Glutathione S-transferase and moderate neonatal hyperbilirubinemia associated with glucose-6-phosphate dehydrogenase deficiency Reply

per1 and for his comments. While we did emphasize the in the pathogenesis of glucose-6-phosphate dehydrogenase there was no intention of designating these as the only genetic factors contributing to the hyperbilirubinemia. binemia has been characterized as a complexity of interaca high degree of genetic polymorphism coinheritance, including G6PD deficiency, genetic polymorphisms of the UDP-glucuronosyltransferase 1A1 promoter, and OATP1B1 coding sequence variants, in determining the factors, genetic or environmental, may interact with G6PD-deficiency to increase the likelihood of neonatal hyperbilirubinemia.