Brunet L. Clin Infect Dis. 2013;doi:10.1093/cid/cit378.
July 10, 2013
Smoking marijuana did not lead to liver disease progression among people coinfected with HIV and hepatitis C, researchers from McGill University have found.
“The literature regarding the effects of cannabis on liver diseases is conflicting,” the researchers wrote in Clinical Infectious Diseases. “Cell culture and animal model studies support that cannabinoids could have a therapeutic effect on liver injury and fibrosis progression. However, three cross-sectional studies in patients with chronic HCV suggest that daily cannabis use is associated with fibrosis and steatosis.”
The study included 690 patients who were positive for HCV but did not have significant fibrosis or end-stage liver disease (ESLD). The patients were part of the Canadian Coinfection Cohort and visited their providers every 6 months, contributing to 1,875.3 person-years of follow-up, with a median follow-up time of 2.7 years. At each visit, they reported their marijuana use, including how often they smoked and the amount they consumed.
At baseline, 53% of the patients reported smoking marijuana in the past 6 months. The median consumption was seven joints per week, and 40% of the patients smoked daily. Among the patients, 19.1% developed liver fibrosis and 14.8% developed cirrhosis, according to APRI score. Eleven patients developed ESLD and eight patients developed clinical cirrhosis.
Multivariate analysis showed that marijuana use was not associated with fibrosis or cirrhosis as measured by APRI score. Smoking marijuana did accelerate progression to clinical cirrhosis (HR=1.33 per 10 joints/week; 95% CI, 1.09-1.62). Marijuana smoking was also associated with an increased risk of clinical cirrhosis and ESLD combined (HR=1.13; 95% CI, 1.01-1.28). However, if the exposure lagged 6 to 12 months before diagnosis, they were no longer associated (HR=1.10; 95% CI, .95-1.26).
“A causal association is unlikely: hazard ratios were weak and most importantly were attenuated when accounting for temporality in the exposure-disease relationship and there was no dose-response relationship,” the researchers wrote. “It is likely that previous studies have been biased by reverse causality as patients use more marijuana to relieve symptoms as liver disease progresses.”
Disclosure: The researchers report no relevant financial disclosures.
Source - Healio
“The literature regarding the effects of cannabis on liver diseases is conflicting,” the researchers wrote in Clinical Infectious Diseases. “Cell culture and animal model studies support that cannabinoids could have a therapeutic effect on liver injury and fibrosis progression. However, three cross-sectional studies in patients with chronic HCV suggest that daily cannabis use is associated with fibrosis and steatosis.”
The study included 690 patients who were positive for HCV but did not have significant fibrosis or end-stage liver disease (ESLD). The patients were part of the Canadian Coinfection Cohort and visited their providers every 6 months, contributing to 1,875.3 person-years of follow-up, with a median follow-up time of 2.7 years. At each visit, they reported their marijuana use, including how often they smoked and the amount they consumed.
At baseline, 53% of the patients reported smoking marijuana in the past 6 months. The median consumption was seven joints per week, and 40% of the patients smoked daily. Among the patients, 19.1% developed liver fibrosis and 14.8% developed cirrhosis, according to APRI score. Eleven patients developed ESLD and eight patients developed clinical cirrhosis.
Multivariate analysis showed that marijuana use was not associated with fibrosis or cirrhosis as measured by APRI score. Smoking marijuana did accelerate progression to clinical cirrhosis (HR=1.33 per 10 joints/week; 95% CI, 1.09-1.62). Marijuana smoking was also associated with an increased risk of clinical cirrhosis and ESLD combined (HR=1.13; 95% CI, 1.01-1.28). However, if the exposure lagged 6 to 12 months before diagnosis, they were no longer associated (HR=1.10; 95% CI, .95-1.26).
“A causal association is unlikely: hazard ratios were weak and most importantly were attenuated when accounting for temporality in the exposure-disease relationship and there was no dose-response relationship,” the researchers wrote. “It is likely that previous studies have been biased by reverse causality as patients use more marijuana to relieve symptoms as liver disease progresses.”
Disclosure: The researchers report no relevant financial disclosures.
Source - Healio
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