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Antioxidant vitamins and glucose-6-phosphate dehydrogenase deficiency in full-term neonates

Khalid K Abdul-Razzak1, Enaam M Almomany, Mohamad K Nusier

  • 1Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan. kkalani@just.edu.jo

German Medical Science : GMS E-Journal
|August 14, 2009
PubMed

Insights

Glucose-6-phosphate dehydrogenase (G6PD) deficiency in neonates may not solely cause hyperbilirubinemia through red blood cell hemolysis. Lower antioxidant vitamin levels were observed in G6PD-deficient infants who developed hyperbilirubinemia, but results were not significant.

Area of Science:

  • Biochemistry
  • Neonatology
  • Genetics

Background:

  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a genetic disorder.
  • G6PD deficiency increases susceptibility to oxidative stress in red blood cells.
  • The exact mechanism linking G6PD deficiency to neonatal hyperbilirubinemia remains unclear.

Purpose of the Study:

  • To investigate the relationship between antioxidant vitamin (E and C) levels and neonatal hyperbilirubinemia in term infants with G6PD deficiency.
  • To explore potential contributing factors to hyperbilirubinemia in G6PD-deficient neonates.

Main Methods:

  • A cohort of 196 neonates was studied, with 12 identified as G6PD deficient.
  • Demographic data, serum total bilirubin, hemoglobin, hematocrit, and plasma levels of vitamins E and C were measured on day one postpartum.
  • Comparison was made between G6PD-deficient neonates who developed hyperbilirubinemia and those who did not.

Main Results:

  • G6PD-deficient neonates who developed hyperbilirubinemia had lower mean serum levels of hemoglobin, hematocrit, vitamin C, and vitamin E compared to those without hyperbilirubinemia.
  • Despite observed differences, none of the measured parameters (including vitamin levels) showed a statistically significant difference between the two groups.
  • Gestational age and birth weight were similar between G6PD-deficient neonates with and without hyperbilirubinemia.

Conclusions:

  • Red blood cell hemolysis due to an insufficient antioxidant system in G6PD-deficient neonates is likely not the sole cause of hyperbilirubinemia.
  • Further research is needed to fully elucidate the multifactorial nature of hyperbilirubinemia in the context of G6PD deficiency.
Abstract

Keywords:
G6PD deficiencybilirubinglucose-6-phosphate dehydrogenase deficiencyvitamin Cvitamin E

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