Cleveland Clinic, Cleveland, OH, USA.
J Hepatol. 2011 Apr;54(4):753-9. doi: 10.1016/j.jhep.2010.07.040. Epub 2010 Sep 22.
BACKGROUND & AIMS: Although many predictors of disease severity of nonalcoholic fatty liver disease (NAFLD) have been proposed, studies of the potential effects of specific environmental exposures on human NAFLD are lacking. Smoking increases insulin resistance. Given the pathophysiological role of insulin resistance in NAFLD, characterization of the influence of smoking in NAFLD is warranted. The aim of this paper was to study the potential association between cigarette smoking and advanced fibrosis in NAFLD.
All adults enrolled in the NASH CRN studies, between October 2004 and February 2008, who had liver biopsies, were included (n=1091). Advanced fibrosis was defined as stages 3-4. Analyses were performed.
Significant bivariate associations were demonstrated between advanced fibrosis and age, gender, ethnicity, diabetes, and smoking history. History of smoking ≥ 10 pack-years was more common (p <0.0001) among patients with advanced fibrosis. Multivariate analysis demonstrated an association between smoking history of ≥ 10 pack-years and advanced fibrosis (OR=1.63). Among non-diabetics, history of ≥ 10 pack-years was associated with an OR of 2.48 for advanced fibrosis. High frequencies of advanced fibrosis were observed among diabetics (with or without ≥ 10 pack-years history) and non-diabetics with ≥ 10 pack-years history as compared to non-diabetics without significant smoking history.
Smoking history was associated with advanced liver fibrosis in this large multicenter cohort of NAFLD patients. The results indicate that smoking may enhance the progression of NAFLD partly through its effect on insulin resistance. Our results are consistent with recent animal studies suggesting that cigarette smoke may aggravate fatty liver. To our knowledge, this is the first study to show that cigarette smoking is associated with increased fibrosis severity in human NALFD, suggesting it may accelerate disease progression. These results may support a formal recommendation of smoking cessation in patients with NAFLD.
虽然已经提出了许多非酒精性脂肪性肝病(NAFLD)严重程度的预测因素,但缺乏关于特定环境暴露对人类 NAFLD 的潜在影响的研究。吸烟会增加胰岛素抵抗。鉴于胰岛素抵抗在 NAFLD 中的病理生理作用,有必要对吸烟在 NAFLD 中的影响进行特征描述。本文旨在研究吸烟与 NAFLD 中晚期纤维化之间的潜在关联。
纳入 2004 年 10 月至 2008 年 2 月期间在 NASH CRN 研究中接受肝活检的所有成年人(n=1091)。晚期纤维化定义为 3-4 期。进行了分析。
显著的双变量关联表明,晚期纤维化与年龄、性别、种族、糖尿病和吸烟史有关。有≥10 包年吸烟史的患者更常见(p<0.0001)。多变量分析表明,有≥10 包年吸烟史与晚期纤维化之间存在关联(OR=1.63)。在非糖尿病患者中,≥10 包年的吸烟史与晚期纤维化的 OR 为 2.48。与无显著吸烟史的非糖尿病患者相比,有≥10 包年吸烟史的糖尿病患者和非糖尿病患者的晚期纤维化发生率较高。
在这项大型多中心 NAFLD 患者队列研究中,吸烟史与晚期肝纤维化有关。结果表明,吸烟可能通过其对胰岛素抵抗的影响来促进 NAFLD 的进展。我们的结果与最近的动物研究一致,表明香烟烟雾可能会加重脂肪肝。据我们所知,这是第一项表明吸烟与人类 NALFD 纤维化严重程度增加相关的研究,提示吸烟可能会加速疾病进展。这些结果可能支持向 NAFLD 患者推荐戒烟。