MATERNAL INFLAMMATORY AND ANGIOGENIC BIOMARKERS IN PROLONGED NEONATAL JAUNDICE

Abstract

Maternal obesity is characterized by low-grade inflammation and endothelial activation, which may influence neonatal metabolic adaptation and hepatic function. This study evaluated maternal C-reactive protein (CRP), procalcitonin (PCT), and vascular endothelial growth factor A (VEGF-A) across prepregnancy body mass index categories and explored their associations with biochemical profiles in term infants with prolonged neonatal jaundice. This single-center observational study included 140 mother-infant pairs examined at the Urgench City Maternity Complex, Uzbekistan, during 2023-2025. Mothers were classified as overweight (n = 57), obese class I-II (n = 21), underweight (n = 25), or normal weight (n = 37). An immunobiochemical subanalysis was performed in 80 pairs. Maternal CRP and PCT were measured using standard serum assays and VEGF-A by sandwich enzyme-linked immunosorbent assay. Infant total, direct, and indirect bilirubin, alanine aminotransferase, aspartate aminotransferase, total protein, and glucose were assessed. Compared with normal-weight mothers, mothers with obesity had higher CRP (2.34 ± 0.21 vs 1.76 ± 0.19 mg/L), PCT (0.28 ± 0.10 vs 0.05 ± 0.02 ng/mL), and VEGF-A (95.8 ± 7.3 vs 72.9 ± 3.9 pg/mL; P < 0.05 for reported comparisons). In the obesity group, infant total bilirubin correlated with maternal total cholesterol (r = 0.49) and atherogenic index (r = 0.45); direct bilirubin correlated with maternal low-density lipoprotein cholesterol (r = 0.52), and infant alanine aminotransferase correlated with maternal PCT (r = 0.42). Maternal obesity was associated with an inflammatory and angiogenic biomarker pattern in mothers of infants with prolonged jaundice. The exploratory maternal-infant correlations support further prospective investigation of metabolic inflammation and neonatal hepatic adaptation.