吸烟,百害而无一利,已经成为公认的事实。然而,吸烟与慢性肝病之间的关系,一直不明确。最近,法国科学家海泽德与美国科学家泽恩的研究分别表明,吸烟不但能导致慢性肝病活动,而且会加快肝硬化进程。这是科学界首次证明吸烟对肝有害。
日前,法国科学家海泽德等对244例慢性丙型肝炎进行了回顾性临床流行病学研究,并经肝组织活检证实,每日吸烟支数越多,肝脏炎症活动越严重,中度或重度炎症患者在不吸烟组的比例为62%,而在每日吸烟超过15支的患者组中则占81.9%,差异非常显著。并且,患者一生的总吸烟量与肝脏炎症活动度也密切相关,中度或重度炎症患者在从不吸烟组的比例为59%,而在每年吸烟超过20包的患者组中占到84.6%。
那么,吸烟能否加快慢性肝病的肝硬化进程?美国科学家给出了答案。2006年12月,泽恩博士等在世界著名肝脏病学杂志《肝病学》(Hepatology)发表的研究报告称,吸烟能够加快原发性胆汁性肝硬化患者的肝纤维化进程。他们对269例原发性胆汁性肝硬化患者进行了流行病学研究。结果发现,与肝纤维化程度较轻的患者相比,在肝纤维化程度较重的患者中吸烟非常常见。并且,在吸烟的患者中,具有严重组织学病变的患者平均消耗的香烟量为每年30包,明显高于组织学病变较轻的患者(每年17包)。
为什么吸烟会促进肝纤维化?科学家分析,烟草中含有大量可能具有肝毒性的物质,如尼古丁,它们会激活很多细胞因子,导致全身炎症、血栓形成和过氧化等,而这些因素都会加快肝硬化的进程。
强有力的证据表明,在影响慢性肝病临床进程的诸多因素中,吸烟是一个完全可以避免的因素。因此,慢性肝病患者不仅要戒酒,还要戒烟。
Hepatology. 2006 Dec;44(6):1564-71.
Smoking and increased severity of hepatic fibrosis in primary biliary cirrhosis: A cross validated retrospective assessment.
Zein CO, Beatty K, Post AB, Logan L, Debanne S, McCullough AJ.
Division of Gastroenterology and Hepatology, University Hospitals of Cleveland, Cleveland, OH, USA.
Division of Gastroenterology and Hepatology, University Hospitals of Cleveland, Cleveland, OH, USA.
An epidemiological association between cigarette smoking and primary biliary cirrhosis (PBC) has been demonstrated. Our aim was to determine the relationship between smoking and severity of liver fibrosis at presentation in patients with PBC. All patients with PBC seen at the three major teaching hospitals of Case Western Reserve University between October 1998 and December 2005 were identified. Data obtained at the time of the first evaluation leading to the PBC diagnosis on 97 patients were collected. The cumulative number of cigarette packs smoked per year (pack-years) was calculated. Advanced histological disease was defined as Ludwig stages 3 or 4. Analyses were performed to determine associations between advanced histological disease, smoking and other variables related to liver fibrosis. Smoking history was more common (P = .0008) in patients with advanced histological disease at presentation compared to those with early disease. Among smokers, mean lifetime tobacco consumption was higher (P = .04) in cases with advanced histological disease at presentation (30 pack-years) compared to cases with early disease (17 pack-years). Logistic regression demonstrated a significant association between a lifetime tobacco consumption of > or =10 pack-years and advanced histological disease at presentation (OR = 13.3). The association remained significant after adjusting for age, gender, and alcohol intake. The validity of these results was corroborated by cross-validation in an independent confirmatory set of 172 patients with PBC. In conclusion, smoking may accelerate the progression of PBC. This could be induced by exposure to chemicals in cigarette smoke.