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From the Department of Obstetrics and Gynecology, University of Medicine and Dentistry of New Jersey—New Jersey Medical School, Newark, New Jersey; and the Reproductive Endocrine Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts
Abstract
We compared serum concentrations of immunoreactive inhibin, hCG, and FSH in normal women with those of two groups of women lacking endogenous luteal function. Twelve functionally agonadal, hypergonadotropic women with premature ovarian failure were given replacement ovarian steroids. Donor oocytes were fertilized in vitro with the husband's semen, and embryos were transferred into these women. A second group of 12 women were normogonadotropic but anovulatory, had undergone previously unsuccessful in vitro fertilization, and possessed cryopreserved embryos. These women were suppressed with a GnRH agonist before sex hormone replacement. Serum samples collected at weeks 2, 3, 4-6, 8-10, and 12-14 of pregnancy were measured for FSH, hCG, and immunoreactive inhibin. Data were compared with concentrations in normally ovulating women with well-established dates of conception. Sex steroid replacement hormone levels did not differ between the ovarian-failure and agonist-suppressed women and approximated that of normal cycles until pregnancy; thereafter, estradiol and progesterone levels remained higher than normal. Despite excessive steroid replacement, FSH remained higher in women with ovarian failure than in agonist-suppressed or normal women. On immunoassay, inhibin failed to show an early rise at 4-6 weeks of pregnancy in either group of aluteal women (0.52 ± 0.05 ng/mL), whereas normal women demonstrated 0.9 ± 0.05 ng/mL inhibin in their sera (P<.001). By 8-10 weeks of pregnancy, women with ovarian failure demonstrated inhibin concentrations identical to those of normal women (1.2 ± 0.1 and 1.2 ± 0.15 ng/mL, respectively), whereas agonist-suppressed women lagged behind (0.7 ± 0.1 ng/mL) (P<.02). In all groups, hCG followed a pattern identical to inhibin. Normal hCG levels were observed in ovarian- failure women by 8-10 weeks, but not in agonist-suppressed women. We conclude the following: 1) Women lacking a corpus luteum do not appear to secrete inhibin until at least 8 weeks of gestation, indicating a luteal source of immunoreactive inhibin in normal early pregnancy; 2) detectable placental inhibin in ovarian failure increases by 8-10 weeks, as does hCG, and appears to be associated with suppressed FSH concentrations, suggesting that placental immunoreactive inhibin may be a biologically active dimer; and 3) both hCG and inhibin secretion are suppressed in GnRH agonistsuppressed women, suggesting a placental "lagZ" in pregnancies derived from cryopreserved embryos or in chronically anovulatory infertile women.
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