2016
Costiniuk, Cecilia T.; Brunet, Laurence; Rollet-Kurhajec, Kathleen C.; Cooper, Curtis; Walmsley, Sharon; Gill, M. John; Martel-Laferriere, Valérie; Klein, Marina B.
In: Open Forum Infectious Diseases, 2016.
Abstract | Links | BibTeX | Tags: Cohort study, HCV, HIV, Liver disease, Tobacco
@article{Costiniuk2016,
title = {Tobacco Smoking Is Not Associated With Accelerated Liver Disease in Human Immunodeficiency Virus-Hepatitis C Coinfection: A Longitudinal Cohort Analysis},
author = {Cecilia T. Costiniuk and Laurence Brunet and Kathleen C. Rollet-Kurhajec and Curtis Cooper and Sharon Walmsley and M. John Gill and Valérie Martel-Laferriere and Marina B. Klein},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27047987},
doi = {10.1093/ofid/ofw050},
year = {2016},
date = {2016-03-04},
journal = {Open Forum Infectious Diseases},
abstract = {Background. 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. Methods. The study population consisted of participants from the Canadian Co-infection Cohort study (CTN 222), a multicenter longitudinal study of HIV-HCV coinfected individuals from 2003 to 2014. Data were analyzed for all participants who did not have significant fibrosis or end-stage liver disease (ESLD) at baseline. The association between time-updated tobacco exposure (ever vs nonsmokers and pack-years) and progression to significant liver fibrosis (defined as an aspartate-to-platelet ratio index [APRI] ≥1.5) or ESLD was assessed by pooled logistic regression. Results. Of 1072 participants included in the study, 978 (91%) had ever smoked, 817 (76%) were current smokers, and 161 (15%) were previous smokers. Tobacco exposure was not associated with accelerated progression to significant liver fibrosis nor with ESLD when comparing ever vs never smokers (odds ratio [OR] = 1.06, 95% confidence interval [CI], 0.43-1.69 and OR = 1.20, 95% CI, 0.21-2.18, respectively) or increases in pack-years smoked (OR = 1.05, 95% CI, 0.97-1.14 and OR = 0.94, 95% CI, 0.83-1.05, respectively). Both time-updated alcohol use in the previous 6 months and presence of detectable HCV ribonucleic acid were associated with APRI score ≥1.5. Conclusions. Tobacco exposure does not appear to be associated with accelerated progression of liver disease in this prospective study of HIV-HCV coinfected individuals.},
keywords = {Cohort study, HCV, HIV, Liver disease, Tobacco},
pubstate = {published},
tppubtype = {article}
}
Background. 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. Methods. The study population consisted of participants from the Canadian Co-infection Cohort study (CTN 222), a multicenter longitudinal study of HIV-HCV coinfected individuals from 2003 to 2014. Data were analyzed for all participants who did not have significant fibrosis or end-stage liver disease (ESLD) at baseline. The association between time-updated tobacco exposure (ever vs nonsmokers and pack-years) and progression to significant liver fibrosis (defined as an aspartate-to-platelet ratio index [APRI] ≥1.5) or ESLD was assessed by pooled logistic regression. Results. Of 1072 participants included in the study, 978 (91%) had ever smoked, 817 (76%) were current smokers, and 161 (15%) were previous smokers. Tobacco exposure was not associated with accelerated progression to significant liver fibrosis nor with ESLD when comparing ever vs never smokers (odds ratio [OR] = 1.06, 95% confidence interval [CI], 0.43-1.69 and OR = 1.20, 95% CI, 0.21-2.18, respectively) or increases in pack-years smoked (OR = 1.05, 95% CI, 0.97-1.14 and OR = 0.94, 95% CI, 0.83-1.05, respectively). Both time-updated alcohol use in the previous 6 months and presence of detectable HCV ribonucleic acid were associated with APRI score ≥1.5. Conclusions. Tobacco exposure does not appear to be associated with accelerated progression of liver disease in this prospective study of HIV-HCV coinfected individuals.
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