Abstract

Background: The enzyme glucose-6-phosphate dehydrogenase (G6PD) deficiency leads to impaired production of reduced glutathione and predisposes the red cells to damage by oxidative metabolites causing hemolysis. Deficient neonates may manifest clinically as indirect hyperbilirubinemia or even kernicterus. G6PD deficiency is the most common enzyme deficiency in humans affecting around 400 million people worldwide which presents in neonatal period as unconjugated hyperbilirubinemia and is inherited as X-linked recessive disorder. It has a high prevalence in persons of African, Asian, and Mediterranean descent. Materials and Methods: Sample size - It was a prospective study conducted in a Military Zonal Hospital of Jodhpur (Rajasthan India). A total of 400 neonates with indirect hyperbilirubinemia were screened for G6PD deficiency from May 2014 to April 2016 in there were 165 female and 235 male neonates. The age of the neonates varied from 2 to 10 days of life. A written informed consent was obtained. Inclusion criteria - All neonates with more than 35 weeks of gestation with total serum bilirubin >12 mg% were included in the study. Exclusion criteria - All neonates with <35 weeks of gestation and serum bilirubin <12 mg% and also neonates with direct hyperbilirubinemia, polycythemia, sepsis, ABO/Rh incompatibility, and physiological jaundice (total serum bilirubin was <12 mg% and jaundice subsided by day 10 of life) were excluded from the study. Results: The result analysis showed ten (2.5%) neonates with indirect hyperbilirubinemia were G6PD deficient. There was a significant statistical difference between G6PD deficient and non-G6PD deficient group in terms of indirect bilirubin levels, duration of phototherapy, and gender as G6PD affect only males. However, there was no difference in terms of onset of jaundice, age and gestational age of neonates, and reticulocyte count.

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