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US Medical Eligibility Criteria (US MEC) for Contraceptive Use

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
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 C1. Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestin-only pills
Condition Category Clarifications/Evidence/Comments
Implants DMPA POPs
Personal Characteristics and Reproductive History
Pregnancy NA NA NA 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.
Age 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 (148).
a. Menarche to <18 years 1 2 1
b. 18–45 years 1 1 1
c. >45 years 1 2 1
Parity
a. Nulliparous 1 1 1
b. Parous 1 1 1
Breastfeeding
a. <21 days postpartum 2 2 2 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.
b. 21 to <30 days postpartum 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.

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) 2 2 2
ii. Without other risk factors for VTE 2 2 2
c. 30–42 days postpartum 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.

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) 1 1 1
ii. Without other risk factors for VTE 1 1 1
d. >42 days postpartum 1 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 (49).
Evidence: Overall, 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 (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.
Postpartum (nonbreastfeeding women)
a. <21 days postpartum 1 1 1
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) 1 1 1
ii. Without other risk factors for VTE 1 1 1
c. >42 days postpartum 1 1 1
Postabortion
a. First trimester 1 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 (5255).

b. Second trimester 1 1 1 Clarification: POCs may be started immediately postabortion.
c. Immediate postseptic abortion 1 1 1 Clarification: POCs may be started immediately postabortion.
Past ectopic pregnancy 1 1 2 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.
History of pelvic surgery 1 1 1
Smoking
a. Age <35 years 1 1 1
b. Age ≥35 years
i. <15 cigarettes per day 1 1 1
ii. ≥15 cigarettes per day 1 1 1
Obesity
a. BMI ≥30 kg/m2 1 1 1
b. Menarche to <18 years and BMI ≥30 kg/m2 1 2 1 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 (5673).
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) 1 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).
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) 1 1 3 Evidence: Limited evidence demonstrated no substantial decrease in effectiveness of oral contraceptives among women who underwent a biliopancreatic diversion; however, evidence from pharmacokinetic studies suggested conflicting results regarding oral contraceptive effectiveness among women who underwent a jejunoileal bypass (74).
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.
Cardiovascular Disease
Multiple risk factors for atherosclerotic cardiovascular disease (e.g., older age, smoking, diabetes, hypertension, low HDL, high LDL, or high triglyceride levels) 2 3 2 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.
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 (https://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 1 2 1 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 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.
b. Elevated blood pressure levels
(properly taken measurements)
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.

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 compared with women who did not use these methods (75).

i. Systolic 140–159 mm Hg or diastolic 90–99 mm Hg 1 2 1
ii. Systolic ≥160 mm Hg or diastolic ≥100 mm Hg 2 3 2
c. Vascular disease 2 3 2 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.
Comment: Concern exists about hypoestrogenic effects and reduced HDL levels, particularly among users of DMPA. However, little concern exists about these effects with regard to POPs. The effects of DMPA might persist for some time after discontinuation.
History of high blood pressure during pregnancy (when current blood pressure is measurable and normal) 1 1 1
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

2 2 2
ii. Lower risk for recurrent DVT/PE (no risk factors) 2 2 2
b. Acute DVT/PE 2 2 2 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 (7577).
c. DVT/PE and established anticoagulant therapy for at least 3 months 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 (7577).

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).

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

2 2 2
ii. Lower risk for recurrent DVT/PE (no risk factors) 2 2 2
d. Family history (first-degree relatives) 1 1 1
e. Major surgery
i. With prolonged immobilization 2 2 2
ii. Without prolonged immobilization 1 1 1
f. Minor surgery without immobilization 1 1 1
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).
2 2 2 Clarification: Routine screening is not appropriate because of the rarity of the conditions and the high cost of screening.
Superficial venous disorders
a. Varicose veins 1 1 1
b. Superficial venous thrombosis (acute or history) 1 1 1
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).

Initiation Continuation Initiation Continuation Comment: Concern exists about hypoestrogenic effects and reduced HDL levels, particularly among users of DMPA. However, little concern exists about these effects with regard to POPs. The effects of DMPA might persist for some time after discontinuation.
2 3 3 2 3
Stroke (history of cerebrovascular accident)
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
Initiation Continuation Initiation Continuation Comment: Concern exists about hypoestrogenic effects and reduced HDL levels, particularly among users of DMPA. However, little concern exists about these effects with regard to POPs. The effects of DMPA might persist for some time after discontinuation.
2 3 3 2 3
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 1 1 1
b. Complicated (pulmonary hypertension, risk for atrial fibrillation, or history of subacute bacterial endocarditis) 1 1 1
Peripartum cardiomyopathy
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
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.

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 1 1 1
ii. ≥6 months 1 1 1
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) 2 2 2
Rheumatic Diseases
Systemic lupus erythematosus
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
Initiation Continuation
a. Positive (or unknown) antiphospholipid antibodies 3 3 3 3 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 (8199).
Evidence: Antiphospholipid antibodies are associated with a higher risk for both arterial and venous thrombosis (100,101).
b. Severe thrombocytopenia 2 3 2 2 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 (8199).
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 2 2 2 2 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 (8199).
d. None of the above 2 2 2 2 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 (8199).
Rheumatoid arthritis
a. Receiving immunosuppressive therapy 1 2/3 1 Clarification (DMPA): DMPA use among women receiving 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, progesterone, or estrogen (102).
b. Not receiving immunosuppressive therapy 1 2 1 Evidence: Limited evidence shows no consistent pattern of improvement or worsening of rheumatoid arthritis with use of oral contraceptives, progesterone, or estrogen (102).
Neurologic Conditions
Headaches
a. Nonmigraine (mild or severe) 1 1 1
b. Migraine 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-Classification-III-ICHD-III-2013-Beta.pdf).

i. Without aura (This category of migraine includes menstrual migraine.) 1 1 1
ii. With aura 1 1 1
Epilepsy
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
1 1 1 Clarification: If a woman is taking anticonvulsants, see Drug Interactions section. Certain anticonvulsants lower POC effectiveness.
Multiple sclerosis 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.
a. With prolonged immobility 1 2 1
b. Without prolonged immobility 1 2 1
Depressive Disorders
Depressive disorders 1 1 1 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 2 2 2 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, although these patterns might persist longer.
b. Heavy or prolonged bleeding (includes regular and irregular patterns) 2 2 2 Clarification: Unusually heavy bleeding should raise the suspicion of a serious underlying condition.
Unexplained vaginal bleeding
(suspicious for serious condition) before evaluation
3 3 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.
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 1 1 1
Benign ovarian tumors (including cysts) 1 1 1
Severe dysmenorrhea 1 1 1
Gestational trophoblastic disease
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
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.
a. Suspected gestational trophoblastic disease (immediate postevacuation)
i. Uterine size first trimester 1 1 1
ii. Uterine size second trimester 1 1 1
b. Confirmed gestational trophoblastic disease (after initial evacuation and during monitoring)
i. Undetectable/nonpregnant β–hCG levels 1 1 1
ii. Decreasing β–hCG levels 1 1 1
iii. Persistently elevated β-hCG levels or malignant disease, with no evidence or suspicion of intrauterine disease 1 1 1
iv. Persistently elevated β-hCG levels or malignant disease, with evidence or suspicion of intrauterine disease 1 1 1
Cervical ectropion 1 1 1
Cervical intraepithelial neoplasia 2 2 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)
2 2 1 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
Breast cancer is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
a. Undiagnosed mass 2 2 2 Clarification: Evaluation should be pursued as early as possible.
b. Benign breast disease 1 1 1
c. Family history of cancer 1 1 1
d. Breast 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.
i. Current 4 4 4
ii. Past and no evidence of current disease for 5 years 3 3 3
Endometrial hyperplasia 1 1 1
Endometrial cancer
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
1 1 1 Comment: While awaiting treatment, women may use POCs. 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).
1 1 1 Comment: While awaiting treatment, women may use POCs. In general, treatment of this condition can render a woman sterile.
Uterine fibroids 1 1 1 Comment: POCs do not appear to cause growth of uterine fibroids.
Pelvic inflammatory disease 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.
a. Past PID
i. With subsequent pregnancy 1 1 1
ii. Without subsequent pregnancy 1 1 1
b. Current PID 1 1 1
Sexually transmitted diseases
a. Current purulent cervicitis or chlamydial infection or gonococcal infection 1 1 1
b. Vaginitis (including Trichomonas vaginalis and bacterial vaginosis) 1 1 1
c. Other factors related to STDs 1 1 1
HIV
High risk for HIV 1 2 1 Clarification (DMPA): There continues to be evidence of a possible increased risk of acquiring HIV among progestin-only injectable users. Uncertainty exists about whether this is due to methodological issues with the evidence or a real biological effect. In many settings, unintended pregnancies and/or pregnancy-related morbidity and mortality are common, and progestin-only injectables are among the few types of methods widely available. Women should not be denied the use of progestin-only injectables because of concerns about the possible increased risk. Women considering progestin-only injectables should be advised about these concerns, about the uncertainty over whether there is a causal relationship, and about how to minimize their risk of acquiring HIV.
Evidence: Evidence from 13 observational studies of DMPA, NET-EN or non-specified progestin-only injectables, which were considered to be “informative but with important limitations”, continues to show some association between use of progestin-only injectables and risk of HIV acquisition, but it remains unclear whether this results from a causal relationship or methodological limitations (108a).

One additional randomized pilot feasibility trial, published subsequently to the systematic review, found no statistically significant difference in risk of HIV acquisition between progestin-only injectable users (DMPA or NET-EN) and copper IUD users; this study had several limitations including lack of power to assess differences in HIV acquisition rates, and problems with ascertainment of hormonal contraception exposure and HIV acquisition outcomes (108b).
Two small studies assessing levonorgestrel implants, which were considered to be “informative but with important limitations”, did not suggest an elevated risk, although the risk estimates were imprecise. One study reported no association between use of progestin-only pills and HIV acquisition (108a).

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).
1 1 1 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 (109111).
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 1 Evidence: Among women with uncomplicated schistosomiasis, limited evidence showed that DMPA use had no adverse effects on liver function (112).
b. Fibrosis of the liver (if severe, see Cirrhosis section) 1 1 1
Tuberculosis
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
Clarification: If a woman is taking rifampin, see Drug Interactions section. Rifampin is likely to decrease the effectiveness of some POCs.
a. Nonpelvic 1 1 1
b. Pelvic 1 1 1
Malaria 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 1 1 1 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 (115118).
b. Nonvascular disease 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 (119122).
i. Non-insulin dependent 2 2 2
ii. Insulin dependent 2 2 2
c. Nephropathy, retinopathy or neuropathy 2 3 2 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 2 3 2 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.
Thyroid disorders
a. Simple goiter 1 1 1
b. Hyperthyroid 1 1 1
c. Hypothyroid 1 1 1
Gastrointestinal Conditions
Inflammatory bowel disease (ulcerative colitis or Crohn’s disease) 1 2 2 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).
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 2 2 2
ii. Medically treated 2 2 2
iii. Current 2 2 2
b. Asymptomatic 2 2 2
History of cholestasis
a. Pregnancy related 1 1 1
b. Past COC related 2 2 2 Comment: Theoretical concern exists that a history of COC-related cholestasis might predict subsequent cholestasis with POC use. However, this has not been documented.
Viral hepatitis
a. Acute or flare 1 1 1
b. Carrier 1 1 1
c. Chronic 1 1 1
Cirrhosis
Severe cirrhosis is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
a. Mild (compensated) 1 1 1
b. Severe (decompensated) 3 3 3
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 2 2 2 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).
ii. Hepatocellular adenoma 3 3 3 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.
b. Malignant (hepatoma) 3 3 3
Respiratory Conditions
Cystic fibrosis
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
1 2 1 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 1 1 1
Sickle cell disease
This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 2).
1 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 (126133).
Iron deficiency anemia 1 1 1 Comment: Changes in the menstrual pattern associated with POC use have little effect on hemoglobin levels.
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 2 2 2
b. Uncomplicated 2 2 2
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.
a. Nucleoside reverse transcriptase inhibitors (NRTIs)
i. Abacavir (ABC) 1 1 1 Evidence: NRTIs do not appear to have significant risk for interactions with hormonal contraceptive methods (134139).
ii. Tenofovir (TDF) 1 1 1
iii. Zidovudine (AZT) 1 1 1
iv. Lamivudine (3TC) 1 1 1
v. Didanosine (DDI) 1 1 1
vi. Emtricitabine (FTC) 1 1 1
vii. Stavudine (D4T) 1 1 1
b. Nonnucleoside reverse transcriptase inhibitors (NNRTIs)
i. Efavirenz (EFV) 2 1 2 Clarification: Evidence suggests drug interactions between EFV and certain hormonal contraceptives. These interactions might reduce the effectiveness of the hormonal contraceptive.
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 (141143); 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 (141,144148). 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.
ii. Etravirine (ETR) 1 1 1
iii. Nevirapine (NVP) 1 1 1 Evidence: Five studies found no significant increase in pregnancy rates among women using implants and NVP compared with implants alone (141144,149). 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 (143,145,147149,151). 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.
iv. Rilpivirine (RPV) 1 1 1
c. Ritonavir-boosted protease inhibitors
i. Ritonavir-boosted atazanavir (ATV/r) 2 1 2 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) 2 1 2 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.
iii. Ritonavir-boosted fosamprenavir (FPV/r) 2 1 2 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.
iv. Ritonavir-boosted lopinavir (LPV/r) 1 1 1 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) 2 1 2 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.
vi. Ritonavir-boosted tipranavir (TPV/r) 2 1 2 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.
d. Protease inhibitors without ritonavir
i. Atazanavir (ATV) 1 1 1 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) 2 2 2 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.
iii. Indinavir (IDV) 1 1 1
iv. Nelfinavir (NFV) 2 1 2 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) 1 1 1
f. HIV integrase strand transfer inhibitors
i. Raltegravir (RAL) 1 1 1
ii. Dolutegravir (DTG) 1 1 1
iii. Elvitegravir (EVG) 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.
g. Fusion inhibitors
i. Enfuvirtide 1 1 1
Anticonvulsant therapy
a. Certain anticonvulsants (phenytoin, carbamazepine, barbiturates, primidone, topiramate, and oxcarbazepine) 2 1 3 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 (154156).
b. Lamotrigine 1 1 1 Evidence: No drug interactions have been reported among women with epilepsy receiving lamotrigine and POCs (157).
Antimicrobial therapy
a. Broad-spectrum antibiotics 1 1 1
b. Antifungals 1 1 1
c. Antiparasitics 1 1 1
d. Rifampin or rifabutin therapy 2 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.
Psychotropic medications 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 1 1 1 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 2 1 2 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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  9. Lopez LM, Grimes DA, Schulz KF, Curtis KM. Steroidal contraceptives: effect on bone fractures in women. Cochrane Database Syst Rev 2011;(7):CD006033. PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  18. 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.http://dx.doi.org/10.1016/S0010-7824(00)00168-2 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  46. Bahamondes L, Espejo-Arce X, Hidalgo MM, Hidalgo-Regina C, Teatin-Juliato 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 PubMed
  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 PubMed
  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 PubMed
  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-and-child-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 PubMed
  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. PubMed
  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 PubMed
  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. PubMed
  54. Lähteenmäki P, Toivonen J, Lähteenmäki PL. Postabortal contraception with norethisterone enanthate injections. Contraception 1983;27:553–62http://dx.doi.org/10.1016/0010-7824(83)90020-3 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  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;160:40–5http://dx.doi.org/10.1001/archpedi.160.1.40 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  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. PubMed
  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 PubMed
  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 PubMed
  70. Pantoja M, Medeiros T, Baccarin MC, Morais SS, Bahamondes L, Fernandes AM. Variations in body mass index of users of depot-medroxyprogesterone acetate as a contraceptive. Contraception 2010;81:107–11.http://dx.doi.org/10.1016/j.contraception.2009.07.008 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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;57:315–24http://dx.doi.org/10.1016/S0010-7824(98)00041-9 PubMed
  76. Heinemann LA, Assmann A, DoMinh T, Garbe E. 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.http://dx.doi.org/10.3109/13625189909064007 PubMed
  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 PubMed
  78. Sönmezer M, Atabekoğlu C, Cengiz B, Dökmeci F, Cengiz SD. Depot-medroxyprogesterone 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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  103. Tepper N, Whiteman M, Zapata L, Marchbanks P, Curtis K. 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 PubMed
  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 E, 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. PubMed
  108. (a) Polis CB, Curtis KM, Hannaford PC, Phillips SJ, Chipato T, Kiarie JN, et al. An updated systematic review of epidemiological evidence on hormonal contraceptive methods and HIV acquisition in women. AIDS 2016 Nov 13;30(17):2665-83.
    (b) Hofmeyr GJ, Singata-Madliki M, Lawrie TA, Bergel E, Temmerman M. Effects of injectable progestogen contraception versus the copper intrauterine device on HIV acquisition: sub-study of a pragmatic randomised controlled trial. J Fam Plann Reprod Health Care 2017 Apr 05.
  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 PubMed
  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 PubMed
  111. Phillips SJ, Polis CB, Curtis KM. The safety of hormonal contraceptives for women living with HIV and their sexual partners. Contraception 2016;93:11–6http://dx.doi.org/10.1016/j.contraception.2015.10.002. PubMed
  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 PubMed
  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. PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  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;46:858–64http://dx.doi.org/10.1016/S0015-0282(16)49825-0. PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  140. Vieira CS, Bahamondes MV, de Souza RM, et al. Effect of antiretroviral therapy including lopinavir/ritonavir or efavirenz on etonogestrel-releasing implant pharmacokinetics in HIV-positive women. J Acquir Immune Defic Syndr 2014;66:378–85.http://dx.doi.org/10.1097/QAI.0000000000000189 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  145. Cohn SE, Park JG, Watts DH, et al; ACTG A5093 Protocol Team. Depo-medroxyprogesterone 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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  149. Hubacher D, Liku J, Kiarie J, et al. Effect of concurrent use of anti-retroviral 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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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 PubMed
  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. PubMed
  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 PubMed
  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.

 

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