large ovarian cysts, also known as endometriomas, may be detected. Sonographic assessment of the latter may enhance the clinician's diagnostic suspicion. In the final analysis, however, the diagnosis of endometriosis requires surgery and is a histologic diagnosis complemented by direct observation of the typical lesion through laparoscopy or laparotomy.

Unanswered questions about the precise etiology of endometriosis notwithstanding, there is little doubt about the hormonal responsiveness of ectopic endometrial tissue. In general, estrogen deprivation, progestin excess, and androgen excess appear to have a favorable, albeit reversible, impact on the disease. Although regression of the lesions in many, but not all, patients can be documented when such regimens are used, the effect is always palliative, not curative. By using these findings therapeutic strategies over the last 30 years have made use of the progestational effect of high-dose combination oral contraceptives to produce pseudopregnancy, the apparent antiendometrial effect of testosterone, the progestational-androgenic effect of danazol, and the hypoestrogenic impact of gonadotropin-releasing hormone (GnRH) agonists to produce pseudomenopause. Surgical therapy has always constituted a component of the treatment regimen, particularly when endometriosis is associated with infertility. Here, too, only palliation can be anticipated. Moreover, significant concerns currently exist as to the very utility of this approach in light of the iatrogenic insult acquired in the process. Clearly then, long-term prevention may well be the best strategy for individuals with known early disease.

Utility of Mifepristone (RU 486) for Treatment of Endometriosis

The first suggestion about the utility of mifepristone to treat endometriosis can be traced to an article by van Uem et al. (1989), who observed that the administration of mifepristone to female monkeys treated with human menopausal gonadotropin and human chorionic gonadotropin resulted in the genesis of an atrophic to weakly proliferative endometrium on menstrual cycle day 25, despite serum estradiol concentrations in excess of 300 pg/ml. These effects were observed whether mifepristone was begun on cycle day 3 or 7. Thus, when administered daily in early or midfollicular phase at a dose of 10 mg/kg, mifepristone elicited a persistent retardation of early proliferative endometrium. Apparently it antagonized the mitogenic effects of estrogens. This observation prompted the investigators to suggest that mifepristone might exhibit noncompetitive antiestrogenic activity.

To elaborate on this action of mifepristone, Wolf and associates (1989) examined its action in estradiol-treated monkeys. Use of mifepristone

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