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Updated: Mar 26, 2026

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Published on: September 25, 2015
Prevalence of glucose-6-phosphate dehydrogenase deficiency in jaundiced Egyptian neonates
Wafaa Moustafa M Abo El Fotoh1, Mohammed Soliman Rizk2
1a Department of Pediatrics , Menoufia University , Shebin El-Kom , Egypt and.
Insights
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a significant cause of neonatal hyperbilirubinemia, particularly in males. This condition impairs red blood cell function, leading to jaundice and potentially kernicterus.
Area of Science:
- Biochemistry
- Pediatrics
- Genetics
Background:
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency impairs reduced glutathione production, increasing red blood cell susceptibility to oxidative damage and hemolysis.
- Neonatal G6PD deficiency can manifest as severe hyperbilirubinemia and kernicterus.
Purpose of the Study:
- To investigate the prevalence and impact of erythrocyte G6PD deficiency in neonates presenting with hyperbilirubinemia.
- To establish a correlation between G6PD deficiency and the severity of neonatal jaundice.
Main Methods:
- A cohort of 202 neonates with indirect hyperbilirubinemia were analyzed.
- G6PD activity was quantified using the UV-Kinetic Method via spectrophotometry.
- Demographic data and clinical parameters, including serum total bilirubin levels, were recorded.
Main Results:
- Eighteen neonates (8.9%) were diagnosed with G6PD deficiency, exclusively in males.
- A positive correlation was observed between the onset of jaundice and G6PD levels in deficient neonates.
- Mean serum total bilirubin was elevated in G6PD-deficient cases.
Conclusions:
- G6PD deficiency is a notable contributor to neonatal jaundice, particularly when jaundice appears on or after the second day of life.
- Early detection of G6PD deficiency is crucial for managing neonatal hyperbilirubinemia and preventing complications.
Background:
The enzyme, Glucose-6-phosphate dehydrogenase (G6PD), deficiency leads to impaired production of reduced glutathione and predisposes the red cells to be damaged by oxidative metabolites, causing hemolysis. Deficient neonates may manifest clinically as hyperbilirubinemia or even kernicterus.
Objective:
This study was carried out to detect erythrocyte G6PD deficiency in neonatal hyperbilirubinemia.
Methods And Design:
To determine the frequency and effect of G6PD deficiency, this study was conducted on 202 neonates with indirect hyperbilirubinemia. All term and preterm babies up to 13 day of age admitted with clinically evident jaundice were taken for the study. G6PD activity is measured by the UV-Kinetic Method using cellular enzyme determination reagents by spectrophotometry according to manufacturer's instructions.
Results:
A total of 202 babies were enrolled in this study. Male babies outnumbered the female (71.3% versus 28.7%). Mean age of the study newborns was 3.75 ± 2.5 days. Eighteen neonates (8.9%) had G6PD deficiency, all are males. One case had combined G6PD deficiency and RH incompatibility. Mean serum total bilirubin was 17.2 ± 4.4 in G6PD deficient cases. There was significant positive correlation between the time of appearance of jaundice in days and G6PD levels in G6PD deficient cases.
Conclusion:
Neonatal hyperbilirubinemia is associated with various clinical comorbidities. G6PD deficiency is found to one important cause of neonatal jaundice developing on day 2 onwards.
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