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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 1 218-222
Copyright © 1997 by The Endocrine Society


Reproductive Endocrinology

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

Euan M. Wallace, Simon C. Riley, Jennifer A. Crossley, Savitri C. Ritoe2, Andrew Horne, Mary Shade, Patricia M. Ellis, David A. Aitken and Nigel P. Groome

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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