Concentrations of immunoactive inhibin in serum during human pregnancy: evidence for an ovarian contribution

Abstract

Immunoactive inhibin (ir-inhibin) concentrations in maternal serum during normal human pregnancy have been established in two separate studies employing cross-sectional and longitudinal sampling regimes. Ir-inhibin concentrations rose from the mid-luteal phase (geometric mean + 95% confidence intervals 1.490 (1.086-2.028) U mL-1) to peak at week 11 of gestation (3.77 (3.26-4.35) U mL-1), declined to a plateau from 14 to 25 weeks with means ranging from 1.8 to 2.3 U mL-1, and subsequently rose slowly to a peak of 6.53 U mL-1 at 41 weeks. In the longitudinal study, similar results were obtained and no differences were found in maternal inhibin levels in women carrying male or female fetuses. Paired cord blood and maternal samples showed no significant difference in ir-inhibin concentrations irrespective of the sex of the fetus. However, in all such pregnancies amniotic fluid ir-inhibin levels were 2-3 fold greater than maternal or fetal levels raising the possibility that the amnion may secrete inhibin. In 12 women without functional ovaries in whom a singleton pregnancy was achieved by donation of oocytes and in vitro fertilization, the ir-inhibin levels showed a similar pattern in the first trimester of pregnancy but the concentrations achieved were markedly lower (peak 1.1 U mL-1 at 9 weeks). In five women from the group in whom samples were available late in gestation, three showed greater than normal levels and two had subnormal levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of Inhibin and Activin in Early Human Pregnancy: Demonstration of Fetoplacental Origin and Role in Prediction of Early-Pregnancy Outcome1

“…Previously reported comparative studies of conceptions on donor egg programs have been in conflict about the source of ir-inhibin; McLachlan et al [17] reported similar levels of ir-inhibin in the maternal circulation of pregnant women with functional ovaries and those conceiving with donor eggs, whereas a study by Yohkaichiya [18] showed decreased levels in women pregnant without corpus luteum function. Both these studies used an RIA for ir-inhibin that cannot distinguish between the free alpha subunit monomer and the dimeric inhibin forms.…”

“…1493 5 ----· 9; i·\ corpus luteum as the major site of ir-inhibin production during the luteal phase of the menstrual cycle [14] and with Yohkaichiya's [18] study showing decreased levels of irinhibin in women conceiving without functional corpora lutea in an egg donation program, which utilized an RIA for inhibin that detects the alpha subunit as the free inactive monomer and as part of the biologically active dimers. Muttukrishna et al [6] found that after surgical first-trimester termination of pregnancy, serum levels of pro-aCcontaining inhibins fell only marginally (-20%) during 4 h following the procedure, indicating that the corpus luteum is the major source in early pregnancy.…”

Source of Inhibin in Ovine Fetal Plasma and Amniotic Fluid during Late Gestation: Half-Life of Fetal Inhibin1

“…However, in view of the transient nature of the rise, it is possible that the sampling regime employed in the present study may have missed this increase. The failure of ovine maternal plasma ir-inhibin levels to rise in late gestation contrasts with the very significant increase in concentrations in the last trimester of human pregnancy [2,8,38], which is presumed to arise from a placental source [8]. Similarly, a rise in ir-inhibin concentrations has been observed in late gestation in rats.…”

“…Similarly, a rise in ir-inhibin concentrations has been observed in late gestation in rats. Maternal ovariectomy demonstrated that this is a product of the maternal ovary associated with resumption of follicular activity in preparation to the postpartum estrus that occurs in this species [8]. The variations in the pattern of inhibin secretion in late gestation in different species may thus reflect the type of placentation as well as the reproductive strategies of each species.…”

“…In this species the placenta does not appear to be a major source of inhibin since, although both bioactive and immunoactive forms of inhibin have been detected in the placenta during gestation [5], uninuclear trophoblast cells in culture produce only minimal amounts of inhibin [6], and there is no significant arteriovenous difference in ir-inhibin concentrations across the placenta in chronically cannulated late-pregnant sheep [7]. During pregnancy in both the human and sheep, no difference has been found in maternal plasma inhibin concentrations in individuals carrying male versus female fetuses [4,8].…”