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Chun Chao,1
Lisa P. Jacobson,2
Frank J. Jenkins,3
Donald Tashkin,4
Otoniel Martínez-Maza,5
Michael D. Roth,4
Leslie Ng,1
Joseph B. Margolick,6
Joan S. Chmiel,7
Zuo-Feng Zhang,1 and
Roger Detels1,4
1Department of Epidemiology and Jonsson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, California 90095.
2Department of Epidemiology, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, Maryland 21205.
3Department of Pathology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15213.
4Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095.
5Departments of Obstetrics and Gynecology and Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095.
6Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, Maryland 21205.
7Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611.
Address reprint request to:
Zuo-Feng Zhang
Department of Epidemiology
University of California at Los Angeles
71-225 CHS
Box 951772
650 Charles E. Young Drive, South
Los Angeles, California 90095-1772
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Abstract
Experimental data suggested that exposure to recreational drugs might adversely affect antitumor immunity, which led us to examine the hypothesis that use of marijuana, cocaine, poppers, and amphetamines might increase the risk of Kaposi's Sarcoma (KS) in HIV- and HHV-8-coinfected homosexual men. We analyzed data prospectively collected from the Multicenter AIDS Cohort Study (MACS) between 1984 and 2002. Among the 1335 HIV- and HHV-8-coinfected white men, 401 KS cases were identified. Multivariable Cox regression models were used to estimate the effects of time-varying recreational drug use on KS risk adjusting for potential confounders. The effects of both recent use (6 months prior) of recreational drugs and lagged exposure (i.e., use from 3 and 5 years prior) were examined. We did not observe any clear association with KS for recent use of any of the four drugs. In the analyses using lagged exposures, KS risk was associated with use of poppers 3–5 years prior [hazard ratio (HR)3 years prior=1.27, 95% CI (0.97–1.67), HR5 years prior=1.46 (1.01–2.13)]. However, no clear dose–response relationship was observed. These findings do not support a biological association between use of these substances and KS development in HIV- and HHV-8-coinfected homosexual men.
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