Sherlock D S
Department of Medicine, Royal Free Hospital School of Medicine, University of London, United Kingdom.
Dis Mon. 1994 Mar;40(3):117-96.
Formerly the diagnosis of acute and chronic non-A, non-B hepatitis was made by the exclusion of other causes. However, in 1989 cloning of an antigenic component of the hepatitis C virus (HCV) was reported. This led to first- and second-generation tests for antibody to HCV (anti-HCV) in serum. HCV has been associated with acute and chronic posttransfusion and sporadic non-A, non-B hepatitis, and with hepatocellular carcinoma. Viral HCV RNA can be estimated with the polymerase chain reaction test, but this technically difficult test is not generally available. The entire viral genome has been sequenced. The envelope region shows considerable variation, and mutant HCV infections are being described already. There are geographic variations in the prevalence of anti-HCV, but usually about 0.5% to 1% of healthy blood donors test positive. Parenteral exposure to blood, especially by transfusion or drug abuse, remains a certain means of acquiring HCV infection. The method by which millions without parenteral risk factors acquire HCV remains uncertain. Vertical transmission and sexual and family spread occur only rarely. Body secretions are free of the virus. The mode of transmission may become clarified when tests for viral HCV as opposed to anti-HCV become generally available. Acute HCV infection usually is mild, and the chronic disease is also indolent. Carriers of hepatitis B virus or alcoholics who also test positive for HCV have more serious disease. Chronic HCV infection must be distinguished from autoimmune chronic active hepatitis. The most important difference is the response to corticosteroid therapy, which is good in autoimmune hepatitis and poor in HCV-related disease. Hepatocellular carcinoma can complicate HCV-related cirrhosis, usually about 20 years after infection with HCV. Recombinant interferon-alpha is used to treat chronic HCV disease, but selection of patients, dose, and duration of therapy are uncertain. In general, 50% of patients respond to the treatment, but 50% of these will have a relapse, with an overall response rate of 25%. Liver transplantation in patients with end-stage HCV disease usually is followed by infection of the graft.
过去,急性和慢性非甲非乙型肝炎的诊断是通过排除其他病因来做出的。然而,1989年有报道称克隆出了丙型肝炎病毒(HCV)的一种抗原成分。这导致了血清中抗HCV的第一代和第二代检测方法。HCV与急性和慢性输血后及散发性非甲非乙型肝炎以及肝细胞癌有关。可用聚合酶链反应检测来估计病毒HCV RNA,但这项技术难度较大的检测方法一般无法普遍使用。整个病毒基因组已被测序。包膜区域显示出相当大的变异,并且已经有突变型HCV感染的相关描述。抗HCV的流行率存在地理差异,但通常约0.5%至1%的健康献血者检测呈阳性。经肠道外接触血液,尤其是通过输血或药物滥用,仍然是感染HCV的一种确定方式。数百万没有肠道外危险因素的人感染HCV的方式仍不确定。垂直传播以及性传播和家庭传播很少发生。身体分泌物中没有该病毒。当针对病毒HCV而非抗HCV的检测方法普遍可用时,传播方式可能会变得清晰。急性HCV感染通常较轻,慢性疾病也进展缓慢。同时检测出HCV呈阳性的乙肝病毒携带者或酗酒者病情更严重。慢性HCV感染必须与自身免疫性慢性活动性肝炎相区分。最重要的区别在于对皮质类固醇治疗的反应,自身免疫性肝炎对此反应良好,而HCV相关疾病则较差。肝细胞癌可使HCV相关肝硬化复杂化,通常在感染HCV后约20年发生。重组干扰素-α用于治疗慢性HCV疾病,但患者的选择、剂量和治疗持续时间尚不确定。一般来说,50%的患者对治疗有反应,但其中50%会复发,总体反应率为25%。终末期HCV疾病患者进行肝移植后,移植物通常会被感染。