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Appendix B

Classifications for Combined Hormonal Contraceptives


Combined hormonal contraceptives (CHCs) include low-dose (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

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

Condition

Category

Clarifications/Evidence/Comments

Personal Characteristics and Reproductive History

Pregnancy

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.

Age

a. Menarche to <40 yrs

1

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.

b. ≥40 yrs

2

Parity

a. Nulliparous

1

b. Parous

1

Breastfeeding

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.

a. <1 mo postpartum

3

b. 1 mo to <6 mos postpartum

2

c. ≥6 mos postpartum

2


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

Condition

Category

Clarifications/Evidence/Comments

Postpartum (in nonbreastfeeding women)

a. <21 days

3

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.

b. ≥21 days

1

Postabortion

Clarification: COCs, P, or R may be started immediately postabortion.

a. First trimester

1

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).

b. Second trimester

1

c. Immediate postseptic abortion

1

Past ectopic pregnancy

1

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.

History of pelvic surgery

1

Smoking

a. Age <35 yrs

2

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).

b. Age ≥35 yrs

i. <15 Cigarettes/day

3

ii. ≥15 Cigarettes/day

4

Obesity

a. ≥30 kg/m2 BMI

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).

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

2

History of bariatric surgery§

a. Restrictive procedures: decrease storage capacity of the stomach (vertical banded gastroplasty, laparoscopic adjustable gastric band, laparoscopic sleeve gastrectomy)

1

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

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)

COCs: 3

P/R: 1

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).

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)


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

Condition

Category

Clarifications/Evidence/Comments

i. Systolic 140--159 mm Hg or diastolic 90--99 mm Hg

3

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).

ii. Systolic ≥160 mm Hg or diastolic ≥100 mm Hg§

4

c. Vascular disease

4

History of high blood pressure during pregnancy (where current blood pressure is measurable and normal)

2

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).

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)

• History of estrogen-associated DVT/PE

• Pregnancy-associated DVT/PE

• Idiopathic DVT/PE

• Known thrombophilia, including antiphospholipid syndrome

• Active cancer (metastatic, on therapy, or within 6 mos after clinical remission), excluding non-melanoma skin cancer

• History of recurrent DVT/PE

4

ii. Lower risk for recurrent DVT/PE (no risk factors)

3

b. Acute DVT/PE

4

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

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

• Known thrombophilia, including antiphospholipid syndrome

• Active cancer (metastatic, on therapy, or within 6 mos after clinical remission), excluding non-melanoma skin cancer

• History of recurrent DVT/PE

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-by-case basis.

ii. Lower risk for recurrent DVT/PE (no risk factors)

3

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-by-case basis.

d. Family history (first-degree relatives)

2

Comment: Some conditions that increase the risk for DVT/PE are heritable.

e. Major surgery

i. With prolonged immobilization

4

ii. Without prolonged immobilization

2

f. Minor surgery without immobilization

1

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

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).

Superficial venous thrombosis

a. Varicose veins

1

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

b. Superficial thrombophlebitis

2

Current and history of ischemic heart disease§

4

Stroke§ (history of cerebrovascular accident)

4


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

Condition

Category

Clarifications/Evidence/Comments

Known hyperlipidemias

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.

Valvular heart disease

a. Uncomplicated

2

b. Complicated§ (pulmonary hypertension, risk for atrial fibrillation, history of subacute bacterial endocarditis)

4

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.

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)

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.

i. <6 mos

4

ii. ≥6 mos

3

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)

4

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.

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 present with 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 (219--237).

a. Positive (or unknown) antiphospholipid antibodies

4

Evidence: Antiphospholipid antibodies are associated with a higher risk for both arterial and venous thrombosis (238,239).

b. Severe thrombocytopenia

2

c. Immunosuppressive treatment

2

d. None of the above

2

Rheumatoid arthritis

a. On immunosuppressive therapy

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).

b. Not on immunosuppressive therapy

2

Neurologic Conditions

Headaches

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.

a. Non-migrainous (mild or severe)

1

2

b. Migraine

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).

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). Available http://www.i-h-s.org/upload/ct_clas/ihc_II_main_no_print.pdf.

i. Without aura

• Age <35 yrs

2

3

• Age ≥35 yrs

3

4

ii. With aura, at any age

4

4

Epilepsy§

1

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.


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

Condition

Category

Clarifications/Evidence/Comments

Depressive Disorders

Depressive disorders

1

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.

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

1

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

b. Heavy or prolonged bleeding (includes regular and irregular patterns)

1

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).

Unexplained vaginal bleeding (suspicious for serious condition)

Before evaluation

2

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

1

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).

Benign ovarian tumors (including cysts)

1

Severe dysmenorrhea

1

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).

Gestational trophoblastic disease

a. Decreasing or undetectable β--hCG levels

1

Evidence: After molar pregnancy evacuation, the balance of evidence found COC use did not increase the risk for postmolar trophoblastic disease, and b-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).

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

1

Cervical ectropion

1

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

Cervical intraepithelial neoplasia

2

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)

2

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

2

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

b. Benign breast disease

1

c. Family history of cancer

1

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).

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 CHC use.

i. Current

4

ii. Past and no evidence of current disease for 5 yrs

3

Endometrial hyperplasia

1

Endometrial cancer§

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.


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

Condition

Category

Clarifications/Evidence/Comments

Ovarian cancer§

1

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

1

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

Pelvic inflammatory disease (PID)

a. Past PID (assuming no current risk factors 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.

i. With subsequent pregnancy

1

ii. Without subsequent pregnancy

1

b. Current PID

1

STIs

a. Current purulent cervicitis or chlamydial infection or gonorrhea

1

b. Other STIs (excluding HIV and hepatitis)

1

c. Vaginitis (including Trichomonas vaginalis and bacterial vaginosis)

1

d. Increased risk for STIs

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).

HIV/AIDS

High risk for HIV

1

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§

1

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§

1

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

Other Infections

Schistosomiasis

a. Uncomplicated

1

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

b. Fibrosis of liver§ (if severe, see cirrhosis)

1

Tuberculosis§

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.

a. Nonpelvic

1

b. Pelvic

1

Malaria

1

Endocrine Conditions

Diabetes

a. History of gestational disease

1

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).

b. Nonvascular disease

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).

i. Noninsulin-dependent

2

ii. Insulin-dependent§

2

c. Nephropathy/retinopathy/ neuropathy§

3/4

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

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

3/4

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


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

Condition

Category

Clarifications/Evidence/Comments

Thyroid disorders

a. Simple goiter

1

b. Hyperthyroid

1

c. Hypothyroid

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

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

i. Treated by cholecystectomy

2

ii. Medically treated

3

iii. Current

3

b. Asymptomatic

2

History of cholestasis

a. Pregnancy-related

2

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

b. Past COC-related

3

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

Viral hepatitis

Initiation

Continuation

a. Acute or flare

3/4

2

Clarification for 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 (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).

b. Carrier

1

1

c. Chronic

1

1

Cirrhosis

a. Mild (compensated)

1

b. Severe§ (decompensated)

4

Liver tumors

a. Benign

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).

i. Focal nodular hyperplasia

2

ii. Hepatocellular adenoma§

4

b. Malignant§ (hepatoma)

4

Anemias

Thalassemia

1

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

Sickle cell disease§

2

Iron deficiency anemia

1

Comment: CHC use may decrease menstrual blood loss.

Solid Organ Transplantation

Solid organ transplantation§

a. Complicated: graft failure (acute or chronic), rejection, cardiac allograft vasculopathy

4

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).

b. Uncomplicated

2

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

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).


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

Condition

Category

Clarifications/Evidence/Comments

Drug Interactions

Antiretroviral (ARV) therapy

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.

a. Nucleoside reverse transcriptase inhibitors (NRTIs)

1

b. Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

2

c. Ritonavir-boosted protease inhibitors

3

Anticonvulsant therapy

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).

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

3

b. Lamotrigine

3

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

1

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

b. Antifungals

1

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

c. Antiparasitics

1

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

d. Rifampicin or rifabutin therapy

3

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.
  10. 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.
  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 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.
  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.
  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, population-based 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.
  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. Oral-contraceptive 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.
  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.
  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 low-dose 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.
  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 case-control 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, Guggenmoos-Holzmann 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 estrogen-porgestin 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 preeclampsia-eclampsia. 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.
  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 gene-environment 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.
  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 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.
  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, low-dose 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 hormone-based 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.
  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 early-onset 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.
  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.
  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.
  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.
  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 male-to-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.
  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 non-intravenous 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 male-female 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 family-planning 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.
  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.
  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 insulin-dependent 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.
  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, placebo-controlled 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.
  509. 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.
  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.
  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.
  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.


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