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Hemolysis and Glucose-6-Phosphate Dehydrogenase Deficiency-Related Neonatal Hyperbilirubinemia

Michael Kaplan1,2, Ronald J Wong3, David K Stevenson3

  • 1Shaare Zedek Medical Center (Emeritus), Jerusalem, Israel.

Neonatology
|June 26, 2018
PubMed

Insights

Hemolysis plays a key role in neonatal hyperbilirubinemia for infants with Glucose-6-phosphate dehydrogenase (G6PD) deficiency. Elevated carbon monoxide levels confirm increased red blood cell breakdown in affected newborns.

Area of Science:

  • Neonatology
  • Hematology
  • Genetics

Background:

  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency affects over 300 million people globally.
  • Neonatal hyperbilirubinemia in G6PD deficiency can lead to severe complications, including bilirubin neurotoxicity and death.
  • The exact pathophysiology of jaundice in G6PD-deficient neonates is debated, with some suggesting limited hemolysis.

Purpose of the Study:

  • To investigate the contribution of hemolysis to neonatal hyperbilirubinemia in cases of G6PD deficiency.
  • To clarify the role of red blood cell breakdown in the development of severe jaundice in newborns with G6PD deficiency.

Main Methods:

  • A review of previously published studies was conducted.
  • Focus was placed on research examining endogenous carbon monoxide (CO) production, a marker of heme catabolism, in hyperbilirubinemic neonates with G6PD deficiency.

Main Results:

  • Three reviewed studies indicated elevated endogenous CO production in G6PD-deficient neonates experiencing extreme hyperbilirubinemia.
  • This finding suggests increased heme breakdown, indicative of hemolysis.

Conclusions:

  • Hemolysis is confirmed as a significant pathogenetic factor in neonatal hyperbilirubinemia associated with G6PD deficiency.
  • Understanding the role of hemolysis is crucial for managing severe jaundice in these infants.
Abstract

Keywords:
Glucose-6-phosphate dehydrogenase deficiencyHemolysisHyperbilirubinemia

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