• Vol. 36 No. 12, 1003–1009
  • 15 December 2007

Identifying Risk of Neonatal Hyperbilirubinaemia and Early Discharge for Glucose-6-Phosphate Dehydrogenase Deficient Newborns in Singapore

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ABSTRACT

Introduction: This study aims to compare and assess usefulness of day 3 and 4 (49 to 96 hours) pre-phototherapy total serum bilirubin (TSB) in predicting subsequent significant hyper-bilirubinaemia (SHB) in glucose-6-phosphate dehydrogenase (G6PD) deficient neonates. Methods: This prospective study was on all the G6PD deficient newborns weighing >2500 g. Day 3 and 4 pre-phototherapy TSB and phototherapy requirements in their first 2 weeks of life were analysed for its value in predicting subsequent SHB. Results: The frequency of G6PD deficiency was 2.4%, 1 per 42 live births (1.3% in males and 1.1% in females). Phototherapy was required in 51% of G6PD deficient infants, all within the first week of life. In the absence of SHB in the first week, the probability of its development in the second week was zero (95% confidence interval, 0 to 0.051). The day 4 pre-phototherapy TSB of <160 umol/L predicted no measurable risk of subsequent SHB (sensitivity, 94%; 95% confidence interval, 83.5% to 97.9%; specificity 82.8%; 95% confidence interval, 71.1% to 90.4%). Conclusions: G6PD deficient newborns without SHB in their first week of life were at no measurable risk of its development in the second week. Day 4 pre-phototherapy has better sensitivity and specificity compared to day 3 pre-phototherapy TSB in predicting the risk of subsequent SHB. Low-risk infants, thus identified, may be eligible for discharge on or before day 7 of life. Infants with Day 4 TSB <160 can be even discharge on day 4 with follow-up appointment. Evidence-based early discharge can decrease the social, emotional and financial burden of G6PD deficiency in Singapore.


Glucose-6-phosphate dehydrogenase (G6PD) deficiency was discovered half a century ago, at the end of World War II.1 It is probably the most common sex-linked Mendelian disease and inherited enzyme defect recorded worldwide and is estimated to affect hundreds of millions of people.2-4 G6PD deficiency is a major cause of severe neonatal hyper-bilirubinaemia with the devastating potential of bilirubin encephalopathy or kernicterus 2,3,5,6 In a report of Kernicterus Registry, 19 of 61 (31.5%) term and near-term neonates who were readmitted for kernicterus within 7 days of life had G6PD deficiency.

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