Fetal bilirubin metabolism
is characterised by accumulation of unconjugated bilirubin because of immature enzymatic activity of bilirubin-uridine-glucuronosyltransferase.
This review offers a perspective on neonatal jaundice by examining bilirubin metabolism
, bilirubin neurotoxicity, the management of neonatal hyperbilirubinemia, and methods for the clinical assessment of neonatal jaundice.
involves transport of the unconjugated insoluble form (bound to albumin) to the hepatocyte where conjugation occurs, increasing its solubility.
Late preterm infants face several vulnerabilities including low energy stores, poor thermoregulation, poor feeding, low muscle tone, immature or wet lungs, immature bilirubin metabolism
, increased infection rate, and poor state regulation.
INTRODUCTION: CNS is a rare autosomal recessive disorder of bilirubin metabolism
, caused by mutation of bilirubin uridine glucoronosyl transferase gene (UGT1A 1) resulting in either complete deficiency of UGT enzyme (CNS type-I) or decreased activity of UGT (Type 2).
Therefore, the genes involved in bilirubin metabolism
as well as red blood cell life span, such as G6PD (glucose-6-phosphate dehydrogenase), are important candidate genes for the control of serum bilirubin concentrations.
Due to immaturity of the bilirubin metabolism
approximately 60% of term new borns and 80% of preterms (1) develop jaundice in the first week of life.