Hossain Sanghi

ABSTRACT

Neonatal hyperbilirubinemia remains one of the most frequent metabolic conditions encountered in the early neonatal period, with potential progression to bilirubin encephalopathy if not identified and managed promptly. From a pharmacotherapeutic standpoint, serum albumin plays a critical role in modulating bilirubin toxicity through high-affinity binding of unconjugated bilirubin, thereby reducing the free bilirubin fraction available for neurotoxic interactions. Consequently, cord serum albumin concentration at birth has been proposed as a clinically relevant biomarker to stratify the risk of hyperbilirubinemia and guide early therapeutic interventions.