Karino Y, Toyota J, Sato T, Ohmura T, Yamazaki K, Suga T, Nakamura K, Sugawara M, Matsushima T, Hino K
Department of Gastroenterology, Sapporo Kosei Hospital, Japan.
Dig Dis Sci. 2000 Nov;45(11):2207-13. doi: 10.1023/a:1026463102104.
To evaluate the relationship between mutations and clinical courses, we investigated precore (preC) and core promoter (CP) mutations and serum HBV DNA levels in HBe-antibody-positive HBV carriers. Fifty-six asymptomatic carriers (ASC), 29 patients with chronic hepatitis who showed normal ALT levels for more than two years (CH-ASC), 31 patients with chronic hepatitis (CH), and 32 patients with hepatocellular carcinoma (HCC) were studied. Almost all patients (99.2%) had mutations in either CP or preC. Mutation only in preC (A1896) was present in 52.2% with ASC, 25.0% with CH-ASC, 16.1% with CH, and 8.0% with HCC, and was significantly higher in ASC (P < 0.01). The patients with only preC mutation showed low HBV DNA levels in each clinical stage. The mutation of preC (A1896) prior to the mutation of CP might control the replication of HBV, which leads to the remission of hepatitis.
为了评估突变与临床病程之间的关系，我们研究了HBe抗体阳性的HBV携带者的前核心（preC）和核心启动子（CP）突变以及血清HBV DNA水平。研究对象包括56例无症状携带者（ASC）、29例慢性肝炎患者（这些患者的ALT水平在两年多时间内一直正常，即CH-ASC）、31例慢性肝炎患者（CH）以及32例肝细胞癌患者（HCC）。几乎所有患者（99.2%）的CP或preC存在突变。仅preC（A1896）突变在ASC中占52.2%，在CH-ASC中占25.0%，在CH中占16.1%，在HCC中占8.0%，且在ASC中显著更高（P < 0.01）。仅存在preC突变的患者在各个临床阶段的HBV DNA水平较低。CP突变之前的preC（A1896）突变可能控制HBV的复制，从而导致肝炎缓解。
