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丙型肝炎的自然史。

Natural history of hepatitis C.

作者信息

Kiyosawa K, Tanaka E, Sodeyama T, Furuta S

机构信息

Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.

出版信息

Intervirology. 1994;37(2):101-7. doi: 10.1159/000150363.

DOI:10.1159/000150363
PMID:7529217
Abstract

With advances in tools for the diagnosis of hepatitis C virus (HCV) infection, it has become easier to evaluate the natural course of hepatitis C. Although HCV infection initially occurs in adult individuals, in most patients with acute hepatitis C (68%) it develops into chronic hepatitis. Once chronic hepatitis is established, the rate of spontaneous cure of the liver disease is very rare (below 2%). The duration from the onset of acute hepatitis until the time of diagnosis of cirrhosis of the liver and of hepatocellular carcinoma is about 20 and 30 years, respectively. The long-term clinical course of hepatitis C is divided into the three phases of acute, silent, and reactivated. The acute phase lasts from the onset of disease until 2-3 years thereafter, and the silent phase which follows lasts for 10-15 years. In the silent phase, the serum transferase level remains relatively low, below 100 IU/l, and is sometimes within the normal range. In the reactivated phase, the level of serum aminotransferase increases and remains at a high or moderate level until hepatocellular carcinoma develops. The mechanism of the chronicity of hepatitis C is unknown. However, recent advances in molecular analysis may soon elucidate this. Successive antigenic change of the HCV E2/NS1 hypervariable domain as a result of mutations may represent a mechanism by which this virus escapes the host immunosurveillance system, as well as a mechanism of its chronicity.

摘要

随着丙型肝炎病毒(HCV)感染诊断工具的进步,评估丙型肝炎的自然病程变得更加容易。虽然HCV感染最初发生在成年人中,但在大多数急性丙型肝炎患者(68%)中,它会发展为慢性肝炎。一旦慢性肝炎形成,肝病自发痊愈的几率非常低(低于2%)。从急性肝炎发作到诊断为肝硬化和肝细胞癌的时间分别约为20年和30年。丙型肝炎的长期临床病程分为急性、静止和再激活三个阶段。急性期从疾病发作持续到此后2至3年,随后的静止期持续10至15年。在静止期,血清转氨酶水平相对较低,低于100 IU/l,有时在正常范围内。在再激活期,血清转氨酶水平升高并保持在高水平或中等水平,直到发展为肝细胞癌。丙型肝炎慢性化的机制尚不清楚。然而,分子分析的最新进展可能很快阐明这一点。由于突变导致的HCV E2/NS1高变区连续抗原变化可能代表该病毒逃避宿主免疫监视系统的一种机制,以及其慢性化的一种机制。

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