Abstract
In STRIDE, slow metabolizer CYP2B6 and NAT2 genotypes were each associated with increased plasma efavirenz concentrations during antituberculosis therapy. Concentrations were greater on therapy than off therapy in 58% with CYP2B6 and 93% with NAT2 slow metabolizer genotypes. Individuals with slow metabolizer genotypes in both genes had markedly elevated concentrations.
Keywords:
HIV/AIDS; efavirenz; pharmacogenetic; rifampin; tuberculosis.
© The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Alkynes
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Antitubercular Agents* / blood
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Antitubercular Agents* / pharmacokinetics
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Antitubercular Agents* / therapeutic use
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Arylamine N-Acetyltransferase / genetics*
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Arylamine N-Acetyltransferase / metabolism
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Benzoxazines / blood*
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Benzoxazines / pharmacokinetics
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Benzoxazines / therapeutic use
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Cyclopropanes
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Cytochrome P-450 CYP2B6 / genetics*
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Cytochrome P-450 CYP2B6 / metabolism
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Female
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Genotype
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HIV Infections / complications
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Humans
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Male
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Peru
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Pharmacogenetics
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Rifampin / therapeutic use*
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South Africa
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Tuberculosis* / complications
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Tuberculosis* / drug therapy
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Tuberculosis* / genetics
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Tuberculosis* / metabolism
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Uganda
Substances
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Alkynes
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Antitubercular Agents
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Benzoxazines
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Cyclopropanes
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Cytochrome P-450 CYP2B6
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Arylamine N-Acetyltransferase
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NAT2 protein, human
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efavirenz
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Rifampin