Hemolysis in Preterm Neonates

Robert D Christensen; Hassan M Yaish

doi:10.1016/j.clp.2016.01.002

Hemolysis in Preterm Neonates

Clin Perinatol. 2016 Jun;43(2):233-40. doi: 10.1016/j.clp.2016.01.002. Epub 2016 Feb 28.

Authors

Robert D Christensen¹, Hassan M Yaish²

Affiliations

¹ Division of Hematology/Oncology, Department of Pediatrics, Primary Children's Hospital, University of Utah School of Medicine, Chipeta Way, Salt Lake City, UT 84108, USA; Women and Newborn's Clinical Program, Division of Neonatology, Department of Pediatrics, Intermountain Healthcare, University of Utah School of Medicine, Chipeta Way, Salt Lake City, UT 84108, USA. Electronic address: robert.christensen@hsc.utah.edu.
² Division of Hematology/Oncology, Department of Pediatrics, Primary Children's Hospital, University of Utah School of Medicine, Chipeta Way, Salt Lake City, UT 84108, USA.

PMID: 27235204
DOI: 10.1016/j.clp.2016.01.002

Abstract

Hemolysis can be an important cause of hyperbilirubinemia in premature and term neonates. It can result from genetic abnormalities intrinsic to or factors exogenous to normal to red blood cells (RBCs). Hemolysis can lead to a relatively rapid increase in total serum/plasma bilirubin, hyperbilirubinemia that is somewhat slow to fall with phototherapy, or hyperbilirubinemia that is likely to rebound after phototherapy. Laboratory methods for diagnosing hemolysis are more difficult to apply, or less conclusive, in preterm infants. Transfusion of donor RBCs can present a bilirubin load that must be metabolized. Genetic causes can be identified by next-generation sequencing panels.

Keywords: Anemia; Bilirubin; End-tidal carbon monoxide; Haptoglobin; Next-generation DNA sequencing; Prematurity.

Publication types

Review

MeSH terms

Bilirubin / metabolism*
Blood Transfusion
Cell Death*
Erythrocytes*
Hemolysis*
Humans
Hyperbilirubinemia, Neonatal / metabolism*
Hyperbilirubinemia, Neonatal / therapy
Infant, Newborn
Infant, Premature
Phototherapy

Substances

Bilirubin