This page is an archive. Its content may no longer be accurate and was last updated on the original publication date. It is intended for reference and as a historical record only. For hep C questions, call Help4Hep BC at 1-888-411-7578.
Tobacco exposure does not appear to be associated with accelerated progression of liver disease in this prospective study of HIV-HCV coinfected individuals.
Well surprise surprise! Although tobacco smoking has been shown to be an independent risk factor for liver fibrosis in hepatitis C virus (HCV) infection in some cross-sectional studies, no longitudinal study has confirmed this relationship, and the effect of tobacco exposure on liver fibrosis in human immunodeficiency virus (HIV)-HCV coinfected individuals is unknown. A recent study of participants from the Canadian Co-infection Cohort study (CTN 222), a multicenter longitudinal study of HIV-HCV coinfected individuals from 2003 to 2014 Canadian Co-infection Cohort study (CTN 222), examined whether or not cigarette smoking affected liver disease progression.
This study was undertaken by MAJOR major institutions and research centres, such as McGill University, UBC, Ottawa University, Canadian HIV Trials Network, University of Toronto, and others involved in the Canadian Co-infection Cohort study.
The authors state, “We did not find evidence that tobacco smoking was associated with a faster progression to significant liver fibrosis, as measured by APRI scores, or to ESLD when comparing ever versus never smokers. Moreover, progression to APRI score ≥1.5 or ESLD was not influenced by number of pack-years of smoking. Of the characteristics examined, the only factors associated with accelerated progression to liver fibrosis were detectable HCV RNA and alcohol use, both of which are well known risk factors for liver disease. Some studies have found that smokers are at increased risk of insulin resistance, which is a risk factor for steatosis, necroinflammation, and fibrosis in nonalcoholic fatty liver disease. A direct effect of tobacco smoking on insulin activity has also been documented in some studies. However, in our analyses, the estimates associated with smoking were unaffected by the inclusion of impaired fasting glucose or impaired glucose tolerance and progression to liver fibrosis or ESLD as a covariate.”
However the authors also point out that this study is not the last word on the subject: “Given the well described health risks of tobacco smoking, the strikingly high smoking rates among HIV-HCV coinfected individuals, and the excess rate of comorbidities in HIV-HCV coinfection, further study is merited to elucidate whether the excess rate of some of these comorbidities may indeed be linked in part to tobacco consumption.”
Open Forum Infect Dis. 2016 Mar; 3(2): ofw050.
Published online 2016 Mar 7. doi: 10.1093/ofid/ofw050
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817089/