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Glucose-6-phosphate dehydrogenase deficiency. WHO Working Group

    Insights

    Glucose-6-phosphate dehydrogenase (G6PD) deficiency, a common enzyme disorder, causes severe neonatal jaundice and hemolytic crises. Prevention through education and simple treatments like phototherapy are key for managing G6PD deficiency complications.

    Area of Science:

    • Genetics
    • Biochemistry
    • Public Health

    Background:

    • Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most prevalent human enzyme disorder globally.
    • It is a significant cause of neonatal jaundice, kernicterus, and life-threatening hemolytic crises.
    • Complications arise from interactions with certain drugs and fava beans.

    Purpose of the Study:

    • To provide an update on Glucose-6-phosphate dehydrogenase (G6PD) deficiency.
    • To review recent advances in characterizing G6PD deficiency.
    • To discuss prevention strategies and implications of DNA-level discoveries.

    Main Methods:

    • Review of current literature and recent advancements.
    • Analysis of diagnostic methodologies for G6PD deficiency.
    • Examination of epidemiological data and community-based prevention strategies.

    Main Results:

    • G6PD deficiency characterization methods have evolved.
    • Newer insights into hemolytic triggers are available.
    • DNA-level advances offer new perspectives on the disorder.

    Conclusions:

    • Complications of G6PD deficiency are largely preventable through education and information.
    • Neonatal jaundice due to G6PD deficiency is treatable with phototherapy.
    • Community approaches and understanding genetic factors are crucial for managing G6PD deficiency.

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