期刊
SEMINARS IN FETAL & NEONATAL MEDICINE
卷 15, 期 3, 页码 169-175出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.siny.2009.11.003
关键词
Compound heterozygosity; Genetics; Glucose-6-phosphate dehydrogenase (G6PD); Hyperbilirubinemia; Solute carrier organic anion transporter polypeptide 1B1 (SLCO1B1); Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1)
类别
资金
- Pediatrix Hyperbilirubinemia Study Group
- Mario Lemieux Centers for Patient Care and Research of the Mario Lemieux Foundation
The potential for genetic variation to modulate neonatal hyperbilirubinemia risk is increasingly being recognized. In particular, polymorphisms across three genes involved in bilirubin production and metabolism [glucose-6-phosphate dehydrogenase (G6PD), uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1), and solute carrier organic anion transporter polypeptide 1B1 (SLCO1B1)] may interact with each other and/or environmental contributors to produce significant hyperbilirubinemia. Variant gene co-expression including compound and synergistic heterozygosity enhances hyperbilirubinemia risk, contributing to the etiologic heterogeneity and complex nature of neonatal jaundice. (C) 2009 Elsevier Ltd. All rights reserved.
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