This review of 23 trials involving 3043 women with endometriosis has shown that there no evidence of benefit with the use of ovulation suppression for women with endometriosis and infertility. Endometriosis is caused by the lining of the uterus (endometrium) spreading to a site outside the uterus. It is associated with subfertility and can cause pain during both sexual intercourse and menstruation. The hormone oestrogen stimulates the growth of endometriosis. For many years, the use of drugs such as danazol to stop ovulation and the production of oestrogen has been standard practice in the treatment of pain and subfertility caused by endometriosis. This works well for pain, but does not appear to improve fertility. In fact, as ovulation and periods are stopped for the time of treatment, fertility may be reduced by this approach.
There is no evidence of benefit in the use of ovulation suppression in subfertile women with endometriosis who wish to conceive.
Endometriosis is the presence of endometrial glands or stroma in sites other than the uterine cavity and appears to be an oestrogen-dependent condition. This dependency has prompted the therapeutic use of ovulation suppression agents in an effort to improve subsequent fertility.
To assess the effectiveness of ovulation suppression agents, including danazol, progestins and oral contraceptives, in the treatment of endometriosis-associated subfertility in improving pregnancy outcomes including live births.
We searched the Cochrane Menstrual Disorders and Subfertility Group Specialised Register of trials (February 2009), Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 1, 2009), MEDLINE (1966 to February 2009), EMBASE (1980 to February 2009), and reference lists of articles.
Randomised trials comparing an ovulation suppression agent with placebo or no treatment, a suppressive agent with danazol, or a gonadotropin-releasing hormone analogue (GnRHa) with oral contraception in women with endometriosis.
Two review authors independently extracted data and assessed quality. We contacted study authors for additional information.
Twenty-five trials were included. Only two studies reported live births. The odds ratios (OR) for pregnancy following ovulation suppression versus placebo or no treatment was 0.97 (95% confidence interval (CI) 0.68 to 1.34, P = 0.8) for all women randomised, and 1.02 (95% CI 0.70 to 1.52, P = 0.82) for subfertile couples only despite the use of a variety of suppression agents. There was no evidence of benefit from the treatment. The common OR for pregnancy following all agents versus danazol was 1.38 (95% CI 1.05 to 1.82, P = 0.02) for all women randomised, and 1.37 (95% CI 0.94 to 1.99, P = 0.10) for subfertile couples only. When GnRHa and danazol were directly compared, the OR was 1.45 (95% CI 1.08 to 1.95, P = 0.01) for all women randomised, and 1.63 (95% CI 1.12 to 2.37, P = 0.01) for subfertile couples only, in favour of GnRHa. No effect was observed for GnRHa compared with oral contraception (OR 0.93, 95% CI 0.41 to 2.12, P = 0.86 for all women randomised; OR 0.83, 95% CI 0.34 to 2.05, P = 0.69 for subfertile couples only).