Evaluation of Maternal Serum Endoglin in preeclampsia and in normotensive pregnant females

Abstract

Pre-eclampsia is a syndrome defined as the onset of hypertension and proteinurea after 20 weeks of gestation in previously normotensive and nonproteinuric women. Though pathogenesis is not yet clear, several theoretical mechanisms have been proposed which result in uteroplacental insufficiency. Endoglin, a co-receptor for transforming growth factor 1 and 3 (TGF- 1 and TGF-3, respectively), is highly expressed on cell membranes of vascular endothelium and syncytiotrophoblasts. Placental endoglin is up-regulated in preeclampsia, releasing soluble endoglin into the maternal circulation. Soluble endoglin is an antiangiogenic protein that may inhibit TGF- 1 signaling in vasculature. The principal pathologic changes of the placenta in PIH include decidual arteriolopathy, infarcts and ischemic change in central portions of the placenta, abruptio placentae, “Tenney-Parker changes,” and restricted fetal growth. These pathologic features are not all invariably present but they are significantly overrepresented in PIH. This study was designed to compare between maternal serum concentration of soluble endoglin in normal pregnancy and those of the preeclampsia.