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Published on: August 2, 2017
Maternal plasma concentrations of soluble endoglin in pregnancies with intrauterine growth restriction
Holger Stepan1, Thomas Krämer, Renaldo Faber
1Department of Obstetrics and Gynecology, University of Leipzig, 04103 Leipzig, Germany. holger.stepan@medizin.uni-leipzig.de
Context:
Soluble endoglin (sEng), a coreceptor for TGF with antiangiogenic properties, acts synergistically with soluble fms-like tyrosine kinase 1 (sFlt1) to induce symptoms of HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome in animal models and to promote a preeclamptic phenotype. Pregnant women with preeclampsia show increased sEng concentrations in circulation, whereas the sEng increase is detectable months before the clinical onset of the disease.
Objective:
The aim of the study was to determine whether maternal sEng is altered in pregnancies with normotensive intrauterine growth restriction (IUGR).
Design:
sEng and sFlt1 were retrospectively determined by a commercial ELISA.
Patients:
The study included 11 normotensive pregnancies with IUGR, 18 pregnancies with manifest preeclampsia, and 15 gestational-age-matched controls.
Results:
Patients with preeclampsia showed significantly higher sEng concentrations compared with controls (57.0 ng/ml vs. 5.3 ng/ml; P < 0.001). Also IUGR pregnancies showed significantly elevated sEng concentrations (25.9 ng/ml; P < 0.001), but the levels were lower compared with the preeclamptic patients. There was a strong positive correlation between the sEng and sFlt1 concentration (Pearson 0.552; P < 0.01). Similar to sEng, the maternal sFlt1 concentration is highest in the preeclamptic patients (8388 vs. 2602 pg/ml; P < 0.01) but also significantly elevated in the IUGR patients (6952 pg/ml; P < 0.01).
Conclusions:
Pregnancy with IUGR, but without maternal symptoms, was characterized by elevated sEng concentrations in circulation. Although this finding is less pronounced when compared with preeclampsia, sEng seems to be involved in different clinical manifestations of placental pathology.
