| Literature DB >> 26417955 |
R S Gammal1, M H Court2, C E Haidar1, O F Iwuchukwu3,4, A H Gaur5, M Alvarellos6, C Guillemette7, J L Lennox8, M Whirl-Carrillo6, S S Brummel9, M J Ratain10, T E Klein6, B R Schackman11, K E Caudle1, D W Haas12.
Abstract
The antiretroviral protease inhibitor atazanavir inhibits hepatic uridine diphosphate glucuronosyltransferase (UGT) 1A1, thereby preventing the glucuronidation and elimination of bilirubin. Resultant indirect hyperbilirubinemia with jaundice can cause premature discontinuation of atazanavir. Risk for bilirubin-related discontinuation is highest among individuals who carry two UGT1A1 decreased function alleles (UGT1A1*28 or *37). We summarize published literature that supports this association and provide recommendations for atazanavir prescribing when UGT1A1 genotype is known (updates at www.pharmgkb.org).Entities:
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Year: 2015 PMID: 26417955 PMCID: PMC4785051 DOI: 10.1002/cpt.269
Source DB: PubMed Journal: Clin Pharmacol Ther ISSN: 0009-9236 Impact factor: 6.875