Abstract
Bilirubin, a neurotoxic pigment, is the end product of heme catabolism in mammals. In adults, bilirubin is extensively metabolized by hepatic UDP-glucuronosyltransferase (UGT) 1A1 and therefore cleared from the body immediately. Meanwhile, the expression and function of UGT1A1 is much less in the neonatal liver, allowing accumulation of unconjugated bilirubin in the body. Mild hyperbilirubinemia is commonly observed in human neonates. However, neonates who develop severe hyperbilirubinemia, in which the serum bilirubin level exceeds 30 mg/dL, have a higher risk for kernicterus, an irreversible brain damage caused by invasion and accumulation of bilirubin into the brain. This chapter summarizes metabolism of bilirubin in the fetus and in neonates, which is highly important in order to understand and prevent neonatal hyperbilirubinemia and kernicterus.
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