Ovarian and endometrial function during hormonal contraception.
This report addresses the balance of benefits and risks from changes in ovarian and endometrial function from hormonal contraception. The main mode of action of hormonal contraception is inhibition of ovulation, due chiefly to the dose of oestrogen in combined oral contraceptives. With 20 microg dosages of ethinyl oestradiol follicular activity is more common so that contraception depends on suppression of the LH surge or disruption of the endometrial cycle. In polycystic ovary syndrome (PCOS) treated with oral contraceptives, cysts become smaller and in time the ovarian volume is reduced, ovarian testosterone secretion is reduced and there are potentially favourable effects on carbohydrate and lipid metabolism. Typical oral contraceptive users in the 1980s had a lower incidence of ovarian cysts, but modern oral contraceptives do not appear to affect the incidence of functional cysts or benign epithelial cysts. Moreover, randomized controlled trials indicate that oral contraception prescriptions are unlikely to prevent the development of functional cysts or to hasten their disappearance. Oral contraceptives, however, greatly reduce pelvic pain in women with symptomatic endometriosis and improve the health-related quality of life. Bleeding is a common response with all types of hormonal contraception, but current methodology is inadequate to make accurate comparisons of different products or of different phasic formulations. With continuing use, however, combined oral contraception is associated with endometrial atrophy, the biological plausibility for a reduced risk of endometrial carcinoma. With progestin-only contraception, a number of endometrial changes are considered as possible mechanisms of the associated bleeding but it remains largely unexplained. Oral contraceptives are frequently used for treatment of dysfunctional uterine bleeding, although only one trial has been reported. Oral contraceptive use confers protection from endometrial [relative risk (RR) 0.5] and ovarian (RR 0.4) cancers and in both cases, the protection lasts for up to 2 decades after stopping use.
D003271:Contraceptive Agents, Female / Q000009:adverse effects; D003277:Contraceptives, Oral, Combined / Q000009:adverse effects; D003278:Contraceptives, Oral, Hormonal / Q000009:adverse effects / Q000627:therapeutic use; D016889:Endometrial Neoplasms / Q000517:prevention & control; D004715:Endometriosis / Q000188:drug therapy; D004717:Endometrium / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006801:Humans; D010048:Ovarian Cysts / Q000188:drug therapy / Q000453:epidemiology / Q000517:prevention & control; D010051:Ovarian Neoplasms / Q000517:prevention & control; D010053:Ovary / Q000187:drug effects / Q000502:physiology*; D011085:Polycystic Ovary Syndrome; D011372:Progestins / Q000009:adverse effects; D018570:Risk Assessment; D014592:Uterine Hemorrhage / Q000139:chemically induced / Q000188:drug therapy
D003271:Contraceptive Agents, Female; D003277:Contraceptives, Oral, Combined; D003278:Contraceptives, Oral, Hormonal; D011372:Progestins