Background: Glucose-6-phosphate dehydrogenase (G6PD) deficiency triggered and
low-bilirubin kernicterus persist despite current prevention strategies.
Objective: Review efforts to eradicate bilirubin induced brain injury in these two conditions
including novel approaches to risk assessment and hyperbilirubinemia evaluation.
Result and Conclusion: In the case of G6PD deficiency, a heightened awareness of populations at
risk and an expanded kernicterus prevention strategy focused on intensified parental engagement,
education and counselling on neonatal jaundice is needed. In the case of low-bilirubin kernicterus,
a renewed focus on identifying infants with hypoalbuminemia and implementation of
hyperbilirubinemia treatment thresholds based on the bilirubin/albumin ratio is needed. Bilirubin
binding panels when commercially available will prove valuable.
Keywords: Jaundice, hyperbilirubinemia, hemolysis, prematurity, genetics, hypoalbuminemia, bilirubin encephalopathy,
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