INHIBIN-B AND PRO-ALPHA-C-CONTAINING INHIBINS IN AMNIOTIC-FLUID FROM CHROMOSOMALLY NORMAL AND DOWN-SYNDROME PREGNANCIES

Citation
Em. Wallace et al., INHIBIN-B AND PRO-ALPHA-C-CONTAINING INHIBINS IN AMNIOTIC-FLUID FROM CHROMOSOMALLY NORMAL AND DOWN-SYNDROME PREGNANCIES, Prenatal diagnosis, 18(3), 1998, pp. 213-217
Citations number
15
Categorie Soggetti
Genetics & Heredity","Obsetric & Gynecology
Journal title
ISSN journal
01973851
Volume
18
Issue
3
Year of publication
1998
Pages
213 - 217
Database
ISI
SICI code
0197-3851(1998)18:3<213:IAPIIA>2.0.ZU;2-0
Abstract
In second-trimester Down syndrome pregnancies, levels of inhibin-A (th e alpha-beta(A) dimer) in maternal serum and amniotic fluid (AF) are s ignificantly higher and lower than in normal pregnancy, respectively. Since AF also contains inhibin-B (the alpha-beta(B) dimer) and precurs or inhibins: we have examined whether the secretion of these inhibin i soforms may also be altered in association with Down syndrome. AF from 45 Down syndrome and 150 chromosomally normal pregnancies between 16 and 19 weeks' gestation were analysed, blinded to whether the sample w as from a Down syndrome or a normal pregnancy. The median (10th-90th p ercentiles) inhibin-B level in the control pregnancies increased from 310.0 (80.8-1112.5) pg/ml at 16 weeks to 459.5 (193.7-1386.8) pg/ml at 19 weeks' gestation. The corresponding figures for precursor inhibins (pro-aC inhibins) were 541.8 (206.9-1322.8) pg/ml at 16 weeks and 139 1.8 (433.3-2652.6) pg/ml at 19 weeks. Expressed as multiples of the me dian (MOM), the levels of inhibin-B and pro-aC inhibins in the Down sy ndrome samples were 0.85 and 0.79; respectively. Neither was significa ntly different from the controls. These data suggest that, of the thre e inhibin subunits, abnormal production or secretion of the inhibin be ta(A)-subunit may underlie the decreased inhibin-A levels previously o bserved in Down syndrome. Confirmation of this by quantitative assessm ent of the inhibin subunit messenger ribonucleic acids would now be us eful. (C) 1998 John Wiley & Sons, Ltd.