Abstract

Introduction Pre-eclampsia (PE) is an important cause of perinatal and maternal morbidity, especially when diagnosed at or before 34 weeks’ gestation (early-onset PE), and is characterised by endothelial dysfunction/inflammation. E-selectin belongs to the selectin family of adhesion molecules involved in guiding non-activated polymorphonuclear cells to areas of inflammation in the endothelial layer. sE-selectin is a sensitive and specific marker of endothelial dysfunction, thus may be important in PE. Objective To determine whether plasma sE-selectin concentrations differed between normotensive controls (NC) and PE, as well as sub-grouped in early- and late-onset (>34 weeks’ gestation) PE in matched maternal and fetal samples. Methods sE-selectin was measured by ELISA in maternal and fetal umbilical venous EDTA plasma from NC ( n = 17) or pre-eclamptic ( n = 17) pregnancy. Distribution-free statistical tests were used. Results In PE overall, maternal sE-selectin concentrations were raised compared to normotensive controls (median [IQR]: 7.6 [6.9, 8.5] vs. 5.0 [3.5, 8.2] ng/ml; P vs. 10.6 [7.9, 15.1] ng/ml; P P n = 5) and late-onset PE ( n = 12), only the early-onset had higher maternal sE-selectin ( P Conclusions The increased maternal plasma sE-selectin in pre-eclampsia reflects the endothelial dysfunction, possible due to oxidative stress, which is apparent only in the more severe early-onset PE. The lower levels in the fetal plasma and the lack of difference between maternal and fetal circulations from the pre-eclampsia suggest there may be a different regulatory mechanism in the fetus.

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