| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3974690 | Seminars in Fetal and Neonatal Medicine | 2010 | 7 Pages |
Abstract
SummaryThe 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.
Related Topics
Health Sciences
Medicine and Dentistry
Obstetrics, Gynecology and Women's Health
Authors
Jon F. Watchko, Zhili Lin,