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[Glucose-6-phosphate dehydrogenase et neonatal jaundice]

C Badens1, M Leclaire, J Collomb

  • 1Laboratoire des Hémoglobines, Centre d'Enseignement et de Recherche en Génétique Médicale, Faculté de Médecine de la Timone, Marseille. badens@medecine.univ-mrs.fr

Presse Medicale (Paris, France : 1983)
|April 25, 2001
PubMed

Insights

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is present in 2.1% of male newborns in Marseille. This deficiency increases the risk of neonatal jaundice by 2.6 times, necessitating early screening.

Area of Science:

  • Medical Genetics
  • Neonatology
  • Public Health

Background:

  • Routine screening for Glucose-6-phosphate dehydrogenase (G6PD) activity has been conducted in Marseille public maternity hospitals since 1986.
  • G6PD deficiency is an inherited condition that can lead to hemolytic anemia.

Purpose of the Study:

  • To determine the prevalence of G6PD deficiency in newborns screened in Marseille.
  • To evaluate the association between G6PD deficiency and the risk of developing neonatal jaundice.

Main Methods:

  • Retrospective study of 7779 newborns.
  • G6PD activity quantified using spectrophotometric measurements on cord blood.
  • Comparison of neonatal jaundice occurrence between 85 G6PD-deficient and 85 non-deficient newborns.

Main Results:

  • The incidence of G6PD deficiency was 2.1% among male newborns.
  • Newborns with G6PD deficiency had a 2.6 times higher relative risk of developing neonatal jaundice compared to those without the deficiency.

Conclusions:

  • G6PD deficiency is a significant risk factor for pathological hyperbilirubinemia and neonatal jaundice.
  • Early G6PD activity testing aids in the etiological diagnosis of neonatal jaundice.
  • Identifying G6PD deficiency allows for crucial family counseling on preventing hemolytic crises.
Abstract

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