Smoking as an independent risk factor of liver fibrosis in primary biliary cirrhosis
Smoking as an independent risk factor of liver fibrosis in primary biliary cirrhosis
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DOI：
10.1016/j.jhep.2011.03.031
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发表时间：
2012-01-01
影响因子：
25.7
通讯作者：
Poupon, Raoul
中科院分区：
文献类型：
--
作者：
Corpechot, Christophe;Gaouar, Farid;Poupon, Raoul
背景与目的：吸烟已被认为是原发性胆汁性肝硬变(PBC)的潜在易感因素。然而，目前尚不清楚它是否与更活跃和更严重的疾病有关。我们的目的是评估吸烟与基本组织学损害的严重程度以及PBC的生化和免疫学特征的关系。方法：采用标准化问卷收集223例PBC患者的吸烟史资料。有164名患者在发病时获得了组织学数据。根据基于METAVIR的分类系统对肝纤维化和组织学炎症活动进行半定量。结果：确诊前有吸烟史的患者58例(26%)。25名患者(11%)在确诊时是活跃的吸烟者。男性(OR，4.5)、饮酒20g/d(OR，4.2)、F3-F4纤维化分期(OR，2.7)与吸烟史相关，但与炎症分级、胆管改变、生化或免疫学特征无关。F3-F4分期的患者吸烟强度显著升高(8.1+/-14.2包年vs.3.0+/-7.0包年；p=0.01)。调整后的Logistic回归分析显示，吸烟史和吸烟强度是晚期纤维化的独立危险因素。吸烟强度每增加一包年，晚期纤维化的可能性增加5.0%(95%CI，1.3-8.7%)。结论：吸烟以剂量依赖的方式增加了PBC的肝纤维化风险，而对疾病的组织学炎症活动、胆管病变、生化和免疫学特征没有明显的增加。应该强烈建议PBC患者不要吸烟。(C)2011年欧洲肝脏研究协会。爱思唯尔出版，版权所有。
Background & Aims: Smoking has been identified as a potential predisposition factor for primary biliary cirrhosis (PBC). However, it remains unclear whether it is associated with more active and severe disease. Our aim was to assess the relationships between smoking and the severity of the elementary histological lesions, as well as the biochemical and immunological features of PBC.Methods: Smoking history data were collected from 223 PBC patients using a standardized questionnaire. Histological data were available in 164 patients at presentation. Liver fibrosis and histological inflammatory activity were semi-quantified according to a METAVIR-based classification system. Odds ratios (OR) were assessed using a logistic regression analysis.Results: Smoking history prior to diagnosis was reported in 58 patients (26%). Twenty-five patients (11%) were active smokers at diagnosis. Male gender (OR, 4.5), alcohol intake >20 g/d (OR, 4.2), and F3-F4 fibrosis stage (OR, 2.7), but not inflammatory grade, bile duct changes, biochemical or immunological features, were associated with smoking history. Smoking intensity was significantly higher in patients with F3-F4 stage (8.1 +/- 14.2 pack-years vs. 3.0 +/- 7.0 pack-years; p = 0.01). Adjusted logistic regression identified smoking history and smoking intensity as independent risk factors of advanced fibrosis. Each pack-year of increase in smoking intensity was associated with a 5.0% (95% CI, 1.3-8.7%) increased likelihood of advanced fibrosis.Conclusions: Smoking increases, in a dose-dependent fashion, the risk of liver fibrosis in PBC without apparent increase in the histological inflammatory activity, bile duct lesions, biochemical, and immunological features of the disease. PBC patients should be strongly encouraged not to smoke. (C) 2011 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.