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  49th ICAAC
San Francisco, CA
September 12-15, 2009
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Tobacco and Marijuana Tied to Lower Atazanavir Concentrations
  49th ICAAC (Interscience Conference on Antimicrobial Agents and Chemotherapy), September 12-15, 2009, San Francisco
Mark Mascolini
HIV-infected people who smoked tobacco or marijuana had significantly lower trough concentrations of the protease inhibitor (PI) atazanavir than people who did not smoke in a 67-person study [1]. But neither tobacco nor marijuana use had a direct effect on viral load or CD4 count in this analysis from the University of Buffalo and other centers.
The study involved 32 people who abused one or more substance and 35 who did not, all of them taking a regimen containing atazanavir for at least 6 months. (The investigators did not specify whether anyone was taking atazanavir without a ritonavir boost.) Study participants lived in the Bronx and Rochester, New York; Cleveland, Ohio; and Miami, Florida. Rates of abuse disorders were 41% for alcohol, 19% for cocaine, 38% for marijuana, 22% opioids, and 91% for tobacco. The multiple substance-abuse rate was 43%.
Substance abusers did not differ significantly from nonabusers in proportion of men (64% overall), age (average 46 years), CD4 count (average 454), viral load (average about 25,000 copies), or proportion with antibodies to hepatitis C virus (25%).
Median atazanavir trough concentrations (reported as micrograms/milliliter and interquartile range) were significantly lower among tobacco and marijuana users than among people who did not smoke:
· Tobacco yes vs no: 0.314 (0.121 to 0.790) vs 0.957 (0.325 to 1.196), P = 0.009
· Marijuana yes vs no: 0.238 (0.050 to 0.801) vs 0.593 (0.272 vs 1.111), P = 0.030
Significantly larger proportions of tobacco and marijuana smokers had atazanavir troughs below the therapeutic range (36% for tobacco and 50% for marijuana, P < 0.05).
Use of alcohol, cocaine, or opioids did not correlate with atazanavir trough concentrations. And none of the studied substances had any measurable impact on CD4-cell or virologic response to the atazanavir regimen.
The investigators speculate that one explanation of lower atazanavir troughs in smokers may be induction of CYP3A PI-metabolizing enzymes. They suggest that "clinicians should consider these pharmacologic findings when developing antiretroviral regimens for HIV+ patients with substance-related disorders."
1. Ma Q, Fehintola F, Zingman B, et al. Tobacco and marijuana uses significantly decrease atazanavir trough concentrations in HIV-infected individuals. 49th ICAAC (Interscience Conference on Antimicrobial Agents and Chemotherapy). September 12-15, 2009. San Francisco. Abstract H-231.