa, CA

3,170

15.65

0.77

$53.62

$111,530

Stockton-Lodi, CA

4,270

17.59

0.86

$52.03

$108,230

Nonmetropolitan areas with the highest employment in this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Piedmont North Carolina
nonmetropolitan area

6,200

24.16

1.18

$28.88

$60,060

North Northeastern Ohio nonmetropolitan area (noncontiguous)

5,420

16.33

0.80

$28.45

$59,190

Northeast Mississippi
nonmetropolitan area

5,340

23.08

1.13

$26.03

$54,150

Southeast Coastal North Carolina
nonmetropolitan area

4,620

18.65

0.91

$28.28

$58,810

4,450

16.53

0.81

$29.87

$62,130

https://www.bls.gov/oes/current/oes291141.htm

4/21/2018

Registered Nurses

Page 8 of 9

North Texas Region of Texas
nonmetropolitan area
Nonmetropolitan areas with the highest concentration of jobs and location quotients in this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

West Central New Hampshire
nonmetropolitan area

2,440

37.79

1.85

$35.73

$74,310

Upper Savannah South Carolina
nonmetropolitan area

2,900

37.15

1.82

$29.32

$60,980

East Kentucky nonmetropolitan
area

3,300

32.94

1.62

$27.01

$56,190

Northwest Kansas
nonmetropolitan area

1,560

26.20

1.28

$26.84

$55,820

Northwest Lower Peninsula of
Michigan nonmetropolitan area

3,190

26.14

1.28

$30.95

$64,380

Top paying nonmetropolitan areas for this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Mother Lode Region of California
nonmetropolitan area

730

17.19

0.84

$48.89

$101,700

Eastern Sierra Region of California
nonmetropolitan area

190

13.54

0.66

$45.04

$93,690

Hawaii / Kauai nonmetropolitan
area

1,610

16.35

0.80

$44.78

$93,130

North Central Massachusetts
nonmetropolitan area

(8)

$44.12

$91,770

Balance of Alaska nonmetropolitan
area

760

10.74

0.53

$43.98

$91,480

(1) Estimates for detailed occupations do not sum to the totals because the totals include occupations not shown separately. Estimates
do not include self-employed workers.
(2) Annual wages have been calculated by multiplying the hourly mean wage by a "year-round, full-time" hours figure of 2,080 hours; for
those occupations where there is not an hourly wage published, the annual wage has been directly calculated from the reported survey
data.
(3) The relative standard error (RSE) is a measure of the reliability of a survey statistic. The smaller the relative standard error, the more
precise the estimate.
(8) Estimate not released.
(9) The location quotient is the ratio of the area concentration of occupational employment to the national average concentration. A
location quotient greater than one indicates the occupation has a higher share of employment than average, and a location quotient less
than one indicates the occupation is less prevalent in the area than average.
Other OES estimates and related information:
May 2017 National Occupational Employment and Wage Estimates
May 2017 State Occupational Employment and Wage Estimates
May 2017 Metropolitan and Nonmetropolitan Area Occupational Employment and Wage Estimates
May 2017 National Industry-Specific Occupational Employment and Wage Estimates
May 2017 Occupation Profiles

https://www.bls.gov/oes/current/oes291141.htm

4/21/2018

Registered Nurses

Page 9 of 9

Technical Notes

Last Modified Date: March 30, 2018

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Medical and Health Services Managers

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Occupational Employment and Wages, May 2017

BROWSE OES
OES HOME
OES OVERVIEW

11-9111 Medical and Health Services Managers

OES NEWS RELEASES

Plan, direct, or coordinate medical and health services in hospitals, clinics, managed care organizations, public health agencies, or similar

OES DATA

organizations.

OES CHARTS

National estimates for this occupation
Industry profile for this occupation
Geographic profile for this occupation

OES MAPS
OES PUBLICATIONS
OES DATABASES

National estimates for this occupation: Top

OES FAQS

Employment estimate and mean wage estimates for this occupation:

CONTACT OES

Employment (1)
SEARCH OES
Go

OES TOPICS

346,980

Employment Mean hourly Mean annual
Wage RSE (3)
RSE (3)
wage
wage (2)
0.5 %

$53.69

$111,680

0.4 %

Percentile wage estimates for this occupation:

RESPONDENTS
DOCUMENTATION

Percentile

10%

25%

50%
(Median)

Hourly Wage

$28.05

$36.22

$47.29

SPECIAL NOTICES
RELATED LINKS

Annual Wage (2) $58,350 $75,340 $98,350

75%

90%

$62.00

$84.68

$128,960 $176,130

Industry profile for this occupation: Top

Subscribe
to the OES
Update

Email Address

Percent of
industry
employment

Industry

Employment
(1)

Hourly mean
wage

Annual mean
wage (2)

General Medical and Surgical Hospitals

116,940

2.13

$57.95

$120,540

Offices of Physicians

40,490

1.59

$50.87

$105,810

Outpatient Care Centers

24,880

2.83

$49.74

$103,460

Nursing Care Facilities (Skilled Nursing Facilities)

22,670

1.40

$44.59

$92,750

Home Health Care Services

20,020

1.43

$47.70

$99,220

Employment
(1)

Percent of
industry
employment

Hourly mean
wage

Annual mean
wage (2)

Industries with the highest concentration of employment in this occupation:

Industry
Outpatient Care Centers

24,880

2.83

$49.74

$103,460

General Medical and Surgical Hospitals

116,940

2.13

$57.95

$120,540

Specialty (except Psychiatric and Substance Abuse)
Hospitals

5,080

1.96

$60.45

$125,730

Medical and Diagnostic Laboratories

5,090

1.92

$58.45

$121,570

Other Ambulatory Health Care Services

5,260

1.76

$46.71

$97,160

Employment
(1)

Percent of
industry
employment

Hourly mean
wage

Annual mean
wage (2)

Pharmaceutical and Medicine Manufacturing

570

0.20

$106.42

$221,360

Scientific Research and Development Services

2,720

0.42

$83.18

$173,020

Top paying industries for this occupation:

Industry

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Page 2 of 9

Navigational, Measuring, Electromedical, and
Control Instruments Manufacturing

0.02

$75.59

$157,220

Computer Systems Design and Related Services

120

0.01

$74.22

$154,380

Business, Professional, Labor, Political, and Similar
Organizations

320

0.07

$73.71

$153,320

States with the highest employment level in this occupation:

State

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

California

34,140

2.05

0.84

$58.90

$122,500

New York

25,850

2.81

1.15

$65.75

$136,770

Texas

23,740

2.00

0.82

$51.58

$107,290

Ohio

15,330

2.85

1.17

$48.21

$100,290

Pennsylvania

14,540

2.52

1.03

$46.35

$96,400

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Page 3 of 9

States with the highest concentration of jobs and location quotients in this occupation:

State

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)
$86,710

Iowa

6,160

4.01

1.65

$41.69

Oklahoma

6,210

3.95

1.62

$42.79

$88,990

Massachusetts

13,770

3.90

1.60

$61.89

$128,730

Maryland

10,210

3.83

1.57

$57.15

$118,860

Arkansas

4,360

3.63

1.49

$39.87

$82,930

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Page 4 of 9

Top paying States for this occupation:
Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

District of Columbia

1,670

2.36

0.97

$69.09

$143,710

New York

25,850

2.81

1.15

$65.75

$136,770

Connecticut

5,440

3.29

1.35

$63.75

$132,600

Delaware

1,010

2.29

0.94

$62.06

$129,070

Massachusetts

13,770

3.90

1.60

$61.89

$128,730

State

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Page 5 of 9

<
Metropolitan areas with the highest employment level in this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

New York-Jersey City-White
Plains, NY-NJ Metropolitan Division

19,870

2.97

1.22

$66.34

$137,980

Los Angeles-Long Beach-Glendale,
CA Metropolitan Division

9,200

2.08

0.85

$54.59

$113,540

Chicago-Naperville-Arlington
Heights, IL Metropolitan Division

7,930

2.16

0.89

$56.99

$118,540

Boston-Cambridge-Newton, MA
NECTA Division

7,130

3.87

1.59

$71.60

$148,930

Houston-The Woodlands-Sugar
Land, TX

5,620

1.92

0.79

$57.01

$118,590

Phoenix-Mesa-Scottsdale, AZ

5,610

2.83

1.16

$55.41

$115,260

Minneapolis-St. Paul-Bloomington,
MN-WI

5,140

2.66

1.09

$55.77

$116,000

Washington-Arlington-Alexandria,
DC-VA-MD-WV Metropolitan
Division

4,920

1.95

0.80

$62.44

$129,880

Dallas-Plano-Irving, TX
Metropolitan Division

4,630

1.86

0.76

$54.02

$112,370

Atlanta-Sandy Springs-Roswell, GA

4,400

1.68

0.69

$55.65

$115,740

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Page 6 of 9

<
Metropolitan areas with the highest concentration of jobs and location quotients in this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Peabody-Salem-Beverly, MA
NECTA Division

700

7.37

3.03

$52.43

$109,060

Silver Spring-Frederick-Rockville,
MD Metropolitan Division

4,010

6.86

2.82

$58.53

$121,730
$100,130

Iowa City, IA

620

6.76

2.78

$48.14

Ann Arbor, MI

1,340

6.24

2.56

$53.31

$110,880

Pittsfield, MA

220

5.54

2.27

$56.19

$116,870

Hot Springs, AR

180

5.22

2.14

$38.11

$79,260

Rochester, MN

590

5.13

2.11

$55.39

$115,210

Lawrence-Methuen Town-Salem,
MA-NH NECTA Division

420

5.11

2.10

$53.87

$112,060

Ames, IA

210

4.76

1.95

$43.98

$91,490

Jackson, TN

310

4.75

1.95

$40.69

$84,630

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Page 7 of 9

<
Top paying metropolitan areas for this occupation:

Metropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

San Francisco-Redwood City-South
San Francisco, CA Metropolitan
Division

2,170

1.94

0.80

$76.56

$159,250

Vallejo-Fairfield, CA

520

3.83

1.57

$73.89

$153,680

Nassau County-Suffolk County, NY
Metropolitan Division

4,120

3.16

1.30

$72.91

$151,660

Boston-Cambridge-Newton, MA
NECTA Division

7,130

3.87

1.59

$71.60

$148,930

Bridgeport-Stamford-Norwalk, CT

1,220

2.93

1.20

$70.30

$146,220

Athens-Clarke County, GA

180

2.15

0.88

$69.37

$144,280

Madera, CA

0.89

0.37

$69.20

$143,940

San Jose-Sunnyvale-Santa Clara,
CA

2,110

1.94

0.80

$68.96

$143,440

Santa Cruz-Watsonville, CA

340

3.50

1.44

$66.45

$138,220

New York-Jersey City-White
Plains, NY-NJ Metropolitan Division

19,870

2.97

1.22

$66.34

$137,980

Nonmetropolitan areas with the highest employment in this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

North Northeastern Ohio nonmetropolitan area (noncontiguous)

730

2.21

0.91

$42.83

$89,090

North Texas Region of Texas
nonmetropolitan area

710

2.63

1.08

$45.24

$94,100

Southern Ohio non-metropolitan
area

690

4.41

1.81

$44.53

$92,620

Southeast Iowa nonmetropolitan
area

690

3.02

1.24

$38.33

$79,730

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Southwest Maine nonmetropolitan
area

Page 8 of 9

630

3.30

1.35

$42.76

$88,940

Nonmetropolitan areas with the highest concentration of jobs and location quotients in this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Southwest Iowa nonmetropolitan
area

520

6.16

2.53

$40.97

$85,210

West Central New Hampshire
nonmetropolitan area

380

5.94

2.44

$65.50

$136,240

Southwest Oklahoma
nonmetropolitan area

290

4.70

1.93

$32.15

$66,880

Northeast Iowa nonmetropolitan
area

470

4.68

1.92

$36.92

$76,800

Northwest Massachusetts
nonmetropolitan area

120

4.46

1.83

$45.46

$94,570

Top paying nonmetropolitan areas for this occupation:

Nonmetropolitan area

Employment
(1)

Employment
per thousand
jobs

Location
quotient (9)

Hourly mean
wage

Annual mean
wage (2)

Eastern Sierra Region of California
nonmetropolitan area

(8)

$65.97

$137,230

West Central New Hampshire
nonmetropolitan area

380

5.94

2.44

$65.50

$136,240

Arizona nonmetropolitan area

360

4.00

1.64

$64.02

$133,170

Mother Lode Region of California
nonmetropolitan area

2.14

0.88

$61.80

$128,530

Balance of Alaska nonmetropolitan
area

180

2.56

1.05

$60.36

$125,540

(1) Estimates for detailed occupations do not sum to the totals because the totals include occupations not shown separately. Estimates
do not include self-employed workers.
(2) Annual wages have been calculated by multiplying the hourly mean wage by a "year-round, full-time" hours figure of 2,080 hours; for
those occupations where there is not an hourly wage published, the annual wage has been directly calculated from the reported survey
data.
(3) The relative standard error (RSE) is a measure of the reliability of a survey statistic. The smaller the relative standard error, the more
precise the estimate.
(8) Estimate not released.
(9) The location quotient is the ratio of the area concentration of occupational employment to the national average concentration. A
location quotient greater than one indicates the occupation has a higher share of employment than average, and a location quotient less
than one indicates the occupation is less prevalent in the area than average.
Other OES estimates and related information:
May 2017 National Occupational Employment and Wage Estimates
May 2017 State Occupational Employment and Wage Estimates
May 2017 Metropolitan and Nonmetropolitan Area Occupational Employment and Wage Estimates
May 2017 National Industry-Specific Occupational Employment and Wage Estimates
May 2017 Occupation Profiles

https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

Medical and Health Services Managers

Page 9 of 9

Technical Notes

Last Modified Date: March 30, 2018

RECOMMEND THIS PAGE USING:

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Glossary
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Contact Us

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Careers @ BLS
Find It! DOL
Join our Mailing Lists
Linking & Copyright Info

Inspector General (OIG)
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USA.gov
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https://www.bls.gov/oes/current/oes119111.htm

4/12/2018

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