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Updated: Jun 17, 2026

Biochemical Measurement of Neonatal Hypoxia
Published on: August 24, 2011
Exploring the genetic architecture of neonatal hyperbilirubinemia
1Division of Newborn Medicine, Department of Pediatrics, Magee-Women's Hospital, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. jwatchko@mail.magee.edu
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.
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