YOLK-SAC CONCENTRATION OF PROSTAGLANDIN E(2) IN DIABETIC PREGNANCY - FURTHER CLUES TO THE ETIOLOGY OF DIABETIC EMBRYOPATHY

Citation
A. Schoenfeld et al., YOLK-SAC CONCENTRATION OF PROSTAGLANDIN E(2) IN DIABETIC PREGNANCY - FURTHER CLUES TO THE ETIOLOGY OF DIABETIC EMBRYOPATHY, Prostaglandins, 50(3), 1995, pp. 121-126
Citations number
13
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00906980
Volume
50
Issue
3
Year of publication
1995
Pages
121 - 126
Database
ISI
SICI code
0090-6980(1995)50:3<121:YCOPEI>2.0.ZU;2-N
Abstract
Fetal malformation associated with maternal diabetes occurs before the seventh week of pregnancy. Current hypotheses suggest that the diabet ic milieu causes a reduction in phosphatidylinositol turnover, leading to a disruption in the arachidonic acid cascade and resulting in a de ficiency of prostaglandins, particularly prostaglandin Eg This in turn results in a wide variety of congenital anomalies. This hypothesis ha s not been tested experimentally in humans. The yolk sac is thought to be the most important source of nutrition in early pregnancy. We soug ht to compare yolk sac prostaglandin levels in normal and diabetic wom en. Under ultrasonographic guidance, yolk sacs were aspirated from 8 n ormal and 12 diabetic women ranging from 8 to 10 weeks gestational age prior to elective abortion. Prostaglandin E(2) levels were determined using RIA. The mean prostaglandin E(2) level in normal controls was 3 605 pg/mL, and was undetected in all of the yolk sacs aspirated from d iabetic women (P < 0.001). Yolk sac diameter in diabetic pregnancies w as 1.2 mm larger than that of normal pregnancies. The functional and m orphological changes demonstrated in this study may increase our under standing of the pathophysiology of diabetic embryopathy.