Journal
SEMINARS IN FETAL & NEONATAL MEDICINE
Volume 15, Issue 3, Pages 169-175Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.siny.2009.11.003
Keywords
Compound heterozygosity; Genetics; Glucose-6-phosphate dehydrogenase (G6PD); Hyperbilirubinemia; Solute carrier organic anion transporter polypeptide 1B1 (SLCO1B1); Uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1)
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Funding
- Pediatrix Hyperbilirubinemia Study Group
- Mario Lemieux Centers for Patient Care and Research of the Mario Lemieux Foundation
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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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