Aim: is to investigate if past exposure to HBV in chronic HCV infection promotes the progression of liver disease and influences Interferon (INF) response or not. Methods: 185 patients with chronic HCV were recruited ...Aim: is to investigate if past exposure to HBV in chronic HCV infection promotes the progression of liver disease and influences Interferon (INF) response or not. Methods: 185 patients with chronic HCV were recruited and randomized into 2 groups, group I was treated with PEG-IFN alfa-2b plus ribavirin and group II with 3 MU/TIW IFN alfa-2b plus ribavirin. All patients had HBsAg negative & patients had HBc Ab positive tested for HBsAb. Patients with HBc Ab (n = 37) were tested for serum HBV DNA. Pretreatment liver biopsy and Immunohistochemistry was performed for detection of HBsAg and HBcAg using monoclonal antibodies. Demographic and laboratory data were collected. Results: 70/185 (38%) patients had Anti-HBc, 37 (20%) had isolated anti-HBc and none of the 37 subjects with isolated anti-HBc had serum HBV DNA. Sustained Viral Response (SVR) was achieved in 32/70 (46%) and 46/115 (40%) in anti-HBc seropositive and seronegative patients respectively, in conventional IFN group SVR was 37% and 39% in past HBV exposed patients and unexposed respectively, in PEG IFN group SVR was 59% and 41% in past HBV exposed patients and unexposed respectively. Among anti-HBc and anti-HBs seropositive patients SVR was 10/12 [83%] and 4/21 [19%] p = 0.004 in PEG and conventional IFN respectively. Marked fibrosis was diagnosed in 20% past HBV exposed patients versus 10% in unexposed patients (p = 0.01). Conclusion: past HBV exposure promotes the progression of liver disease but has no effect on the SVR to antiviral therapy in chronic HCV genotype 4 patients.展开更多
文摘Aim: is to investigate if past exposure to HBV in chronic HCV infection promotes the progression of liver disease and influences Interferon (INF) response or not. Methods: 185 patients with chronic HCV were recruited and randomized into 2 groups, group I was treated with PEG-IFN alfa-2b plus ribavirin and group II with 3 MU/TIW IFN alfa-2b plus ribavirin. All patients had HBsAg negative & patients had HBc Ab positive tested for HBsAb. Patients with HBc Ab (n = 37) were tested for serum HBV DNA. Pretreatment liver biopsy and Immunohistochemistry was performed for detection of HBsAg and HBcAg using monoclonal antibodies. Demographic and laboratory data were collected. Results: 70/185 (38%) patients had Anti-HBc, 37 (20%) had isolated anti-HBc and none of the 37 subjects with isolated anti-HBc had serum HBV DNA. Sustained Viral Response (SVR) was achieved in 32/70 (46%) and 46/115 (40%) in anti-HBc seropositive and seronegative patients respectively, in conventional IFN group SVR was 37% and 39% in past HBV exposed patients and unexposed respectively, in PEG IFN group SVR was 59% and 41% in past HBV exposed patients and unexposed respectively. Among anti-HBc and anti-HBs seropositive patients SVR was 10/12 [83%] and 4/21 [19%] p = 0.004 in PEG and conventional IFN respectively. Marked fibrosis was diagnosed in 20% past HBV exposed patients versus 10% in unexposed patients (p = 0.01). Conclusion: past HBV exposure promotes the progression of liver disease but has no effect on the SVR to antiviral therapy in chronic HCV genotype 4 patients.
