{"title":"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","authors":"S. Shrestha","doi":"10.30654/mjgh.10019","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":209275,"journal":{"name":"Mathews Journal of Gastroenterology and Hepatology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Liver Cirrhosis & Hepatocellular Carcinoma in Chronic Hepatitis B: Role of Hepatic Vena Cava Syndrome in the Pathogenesis\",\"authors\":\"S. Shrestha\",\"doi\":\"10.30654/mjgh.10019\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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.\",\"PeriodicalId\":209275,\"journal\":{\"name\":\"Mathews Journal of Gastroenterology and Hepatology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-03-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Mathews Journal of Gastroenterology and Hepatology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.30654/mjgh.10019\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mathews Journal of Gastroenterology and Hepatology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.30654/mjgh.10019","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.