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).
© 2015 American Society for Clinical Pharmacology and Therapeutics.
Publication types
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Practice Guideline
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Research Support, N.I.H., Extramural
MeSH terms
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Atazanavir Sulfate / adverse effects*
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Genetic Predisposition to Disease
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Genotype
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Glucuronosyltransferase / antagonists & inhibitors*
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Glucuronosyltransferase / genetics
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Glucuronosyltransferase / metabolism
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HIV Protease Inhibitors / adverse effects*
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Humans
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Hyperbilirubinemia / chemically induced*
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Hyperbilirubinemia / enzymology
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Hyperbilirubinemia / genetics
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Jaundice / chemically induced*
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Jaundice / enzymology
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Jaundice / genetics
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Liver / drug effects*
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Liver / enzymology
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Pharmacogenetics / standards*
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Phenotype
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Risk Assessment
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Risk Factors
Substances
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HIV Protease Inhibitors
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Atazanavir Sulfate
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UGT1A1 enzyme
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Glucuronosyltransferase