Wiley T E, McCarthy M, Breidi L, McCarthy M, Layden T J
Section of Digestive and Liver Diseases, University of Illinois at Chicago Medical Center, USA.
Hepatology. 1998 Sep;28(3):805-9. doi: 10.1002/hep.510280330.
In patients infected with the hepatitis C virus (HCV), 20% to 30% will progress to cirrhosis in over two to three decades. Viral and host factors that are important in the clinical and histologic progression of HCV infection are not entirely certain. It has been suggested that liver disease is worse in alcoholics infected with HCV. In the present retrospective study, we examined the effect of moderate alcohol intake on the histologic and clinical progression of HCV infection and assessed whether other variables such as gender, length of exposure, mode of exposure, HCV RNA levels, and ferritin levels also independently impacted disease progression. Liver biopsies were analyzed for the degree of fibrosis, presence of cirrhosis, and histologic activity by using the Histologic Activity Index of Knodell. Patients were divided into two groups based on whether their alcohol intake was significant or not significant. Significant alcohol intake was defined as > 40 g alcohol/day in women and > 60 g of alcohol/day in men for > 5 years. Groups were further divided based on the decades of exposure to HCV. There was no difference in the age or length of exposure to HCV in the alcohol and the alcohol-free group. HCV RNA serum levels, ferritin levels, and viral genotypes were similar in both groups. There was a two- to threefold greater risk of liver cirrhosis and decompensated liver disease in the alcohol group. Also, the rate to which subjects developed cirrhosis was faster in the alcohol group with 58% being cirrhotic by the second decade as opposed to 10% being cirrhotic in the nonalcohol group by the second decade. The histologic and clinical acceleration of liver disease was independent of the mode of exposure or sex. In summary, alcohol intake is an independent risk factor in the clinical and histologic progression of HCV infection.
在丙型肝炎病毒（HCV）感染患者中，20%至30%的人在二三十年内会发展为肝硬化。在HCV感染的临床和组织学进展中起重要作用的病毒和宿主因素尚不完全明确。有人提出，感染HCV的酗酒者的肝病更严重。在本回顾性研究中，我们研究了适度饮酒对HCV感染的组织学和临床进展的影响，并评估了其他变量，如性别、接触时间长度、接触方式、HCV RNA水平和铁蛋白水平是否也独立影响疾病进展。通过使用Knodell组织学活动指数分析肝活检标本的纤维化程度、肝硬化的存在情况和组织学活性。根据饮酒量是否显著，将患者分为两组。显著饮酒定义为女性每天饮酒量>40克，男性每天饮酒量>60克，持续时间>5年。根据接触HCV的十年数进一步对组进行划分。饮酒组和不饮酒组在年龄或接触HCV的时间长度上没有差异。两组的HCV RNA血清水平、铁蛋白水平和病毒基因型相似。饮酒组发生肝硬化和失代偿性肝病的风险高出两到三倍。此外，饮酒组患者发展为肝硬化的速度更快，到第二个十年时，58%的患者出现肝硬化，而非饮酒组在第二个十年时只有10%的患者出现肝硬化。肝病的组织学和临床加速进展与接触方式或性别无关。总之，饮酒是HCV感染临床和组织学进展的一个独立危险因素。
