Soluble endoglin for the prediction of preeclampsia in a high risk cohort

Department of Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC 20037, USA.
Hypertension in Pregnancy (Impact Factor: 1.19). 08/2010; 29(3):330-41. DOI: 10.3109/10641950902968684
Source: PubMed

ABSTRACT To evaluate soluble endoglin (sEng) and the soluble fms-like tyrosine kinase 1 (sFlt1) to placental growth factor (PlGF) ratio for the prediction of preeclampsia in high-risk women, and to evaluate differences in sEng between women with high-risk singleton and multiple gestation pregnancies.
We collected serial serum specimens from 119 women at high preeclampsia risk. sEng, sFlt1 and PlGF were measured by ELISA.
Among subjects who did not develop preeclampsia, mean serum sEng was significantly higher in those with multiple gestation pregnancies vs. high-risk singletons. Among women with singleton gestations, mean serum sEng was higher in subjects who developed early-onset (<34 weeks) and late-onset (>or= 34 weeks) preeclampsia, as compared with subjects without preeclampsia, from 22 weeks and 28 weeks gestation onward, respectively. The within-woman rate of change of sEng was also higher in women who later developed preeclampsia.
sEng is higher in women with multiple gestations vs. high-risk singleton pregnancies. In high-risk women, serum sEng is increased prior to preeclampsia onset.

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    • "In the second stage, the ischemic and hypoxic placenta releases anti-angiogenic factors such as soluble Fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), prostaglandins and cytokines into the maternal circulation and dysregulates the production of pro-angiogenic factors including vascular endothelial growth factor (VEGF), placental growth factor (PlGF), fibroblast growth factor (FGF), transforming growth factor-B (TGF-B) and insulin-like growth factor I (IGF-I) [5] [6] [7] [8]. It is clear that the levels of sFlt1, sEng and other anti-angiogenic factors are increased and the concentrations of VEGF, PlGF and other pro-angiogenic factors are decreased in preeclampsia [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22]. These changes induce systemic endothelial dysfunction and inflammatory response leading to elevated systemic vascular resistance, vasoconstriction, and activation of the coagulation cascade [23]. "
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