Roudot-Thoraval F, Bastie A, Pawlotsky J M, Dhumeaux D
Département de Santé Publique, Hôpital Henri Mondor, Université Paris XII, Creteil, France.
Hepatology. 1997 Aug;26(2):485-90. doi: 10.1002/hep.510260233.
Cirrhosis is a frequent and severe event in the course of chronic hepatitis C, but it is unclear why some patients develop cirrhosis after a given period whereas others do not. We studied a large cohort of patients with chronic hepatitis C to determine the role of the route of transmission of hepatitis C virus (HCV) in the onset of cirrhosis. Six thousand six hundred sixty-four patients were enrolled in a nationwide survey of chronic hepatitis C in France. We first randomly defined a representative sample of 30 hospitals with medical units managing patients with HCV infection. All patients with chronic hepatitis C were enrolled if hepatitis C was diagnosed or treated in these units in 1991, 1992, or 1993. A questionnaire was filled in from the patients' charts and covered demographic data, risk factors for HCV infection, clinical and histological data, hepatitis B virus (HBV) and human immunodeficiency virus status, and alcohol intake. Descriptive statistics were prepared, and factors potentially related to the onset of cirrhosis were identified by means of univariate analysis followed by stepwise logistic regression analysis. Among the patients enrolled, 21.4% had biopsy-proven cirrhosis. Prevalence of cirrhosis markedly varied according to the route of transmission of HCV. It was significantly more frequent in blood recipients (23.4%) than in drug users (7.0%). Although the occurrence of cirrhosis was dependent on disease duration, it remained more frequent in blood recipients than in drug users for a given duration. Apart from the route of transmission, excessive alcohol intake was also associated with a higher risk of cirrhosis (34.9% vs. 18.2%; P < .001), and so was HBV infection (24.6% vs. 21.1%; P < .05). These factors acted independently of the route of transmission. Hepatocellular carcinoma was observed in 3.6% of all patients and in 17.8% of cirrhotic patients, and its occurrence was strongly and mainly related to the presence of cirrhosis. In conclusion, cirrhosis occurred in about 20% of the HCV-infected patients in this study and was more frequent in blood recipients than in drug users, independently of disease duration. Expected changes in the epidemiology of HCV infection might modify the risk of developing cirrhosis and, thereafter, cancer.
肝硬化是慢性丙型肝炎病程中常见且严重的事件,但尚不清楚为何一些患者在特定时期后会发展为肝硬化,而另一些患者则不会。我们研究了一大群慢性丙型肝炎患者,以确定丙型肝炎病毒(HCV)传播途径在肝硬化发病中的作用。6664名患者参与了法国一项全国性慢性丙型肝炎调查。我们首先随机确定了30家设有管理HCV感染患者医疗科室的医院作为代表性样本。所有在1991年、1992年或1993年在这些科室被诊断或治疗过丙型肝炎的慢性丙型肝炎患者均被纳入研究。根据患者病历填写了一份问卷,内容涵盖人口统计学数据、HCV感染的危险因素、临床和组织学数据、乙型肝炎病毒(HBV)和人类免疫缺陷病毒状况以及酒精摄入量。进行了描述性统计,并通过单因素分析及逐步逻辑回归分析确定了可能与肝硬化发病相关的因素。在纳入的患者中,21.4%经活检证实患有肝硬化。肝硬化的患病率根据HCV传播途径的不同有显著差异。在输血者中(23.4%)比在吸毒者中(7.0%)更为常见。尽管肝硬化的发生取决于病程,但在相同病程下,输血者中肝硬化的发生率仍高于吸毒者。除传播途径外,过量饮酒也与更高的肝硬化风险相关(34.9%对18.2%;P <.001),HBV感染也是如此(24.6%对21.1%;P <.05)。这些因素的作用独立于传播途径。在所有患者中,3.6%观察到肝细胞癌,在肝硬化患者中为17.8%,其发生与肝硬化的存在密切且主要相关。总之,在本研究中,约20%的HCV感染患者发生了肝硬化,且在输血者中比在吸毒者中更为常见,与病程无关。HCV感染流行病学的预期变化可能会改变发生肝硬化以及随后发生癌症的风险。