Abstract
Purpose: Tobacco smoking can acclerate liver fibrosis in those with viral hepatitis, alcohol abuse or obesity (1). Additionally, El-Zayadi et al. (2) showed reduced response to interferon monotherapy in smokers compared to non smokers. Pauly et al. (3) demonstrated reduced Sustained Viral Response (SVR) in smokers to combined interferon/ribavarin treatment in genotype 2/3 but not genotype 1 patients. Neither study commented on tobacco dose amounts or ex smoking history effect on SVR. We wished to ascertain if current or prior tobacco exposure impacted SVR rates in patients with genotype 1 or genotype 2/3 when treated with pegylated interferon/ribavarin. Methods: A Retrospective chart analysis of electronic records matching inclusion criteria was performed and patients divided into smokers, ex smokers, and non smokers at treatment time. Non SVR and SVR was evaluated in each group. Amount of tobacco smoked was measured in pack years (packs per day * years smoked). Results: Of 311 medical charts reviewed, 229 met the inclusion criteria. Pack year smoking amounts was documented in 158 charts. Figure 1 reveals genotype 2/3 had better treatment response than genotype 1. There was no real difference amongst groups when smoking history was taken into account. Amongst smokers the mean pack year smoking amount was 21 in the SVR group and 18.8 in the non SVR group (p=0.24).[254] Figure 1: SVR between G1 and G2/3 groups.Conclusion: This study suggests that current or prior tobacco smoking does not have a significant effect on SVR rates in hepatitis C patients treated with interferon/ribavarin. Additionally, response rates do not appear to depend on amount of cigarettes smoked. Larger studies need to be done to validate these findings. Smoking cessation should still be encouraged as part of health promotion efforts.Table 1: DemographicsTable 2: Odds ratio estimates for SVR vs. Non SVR rates for selected variables
Published Version
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