METHODOLOGY: During this study, enzyme activity was measured in 53/59 (89.8%) hospital-diagnosed G6PD-deficient neonates (34 Malays, 12 Chinese, and seven other ethnic groups) born consecutively in the Kuala Lumpur Maternity Hospital. All neonates, except one, were males.

RESULTS: The mean level of enzyme activity of the 52 males G6PD-deficient neonates (0.47 iu/g Hb, 95% confidence intervals: 0.37, 0.57) was less than 10% of that of normal Malaysian male neonates. The enzyme activity of the only female G6PD-deficient infant, at 1.11 iu/g Hb, was 12.5% of the mean G6PD enzyme activity of normal females.

METHODOLOGY: This was a prospective cohort study. Shortly after birth, cranial ultrasonography was carried out via the anterior fontanelles of 70 normal control infants and 104 asphyxiated infants with a history of fetal distress and Apgar scores of less than 6 at 1 and 5 min of life, or requiring endotracheal intubation and manual intermittent positive pressure ventilation for at least 5 min after birth. Neurodevelopmental assessment was carried out on the survivors at 1 year of age.

RESULTS: Abnormal cranial ultrasound changes were detected in a significantly higher proportion (79.8%, or n = 83) of asphyxiated infants than controls (39.5%, or n = 30) (P < 0.0001). However, logistic regression analysis showed that only three factors were significantly associated with adverse outcome at 1 year of life among the asphyxiated infants. These were: (i) decreasing birthweight (for every additional gram of increase in birthweight, adjusted odds ratio (OR) = 0.999, 95% confidence interval (CI) 0.998, 1.000; P = 0.047); (ii) a history of receiving ventilatory support during the neonatal period (adjusted OR = 8.3; 95%CI 2.4, 28.9; P = 0.0009); and (iii) hypoxic-ischaemic encephalopathy stage 2 or 3 (adjusted OR = 5.8; 95%CI 1.8, 18.6; P = 0.003). None of the early cranial ultrasound changes was a significant predictor.