L. Zhuang

Impact of viral replication inhibition by entecavir on peripheral T lymphocyte subpopulations in chronic hepatitis B patients

BackgroundTo investigate dynamic fluctuations of serum viral load and peripheral T-lymphocyte subpopulations of chronic hepatitis B patients and their correlation during entecavir therapy.MethodsFifty-five patients received entecavir 0.5 mg/d therapy. Serum HBV DNA load was measured by Real-Time-PCR, and the levels of peripheral T-lymphocyte subpopulations by flow cytometry biweekly, every four weeks and every eight weeks during weeks 1–12, 13–24 and 24–48, respectively. Multilevel modelling was used to analyse the relationship between these variables.ResultsOf the 55 patients, all HBeAg positive and with detectable HBV DNA, the majority (81.8%) had serum levels of HBV DNA over 107 copies per milliliter. HBV viral load dropped sharply during the first two weeks. In 28 and 43 patients, the level became undetectable from week 24 and 48, respectively. Using pre-therapy level as the reference, a significant decrease in CD8+ T cells and increase in CD4+ T cells were found from week 12. Both parameters and CD4+/CD8+ ratio steadily improved throughout the 48 weeks. Multilevel analyses showed that the level of decrement of HBV DNA was associated with the increment of T-lymphocyte activities only in the later period (4–48 week). After 4 weeks of therapy, for each log10 scale decrement of HBV DNA, the percentage of CD4+ lymphocyte was increased by 0.49 and that of CD8+ decreased by 0.51.ConclusionT-lymphocyte subpopulations could be restored partially by entecavir treatment in patients with chronic hepatitis B concurrently with reduction of viremia.

PP-108 Prevalence of transfusion-transmitted virus in patients with viral liver disease

Introduction: Primary liver cancer accounts for only 1 2% of malignant tumors found at autopsy in western countries. However, in some parts of Africa and Asia it may account for up to 20 30% of all types of malignancy. The high frequency of HBsAg positivity in individuals with Hepatocellular Carcinoma (HCC) strongly suggests that chronic HBV infection may contribute in some way towards the development of 1ry liver cell carcinoma. Although HCC is probably caused by one or more environmental carcinogens, a hereditary predisposition to the tumor has not been excluded. Aim: Determine the incidence of HBsAg carriers patients suffering from primary HCC and detect the association between primary HCC and HLA. Subjects and Methods: The material consisted of twenty patients diagnosed as HCC based on Ultrasonographic examination and by Histopathology. Laboratory investigations; liver biopsy, HBsAg, Anti-HBcAg (IgM) and HLA typing using lymphocyte microcytotoxicity technique. Results: The 20 studied cases were negative for HBcAb IgM and 10 patients were positive for HBsAg. HLA typing revealed significant rise of HLA-A9, HLA-B5 among HCC patients. HLAA9 was significantly increased in HBsAg positive and negative cases. HLA-B5 was significantly increased in HBsAg positive cases only while HLA-B8 was significantly increased in HBsAg negative cases only. In cases with mixed hepatic cirrhosis and Schistosomal hepatic fibrosis which were negative for HBsAg showed significant increase in HLA-A9. Conclusions: 1. Significant association of HBsAg positivity in patients with HCC. 2. Significant association of HLA-A9 and HLA-B5 with HCC. 3. HLA-A9 in patients mixed cirrhosis and Schistosomal hepatic fibrosis may be predisposing to HCC.