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Dimeric Inhibins in Amniotic Fluid, Maternal Serum, and Fetal Serum in Human Pregnancy¹

Department of Obstetrics and Gynecology, University of Edinburgh, Center for Reproductive Biology; Simpson Memorial Maternity Pavilion (A.H.); the and Department of Pediatric Pathology and Cytogenetics, Royal Hospital for Sick Children (M.S., P.M.E.), Edinburgh; Duncan Guthrie Institute (J.A.C., D.A.A.), Glasgow; and School of Biological and Molecular Sciences, Oxford Brookes University (N.P.G.), Oxford, United Kingdom

Address all correspondence and requests for reprints to: Dr. E. M. Wallace, Department of Obstetrics and Gynecology, Monash University, Monash Medical Center, 246 Clayton Road, Clayton, Victoria 3168, Australia. E-mail: Euan.Wallace{at}med.monash.edu.au

Using new specific and sensitive enzyme-linked immunosorbent assays for inhibin A and inhibin B, we measured these proteins in amniotic fluid (AF), maternal serum (MS), and umbilical cord serum in normal pregnancies.

Inhibin A levels in AF rose from a median (10–90th percentile) level of 615 (158.2–1124.6) pg/mL at 14 weeks to 1336.0 (489.4–2084.1) pg/mL at 20 weeks, and inhibin B rose from 216.6 (67.4–554.6) to 1078.2 (439.3–2482.2) pg/mL over the same period. In MS, inhibin A levels fell from a median (10–90th percentile) level of 177.5 (101.4–290.7) pg/mL at 10 weeks to a nadir of 111.9 (59.5–200.3) pg/mL at 17 weeks, rising again to 180.3 (74.1–327.2) pg/mL at 20 weeks. No inhibin B was detectable in MS. In 47 pairs of matched samples (14–16 weeks gestation) there was no correlation of inhibin A levels in AF with those in MS (r = 0.19; P > 0.05). In 45 term umbilical cord serum samples, no dimeric inhibin was detectable in serum from female babies, but inhibin B was detectable in male sera; the median (10–90th percentile) concentration was 167.4 (111.2–224.8) pg/mL.

These data suggest that for the gestation periods studied, although the placenta secretes inhibin A, another source, probably the fetal membranes, secretes both inhibin A and inhibin B. Further, the presence of inhibin B in male fetuses is consistent with a testicular origin, suggesting that inhibin B may be important in the development of the fetal hypothalamo-pituitary-testicular axis.

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