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Neonatal jaundice and glucose-6-phosphate dehydrogenase deficiency in Basrah

L M Al-Naama, I A Al-Sadoon, M M Al-Naama

    Annals of Tropical Paediatrics
    |June 1, 1987
    PubMed

    Insights

    Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is common in newborns with jaundice. This red cell defect significantly increases the risk of severe hyperbilirubinaemia and kernicterus.

    Area of Science:

    • Neonatal Medicine
    • Hematology
    • Genetics

    Background:

    • Neonatal jaundice is a common clinical presentation in newborns.
    • Erythrocyte glucose-6-phosphate dehydrogenase (G6PD) deficiency is a prevalent genetic disorder.
    • G6PD deficiency is associated with hemolytic anemia and hyperbilirubinemia.

    Purpose of the Study:

    • To investigate the association between G6PD deficiency and severe hyperbilirubinaemia in jaundiced newborns.
    • To determine the incidence of G6PD deficiency in this population.
    • To evaluate the impact of G6PD deficiency on the severity of neonatal jaundice and outcomes.

    Main Methods:

    • A study was conducted on 186 newborn babies presenting with jaundice.
    • Erythrocyte G6PD deficiency was detected in the participants.
    • Incidence of severe hyperbilirubinaemia and need for exchange transfusion were recorded.

    Main Results:

    • G6PD deficiency was detected in 51% of the jaundiced newborns.
    • Severe hyperbilirubinaemia was significantly more frequent in G6PD-deficient infants (46%) compared to non-deficient infants (15%).
    • Phototherapy did not decrease the need for exchange transfusion; 27 infants required it, and 8 developed kernicterus.

    Conclusions:

    • G6PD deficiency is a significant risk factor for severe neonatal jaundice and kernicterus in Basrah.
    • Early detection and close monitoring of G6PD-deficient newborns are crucial.
    • Interventions should be tailored to reduce the risk of severe outcomes in affected infants.

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