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Abstract
Pre-eclampsia is a pregnancy-specific hypertensive syndrome that causes substantial maternal and fetal morbidity and mortality. It complicates 5% of all pregnancies worldwide.
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The placenta has a central role in preeclampsia, as evidenced by rapid disappearance of disease syndromes after delivery. The clinical manifestations of preeclampsia reflect widespread endothelial dysfunction, resulting in vasoconstriction, end-organ ischemia and increased vascular permeability. Therefore, it has been suggested that placenta- derived circulating factors may induce the endothelial defects leading to pre-eclampsia. The aim of our prospective study was to confirm that second trimester pregnancies with abnormal uterine perfusion who developed preeclampsia and IUGR have increased sEng level. In our study 50 pregnant women in the second trimester with abnormal uterine blood flow were included. All pregnancies with abnormal uterine perfusion were singleton at time of examination (24-28 weeks gestation), the women were healthy and normotensive ,the fetal growth was normal, and there were no obvious fetal anomalies.