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Marijuana Use Is Not Associated With Progression to Advanced Liver Fibrosis in HIV/Hepatitis C Virus-coinfected Women.

Marijuana Use Is Not Associated With Progression to Advanced Liver Fibrosis in HIV/Hepatitis C Virus-coinfected Women.
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Kelly EM, Dodge JL, Sarkar M, French AL, Tien PC, Glesby MJ, Golub ET, Augenbraun M, Plankey M, Peters MG,


Kelly EM, Dodge JL, Sarkar M, French AL, Tien PC, Glesby MJ, Golub ET, Augenbraun M, Plankey M, Peters MG, (click to view)

Kelly EM, Dodge JL, Sarkar M, French AL, Tien PC, Glesby MJ, Golub ET, Augenbraun M, Plankey M, Peters MG,

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Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2016 05 2563(4) 512-8 doi 10.1093/cid/ciw350

Abstract
BACKGROUND
Marijuana (hereafter "tetrahydrocannabinol [THC]") use has been associated with liver fibrosis progression in retrospective analyses of patients with chronic hepatitis C (HCV). We studied long-term effects of THC on fibrosis progression in women coinfected with human immunodeficiency virus (HIV)/HCV enrolled in the Women’s Interagency HIV Study (WIHS).

METHODS
Liver fibrosis was categorized according to FIB-4 scores as none, moderate, or significant. THC and alcohol use were quantified as average exposure per week. Associations between THC use and progression to significant fibrosis were assessed using Cox proportional hazards regression.

RESULTS
Among 575 HIV/HCV-coinfected women followed for a median of 11 (interquartile range, 6-17) years, 324 (56%) reported no THC use, 141 (25%) less than weekly use, 70 (12%) weekly use, and 40 (7%) daily use at WIHS entry. In univariable analysis, entry FIB-4 score (hazard ratio [HR], 2.26 [95% confidence interval {CI}, 1.88-2.73], P < .001), log HCV RNA (HR, 1.19 [95% CI, 1.02-1.38], P = .02), tobacco use (HR, 1.37 [95% CI, 1.02-1.85], P = .04), CD4(+) count (risk per 100-cell increase: HR, 0.90 [95% CI, .86-.95], P < .001), and log HIV RNA (HR, 1.18 [95% CI, 1.05-1.32], P = .005) were associated with progression to significant fibrosis, as was cumulative alcohol use in follow-up (HR, 1.03 [95% CI, 1.02-1.04], P < .001). In multivariable analysis, entry FIB-4, entry CD4(+) count, and cumulative alcohol use remained significant. Cumulative THC use was not associated with fibrosis progression (HR, 1.01 [95% CI, .92-1.10], P = .83). CONCLUSIONS
In this large cohort of HIV/HCV-coinfected women, THC was not associated with progression to significant liver fibrosis. Alcohol use was independently associated with liver fibrosis, and may better predict fibrosis progression in HIV/HCV-coinfected women.

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