Literature DB >> 20022574

Exploring the genetic architecture of neonatal hyperbilirubinemia.

Jon F Watchko1, Zhili Lin.   

Abstract

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. Copyright 2009 Elsevier Ltd. All rights reserved.

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Year:  2009        PMID： 20022574     DOI： 10.1016/j.siny.2009.11.003

Source DB:  PubMed          Journal:  Semin Fetal Neonatal Med        ISSN： 1744-165X            Impact factor:   3.926


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