Abstract

Introduction: Soluble Endoglin (sEng) has an anti-angiogenic effect, by inhibiting of Transforming Growth Factor (TGF)-β1 bond at endoglin receptors and inhibiting vasodilatation. sEng levels increase in Pre-eclampsia (PE) due to hypoxic placenta and there have been possible role of it in the pathogenesis of PE and its therapeutic implications. Aim: To compare serum sEng levels in pre-eclamptic patients (cases) versus control. Materials and Methods: This case-control study was carried out November 2019 to October 2021, in the Department of Obstetrics and Gynecology, University College of Medical Sciences, Delhi. On 40 cases with a singleton pregnancy with diagnosis of PE enrolled as cases and 40 normal healthy pregnant women matched for age and gestational age as controls. sEng was estimated using commercially available Enzyme- Linked Immunosorbent Assay (ELISA) kit. Last uterine (Ut) and Umbilical Artery (UA) doppler findings were noted and sEng levels were compared with doppler studies. The analysis was done using student t-test and Chi-square test. Results: A total of 80 participants were included in the study, 40 in case group (mean age 26.53±4.93 years) and 40 in control group (mean age: 25.35±3.10 years). A total of 21 PE cases were Non Severe PE (NSPE) (52.5%) and 19 were Severe PE (SPE) (47.5%). Early-onset PE was observed in n=11 (28%) and the remaining n=29 (72%) had late-onset PE. sEng was significantly higher in pre-eclamptic women 55.08±21.42 ng/mL as compared to controls 44.15±12.02 ng/mL (p=0.006). Higher levels of sEng were seen in SPE 59.20±28.44 ng/mL vs NSPE 51.36±11.66 ng/mL (p 0.066). sEng levels between early onset PE (50.93±5.89 ng/mL) and late onset PE (56.66±24.84 ng/ ml) (p= 0.832). sEng levels were higher in cases with abnormal Resistance Index (RI) of Ut artery 54.23±6.68 ng/mL than in normal RI of Ut artery 54.23±6.68 ng/mL, though not significant. Abnormal Ut artery RI doppler was seen more in early-onset (n=2, 33%) than in late onset PE (n=1, 7%). Conclusion: PE cases had significantly higher levels of sEng compared to controls. Thus, it can be concluded that, there is a definitive role of sEng in pathogenesis of PE due to its antiangiogenic action.

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