慢性乙型肝炎肝硬化及肝细胞癌:肝腔静脉综合征在发病机制中的作用

S. Shrestha
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引用次数: 0

摘要

背景:慢性乙型肝炎(CHB)在一些亚非国家非常普遍,并与肝硬化(LC)和肝细胞癌(HCC)的高发病率相关,而在发病率低的西方,它有一个良性病程。慢性乙型肝炎中LC的发病机制尚不明确。材料与方法:肝腔静脉综合征(HVCS)是一种肝静脉流出梗阻疾病,是尼泊尔CHB患者的合并症。HVCS的存在是通过下腔静脉和肝脏的超声和彩色多普勒(US/CD)检查确定的。这是一项对1542例慢性乙型肝炎患者进行长期随访以评估其临床病程的回顾性研究。其中,988例患者根据HBeAg检测分为两组:HBeAg阳性19%进入复制期,HBeAg阴性81%进入非复制期。结果:80%的患者在诊断时无症状。细菌感染导致急性加重(AE), 80%的患者血清转氨酶升高,11.6%的患者出现腹水,US/CD显示HVOO。约14%发生轻度脾肿大,伴脾功能亢进的血液学特征。这些特征与HVCS的自然历史相一致。21.3%的患者发生LC, 4.7%的患者发生HCC。慢性乙型肝炎复制期和非复制期LC和HCC的发生率相似。但LC和HCC患者的ae、腹水和脾功能亢进发生率高。结论:HVCS对慢性乙型肝炎患者LC和HCC的症状性临床病程和发展有促进作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Liver Cirrhosis & Hepatocellular Carcinoma in Chronic Hepatitis B: Role of Hepatic Vena Cava Syndrome in the Pathogenesis
Background: Chronic hepatitis B (CHB) is highly prevalent in some Afro-Asian countries and is associated with high incidence of liver cirrhosis (LC) and hepatocellular carcinoma (HCC), whereas in the West with low prevalence it has a benign course. Pathogenesis of LC in CHB is not well-defined. Materials & Method: Hepatic vena cava syndrome (HVCS), a disease of hepatic venous outflow obstruction is a comorbid condition of CHB patients in Nepal. Presence of HVCS is ascertained by ultrasonography and color Doppler (US/CD) examination of inferior vena cava and liver. This is a retrospective study of a 1542 CHB patients followed for a long period to assess its clinical course. Of these, 988 patients were categorized into two groups based on assay of HBeAg: HBeAg-positive 19% into replicative phase, HBeAg-negative 81% in non-replicative phase. Results: Eighty per cent of the patients were asymptomatic at the time of diagnosis. Acute exacerbations (AE) developed precipitated by bacterial infection with elevation of serum aminotransferases in 80%, and in 11.6 % it was followed by ascites with US/CD evidence of HVOO. About 14% developed mild splenomegaly with hematological features of hypersplenism. These features were consistent with natural history of HVCS. LC developed in 21.3% and HCC in 4.7 % of patient. The incidences of LC and HCC in replicative and non-replicative phases of CHB were similar. But patients with LC and HCC had high incidence of AEs, ascites and hypersplenism. Conclusion: HVCS contributed to the symptomatic clinical course and development of LC and HCC in CHB.
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