title: Gonadotropin, steroid, and inhibin levels in women with incipient ovarian failure during anovulatory and ovulatory rebound cycles.
abstract: We have identified a group of women with infertility and regular menses who have persistently raised FSH levels and probable incipient ovarian failure (IOF). Thirteen such women (19 cycles) had serum samples taken for RIA of LH, FSH, estradiol, and progesterone (P) 3 times a week over 1 menstrual cycle. Sixty infertile women with normal ovulatory cycles (as determined by hormones and ultrasound scan) served as controls. Overall, the FSH was higher (P less than 0.01) on all days of the cycle in the IOF group, serum LH was raised on days-14 to-5 before and days 5-11 after the LH surge. There was no difference between estradiol and P levels in the two groups. Ultrasound scanning showed failure of normal ovulation in the IOF group. Inhibin, measured by RIA in 9 cycles in the IOF group was lower (P less than 0.01) during the follicular phase than in 43 normal cycles. The highest inhibin level was seen in the luteal phase, as in normal cycles, but levels were still lower (P less than 0.01) in the IOF group. Inhibin was inversely correlated with FSH (P less than 0.05) during the follicular and luteal phases and was correlated with P during the luteal phase (P less than 0.05) in the IOF group. After 3 weeks of suppression (39 cycles) with an estrogen-progestogen preparation in the IOF group, LH and FSH fell to normal values. Ovulation occurred in 22 cycles on withdrawal of suppression in the presence of high FSH levels and low inhibin levels. No pregnancies occurred. These findings are consistent with the suggestion that diminished ovarian inhibin secretion may contribute to the elevated FSH levels of IOF and indicate that ovulation in the rebound cycle after suppression occurs in the presence of high FSH and low inhibin levels. Such cycles, however, still appear to be subfertile.
authors.affiliation: Department of Medicine (Endocrinology), Hope Hospital (University of Manchester School of Medicine), Salford, United Kingdom.
authors.forename: H M
authors.initials: HM
authors.lastname: Buckler
authors.forename: C A
authors.initials: CA
authors.lastname: Evans
authors.forename: H
authors.initials: H
authors.lastname: Mamtora
authors.forename: H G
authors.initials: HG
authors.lastname: Burger
authors.forename: D C
authors.initials: DC
authors.lastname: Anderson
mesh_terms: D000328:Adult; D000858:Anovulation / Q000097:blood; D017135:Desogestrel; D004958:Estradiol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D004997:Ethinyl Estradiol / Q000008:administration & dosage / Q000494:pharmacology; D019304:Ethinyl Estradiol-Norgestrel Combination; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood*; D006801:Humans; D007247:Infertility, Female / Q000097:blood*; D007265:Inhibins / Q000097:blood*; D007986:Luteinizing Hormone / Q000097:blood*; D008525:Medroxyprogesterone / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D017258:Medroxyprogesterone Acetate; D008593:Menopause / Q000502:physiology; D009644:Norgestrel / Q000008:administration & dosage / Q000494:pharmacology; D009652:Norpregnenes / Q000008:administration & dosage / Q000494:pharmacology; D010049:Ovarian Diseases / Q000097:blood*; D010060:Ovulation / Q000502:physiology*; D011374:Progesterone / Q000097:blood; D011372:Progestins / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D009652:Norpregnenes; D011372:Progestins; D009644:Norgestrel; D004997:Ethinyl Estradiol; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D019304:Ethinyl Estradiol-Norgestrel Combination; D017135:Desogestrel; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D017258:Medroxyprogesterone Acetate; D008525:Medroxyprogesterone