[Can glucose-6-phosphate dehydrogenase deficiency alone explain neonatal jaundice].
Several authors have insisted on the role of a glucose 6-phosphate deshydrogenase (G6PD) deficiency in the occurrence of neonatal jaundice which can be severe, leading to exchange transfusion. Considering the fact that haemolysis, occuring in deficient patients, is most of the time induced, our aim was to search if a neonatal hyperbilirubinemia could be explained by the sole G6PD deficiency or by extra "oxidant stress". Red blood cell G6PD activity of 289 newborn babies of African or Antillian origin was tested by a Tetrazolium linked method. 21 newborns were deficient. 8 female babies were heterozygous for G6PD deficiency. No neonatal jaundice was observed. With Bienzle and all., we can suppose that the "environment" takes an important part in the incidence of neonatal jaundice among G6PD deficient newborn of African or Antillian origin. However as triggering factors could be ignored, we think compulsary to search a G6PD deficiency in every neonatal jaundice necessitating an exchange-transfusion.
D000349:Africa; D044383:Black People; D004912:Erythrocytes / Q000201:enzymology; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000097:blood; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000150:complications* / Q000235:genetics; D006801:Humans; D007231:Infant, Newborn; D007567:Jaundice, Neonatal / Q000209:etiology*; D008297:Male; D014900:West Indies
D005954:Glucosephosphate Dehydrogenase
Un déficit en glucose 6 phosphate déshydrogénase peut-il à lui seul expliquer un ictère néo-natal?