Antioxidant vitamins and glucose-6-phosphate dehydrogenase deficiency in full-term neonates.

OBJECTIVE: The mechanism by which glucose-6-phosphate dehydrogenase (G6PD) deficiency causes neonatal hyperbilirubinemia is not completely understood. However, the genetic disorder G6PD deficiency predisposes red blood cells to oxidative stress. The aim of this study was to establish the relationship between plasma antioxidant vitamin (E and C) levels and the development of hyperbilirubinemia in full-term neonates with deficient G6PD.

METHODS: A total of 196 live birth neonates of healthy mothers were included in this study. Twelve of them were deficient in G6PD. In addition to demographic data, serum total bilirubin, hemoglobin, hematocrit, and vitamin E and C levels were measured on the first day after birth.

RESULTS: Neonates with G6PD deficiency (n=7) who did not develop hyperbilirubinemia (mean serum bilirubin level of 70.8+/-23 micromol/l, median 71.8) and neonates with G6PD deficiency (n=4) who developed hyperbilirubinemia (mean serum bilirubin level of 226.7+/-79 micromol/l, median 233.4) on the first day of life had similar gestational weights and age. The second group, however, had lower hemoglobin and hematocrit as well as plasma vitamin C and E levels. None of these results showed significant difference.

CONCLUSION: The results of the present study indicate that red blood cell hemolysis as a result of inadequate antioxidants system in G6PD-deficient neonates is not the only contributing factor for hyperbilirubinemia.