Author/Authors :
EL-GAYAR, ALI Al-Galaa Teaching Hospital - Neonatal Department, Egypt , HAMDI, NAGWA Al-Galaa Teaching Hospital - Neonatal Department, Egypt , EL-KHASHAB, AMR Al-Galaa Teaching Hospital - Department of Neonatal, Egypt , SALAH, MOHAMMED HOSSAM Al-Galaa Teaching Hospital - Department of Neonatal, Egypt , AMIN, WAFAA Al-Galaa Teaching Hospital - Neonatal Department, Egypt , FAROUK, HANAN Al-Galaa Teaching Hospital - Department of Clinical Pathology, Egypt
Abstract :
Glucose-6-PD deficiency is a common clinically significant enzyme defect, causing severe indirect hyperbilirubinemia in neonates. Patients and Methods: A total of 324 term neonates with hyperbilirubinemia were screened for G6PD-deficiency, from January to December 2010. The conversion of nicotinamide adenine dinucleotide phosphate to its reduced form in erythrocytes is the basis of diagnostic testing for the deficiency. Results: The analysis of the results indicated that 10 (3.35%) neonates with indirect hyperbilirubinemia were G6PD-deficient. No statistically significant difference was detected between G6PD-deficient and non-G6PD deficiency groups in relation to the time of onset of jaundice, reticulocyte count, hematocrit level, serum bilirubin at admission and maximum serum bilirubin level. Phototherapy duration, duration of hospitalization and the need for exchange transfusion were higher in the G6PD-deficient group. Conclusion: From this study we conclude that G6PD deficiency is a common enzyme defect in our neonatal population, which need early screening to provide the appropriate early management.
