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Updated: Aug 17, 2026

Biochemical Measurement of Neonatal Hypoxia
Published on: August 24, 2011
Glucose-6-phosphate dehydrogenase deficiency in neonatal indirect hyperbilirubinemia
Enver Atay1, Abdulkadir Bozaykut, Ilke Ozahi Ipek
1Zeynep Kamil Maternity and Children's Research Hospital, Istanbul, Turkey. enveratay@e-kolay.net
Insights
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is common in newborns with severe jaundice. G6PD deficiency increases the risk of severe hyperbilirubinemia and kernicterus, necessitating early screening.
Area of Science:
- Neonatal Medicine
- Pediatric Hematology
- Clinical Biochemistry
Background:
- Neonatal hyperbilirubinemia is a common clinical problem.
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a prevalent genetic disorder.
- The association between G6PD deficiency and the severity of neonatal hyperbilirubinemia requires further investigation.
Purpose of the Study:
- To determine the prevalence of G6PD deficiency in neonates with indirect hyperbilirubinemia.
- To compare the clinical presentation and outcomes of G6PD-deficient neonates versus those with normal G6PD levels.
Main Methods:
- A cohort of 624 term neonates with indirect hyperbilirubinemia was studied.
- Clinical data including bilirubin levels, phototherapy duration, and hospitalization were recorded.
- Erythrocyte G6PD levels were measured to identify deficient neonates.
Main Results:
- Twenty-four neonates (3.8%) were diagnosed with G6PD deficiency.
- G6PD-deficient neonates exhibited higher serum bilirubin levels and a greater need for exchange transfusion.
- No significant differences were observed in the onset of jaundice, reticulocyte count, hematocrit, phototherapy duration, or hospitalization duration.
Conclusions:
- G6PD deficiency is a significant risk factor for severe indirect hyperbilirubinemia in neonates.
- This enzyme defect can lead to kernicterus if not identified and managed promptly.
- Implementing early neonatal screening for G6PD deficiency is recommended in high-prevalence regions.
Abstract:
The aim of this article is to investigate the prevalence of Glucose-6-phosphate dehydrogenase (G6PD) deficiency in neonatal hyperbilirubinemia and to compare the clinical presentation and course of G6PD-deficient and normal patients. This study included a total of 624 term neonates with indirect hyperbilirubinemia from March 2001 to September 2004. Birth weight, sex, weight at admission, serum bilirubin at admission, maximum bilirubin, phototherapy duration, duration of hospitalization and the need for exchange transfusion were recorded. Laboratory evaluations included blood group typing of mother and newborn, complete blood count, peripheral blood smear, serum total and direct bilirubin, direct coombs test, reticulocyte count, serum-free T4 and TSH, urine analysis, urinary reducing substance and erythrocyte G6PD level. The analysis of the results indicated that 24 neonates with indirect hyperbilirubinemia were G6PD-deficient. No statistically significant difference was detected between G6PD-deficient and normal groups in relation to the time of onset of jaundice, reticulocyte count, hematocrit level, phototherapy duration and duration of hospitalization. Serum bilirubin at admission, maximum serum bilirubin level and the need for exchange transfusion were higher in G6PD-deficient group. From this study our conclusion is that the G6PD deficiency is a common enzyme defect causing severe indirect hyperbilirubinemia which may result in kernicterus. Early neonatal screening programmes should be instituted in countries where the deficiency is prevalent.
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