| Subject: Connecting the dots.... |
Author:
Teresa Hanbey
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Date Posted: Thu, October 03 2002, 12:29:43 PDT
In reply to:
CNN reports on UCLA study
's message, "Marijuana may be greater cancer risk than tobacco, research suggests" on Thu, October 03 2002, 12:20:44 PDT
For some time an article on the chemical similarities of marijuana and of tobacco has raised concern conmcerning the use of marijuana by patients with liver disease or who are being treated for hepatiti C with interferon, which may cause anorexia and other uncomfortable side effects.
While there is no disputing that people feel better when on drugs (otherwise why bother?) it still seems that the question of what chemicals, besides the TCH, is actually being taken into the body is of critical importance before making a decision about whether to accept the risks of using marijuana. Marijuana has many times the amounts of some very harmful chemicals also found in tobacco products. These substances have been repeatedly shown to be harmful to those with healthy bodies, so we could anticipate that they would be eben more deleterious to those with hepatitis C and other liver diseases.
Wouldn't inhaling chemical compounds similar to (or in excess of) tobacco (which at least has quality control going for it) have similar (or even worse)consequences to the liver as tobacco?
The basic question is, even IF the marijuana leads to increased SVR (which is not a given by any means) by maintianing the patient's ability to tolerate the treatment, would the risk of increased damage to the liver and risk of liver cancer (or any other type oc cancer, for that matter) be worth it? And, if inteferon has even a CHANCE of improving histology of the liver, wouldn't smoking marijuana (and-or tobaco) be DECREASING the odds of improvement to the liver"s architecture?
These are the basic and critical questions. Until there is research proving the safety of marijuana use, I will continue to recommend that people do not smoke anything.
thanbey
www.hcop.org
Cigarette smoking and hepatic lesions in patients with chronic hepatitis C
Abstract
A possible hepatotoxicity of cigarette smoke has been recently suggested by epidemiological and experimental studies. Our aim was to study the possible relationships between smoking and liver fibrosis and activity in patients with chronic hepatitis C.
A cross-sectional study was performed in a group of 310 patients with chronic hepatitis C consecutively hospitalized for their first liver biopsy.
The relationships between age, gender, alcohol consumption, route of contamination, tobacco consumption, and Knodell fibrosis and activity scores were examined in univariate, age-adjusted, and multivariate analyses.
One hundred and seventy-six patients (57%) were current smokers. Smokers were younger (P < .001), more often of male gender (P = .001), more often alcohol consumers (P = .001), and more often had a history of intravenous drug use (P = .0001) than never smokers.
Smoking was related to increased fibrosis and activity scores in age-adjusted (P = .009 and P = .005, respectively) and multivariate analyses (P = .03 and P = .04, respectively).
Smoking increases the severity of hepatic lesions in patients with chronic hepatitis C.
(HEPATOLOGY 2001;34:121-125.)
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