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Bashu Dev Pardhe*, Mukund Joshi, Rajesh Pandey, P D Sharma, Jasbir Singh, Prem Paudyal


G6PDdeficiencyis one of the most common inherited disorders of mankind, with more than 400 million people being affected worldwide. It is probably the most common inborn error of metabolism in human which in adults can cause chronic haemolytic anemia or drug induced or stress induced acute hemolysis, whereas in neonates it is one of the common cause of neonatal hyperbilirubinemia. Purpose: The aim of the study was to find out the extend of G6PD deficiency and to make a correlation between G6PD activity and serum bilirubin levels in neonates. Patients and methods: A total of 100 neonates of age 1-7 days were selected for the study in which 57 were males and 43 were females. Quantitative estimation of Total serum bilirubin, Direct serum bilirubin and Indirect serum bilirubin were done by end point method. G6PD activity was measured by kinetic (increasing) method. Results: Extend of G6PD deficiency was found to be 3% in which male female ratio was 2:1. 40% of the neonates were found to have hyperbilirubinemia and another 40% were normal. Only the direct serum bilirubin was statistically significant (p=0.013) with G6PD activity. Total serum bilirubin was statistically higher in G6PD deficient cases (mean= 9.90 ±6.57 mg/dl) than normal G6PD (5.65±3.56 mg/dl). Total and indirect serum bilirubin were found to be statistically significantly different between G6PD deficient and normal cases with p=0.015, 0.023 respectively. Conclusion: The prevalence of G6PD deficiency was found to be 3%, thus early detection of this enzymopathy regardless of sex and close surveillance of the newborns is important.

Keywords: G6PD, hemolytic anemia, neonatal hyperbilirubinemia, serum bilirubin.

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