Red Cell Metabolism and Severe Neonatal Jaundice in West Malaysia

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Abstract
A study was carried out on 332 babies suffering from severe neonatal jaundice who were admitted to the General Hospital, Kuala Lumpur, Malaysia. Of the 332 neonates, 51 were premature and 281 were full-term babies, 178 (110 Chinese, 58 Malay, 9 Indian and 1 European-Pakistani) had bilirubin levels of 20 mg% or higher, requiring exchange blood transfusion. Of the Chinese neonates, 23 (20.9%) had G6PD [glucose-6-phosphate dehydrogenase] deficiency, 9 (8.2%) had Hb Bart''s and 2 (1.8%) had an abnormal Hb, one Hb Q and 1 fetal variant. Among the Malay infants, 10 (17.2%) had G6PD deficiency, 7 (12.1%) had Hb Bart''s and 10 (17.2%) had abnormal Hb (4 had Hb E trait, 1 had Hb K and Bart''s addition to Hb E, 3 had Hb CoSp with Hb Bart''s, 1 had Hb Q and 1 Hb Tak). One of the 9 Indian neonates had G6PD deficiency and 1 had Hb S trait. The 1 European-Pakistani baby was a carrier of Hb D Punjab. In addition to G6PD deficiency, abnormal Hb seem to have contributed to the high incidence of severe neonatal jaundice in Malaysia. The mean activities of GP [glutathione peroxidase], GR [glutathione reductase] and GR after stimulation with FAD were higher, while the mean activity of PK [pyruvate kinase] and mean level of reduced glutathione were lower than in normal cord bloods. The percent increase of GR after FAD stimulation was significantly lower; fewer in this group had increases above 20% than in normal cord blood. The possible significance of the findings is discussed.