Abstract
Preeclampsia is a placental disease characterized by hypertension and proteinuria in pregnant women, and it is associated with a high maternal and neonatal morbidity. However, circulating biomarkers that are able to predict the prognosis of preeclampsia are lacking. Thirty-eight women were included in the current study. They consisted of 19 patients with preeclampsia (13 with severe preeclampsia and 6 with non-severe preeclampsia) and 19 gestational age-matched women with normal pregnancies as controls. We measured circulating factors that are associated with the coagulation pathway (including fibrinogen, fibronectin, factor VIII, antithrombin, protein S and protein C), endothelial activation (such as soluble endoglin and CD146), and the release of total and platelet-derived microparticles. These markers enabled us to discriminate the preeclampsia condition from a normal pregnancy but were not sufficient to distinguish severe from non-severe preeclampsia. We then used a microarray to study the transcriptional signature of blood samples. Preeclampsia patients exhibited a specific transcriptional program distinct from that of the control group of women. Interestingly, we also identified a severity-related transcriptional signature. Functional annotation of the upmodulated signature in severe preeclampsia highlighted two main functions related to “ribosome” and “complement”. Finally, we identified 8 genes that were specifically upmodulated in severe preeclampsia compared with non-severe preeclampsia and the normotensive controls. Among these genes, we identified VSIG4 as a potential diagnostic marker of severe preeclampsia. The determination of this gene may improve the prognostic assessment of severe preeclampsia.
Highlights
Preeclampsia (PE) is a placental disease characterized by the onset of hypertension and proteinuria after 20 weeks of gestation [1]
A comparison of the two groups revealed that proteinuria was higher in the severe PE than in the non-severe PE patients (1.00 [0.53-3.00] g/24h vs. 0.38 [0.20-0.38]; p = 0.02), but that other clinical (Table 1) and biological (Table 2) parameters were similar between these patients
We found that potential biomarkers, such as sEndoglin and Soluble CD146 (sCD146), were not significantly modulated in PE patients
Summary
Preeclampsia (PE) is a placental disease characterized by the onset of hypertension and proteinuria after 20 weeks of gestation [1]. PE occurs in 2-8% of pregnancies [2] and is a leading cause of feto-maternal morbidity and mortality [1]. The clinical presentations of PE are heterogeneous, which makes effective treatment difficult. Two nonexclusive theories account for the pathophysiology of PE. The first emphasizes the vascular aspect of the pathophysiology, including placental hypoxia, enhanced platelet aggregation and endothelial dysfunction. Endothelial dysfunction is believed to persist after delivery, explaining maternal and neonatal complications
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
