Tim Zimmermann1, Dietrich Hueppe2, Stefan Mauss3, Peter Buggisch4, Heike Pfeiffer-Vornkahl5, Daniel Grimm6, Peter R Galle6, Ulrich Alshuth7. 1. First Department of Medicine, Johannes Gutenberg University, Mainz, Germany. tim.zimmermann@unimedizin-mainz.de. 2. Center of Gastroenterology, Herne, Germany. 3. Center for HIV and Hepatogastroenterology, Duesseldorf, Germany. 4. Ifi-Institute for Interdisciplinary Medicine, Hamburg, Germany. 5. Factum GmbH, Offenbach/Main, Germany. 6. First Department of Medicine, Johannes Gutenberg University, Mainz, Germany. 7. Roche Pharma AG, Medical Affairs Virology, Grenzach-Wyhlen, Germany.
Abstract
BACKGROUND AND AIMS: Smoking has multiple effects on factors influencing hepatitis C and antiviral therapy, including lipid metabolism, fibrosis, platelet count and adherence aspects. The aim of this analysis was to determine the impact of smoking on hepatitis C virus antiviral therapy. METHODS: Data of two cohorts of an observational multicenter study including therapy-naïve patients infected with genotype 1 hepatitis C virus (HCV) treated with dual antiviral therapy (n=7,796) with pegylated interferon alpha 2a in combination with ribavirin, or triple antiviral therapy (n=1,122) containing telaprevir or boceprevir, were analysed. RESULTS: In the univariate matched pair analysis of dual antiviral therapy patients (n=584), smoking was significantly associated with lower sustained viral response rates (p=0.026, OR 0.69 CI: 0.50 - 0.96). The effect of smoking on sustained viral response remained significant (p=0.028, OR 0.67 CI: 0.47 - 0.96) in the multivariate analysis when adjusting for all other baseline parameters with a significant association in the univariate analysis, i.e. diabetes, fibrosis, body mass index, transaminases and baseline viral load. Under protease inhibitors the influence of smoking on virological response did not arise. CONCLUSIONS: Smoking has a negative impact on antiviral therapy in naïve patients infected with HCV genotype 1 independently of age, gender, history of drug use or alcoholic liver disease. The effects of smoking might be overcome by the new antiviral agents.
BACKGROUND AND AIMS: Smoking has multiple effects on factors influencing hepatitis C and antiviral therapy, including lipid metabolism, fibrosis, platelet count and adherence aspects. The aim of this analysis was to determine the impact of smoking on hepatitis C virus antiviral therapy. METHODS: Data of two cohorts of an observational multicenter study including therapy-naïve patients infected with genotype 1 hepatitis C virus (HCV) treated with dual antiviral therapy (n=7,796) with pegylated interferon alpha 2a in combination with ribavirin, or triple antiviral therapy (n=1,122) containing telaprevir or boceprevir, were analysed. RESULTS: In the univariate matched pair analysis of dual antiviral therapy patients (n=584), smoking was significantly associated with lower sustained viral response rates (p=0.026, OR 0.69 CI: 0.50 - 0.96). The effect of smoking on sustained viral response remained significant (p=0.028, OR 0.67 CI: 0.47 - 0.96) in the multivariate analysis when adjusting for all other baseline parameters with a significant association in the univariate analysis, i.e. diabetes, fibrosis, body mass index, transaminases and baseline viral load. Under protease inhibitors the influence of smoking on virological response did not arise. CONCLUSIONS: Smoking has a negative impact on antiviral therapy in naïve patients infected with HCV genotype 1 independently of age, gender, history of drug use or alcoholic liver disease. The effects of smoking might be overcome by the new antiviral agents.
Authors: Mirna Becevic; Emmanuelle Wallach; Lincoln R Sheets; Hope Misterovich; Susan Norris; Evelyn Aboagye; Jonathan A Dyer; Bruce R Bacon; Karen Edison; Kristin Sohl Journal: Mo Med Date: 2020 May-Jun