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

被引：0
|
作者：
Kaplan, Michael [1 ,2 ]
Hammerman, Cathy [1 ,2 ]
Shapiro, Steven M. [3 ]
机构：
[1] Shaare Zedek Med Ctr MK Emeritus, Dept Neonatol, Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Fac Med, Jerusalem, Israel
[3] Univ Kansas, Dept Neurol, Med Ctr, Kansas City, MO USA
来源：
JOURNAL OF PEDIATRICS | 2024年 / 265卷
关键词：
D O I：
10.1016/j.jpeds.2023.113810
中图分类号：
R72 [儿科学];
学科分类号：
100202 ;
摘要：
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.
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