This nonconcurrent cohort study was carried out to evaluate the association of neonatal jaundice with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and its interactions with other risk factors. The G-6-PD enzyme activity of 12,379 neonates was screened by a semi-quantitative fluorometric assay and double-checked by a quantitative method to identify a G-6-PD deficient cohort of 333 neonates. Matched with these on birth date, sex and delivery hospital were a G-6-PD normal cohort of 653 neonates. Neonatal jaundice was defined by a peak serum bilirubin (PSB) level of > or = 15 mg/dl. A significant association between G-6-PD deficiency and neonatal jaundice was observed in male but not female neonates. There was an inverse dose-response relation between G-6-PD activity and neonatal jaundice among male neonates. Both hypoxia/asphyxia and maternal hepatitis B surface antigen (HBsAg) carrier status were associated with an increased risk of neonatal jaundice among G-6-PD deficient but not G-6-PD normal male neonates. Based on multiple regression analyses, an additively synergistic effect on PSB level and severe jaundice (PSB > or = 20 mg/dl) was observed for G-6-PD deficiency and maternal HBsAg carrier status.
PIP: Researchers compared data on 333 newborns with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency at 5 public and 5 private hospitals in Taiwan with data on 653 birth date, sex, and delivery hospital matched newborns to examine the peak serum bilirubin (PSB) level and incidence of neonatal jaundice of both G-6-PD deficient and G-6-PD normal newborns. They also wanted to determine whether an association exists between G-6-PD activity level and incidence of neonatal jaundice and associations between G-6-PD deficiency and other likely risk factors of neonatal jaundice. A significant association between G-6-PD deficiency and neonatal jaundice existed among male neonates but not female neonates. Male neonates had a considerably higher incidence of neonatal jaundice than did female neonates (11.6% vs. 6.2%). There was a significant inverse dose-response relationship between G-6-PD activity and neonatal jaundice among the male neonates (p.01). For example, the relative risk was 1.78 for 20.1-29.9 relative intensity, 2.01 for 15.1-20, 2.61 for 10.1-15, and 4.07 for 10. Maternal hepatitis B surface antigen (HBsAg) carrier status and hypoxia/asphyxia significantly increased the risk for G-6-PD deficiency in male neonates (p.05). The multiple regression analysis indicated a significant effect of G-6-PD deficiency on the PSB level and the incidence rate of severe neonatal jaundice. There was a similar significant interaction between G-6-PD deficiency and maternal HBsAg carrier status.