. "B8. Use of Antiprogestins in the Management of Endometriosis and Leiomyoma." Clinical Applications of Mifepristone (RU486) and Other Antiprogestins: Assessing the Science and Recommending a Research Agenda. Washington, DC: The National Academies Press, 1993.
The following HTML text is provided to enhance online
readability. Many aspects of typography translate only awkwardly to HTML.
Please use the page image
as the authoritative form to ensure accuracy.
Clinical Applications of Mifepristone (RU 486) and other Antiprogestins: Assessing the Science and Recommending a Research Agenda
Antiprogestin in the Treatment of Endometriosis
Rationale. Since ectopic endometrial tissue contains both ER and PR, and is sensitive to the hormonal agents that affect these receptors (Lessey et al., 1989), it prompted us to evaluate whether the antiprogestin RU 486 could have some beneficial effects in women with symptomatic pelvic endometriosis (Kettel et al., 1991).
Protocol. Six normal-cycling women with pelvic pain due to endometriosis participated in the pilot study. Their mean age was 29 years (range: 17–40 years). Four of them had failed other hormonal treatments, and none had taken any hormonal medication for at least two months prior to the study. All patients used barrier contraceptives throughout the study. Informed consent was obtained prior to enrollment.
RU 486 was given as two 50-mg tablets per day for three months, starting on cycle day 1. Staging of the disease was assessed at pre- and posttreatment laparoscopy by the American Fertility Society (AFS) Revised Classification (AFS, 1985). Pelvic pain was graded as minimal (+), mild (++), moderate (+++), or severe (++++).
Baseline blood samples were obtained in the early follicular phase of the pretreatment cycle and again during the last month of treatment. Ovarian function was monitored by daily determinations of estrone 3a-glucuronide (E1G), an estrogen metabolite, and pregnanediol 3a-glucuronide (PdG), a progesterone metabolite, on the first void urine samples throughout the treatment period. Values were compared with data collected from 13 regularly cycling women during the menstrual cycle. In addition, 24-hour frequent sampling (10–20 minutes) for luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), and cortisol measurements was performed in the early follicular phase of the pretreatment cycle and in the third month of treatment. Analytical methods are well established in our laboratory.
Outcome. All women became amenorrheic during treatment. Concentrations of PdG were acyclic and remained relatively constant throughout the treatment period. After an initial transient rise in E1G levels during the first month of treatment, values comparable to the early to midfollicular phase range of normal-cycling women (Figure B8.1) were maintained. Serum estradiol (E2) and estrone (E1), testosterone (T), and androstenedione (A) as well as serum follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), and prolactin were unchanged. LH pulse amplitude (but not frequency) was increased