© 1992 Oxford University Press
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Association between Glucose-6-Phosphate Dehydrogenase Deficiency and Neonatal Jaundice: Interaction with Multiple Risk Factors
*Institute of Public Health, National Taiwan University College of Medicine Taipei, Taiwan, Republic of China (ROC)
**Clinical Biochemistry Research Laboratory, Veterans General Hospital Taipei, Taiwan, ROC
Institute of Genetics, National Yang-Ming Medical College Taipei, Taiwan, ROC
Institute of Biomedical Sciences, Academia Sinica Taipei, Taiwan, ROC
Yu M-W (Institute of Public Health, National Taiwan University College of Medicine, 1, Jen-Ai Road Section 1. Taipei 10018, Taiwan, ROC), Hsiao K-J, Wuu K-D, and Chen C-J. Association between glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice: interaction with multiple risk factors. International Journal of Epidemiology 1992; 21: 947–952.
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 12379 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 
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} earner 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 20 mg/dI) was observed for G-6-PD deficiency and maternal HBSAg carrier status.
Received 1 April 1992
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