Maternal and Early Neonatal Serum Cytokine and Endothelin-1 Concentrations in Preeclampsia: A Single-Center Observational Cohort Study

Background/Objectives: Preeclampsia (PE) may be associated with maternal endothelial activation and altered early neonatal inflammation. The primary objective was to compare maternal and early neonatal serum interleukin 2 (IL2), IL6, IL8, tumor necrosis factor α (TNFα), and endothelin 1 (ET1) concentrations between PE and control mother–neonate pairs. Methods: This secondary report from a single-center observational cohort included 31 women with PE (34 neonates) and 45 control women (47 neonates). Biomarker concentrations were log-transformed, and PE–control differences were estimated using linear models, with results expressed as geometric mean ratios (GMRs). Neonatal models used pregnancy-clustered standard errors to account for twins. The Benjamini–Hochberg procedure was applied to control the false discovery rate (FDR). Additional neonatal models adjusted for gestational age at birth served as sensitivity analyses. Selected biomarker–outcome associations were explored post hoc using univariable Firth bias-reduced logistic regression. Results: Maternal ET1 was higher in PE (GMR = 1.79, 95% confidence interval—CI—1.53–2.09; q < 0.001). Neonatal IL2 (GMR = 1.37, 95% CI 1.11–1.71; q = 0.016) and TNFα (GMR = 1.49, 95% CI 1.22–1.82; q < 0.001) were higher in PE-exposed neonates. After gestational age at birth adjustment, the TNFα difference persisted (GMR = 1.33, 95% CI 1.14–1.55; q = 0.003), whereas IL2 was attenuated (GMR = 1.20, 95% CI 0.99–1.45; q = 0.164). None of the exploratory Firth associations remained significant after FDR correction. Thrombocytopenia at birth occurred in 5/33 PE-exposed and 1/47 control neonates; intraventricular hemorrhage occurred in 2/34 and 2/47, respectively. Conclusions: PE was associated with between-group differences in maternal endothelial and early neonatal inflammatory biomarkers, with maternal ET1 and neonatal TNFα as the most robust signals. Complication-related findings remain hypothesis-generating and do not support predictive cut-offs, risk stratification, or causal inference.