GONADOTROPIN AND INHIBIN CONCENTRATIONS IN EARLY-PREGNANCY IN WOMEN WITH AND WITHOUT CORPORA-LUTEA

We compared serum concentrations of immunoreactive inhibin, hCG, and F SH in normal women with those of two groups of women lacking endogenou s luteal function. Twelve functionally agonadal, hypergonadotropic wom en with premature ovarian failure were given replacement ovarian stero ids. Donor oocytes were fertilized in vitro with the husband's semen, and embryos were transferred into these women. A second group of 12 wo men were normogonadotropic but anovulatory, had undergone previously u nsuccessful in vitro fertilization, and possessed cryopreserved embryo s. 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 w ith well-established dates of conception. Sex steroid replacement horm one levels did not differ between the ovarian-failure and agonist-supp ressed women and approximated that of normal cycles until pregnancy; t hereafter, estradiol and progesterone levels remained higher than norm al. Despite excessive steroid replacement FSH remained higher in women with ovarian failure than in agonist-suppressed or normal women. On i mmunoassay, inhibin failed to show an early rise at 4-6 weeks of pregn ancy in either group of aluteal women (0.52 +/- 0.05 ng/mL), whereas n ormal women demonstrated 0.9 +/- 0.05 ng/mL inhibin in their sera (P < .001). By 8-10 weeks of pregnancy, women with ovarian failure demonst rated inhibin concentrations identical to those of normal women (1.2 /- 0.1 and 1.2 +/- 0.15 ng/mL, respectively), whereas agonist-suppress ed women lagged behind (0.7 +/- 0.1 ng/mL) (P < .02). In all groups, h CG followed a pattern identical to inhibin. Normal hCG levels were obs erved in ovarian-failure women by 8-10 weeks, but not in agonist-suppr essed women. We conclude the following: 1) Women lacking a corpus lute um do not appear to secrete inhibin until at least 8 weeks of gestatio n, indicating a luteal source of immunoreactive inhibin in normal earl y pregnancy; 2) detectable placental inhibin in ovarian failure increa ses by 8-10 weeks, as does hCG, and appears to be associated with supp ressed FSH concentrations, suggesting that placental immunoreactive in hibin may be a biologically active dimer; and 3) both hCG and inhibin secretion are suppressed in GnRH agonist-suppressed women, suggesting a placental "lag" in pregnancies derived from cryopreserved embryos or in chronically anovulatory infertile women.