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.
Abstract

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