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Cannabis Worsens Fibrosis (Liver Disease) in HCV By 3 to 7 Times
 
 
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here are a few that found cannabis worsened HCV fibrosis:

 
Back in the earlier years around 2005 many studies of cannabis in HCV & its affect on HCV fibrosis were conducted and it was a common topic of discussion at hepatitis conferences....
 
(Marijuana/Hash) Endocannabinoids and liver disease - review.... http://www.natap.org/2005/HCV/091905_01.htm
 
Conclusions: Endocannabinoids appear to be involved in several aspects of acute and chronic liver disease, including vascular changes, modulation of inflammatory process and neurological function, Further research may provide new insights into the pathophysiology of liver disease, as well as a basis for novel treatment modalities.
 
Daily Cannabis Use by HCV+ Increased Odds of Moderate to Severe Fibrosis by 7- Fold.....http://www.natap.org/2006/AASLD/AASLD_07.htm
 
This study was conducted by French INSERM Group
 
Daily Cannabis Smoking as a Risk Factor for Fibrosis Progression in Chronic Hepatitis C .....http://www.natap.org/2005/HCV/062705_01.htm
 
These results support experimental data demonstrating the profibrogenic role of CB1 receptors, see below (Grenart et al). Daily cannabis consumption should be avoided in patients with chronic hepatitis C. In multivariate analysis, fibrosis progression rate >0.08 U per year was independently related to a 4 times greater risk from daily cannabis smoking; alcohol intake >30 grams/day showed double the risk for faster fibrosis progression
 
In their publication daily cannabis use was associated with 3.5 increased risk for faster fibrosis progression rate (FBR) and daily cannabis use independent predictor of rapid FPR, excessive alcohol with 2.21 faster rte,
 
Daily Cannabis Smoking as a Risk Factor for Progression of Fibrosis in Chronic Hepatitis C....."Daily cannabis use was also an independent predictor of a rapid FPR" pdf attached above
 
Hepatology 2005- Christophe Hezode,1,6 Franc¬łoise Roudot-Thoraval,2,6 Son Nguyen,1,5 Pascale Grenard,5 Boris Julien,5 Elie-Serge Zafrani,3,5 Jean-Michel Pawlostky,4,6 Daniel Dhumeaux,1 Sophie Lotersztajn,5 and Ariane Mallat1,5
 
Abstract
 
Cannabinoids present in Cannabis sativa (marijuana) exert biological effects via cannabinoid receptors CB1 and CB2. We recently demonstrated that CB1 and CB2 receptors regulate progression of experimental liver fibrosis. We therefore investigated the impact of cannabis smoking on fibrosis progression rate in patients with chronic hepatitis C (CHC). Two hundred seventy consecutive untreated patients with CHC of known duration undergoing liver biopsy were studied. Demographic, epidemiological, metabolic, and virological data were recorded, and detailed histories of cannabis, alcohol, and tobacco use over the span of hepatitis C virus infection were obtained. Fibrosis stage, steatosis, and activity grades were scored according to Metavir system. Patients were categorized as noncannabis users (52.2%), occasional users (14.8%), or daily users (33.0%), and the relationship between cannabis use and fibrosis progression rate (FPR) or fibrosis stage was assessed. On multivariate analysis, six factors were independently related to a FPR greater than 0.074 (median value of the cohort): daily cannabis use (OR = 3.4 [1.5-7.4]), Metavir activity grade A2 or higher (OR = 5.4 [2.9-10.3]), age at contamination of more than 40 years (OR = 10.5 [3.0-37.1]), genotype 3 (OR = 3.4 [1.5-7.7]), excessive alcohol intake (OR = 2.2 [1.1-4.5]), and steatosis (OR = 2.0 [1.0-4.1]). Daily cannabis use was also an independent predictor of a rapid FPR (>0.15) (OR = 3.6 [1.5-7.5]). Finally, severe fibrosis (≥F3) was also predicted by daily cannabis use (OR = 2.5 [1.1-5.6]; P = .034), independently of Metavir activity grade, excessive alcohol intake, age at liver biopsy, steatosis, and tobacco smoking. In conclusion, daily cannabis smoking is significantly associate
 
 
 
 
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