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Marijuana Does Not Promote Liver Disease Progression in HIV/HCV Coinfected People

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Smoking cannabis was not associated with liver fibrosis progression in a study of nearly 700 people with HIV and hepatitis C coinfection, according to a study described in the June 28, 2013, advance edition of Clinical Infectious Diseases.

Many people with HIV and hepatitis C use marijuana medically or recreationally. Studies looking at the link between cannabis use and liver disease progression have produced mixed results, with some showing worse fibrosis or steatosis (fatty liver), while others saw reduced fibrosis and better treatment response.

Laurence Brunet from McGill University and fellow investigators with the Canadian Co-infection Cohort sought to estimate the effect of regular marijuana smoking on liver disease progression among 690 HIV/HCV coinfected people from 17 HIV clinics across Canada who did not have significant fibrosis or end-stage liver disease at baseline.

A majority of participants (73%) in this prospective cohort study were men and the median age was 44 years. They had been infected with HIV for 10 years and HCV for 18 years on average. They had a median CD4 count of 400 cells/mm3, though only about half had undetectable HIV viral load at baseline.

At study entry, 53% said they had smoked marijuana during the past 6 months, consuming a median of 7 joints per week; 40% reported daily smoking. In addition to cannabis, half also drank alcohol (with 15% classified as "alcohol abuse") and 40% reported injection drug use during the past 6 months. Just over 40% reported using marijuana for symptom relief at baseline, rising to about 50% during follow-up.

Liver disease progression was assessed using the non-invasive biomarker aspartate aminotransferase-to-platelet ratio index (APRI), with scores of 1.5 or higher indicating significant liver fibrosis and scores of 2.0 or higher indicating cirrhosis.

Results

  • Over a median follow-up period of 32 months, 19% of participants reached APRI scores of 1.5 or higher, 15% reached scores of 2.0 or higher, 1% developed clinical cirrhosis, and 2% developed end-stage liver disease.
  • Incidence rates for these 4 outcomes were 39.2, 29.2, 2.1, and 2.9 events per 1000 person-visits, respectively.
  • There were no differences between marijuana users and nonusers in crude rates for any of these outcomes.
  • The study found no evidence that marijuana smoking was associated with accelerated progression to significant liver fibrosis (hazard ratio 1.02, where 1.0 indicates no difference) or cirrhosis (hazard ratio 0.99) according to APRI scores.
  • There was no evidence of any dose-response relationship between increased cannabis use and APRI score.
  • Smoking an additional 10 joints per week was associated with a slight increase in the risk of clinical cirrhosis, or cirrhosis and end-stage liver disease combined (hazard ratios 1.33 and 1.13 -- or 33% and 13% higher risk -- respectively).
  • However, when exposure was "lagged," or limited to 6-12 months before diagnosis, marijuana use no longer showed a significant association with either outcome.

Based on these findings, the study authors concluded, "In this prospective analysis we found no evidence for an association between marijuana smoking and significant liver fibrosis progression in HIV/HCV coinfection."

"Reported use for symptom relief was very prevalent suggesting that the association of daily cannabis use and more advanced fibrosis may, in fact, be related to an increased use for symptom management as disease advances," they elaborated in their discussion. "It is likely that previous studies have been biased by reverse causality as patients use more marijuana to relieve symptoms as liver disease progresses.

7/16/13

Reference

L Brunet, EEM Moodie, K Rollet, et al. Marijuana Smoking Does Not Accelerate Progression of Liver Disease in HIV-Hepatitis C Coinfection: A Longitudinal Cohort Analysis. Clinical Infectious Diseases. June 28, 2013 (Epub ahead of print).