PWE-132 Association Between Smoking And Liver Fibrosis In Primary Biliary Cirrhosis. (9th June 2014)

• Record Type: Journal Article
• Authors: Mantaka, A; Koulentaki, M; Sifaki-Pistolla, D; Voumvouraki, A; Marinidou, E; Papiamonis, N; Tzardi, M; Kouroumalis, E
• Is Part Of: Gut. Volume 63(2014)Supplement 1
• Page Start: A182
• Page End: A183
• Publication Date: 2014-06-09
• Subjects: Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gutjnl-2014-307263.392
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : Introduction: Conflicting data for the role that cigarette smoking may play in Primary Biliary Cirrhosis (PBC) have been reported. Some studies have suggested an association of smoking with a more advanced fibrotic stage. The aim of the present study therefore was to assess the association between smoking and a) the severity of histological findings at the time of diagnosis, b) the immunological features of a genetically homogeneous and geographically defined population of PBC patients. Methods: Smoking history data were collected from 171 PBC patients of Cretan origin (163 female) using a standardised questionnaire. Diagnosis was based on standard biochemical, Immunological and histological criteria. Liver biopsy was performed in 148 patients at diagnosis. Liver fibrosis and histological inflammatory activity were semi-quantified according to a METAVIR-based classification system. Odds ratios (OR) were assessed using logistic regression analysis. Results: Smoking history prior to diagnosis was reported in 56 patients (32, 7%%). Twenty-six patients (15, 2%) were active smokers at diagnosis. Male gender (AOR 8.19, 95% CI: 3.014–11.937), alcohol intake >20 g/d (AOR, 2.20, 95% CI: 1.029–4.099), severe steatosis (AOR, 5.31, 95% CI: 2.019–9.919)), and F3–F4 fibrosis stage (AOR 1.21 95% CI: 1.015–3.031), but not piecemeal necrosis grade, bile duct paucity and cholangitis, or immunological laboratory data, were associated with smoking history. Multiple logistic regression analysis identified smoking intensity, years of passive smoking and significant necroinflammatory histological activity as independent risk factors of advanced liver fibrosis (F3–F4 stage) at diagnosis, adjusted for age, gender, BMI and alcohol consumption. For every pack-year increase in smoking intensity there was a 3.2 times higher likelihood of advanced fibrosis (95% CI: 2.018–6.294). Conclusion: Our study results confirm the previously reported link between smoking history and the risk of advanced liver fibrosis at diagnosis in PBC. The mechanism by which smoking may accelerate the histological progression of PBC is unknown and larger studies are needed to define it. Disclosure of Interest: None Declared.