2024, Vol. 7, Issue 1, Part B

Background: Neonatal jaundice, characterized by yellow skin, sclera and conjunctiva due to hyperbilirubinemia. Bilirubin can cross the blood-brain barrier, leading to severe hyperbilirubinemia, acute bilirubin encephalopathy, nuclear jaundice, and even permanent brain damage. This study aims to analyses risk factors for baby hyperbilirubinemia and assess the role of G6PD deficiency in neonatal jaundice.

Method: The term infants with neonatal hyperbilirubinemia in Al elwyia teaching hospital for children and in Iraq from June 2018 to July 2022 were recruited for the retrospective analysis. All the infants underwent quantitative detection of the G6PD enzyme. The etiology was determined through laboratory tests and clinical manifestations.

Results: In a study of 1,119 term newborns, 435 had jaundice, with infection and G6PD deficiency being the main identifiable causes. Jaundiced newborns showed a significantly higher incidence of G6PD deficiency than non-jaundiced ones (19.54% vs. 10.23%, p<0.001), and those with G6PD deficiency had significantly lower hemoglobin levels. Among the jaundiced group, 35.63% had unknown causes, and six G6PD deficiency-related genotypes were identified.

Conclusion: In newborns with G6PD deficiency, infection, and neonatal hemolytic disease were identified as the main causes of hyperbilirubinemia and acute bilirubin encephalopathy. Specifically, Hemolytic factors in infants with G6PD deficiency may lead to reduced hemoglobin and increased bilirubin levels in jaundiced infants.