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Bilateral cataracts associated with glucose-6-phosphate dehydrogenase deficiency

V Nair1, S U Hasan, K Romanchuk

  • 1Faculty of Medicine, Department of Pediatrics, Division of Neonatology, University of Calgary, Calgary, AB, Canada.

Journal of Perinatology : Official Journal of the California Perinatal Association
|June 28, 2013
PubMed

Insights

Glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause neonatal jaundice and hemolysis. This case highlights a rare instance of G6PD deficiency leading to bilateral cataracts in a preterm infant after severe hemolysis.

Area of Science:

  • Biochemistry
  • Ophthalmology
  • Neonatology

Background:

  • Glucose-6-phosphate dehydrogenase (G6PD) is crucial for cellular defense against oxidative stress.
  • G6PD deficiency commonly presents in neonates with jaundice and hemolysis, but ocular complications like cataracts are less recognized.
  • Oxidative damage to lens proteins is a known mechanism in cataract formation.

Observation:

  • This report details a preterm male neonate diagnosed with G6PD deficiency.
  • The infant experienced neonatal sepsis and severe hemolysis requiring exchange transfusion.
  • Following these events, the neonate developed bilateral cataracts.

Findings:

  • The case presents a rare association between G6PD deficiency, neonatal sepsis, severe hemolysis, and the subsequent development of bilateral cataracts in an infant.
  • This observation suggests a potential link between severe oxidative stress in G6PD-deficient neonates and cataractogenesis.

Implications:

  • This case underscores the importance of considering ocular complications, particularly cataracts, in neonates with G6PD deficiency, especially following episodes of significant oxidative stress.
  • Further research is warranted to elucidate the precise mechanisms and prevalence of cataracts in infants with G6PD deficiency.
  • Early ophthalmological screening may be beneficial for G6PD-deficient neonates experiencing severe hemolytic episodes.

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