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Smoking cannabis does not accelerate progression of liver disease in people with HIV/HCV co-infection
Michael Carter, 2013-07-31 07:20:00
does not worsen liver disease in people with HIV and hepatitis C virus (HCV)
co-infection, Canadian research published in the online edition of Clinical Infectious Diseases shows.
“We found no
evidence that cannabis smoking increases the risk of progression to significant
liver fibrosis or cirrhosis,” write the authors. Results also showed that
cannabis was widely used for pain relief by co-infected people.
Up to 30% of
people with HIV in resource-rich countries are co-infected with HCV. Liver
disease caused by HCV is a leading cause of serious illness and death in these
(marijuana) is believed to be widely used by people with HIV. In a study conducted in
Ontario, Canada, 43% of participants reported use of cannabis in the previous year,
29% saying they had self-medicated with the drug.
examining the effects of cannabis consumption on liver disease outcomes has produced
conflicting results. Three cross-sectional – or 'snapshot' – studies involving
people with chronic HCV infection found an association between cannabis use
and liver cirrhosis. In contrast, a small study involving 58 people with HIV
showed no association between cannabis use and significant changes in liver
enzyme levels over one year.
uncertainty, investigators in Canada designed a prospective study involving 690
HIV-positive people with chronic HCV co-infection and no significant fibrosis
at baseline enrolled in the Canadian Coinfection Cohort study. Every six months,
participants were asked if they had used cannabis. Users of the drug were asked how
often they smoked cannabis and the number of joints they consumed on the days
then examined the association between cannabis use and progression to
significant fibrosis, cirrhosis and end-stage liver disease. Significant
fibrosis was defined as an AST platelet ratio index (APRI) score of 1.5 or above. An APRI score of 2.0 was
used to diagnose cirrhosis and the authors also looked at the relationship
between cannabis use and progression to a clinical cirrhosis diagnosis.
were concerned that participants might start to consume cannabis – or intensify their use of the drug – to alleviate symptoms related to advancing
liver disease. By collecting concurrent data on exposure to cannabis and
disease outcomes it could appear that cannabis caused liver disease when in
fact this was present before the participant changed their drug-use behaviour. The
investigators therefore repeated their analyses looking at cannabis use in the six
to twelve month period before liver disease assessments. They called this
method of analysis “lagging”.
The participants were
followed for a median of 2.7 years and contributed a total of 1875 person-years
of follow-up. The majority of participants were male and the median age at baseline
was 44 years. Most of the participants had an undetectable HIV viral load and the
median CD4 cell count at the start of the study was 400 cells/mm3.
Injecting drug use was reported by 38% of participants and 15% had alcohol abuse
Over half (53%) of
participants reported use of cannabis at baseline with similar proportion of
individuals using the drug through follow-up. On entry to the study, approximately
40% of participants who used cannabis said they did so for symptom relief, and this
proportion increased to over 50% during follow-up. Turning to frequency of use,
the investigators found that 40% of cannabis smokers consumed the drug on a
19% of participants developed significant fibrosis, 15% cirrhosis (diagnosed by
APRI score), 1% received a clinical diagnosis of cirrhosis and 2% progressed to
end-stage liver disease.
The incidence rate
of progression to APRI 1.5 or above was 39.2 per 1000 person-visits; incidence
of progression to APRI 2.0 or above was 29.2 per 1000 person-visits; incidence
of progression to a clinical cirrhosis diagnosis was 2.1 per 1000
person-visits; and incidence of progression to end-stage liver disease was 2.9
per 1000 person-visits. There were no differences in these incidence rates
between users and non-users of cannabis.
investigators’ initial analysis appeared to show that smoking cannabis
accelerated progression to a clinical diagnosis of cirrhosis (HR = 1.33; 95%
CI, 1.09-1.62 per ten joints/week). However, after lagging this association
ceased to be significant. Smoking cannabis was also initially associated with a
combined outcome of clinically diagnosed cirrhosis and end-stage liver disease
(HR = 1.13; 95% CI, 1.01-1.28). But once again this association ceased to be significant
when the researchers looked at cannabis consumption in the six to twelve months
before the clinical outcomes were diagnosed.
“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 symptoms management of the disease,” the authors suggest.
“Previous cross-sectional studies reporting an association between marijuana
smoking and liver fibrosis may be biased by reverse causation due to
self-medication with marijuana for relief of symptoms related to significant
They conclude, “We
could not demonstrate any important effect of marijuana on liver disease