Evaluation of endothelial function in pregnant women with preeclampsia

Objective: Preeclampsia is a disease that can cause serious maternal and fetal problems in pregnant women. Many complications such as fetal growth retardation and early placental dissociation may be relevant in preeclampsia. A screening test is needed to detect the disease before early symptoms appear. Endothelial dysfunction plays a key role in the pathogenesis of the disease. Previous studies have indicated that bioactive molecules such as adropine, preptin, autotaxin and lysophosphatidic acid might take a part in the mechanisms of pathologies accompanied by endothelial dysfunction. In this study, we aimed to evaluate the possible role of these molecules in preeclampsia and their relation with endothelial dysfunction. Materials and Methods: 42 preeclampsia patients and 42 healthy pregnant women diagnosed according to the ACOG 2013 criteria were included in the study. Blood pressure, height and weight were measured in all individuals. Sera were collected from each patient. Routine biochemical parameters were studied on the same day, and aliquotes of samples were stored at -80°C for further analyses. Adropine, preptin, ATX and LPA measurements were carried on by the "ELISA" method. Flow-mediated dilation of the brachial artery (FMD) was measured by ultrasonography to evaluate the endothelial function. Results: While the BUN, creatinine, uric acid, triglyceride, AST, ALT, ALP, WBC, systolic blood pressure (SBP) and diastolic blood pressure (DBP) values of the preeclampsia (PE) group were significantly higher than the control; total protein, albumin, Na⁺ and platelet values were significantly low (p <0.005). The mean adropin values were significantly lower in the patient group compared to the control group (p= 0.031). When the control group and the preeclampsia group were compared with regard to their FMD %, it was found to be significantly lower in preeclampsia patients (p <0.001). In the early-onset PE (<34 weeks), ATX and LPA values were significantly lower than late-onset PE (p <0.001). Adropin levels were found to be significantly lower in moderate PE than that in severe PE. while in control patients, they were significantly higher than the patients in both PE groups (p = 0.03). Circulating adropin levels were closely related to the FMD %; and women with endothelial dysfunction had significantly lower adropin levels than their counterparts free of ED. ATX and LPA levels were significantly high in patients with ED. Conclusion: Significantly lower serum adropin levels in PE and in the group with endothelial dysfunction compared to the corresponding controls suggests that adropine may be helpful for an early detection of PE in the future. The close association between adropin levels and FMD test implies that adropin measurements might be a tool for diagnosing and follow-up of the disorders related to ED. Also, ATX levels were found to be significantly lower in the early-onset PE compared to control and late-onset PE. Considering the placental pathology and inadequate formation of trophoblasts in early-onset PE, the decrease in ATX synthesis is likely to be related to placental dysfunction.