Document Type: Original Article
Pediatrics Department,17 Shahrivar Hospital, Guilan University Of Medical Science, Rasht, Iran
Objective: Recently, the role of hemolysis in the pathophysiology of hyperbilirubinemia in glucose-6phosphate dehydrogenase (G6PD) deficient neonates has been questioned and decreased bilirubin conjugation has been suggested. We conducted a study to evaluate the effect of hemolysis on these neonates at the 17-Shahrivar Children Hospital in Rasht.
Methods: In this cross-sectional study, from March 2007 to September 2008, 483 healthy term neonates with icter who were admitted to our hospital were assessed. Sex, gestational age, mode of delivery, kind of milk (breast milk or formula), blood group and RH of mother and newborn, Coombs test (both direct and indirect), hemoglobin level at admission, reticulocyte count, total and direct bilirubin at admission, peripheral blood smear, G6PD activity and duration of admission, were evaluated. They were divided into two groups :G6PD deficient group and G6PD with normal activity group. The afore-mentioned variants were compared between the two groups. The results were analyzed by chi-square, t-test and Pearson’s correlation test, via SPSS version 15 software.
Results: G6PD deficiency was significantly more common in male neonates than females(p< 0.001). Hemoglobin level at admission was significantly lower in G6PD deficient group (p< 0.001). Mean serum bilirubin at admission in G6PD deficient neonates was higher than normal neonats ( 18.48 3.65 versus 17.93 2.58 mg/dl) but this difference is not significant (p= 0.289) Also there was strong positive correlation between direct and total bilirubin in both groups. Severe anemia was not reported in either group.
Conclusion: Hemolysis is the main mechanism of hyperbilirubinemia in G6PD deficient neonates and there were no findings of diminished bilirubin conjugation in our study.