Neonatal Hemolysis and Risk of Bilirubin-Induced Neurologic Dysfunction

Semin Fetal Neonatal Med. 2015 Feb;20(1):26-30. doi: 10.1016/j.siny.2014.12.005. Epub 2015 Jan 2.

Abstract

The pathologic phenotype of severe hyperbilirubinemia in the newborn infant is primarily due to excessive bilirubin production and/or impaired conjugation, resulting in an increased bilirubin load. This may, in turn, increase an infant's risk for the development of bilirubin-induced neurologic dysfunction (BIND). The highest-risk infants are those with increased bilirubin production rates due to hemolysis. Several immune and non-immune conditions have been found to cause severe hemolysis, and these are often exacerbated in those infants with perinatal sepsis and genetic predispositions. Therefore, identification of these infants, with novel technologies, is paramount in reducing the incidence of BIND and the long-term neurologic sequelae for these at-risk infants.

Keywords: Carbon monoxide; Hyperbilirubinemia; Jaundice; Kernicterus.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Carbon Monoxide / analysis
  • Genetic Predisposition to Disease
  • Glucosephosphate Dehydrogenase Deficiency / blood
  • Glucosephosphate Dehydrogenase Deficiency / complications
  • Glucosephosphate Dehydrogenase Deficiency / genetics
  • Hemolysis* / genetics
  • Humans
  • Hyperbilirubinemia, Neonatal / blood
  • Hyperbilirubinemia, Neonatal / complications*
  • Hyperbilirubinemia, Neonatal / genetics
  • Infant, Newborn
  • Nervous System Diseases / etiology*
  • Nervous System Diseases / genetics
  • Nervous System Diseases / prevention & control
  • Polymorphism, Genetic
  • Risk Factors

Substances

  • Carbon Monoxide