Drug: Desogen

Desogen® (desogestrel and ethinyl estradiol tablets) (desogestrel and ethinyl estradiol) Tablets provide an oral contraceptive regimen of 21 white round tablets each containing 0.15 mg desogestrel (13-ethyl-11-methylene-18,19-dinor-17 alpha-pregn-4-en-20-yn-17-ol) and 0.03 mg ethinyl estradiol (19-nor-17 alpha-pregna-1,3,5 (10)-trien-20-yne-3,17-diol). Inactive ingredients include vitamin E, corn starch, povidone, stearic acid, colloidal silicon dioxide, lactose, hydroxypropyl methyl-cellulose, polyethylene glycol, titanium dioxide, and talc. Desogen® (desogestrel and ethinyl estradiol tablets) also contains 7 green round tablets containing the following inactive ingredients: lactose, corn starch, magnesium stearate, FD&C Blue No. 2 aluminum lake, ferric oxide, hydroxypropyl methylcellulose, polyethylene glycol, titanium dioxide, and talc. The molecular weights for desogestrel and ethinyl estradiol are 310.48 and 296.41, respectively. The structural formulas are as follows:

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An increased risk of the following serious adverse reactions has been associated with the use of oral contraceptives (see WARNINGS):
  • Thrombophlebitis and venous
  • thrombosis with or without embolism
  • Arterial thromboembolism
  • Pulmonary embolism
  • Myocardial infarction
  • Cerebral hemorrhage
  • Cerebral thrombosis
  • Hypertension
  • Gallbladder disease
  • Hepatic adenomas or
  • benign liver tumors
There is evidence of an association between the following condi-tions and the use of oral contraceptives:
  • Mesenteric thrombosi
  • Retinal thrombosi
The following adverse reactions have been reported in patients receiving oral contraceptives and are believed to be drug-related:
  • Nausea
  • Vomiting
  • Gastrointestinal symptoms
  • (such as abdominal cramps and bloating)
  • Breakthrough bleeding
  • Change in cervical
  • erosion and secretion
  • Diminution in lactation when given immediately postpartum
  • Cholestatic jaundice
  • Spotting
  • Change in menstrual flow
  • Amenorrhea
  • Temporary infertility after discontinuation of treatment
  • Edema
  • Melasma which may persist
  • Breast changes: tenderness,
  • enlargement, secretion
  • Change in weight (increase or decrease)
  • Migraine
  • Rash (allergic)
  • Mental depression
  • Reduced tolerance to carbohydrates
  • Vaginal candidiasis
  • Change in corneal curvature steepening)
  • Intolerance to contact lenses
The following adverse reactions have been reported in users of oral contraceptives and a causal association has been neither confirmed nor refuted:
  • Pre-menstrual syndrome
  • Cataracts
  • Changes in appetite
  • Cystitis-like syndrome
  • Headache
  • Nervousness
  • Dizziness
  • Hirsutism
  • Loss of scalp hair
  • Erythema multiforme
  • Erythema nodosum
  • Hemorrhagic eruption
  • Vaginitis
  • Porphyria
  • Impaired renal function
  • Hemolytic uremic syndrome
  • Acne
  • Changes in libido
  • Colitis
  • Budd-Chiari Syndrome
Read the Desogen (desogestrel and ethinyl estradiol tablets) Side Effects Center for a complete guide to possible side effectsLearn More »

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To achieve maximum contraceptive effectiveness, Desogen® (desogestrel and ethinyl estradiol tablets) (desogestrel and ethinyl estradiol) Tablets must be taken exactly as directed and at intervals not exceeding 24 hours. Desogen® (desogestrel and ethinyl estradiol tablets) may be initiated using either a Sunday start or a Day 1 start. NOTE: Each cycle pack dispenser is preprinted with the days of the week, starting with Sunday, to facilitate a Sunday start regimen. Six different "day label strips" are provided with each cycle pack dispenser in order to accommodate a Day 1 start regimen. In this case, the patient should place the self-adhesive "day label strip" that corresponds to her starting day over the preprinted days. IMPORTANT: The possibility of ovulation and conception prior to initiation of use of Desogen® (desogestrel and ethinyl estradiol tablets) should be considered. The use of Desogen® (desogestrel and ethinyl estradiol tablets) for contraception may be initiated 4 weeks postpartum in women who elect not to breast-feed. When the tablets are administered during the postpartum period, the increased risk of thromboembolic disease associated with the postpartum period must be considered (see CONTRAINDICATIONS and WARNINGS concerning thromboembolic disease. See also PRECAUTIONS for "Nursing Mothers"). If the patient starts on Desogen® (desogestrel and ethinyl estradiol tablets) postpartum, and has not yet had a period, she should be instructed to use another method of contra-ception, such as condoms, diaphragms, or spermicides, until a white tablet has been taken daily for 7 days. SUNDAY START When initiating a Sunday start regimen, another method of contra-ception, such as condoms, diaphragms, or spermicides, should be used until after the first 7 consecutive days of administration. Using a Sunday start, tablets are taken daily without interruption as follows: The first white tablet should be taken on the first Sunday after menstruation begins (if menstruation begins on Sunday, the first white tablet is taken on that day). One white tablet is taken daily for 21 days, followed by 1 green (inert) tablet daily for 7 days. For all subsequent cycles, the patient then begins a new 28-tablet regimen on the next day (Sunday) after taking the last green tablet. [If switching from a different Sunday Start oral contraceptive, the first Desogen® (desogestrel and ethinyl estradiol tablets) (desogestrel and ethinyl estradiol) tablet should be taken on the same day that a new pack of the previous oral contra-ceptive would have been started.] If a patient misses 1 white tablet, she should take the missed tablet as soon as she remembers. If the patient misses 2 consecutive white tablets in Week 1 or Week 2, the patient should take 2 tablets the day she remembers and 2 tablets the next day; thereafter, the patient should resume taking 1 tablet daily until she finishes the cycle pack. The patient should be instructed to use a back-up method of birth control, such as condoms, diaphragms, or spermi-cides, if she has intercourse in the 7 days after missing pills. If the patient misses 2 consecutive white tablets in the third week or misses 3 or more white tablets in a row at any time during the cycle, the patient should keep taking 1 white tablet daily until the next Sunday. On Sunday the patient should throw out the rest of that cycle pack and start a new cycle pack that same day. The patient should be instructed to use a back-up method of birth control, such as condoms, diaphragms, or spermicides, if she has intercourse in the 7 days after missing pills. DAY 1 START Counting the first day of menstruation as "Day 1", tablets are taken without interruption as follows: One white tablet daily for 21 days, then one green (inert) tablet daily for 7 days. For all subsequent cycles, the patient then begins a new 28-tablet regimen on the next day after taking the last green tablet. [If switching directly from another oral contraceptive, the first white tablet should be taken on the first day of menstruation which begins after the last ACTIVE tablet of the previous product.] If a patient misses 1 white tablet, she should take the missed tablet as soon as she remembers. If the patient misses 2 consecutive white tablets in Week 1 or Week 2, the patient should take 2 tablets the day she remembers and 2 tablets the next day; thereafter, the patient should resume taking 1 tablet daily until she finishes the cycle pack. The patient should be instructed to use a back-up method of birth control, such as condoms, diaphragms, or spermi-cides, if she has intercourse in the 7 days after missing pills. If the patient misses 2 consecutive white tablets in the third week or misses 3 or more white tablets in a row at any time during the cycle, the patient should throw out the rest of that cycle pack and start a new cycle pack that same day. The patient should be instructed to use a back-up method of birth control, such as condoms, diaphragms, or spermicides, if she has intercourse in the 7 days after missing pills. ALL ORAL CONTRACEPTIVES Breakthrough bleeding, spotting, and amenorrhea are frequent reasons for patients discontinuing oral contraceptives. In break-through bleeding, as in all cases of irregular bleeding from the vagina, non-functional causes should be borne in mind. In undiag-nosed persistent or recurrent abnormal bleeding from the vagina, adequate diagnostic measures are indicated to rule out pregnancy or malignancy. If both pregnancy and pathology have been excluded, time or a change to another preparation may solve the problem. Changing to an oral contraceptive with a higher estrogen content, while potentially useful in minimizing menstrual irregularity, should be done only if necessary since this may increase the risk of thromboembolic disease. Use of oral contraceptives in the event of a missed menstrual period:
  1. If the patient has not adhered to the prescribed schedule, the possibility of pregnancy should be considered at the time of the first missed period and oral contraceptive use should be discon-tinued if pregnancy is confirmed.
  2. If the patient has adhered to the prescribed regimen and misses two consecutive periods, pregnancy should be ruled out.

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Changes in Contraceptive Effectiveness Associated with Co-Administration of Other Drugs Contraceptive effectiveness may be reduced when hormonal contraceptives are co-administered with some antibiotics, anticonvulsants, and other drugs that increase metabolism of contraceptive steroids. This could result in unintended pregnancy or breakthrough bleeding. Examples include barbi-turates, griseofulvin, rifampin, phenylbutazone, phenytoin, carbamazepine, felbamate, oxcarbazepine, and topiramate. Several cases of contraceptive failure and breakthrough bleeding have been reported in the literature with concomitant administration of antibiotics such as ampicillin and tetracy-clines. However, clinical pharmacology studies investigating drug interaction between combined oral contraceptives and these antibiotics have reported inconsistent results. Several of the anti-HIV protease inhibitors have been studied with co-administration of oral combination hormonal contra-ceptives; significant changes (increase and decrease) in the plasma levels of the estrogen and progestin have been noted in some cases. The safety and efficacy of oral contraceptive products may be affected with co-administration of anti-HIV protease inhibitors. Health care providers should refer to the label of the individual anti-HIV protease inhibitors for further drug-drug interaction information. Herbal products containing St. John's Wort (hypericum per-foratum) may induce hepatic enzymes (cytochrome P450) and p-glycoprotein transporter and may reduce the effectiveness of contraceptive steroids. This may also result in breakthrough bleeding. Increase in Plasma Hormone Levels Associated with Co-Administered Drugs Co-administration of atorvastatin and certain oral contraceptives containing ethinyl estradiol increase AUC values for ethinyl estradiol by approximately 20%. Ascorbic acid and aceta-minophen may increase plasma ethinyl estradiol levels, possibly by inhibition of conjugation. CYP 3A4 inhibitors such as itra-conazole or ketoconazole may increase plasma hormone levels. Changes in Plasma Levels of Co-Administered Drugs Combination hormonal contraceptives containing some synthetic estrogens (e.g., ethinyl estradiol) may inhibit the metabolism of other compounds. Increased plasma concen-trations of cyclosporine, prednisolone, and theophylline have been reported with concomitant administration of oral contra-ceptives. Decreased plasma concentrations of acetaminophen and increased clearance of temazepam, salicylic acid, morphine, and clofibric acid, due to induction of conjugation, have been noted when these drugs were administered with oral contraceptives. 8. INTERACTIONS WITH LABORATORY TESTS Certain endocrine and liver function tests and blood compo-nents may be affected by oral contraceptives: a. Increased prothrombin and factors VII, VIII, IX and X; decreased antithrombin 3; increased norepinephrine-induced platelet aggregability. b. Increased thyroid binding globulin (TBG) leading to increased circulating total thyroid hormone, as measured by protein-bound iodine (PBI), T4 by column or by radioim-munoassay. Free T3 resin uptake is decreased, reflecting the elevated TBG; free T4 concentration is unaltered. c. Other binding proteins may be elevated in serum. d. Sex hormone-binding globulins are increased and result in elevated levels of total circulating sex steroids; however, free or biologically active levels either decrease or remain unchanged. e. Triglycerides may be increased and levels of various other lipids and lipoproteins may be affected. f.  Glucose tolerance may be decreased. g. Serum folate levels may be depressed by oral contraceptive therapy. This may be of clinical significance if a woman becomes pregnant shortly after discontinuing oral contra-ceptives. Last reviewed on RxList: 7/9/2007
This monograph has been modified to include the generic and brand name in many instances.

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Desogen® (desogestrel and ethinyl estradiol tablets) (desogestrel and ethinyl estradiol) Tablets are indicated for the prevention of pregnancy in women who elect to use this product as a method of contraception. Oral contraceptives are highly effective. Table I lists the typical accidental pregnancy rates for users of combination oral contraceptives and other methods of contraception. The efficacy of these contraceptive methods, except sterilization, the IUD, and the NORPLANT® System, depends upon the reliability with which they are used. Correct and consistent use of these methods can result in lower failure rates. TABLE I: PERCENTAGE OF WOMEN EXPERIENCING AN UNINTENDED PREGNANCY DURING THE FIRST YEAR OF TYPICAL USE AND THE FIRST YEAR OF PERFECT USE OF CONTRACEPTION AND THE PERCENTAGE CONTINUING USE AT THE END OF THE FIRST YEAR: UNITED STATES.   % of Women Experiencing an Unintended Pregnancy within the First Year of Use % of Women Continuing Use at Method
(1) Typical Use1 (2) Perfect Use2
(3) One Year3
(4) Chance4 85 85   Spermicides5 26 6 40 Periodic abstinence 25   63   Calendar   9     Ovulation Method   3     Sympto-Thermal6   2     Post-Ovulation   1   Cap7         Parous Women 40 26 42   Nulliparous Women 20 9 56 Sponge         Parous Women 40 20 42   Nulliparous Women 20 9 56 Diaphragm7 20 6 56 Withdrawal 19 4   Condom8         Female (Reality) 21 5 56   Male 14 3 61 Pill 5   71   Progestin Only   0.5     Combined   0.1   IUD         Progesterone T 2.0 1.5 81   Copper T 380A 0.8 0.6 78   LNg 20 0.1 0.1 81 Depo-Provera 0.3 0.3 70 Norplant and Norplant-2 0.05 0.05 88 Female sterilization 0.5 0.5 100 Male sterilization 0.15 0.10 100 Emergency Contraceptive Pills: Treatment initiated within 72 hours after unprotected intercourse reduces the risk of pregnancy by at least 75%.
9 Lactation Amenorrhea Method: LAM is a highly effective temporary method of contraception.10
Adapted from Hatcher et al., Contraceptive Technology, 17th Revised Edition. New York, NY: Irvington Publishers, 1998.
1 Among typical couples who initiate use of a method (not necessarily for the first time), the percentage who experience an accidental pregnancy during the first year if they do not stop use for any other reason.
2 Among couples who initiate use of a method (not necessarily for the first time) and who use it perfectly (both consistently and correctly), the percentage who experience an accidental pregnancy during the first year if they do not stop use for any other reason.
3 Among couples attempting to avoid pregnancy, the percentage who continue to use a method for one year.
4 The percents becoming pregnant in columns (2) and (3) are based on data from populations where contraception is not used and from women who cease using contraception in order to become pregnant. Among such populations, about 89% become pregnant within one year. This estimate was lowered slightly (to 85%) to represent the percent who would become pregnant within one year among women now relying on reversible methods of contraception if they abandoned contraception altogether.
5 Foams, creams, gels, vaginal suppositories, and vaginal film.
6 Cervical mucus (ovulation) method supplemented by calendar in the pre-ovulatory and basal body temperature in the post-ovulatory phases.
7 With spermicidal cream or jelly.
8 Without spermicides.
9 The treatment schedule is one dose within 72 hours after unprotected intercourse, and a second dose 12 hours after the first dose. The FDA has declared the following brands of oral contraceptives to be safe and effective for emergency contraception: Ovral (one dose is two white pills), Alesse (one dose is five pink pills), Nordette or Levlen (one dose is four yellow pills). Two FDA-approved products for emergency contraception include Plan B® and Preven®.a,b
10 However, to maintain effective protection against pregnancy, another method of contraception must be used as soon as menstruation resumes, the frequency or duration of breast-feeds is reduced, bottle feeds are introduced, or the baby reaches six months of age.
a Plan B® [package insert]. Washington DC: Women's Capital Corporation.
b Preven® [package insert]. Somerville, NJ: Gynetics Inc;1998.

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Oral contraceptives should not be used in women who currently have the following conditions:
  • Thrombophlebitis or thromboembolic disorders
  • A past history of deep vein thrombophlebitis or thromboembolic disorders
  • Cerebral vascular or coronary artery disease
  • Valvular heart disease with complications
  • Severe hypertension
  • Diabetes with valvular involvement
  • Headaches with focal neurological symptoms
  • Major surgery with prolonged immobilization
  • Known or suspected carcinoma of the breast or history of breast cancer
  • Carcinoma of the endometrium or other known or suspected estrogen-dependent neoplasia
  • Undiagnosed abnormal genital bleeding
  • Cholestatic jaundice of pregnancy or jaundice with prior pill use
  • Hepatic adenomas or carcinomas
  • Known or suspected pregnancy
  • Hypersensitivity to any component of this product
REFERENCES 73. The Cancer and Steroid Hormone Study of the Centers for Disease Control and the National Institute of Child Health and Human Development: Oral contraceptive use and the risk of ovarian cancer. JAMA 1983; 249:1596-1599.
74. The Cancer and Steroid Hormone Study of the Centers for Disease Control and the National Institute of Child Health and Human Development: Combi-nation oral contraceptive use and the risk of endometrial cancer. JAMA 1987; 257:796-800.
75. Ory HW. Functional ovarian cysts and oral contraceptives: negative association confirmed surgically. JAMA 1974; 228:68-69.
76. Ory HW, Cole P, Macmahon B, Hoover R. Oral contraceptives and reduced risk of benign> breast disease. N Engl J Med 1976; 294:419-422.
77. Ory HW. The noncontraceptive health benefits from oral contraceptive use. Fam Plann Perspect 1982; 14:182-184.
78. Ory HW, Forrest JD, Lincoln R. Making Choices: Evaluating the health risks and benefits of birth control methods. New York, The Alan Guttmacher Institute, 1983; p. 1.
Last reviewed on RxList: 7/9/2007
This monograph has been modified to include the generic and brand name in many instances.

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Serious ill effects have not been reported following acute ingestion of large doses of oral contraceptives by young children. Overdosage may cause nausea, and withdrawal bleeding may occur in females. Non-Contraceptive Health Benefits The following non-contraceptive health benefits related to the use of oral contraceptives are supported by epidemiologic studies which largely utilized oral contraceptive formulations containing estrogen doses exceeding 0.035 mg of ethinyl estradiol or 0.05 mg of mestranol (73-78). Effects on menses:
  • increased menstrual cycle regularity
  • decreased blood loss and decreased incidence of irondeficiency anemia
  • decreased incidence of dysmenorrhea
Effects related to inhibition of ovulation:
  • decreased incidence of functional ovarian cysts
  • decreased incidence of ectopic pregnancies
Effects from long-term use:
  • decreased incidence of fibroadenomas and fibrocystic disease of the breast
  • decreased incidence of acute pelvic inflammatory disease
  • decreased incidence of endometrial cancer
  • decreased incidence of ovarian cancer

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Desogen® (desogestrel and ethinyl estradiol tablets) (desogestrel and ethinyl estradiol) Tablets contain 21 round white tablets and 7 round green tablets in a blister card within a recyclable plastic dispenser. Each white tablet (debossed with "T5R" on one side and "Organon" on the other side) contains 0.15 mg desogestrel and 0.03 mg ethinyl estradiol. Each green tablet (debossed with "K2H" on one side and "Organon" on the other side) contains inert ingredients. Boxes of 6 NDC 0052-0261-06 STORAGE: Store below 86°F (30°C) Manufactured for Organon USA Inc., West Orange, NJ 07052 by N.V. Organon, Oss, The Netherlands or Organon (Ireland) Ltd., Swords, Co. Dublin, Ireland
FDA rev date: 6/7/2007Last reviewed on RxList: 7/9/2007
This monograph has been modified to include the generic and brand name in many instances.

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1. GENERAL Patients should be counseled that this product does not protect against HIV infection (AIDS) and other sexually transmitted diseases. 2. PHYSICAL EXAMINATION AND FOLLOW UP It is good medical practice for all women to have annual history and physical examinations, including women using oral con-traceptives. The physical examination, however, may be deferred until after initiation of oral contraceptives if requested by the woman and judged appropriate by the clinician. The physical examination should include special reference to blood pressure, breasts, abdomen and pelvic organs, including cervical cytology, and relevant laboratory tests. In case of undiagnosed, persis-tent or recurrent abnormal vaginal bleeding, appropriate measures should be conducted to rule out malignancy. Women with a strong family history of breast cancer or who have breast nodules should be monitored with particular care. 3. LIPID DISORDERS Women who are being treated for hyperlipidemias should be followed closely if they elect to use oral contraceptives. Some progestogens may elevate LDL levels and may render the control of hyperlipidemias more difficult. 4. LIVER FUNCTION If jaundice develops in any woman receiving such drugs, the medication should be discontinued. Steroid hormones may be poorly metabolized in patients with impaired liver function. 5. FLUID RETENTION Oral contraceptives may cause some degree of fluid retention. They should be prescribed with caution, and only with careful monitoring, in patients with conditions which might be aggra-vated by fluid retention. 6. EMOTIONAL DISORDERS Women with a history of depression should be carefully observed and the drug discontinued if depression recurs to a serious degree. 7. CONTACT LENSES Contact lens wearers who develop visual changes or changes in lens tolerance should be assessed by an ophthalmologist. 9. CARCINOGENESIS See WARNINGS section. 10. PREGNANCY Pregnancy Category X (see CONTRAINDICATIONS and WARNINGS). 11. NURSING MOTHERS Small amounts of oral contraceptive steroids have been identified in the milk of nursing mothers and a few adverse effects on the child have been reported, including jaundice and breast enlargement. In addition, oral contraceptives given in the postpartum period may interfere with lactation by decreasing the quantity and quality of breast milk. If possible, the nursing mother should be advised not to use oral contra-ceptives but to use other forms of contraception until she has completely weaned her child. 12. PEDIATRIC USE Safety and efficacy of Desogen® (desogestrel and ethinyl estradiol tablets) (desogestrel and ethinyl estradiol) Tablets have been established in women of repro-ductive age. Safety and efficacy are expected to be the same for postpubertal adolescents under the age of 16 and for users 16 years and older. Use of this product before menarche is not indicated. 13. GERIATRIC USE This product has not been studied in women over 65 years of age and is not indicated in this population. Information For The Patient See Patient Labeling Printed Below REFERENCES 1. Hatcher RA, Trussell J, Stewart F et al. Contraceptive Technology: Seventeenth Revised Edition, New York: Irvington Publishers, 1998.
2. Stadel BV. Oral contraceptives and cardio-vascular disease. (Pt. 1). N Engl J Med 1981; 305:612-618.
3. Stadel BV. Oral contraceptives and cardiovascular disease. (Pt. 2). N Engl J Med 1981; 305:672-677.
4. Adam SA, Thorogood M. Oral contraception and myocardial infarction revisited: the effects of new preparations and prescribing patterns. Br J Obstet and Gynecol 1981; 88:838-845.
5. Mann JI, Inman WH. Oral contraceptives and death from myocardial infarction. Br Med J 1975; 2(5965):245-248.
6. Mann JI, Vessey MP, Thorogood M, Doll R. Myocardial infarction in young women with special reference to oral contraceptive practice. Br Med J 1975; 2(5956):241-245.
7. Royal College of General Practitioners' Oral Contraception Study: Further analyses of mortality in oral contraceptive users. Lancet 1981; 1:541-546.
8. Slone D, Shapiro S, Kaufman DW, Rosenberg L, Miettinen OS, Stolley PD. Risk of myocardial infarction in relation to current and discontinued use of oral contraceptives. N Engl J Med 1981; 305:420-424.
9. Vessey MP. Female hormones and vascular disease-an epidemiological overview. Br J Fam Plann 1980; 6:1-12.
10 . Russell-Briefel RG, Ezzati TM, Fulwood R, Perlman JA, Murphy RS. Cardiovascular risk status and oral contraceptive use, United States, 1976-80. Prevent Med 1986; 15:352-362.
11. Goldbaum GM, Kendrick JS, Hogelin GC, Gentry EM. The relative impact of smoking and oral contraceptive use on women in the United States. JAMA 1987; 258:1339-1342.
12. Layde PM, Beral V. Further analyses of mortality in oral contraceptive users: Royal College General Practitioners' Oral Contraception Study. (Table 5) Lancet 1981; 1:541-546.
13. Knopp RH. Arteriosclerosis risk: the roles of oral contraceptives and postmenopausal estrogens. J Reprod Med 1986; 31(9) (Supplement):913-921.
14. Krauss RM, Roy S, Mishell DR, Casagrande J, Pike MC. Effects of two low-dose oral contraceptives on serum lipids and lipoproteins: Differ-ential changes in high-density lipoproteins subclasses. Am J Obstet 1983; 145:446-452.
15. Wahl P, Walden C, Knopp R, Hoover J, Wallace R, Heiss G, Rifkind B. Effect of estrogen/ progestin potency on lipid/lipoprotein cholesterol. N Engl J Med 1983; 308:862-867.
16. Wynn V, Niththyananthan R. The effect of progestin in combined oral contraceptives on serum lipids with special reference to high-density lipoproteins. Am J Obstet Gynecol 1982; 142:766-771.
17. Wynn V, Godsland I. Effects of oral contra-ceptives and carbohydrate metabolism. J Reprod Med 1986; 31 (9) (Supplement):892-897.
18 . LaRosa JC. Atherosclerotic risk factors in cardiovascular disease. J Reprod Med 1986; 31 (9) (Supple-ment):906-912.
19. Inman WH, Vessey MP. Investigation of death from pulmonary, coronary, and cerebral thrombosis and embolism in women of child-bearing age. Br Med J 1968; 2 (5599):193-199.
20. Maguire MG, Tonascia J, Sartwell PE, Stolley PD, Tockman MS. Increased risk of thrombosis due to oral contraceptives: a further report. Am J Epidemiol 1979; 110 (2):188-195.
21. Pettiti DB, Wingerd J, Pellegrin F, Ramacharan S. Risk of vascular disease in women: smoking, oral contraceptives, noncontraceptive estrogens, and other factors. JAMA 1979; 242:1150-1154.
22. Vessey MP, Doll R. Investigation of relation between use of oral contraceptives and thromboembolic disease. Br Med J 1968; 2 (5599):199-205.
23. Vessey MP, Doll R. Investigation of relation between use of oral contraceptives and thromboembolic disease. A further report. Br Med J 1969; 2 (5658):651-657.
24. Porter JB, Hunter JR, Danielson DA, Jick H, Stergachis A. Oral contracep-tives and non-fatal vascular disease-recent experience. Obstet Gynecol 1982; 59 (3):299-302.
25. Vessey M, Doll R, Peto R, Johnson B, Wiggins P. A long-term follow-up study of women using different methods of contraception: an interim report. Biosocial Sci 1976; 8:375-427.
26. Royal College of General Practitioners: Oral contraceptives, venous thrombosis, and varicose veins. J Royal Coll Gen Pract 1978; 28:393-399.
27. Collaborative Group for the Study of Stroke in Young Women: Oral contraception and increased risk of cerebral ischemia or thrombosis. N Engl J Med 1973; 288:871-878.
28. Petitti DB, Wingerd J. Use of oral contraceptives, cigarette smoking, and risk of subarachnoid hemorrhage. Lancet 1978; 2:234-236.
29. Inman WH. Oral contraceptives and fatal subarachnoid hemorrhage. Br Med J 1979; 2 (6203):1468-70.
30. Collaborative Group for the Study of Stroke in Young Women: Oral contraceptives and stroke in young women: associated risk factors. JAMA 1975; 231:718-722.
31. Inman WH, Vessey MP, Westerholm B, Engelund A. Thromboembolic disease and the steroidal content of oral contraceptives. A report to the Committee on Safety of Drugs. Br Med J 1970; 2:203-209.
32. Meade TW, Greenberg G, Thompson SG. Progestogens and cardiovascular reactions associated with oral contraceptives and a comparison of the safety of 50- and 35-mcg oestrogen preparations. Br Med J 1980; 280 (6224):1157-1161.
33. Kay CR. Progestogens and arterial disease-evidence from the Royal College of General Practitioners' Study. Am J Obstet Gynecol 1982; 142:762-765.
34. Royal College of General Practitioners: Incidence of arterial disease among oral contraceptive users. J Royal Coll Gen Pract 1983; 33:75-82.
35. Ory HW. Mortality associated with fertility and fertility control: 1983. Family Planning Perspectives 1983; 15:50-56.
36. The Cancer and Steroid Hormone Study of the Centers for Disease Control and the National Institute of Child Health and Human Development: Oral-contraceptive use and the risk of breast cancer. N Engl J Med 1986; 315:405-411.
37. Pike MC, Henderson BE, Krailo MD, Duke A, Roy S. Breast cancer risk in young women and use of oral contraceptives: possible modifying effect of formulation and age at use. Lancet 1983; 2:926-929.
38. Paul C, Skegg DG, Spears GFS, Kaldor JM. Oral contraceptives and breast cancer: A national study. Br Med J 1986; 293:723-725.
39. Miller DR, Rosenberg L, Kaufman DW, Schottenfeld D, Stolley PD, Shapiro S. Breast cancer risk in relation to early oral contra-ceptive use. Obstet Gynecol 1986; 68:863-868.
40. Olson H, Olson KL, Moller TR, Ranstam J, Holm P. Oral contraceptive use and breast cancer in young women in Sweden (letter). Lancet 1985; 2:748-749.
41. McPherson K, Vessey M, Neil A, Doll R, Jones L, Roberts M. Early contraceptive use and breast cancer: Results of another case-control study. Br J Cancer 1987; 56: 653-660.
42. Huggins GR, Zucker PF. Oral contraceptives and neoplasia: 1987 update. Fertil Steril 1987; 47:733-761.
43. McPherson K, Drife JO. The pill and breast cancer: why the uncer-tainty? Br Med J 1986; 293:709-710.
44. Shapiro S. Oral contra-ceptives-time to take stock. N Engl J Med 1987; 315:450-451.
45. Ory H, Naib Z, Conger SB, Hatcher RA, Tyler CW. Contraceptive choice and prevalence of cervical dysplasia and carcinoma in situ. Am J Obstet Gynecol 1976; 124:573-577.
46. Vessey MP, Lawless M, McPherson K, Yeates D. Neoplasia of the cervix uteri and contraception: a possible adverse effect of the pill. Lancet 1983; 2:930.
47. Brinton LA, Huggins GR, Lehman HF, Malli K, Savitz DA, Trapido E, Rosenthal J, Hoover R. Long-term use of oral contraceptives and risk of invasive cervical cancer. Int J Cancer 1986; 38:339-344.
48. WHO Collaborative Study of Neoplasia and Steroid Contraceptives: Invasive cervical cancer and combined oral contraceptives. Br Med J 1985; 209:961-965.
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