{"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}
引用次数: 0
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.