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COMBINED EFFECT OF CYP2B6 AND NAT2 GENOTYPE ON PLASMA EFAVIRENZ EXPOSURE DURING RIFAMPIN-BASED ANTITUBERCULOSIS THERAPY IN THE STRIDE STUDY
Author
Affilliation
University of California. San Francisco General Hospital. HIV/AIDS Division. San Francisco, USA.
Harvard School of Public Health. Center for Biostatistics in AIDS Research. Boston, Massachusetts, USA.
Harvard School of Public Health. Center for Biostatistics in AIDS Research. Boston, Massachusetts, USA.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Laboratório de Pesquisa Clínica em DST/AIDS. Rio de Janeiro, RJ, Brasil.
IMPACTA. Lima, Peru.
Joint Clinical Research Center. Kampala, Uganda.
University of the Witwatersrand. Faculty of Health Sciences. Johannesburg, South Africa.
University of Cape Town. Department of Medicine. Division of Clinical Pharmacology Cape Town, South Africa.
University of California. San Francisco General Hospital. HIV/AIDS Division. San Francisco, USA.
Vanderbilt University School of Medicine. Department of Medicine. Nashville, Tennessee, USA.
Harvard School of Public Health. Center for Biostatistics in AIDS Research. Boston, Massachusetts, USA.
Harvard School of Public Health. Center for Biostatistics in AIDS Research. Boston, Massachusetts, USA.
Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Laboratório de Pesquisa Clínica em DST/AIDS. Rio de Janeiro, RJ, Brasil.
IMPACTA. Lima, Peru.
Joint Clinical Research Center. Kampala, Uganda.
University of the Witwatersrand. Faculty of Health Sciences. Johannesburg, South Africa.
University of Cape Town. Department of Medicine. Division of Clinical Pharmacology Cape Town, South Africa.
University of California. San Francisco General Hospital. HIV/AIDS Division. San Francisco, USA.
Vanderbilt University School of Medicine. Department of Medicine. Nashville, Tennessee, USA.
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.
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