Abstract
The role of G6PD deficiency in the etiology of neonatal hyperbilirubinemia has beeninvestigated in a group of South African Bantu infants. The incidence of this enzyme defect was found to be significantly greater in full-term male babies with jaundice with no blood group incompatibility (14 per cent) than in a control group of male newborn infants (1.3 per cent). Evidence of perinatal hypoxia was found in 5 of 7 G6PD-deficient full-term male jaundiced infants with no Rh or ABO incompatibility. It would appear that the combination of an increased bilirubin load from the shortened red cell life span in G6PD deficiency, together with hypoxic liver damage, is responsible for icterus in this group.
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