Second-trimester maternal serum progesterone levels in Turner syndrome with and without hydrops and in trisomy 18

Citation
Gm. Lambert-messerlian et al., Second-trimester maternal serum progesterone levels in Turner syndrome with and without hydrops and in trisomy 18, PRENAT DIAG, 19(5), 1999, pp. 476-479
Citations number
25
Categorie Soggetti
Reproductive Medicine","Medical Research Diagnosis & Treatment
Journal title
PRENATAL DIAGNOSIS
ISSN journal
01973851 → ACNP
Volume
19
Issue
5
Year of publication
1999
Pages
476 - 479
Database
ISI
SICI code
0197-3851(199905)19:5<476:SMSPLI>2.0.ZU;2-7
Abstract
Placental proteins, such as inhibin A and hCG and its subunits, as well as the placental steroid progesterone, are elevated in second-trimester matern al serum from cases of fetal Down syndrome. Since different cellular mechan isms are required for protein versus steroid synthesis and secretion, these data suggest that a generalized placental hypersecretory phenomenon is ass ociated with Down syndrome. Inhibin A and hCG are also elevated in cases of Turner syndrome with hydrops, and are reduced in cases of Turner syndrome without hydrops and in trisomy 18. The objective of the present study was t o determine maternal serum levels of the placental steroid progesterone in cases of Turner syndrome and trisomy 18. Twenty-one cases of trisomy 18, 10 cases of Turner syndrome without hydrops and 12 cases of Turner syndrome w ith hydrops were identified and each matched to five control samples. Maternal serum progesterone levels were significantly elevated in Turner sy ndrome with hydrops (2.11 MoM), slightly reduced in Turner syndrome without hydrops (0.90 MoM) and modestly, though significantly, reduced in trisomy 18 (0.73 MoM). These data are similar to the patterns seen for inhibin A an d hCG, suggesting that the overall synthetic and/or secretory activity of t he placenta is increased in Turner syndrome with hydrops and decreased in T urner syndrome without hydrops and in trisomy 18. These data may be helpful in understanding the pathophysiological basis of Serum marker patterns in these aneuploidies. Copyright (C) 1999 John Wiley & Sons, Ltd.