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Biochemical Measurement of Neonatal Hypoxia
Published on: August 24, 2011
Hyperbilirubinemia among African American, glucose-6-phosphate dehydrogenase-deficient neonates
Michael Kaplan1, Marguerite Herschel, Cathy Hammerman
1Department of Neonatology, Shaare Zedek Medical Center, PO Box 3525, Jerusalem 91031, Israel. kaplan@cc.huji.ac.il
Insights
African American neonates with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency face a higher risk of hyperbilirubinemia and require more phototherapy. Vigilant monitoring is crucial for these G-6-PD-deficient infants.
Area of Science:
- Neonatal Medicine
- Genetics
- Pediatrics
Background:
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is common in African Americans.
- The risk of neonatal hyperbilirubinemia in this population has not been prospectively evaluated.
- G-6-PD deficiency can lead to hemolytic anemia.
Purpose of the Study:
- To compare hemolysis and hyperbilirubinemia risk in G-6-PD-deficient African American neonates versus G-6-PD-normal controls.
- To assess the need for phototherapy in these groups.
Main Methods:
- Prospective study of healthy, term/near-term male African American neonates.
- G-6-PD testing via umbilical cord blood.
- Hemolysis assessed by end-tidal carbon monoxide (ETCOc); bilirubin levels and phototherapy needs monitored.
Main Results:
- 12.8% of 500 neonates were G-6-PD-deficient.
- G-6-PD-deficient neonates showed higher ETCOc levels, indicating increased hemolysis.
- Significantly higher incidence of hyperbilirubinemia (21.9% vs 6.7%) and phototherapy (20.3% vs 5.7%) in G-6-PD-deficient infants.
Conclusions:
- G-6-PD-deficient African American neonates have increased hemolysis and hyperbilirubinemia risk.
- These infants require more phototherapy compared to G-6-PD-normal infants.
- Vigilant monitoring for hyperbilirubinemia is recommended for G-6-PD-deficient newborns.
Background:
Although glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is prevalent in African Americans, their risk of associated neonatal hyperbilirubinemia has not been prospectively studied.
Objective:
To compare hemolysis and the risk of hyperbilirubinemia among African American, G-6-PD-deficient neonates (study group) and G-6-PD-normal control subjects.
Methods:
Consecutive, healthy, term and near-term, male neonates born to African American mothers comprised the patient cohort. G-6-PD testing was performed with umbilical cord blood samples. Routine management included measurement of the end tidal carbon monoxide level corrected for ambient carbon monoxide level (ETCOc) within 4 hours after delivery (assessment of hemolysis), > or =1 predischarge bilirubin determination, and additional bilirubin testing as clinically indicated. Indications for phototherapy were identical for study patients and control subjects. Neonates were monitored for the first 1 week of life. ETCOc results, the incidence of hyperbilirubinemia (defined as a transcutaneous or plasma total bilirubin concentration of > or =95th percentile for the hour of life), and the need for phototherapy were compared between the G-6-PD-deficient and G-6-PD-normal groups.
Results:
Five hundred male patients were enrolled, of whom 64 (12.8%) were G-6-PD-deficient. ETCOc values (median and interquartile range) were higher among G-6-PD-deficient neonates than among control neonates (2.4 ppm [2.0-2.9 ppm] vs 2.1 ppm [1.7-2.5 ppm]). More G-6-PD-deficient neonates developed hyperbilirubinemia than did control subjects (14 of 64, 21.9%, vs 29 of 436, 6.7%; relative risk: 3.27; 95% confidence interval: 1.83-5.86), whereas 13 (20.3%) met the criteria for phototherapy, compared with 25 control subjects (5.7%) (relative risk: 3.53; 95% confidence interval: 1.91-6.56). No cases of kernicterus were observed.
Conclusions:
Within the African American neonatal population, there is a subgroup of G-6-PD-deficient infants with elevated rates of hemolysis, a higher incidence of hyperbilirubinemia, and a greater requirement for phototherapy, compared with G-6-PD-normal control subjects. These newborns should be monitored vigilantly for the development of hyperbilirubinemia.
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