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Neonatal hemolysis and risk of bilirubin-induced neurologic dysfunction.
Semin Fetal Neonatal Med. 2015 Feb; 20(1):26-30.SF

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.

Authors+Show Affiliations

Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: rjwong@stanford.edu.Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.

Pub Type(s)

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

Language

eng

PubMed ID

25560401

Citation

Wong, Ronald J., and David K. Stevenson. "Neonatal Hemolysis and Risk of Bilirubin-induced Neurologic Dysfunction." Seminars in Fetal & Neonatal Medicine, vol. 20, no. 1, 2015, pp. 26-30.
Wong RJ, Stevenson DK. Neonatal hemolysis and risk of bilirubin-induced neurologic dysfunction. Semin Fetal Neonatal Med. 2015;20(1):26-30.
Wong, R. J., & Stevenson, D. K. (2015). Neonatal hemolysis and risk of bilirubin-induced neurologic dysfunction. Seminars in Fetal & Neonatal Medicine, 20(1), 26-30. https://doi.org/10.1016/j.siny.2014.12.005
Wong RJ, Stevenson DK. Neonatal Hemolysis and Risk of Bilirubin-induced Neurologic Dysfunction. Semin Fetal Neonatal Med. 2015;20(1):26-30. PubMed PMID: 25560401.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neonatal hemolysis and risk of bilirubin-induced neurologic dysfunction. AU - Wong,Ronald J, AU - Stevenson,David K, Y1 - 2015/01/02/ PY - 2015/1/7/entrez PY - 2015/1/7/pubmed PY - 2016/1/1/medline KW - Carbon monoxide KW - Hyperbilirubinemia KW - Jaundice KW - Kernicterus SP - 26 EP - 30 JF - Seminars in fetal & neonatal medicine JO - Semin Fetal Neonatal Med VL - 20 IS - 1 N2 - 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. SN - 1878-0946 UR - https://wwww.unboundmedicine.com/medline/citation/25560401/Neonatal_hemolysis_and_risk_of_bilirubin_induced_neurologic_dysfunction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1744-165X(14)00100-0 DB - PRIME DP - Unbound Medicine ER -