First Trimestric Maternal Serum Omentin-1 as an Early Predictor of Preeclampsia

Abstract

PE is multisystem disease unique to human pregnancy affecting 5% to 10% of pregnancies and resolving by 6-12 weeks postpartum in a previous normotensive woman. PE is a major cause of maternal and neonatal morbidity and mortality. Although the pathogenesis of PE remains unclear, the syndrome is characterized by impaired trophoblastic invasion of the spiral artery at 16-20 weeks of pregnancy resulting in the release of factors from the placenta that activates the maternal vascular endothelium. Locally acting angiogenic factors like PIGF regulate the development of the placental villi during early gestation, which involves branching angiogenesis of immature intermediate villous vessels. This is essential for establishing placental blood circulation in a physiological environment of low oxygen tension. Furthermore to stimulate cytotrophoblast proliferation, inhibit trophoblast invasion and promote endothelial cell mitosis. All these factors are essential to ensure a normal pregnancy outcome. Omentin has been shown to act as an anti-inflammatory mediator and in one study has been shown to inhibit TNF-induced vascular inflammation in human endothelial cells. In another report, omentin also inhibited TNF-a-induced vascular cell adhesion molecule-1 expression by preventing the activation of p38 and JNK at least in part through the inhibition of superoxide production. In addition, serum omentin-1 concentrations have been shown to be negatively correlated with concentrations of inflammatory molecules including TNF-a, IL-6 and C-reactive protein. Taken together, these results suggest that omentin may play a role in the process of anti-inflammation. Given that inflammation may have a potential role in preeclampsia, omentin-1 may be therefore involved in the development of preeclampsia via the inhibitory function of the inflammatory pathway. The aim of this study was to evaluate the accuracy of serum omentin 1 in prediction of PE.