Abstract
BACKGROUND: Preeclampsia (PE) is a complex hypertensive pregnancy disorder with a multifaceted aetiology. The current study focuses on determining the role of potent oxidative stress markers and sEng in susceptibility to PE, as well as investigating the morphometric and histopathological alterations induced in the fetal membranes of women with PE. METHODS: The current case-control study involves 200 participants, 100 with Preeclampsia and 100 normotensive control women. A total of 200 urine (PE/Control = 100), 200 blood (PE/Control = 100), 200 placenta (PE/Control = 100), and 100 fetal membrane samples (PE/Control = 50) were collected. Urine samples were analysed to measure protein concentrations. Reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), and guaiacol peroxidase (POD) levels were analysed through a spectrophotometer in both serum and placental samples. sEng levels were observed through ELISA. Histomorphological and histomorphometric analyses were performed on fetal membranes. Data was statistically analysed using the independent sample t-test, the Mann-Whitney test, Chi-square, logistic regression, and Fisher's exact test. Receiver operating characteristic (ROC) analysis was performed to assess the diagnostic accuracy of sEng and potent oxidative stress markers in serum and placental tissues of both groups. RESULTS: Significantly increased urine proteinuria (p < 0.001) was observed in the PE group. The serum and placental samples of the PE group showed elevated ROS and TBARS levels. sEng levels showed significant elevations in both serum (p < 0.05) and placental tissues (p < 0.01) of PE patients when compared to the control group. ROC analysis identified sEng, ROS, and TBARS as the strongest diagnostic biomarkers for preeclampsia, demonstrating high diagnostic value. The histological analysis of fetal membranes revealed complex decidual vasculopathy in the PE group. CONCLUSION: The present study revealed that elevated oxidative stress markers and sEng levels might be involved in the pathophysiology of PE. These findings suggest a strong association between oxidative stress, angiogenic imbalance, and vascular pathology in preeclampsia.