Background/Aim: We compared the prevention of HBV reactivation in (HBsAg)-positive patients with HBsAg-negative patients who were positive for antibody to (anti-HBc) and/or (anti-HBs) undergoing immunosuppressive, anticancer or molecular target therapy. Methods: From Sep 2004 to Nov 2008 HBsAg-positive patients and 22 anti-HBc and/or anti-HBs-positive patients were enrolled in this study. We compared with 2 groups about background disease, age, blood examination, and nucleoside analogues. Results: In HBsAg-positive patients mean age were 56.6±10.2 years old, median AST levels were 30 (18-706) IU/L, and median ALT levels were 36 (13-544) IU/L for 8 (47%) haematological disease and 9 (53%) collagenosis disease. In anti-HBc and/or anti-HBs-positive patients mean age were 71.3±9.6 years old, median AST levels were 20 (9-106) IU/L, median ALT levels were 16.5 (5-247) IU/L for 17 (77%) haematological disease and 5 (23%) collagenosis disease. Serum HBV-DNA levels >5.0 log copies/ml were 8 (47%), 2.6~5.0 were 7 (41%), <2.6 were 2 (12%) in HBsAg-positive patients, and serum HBV-DNA levels <2.6 were all cases in anti-HBc and/or anti-HBs-positive patients. 14 (82%) of HBsAg-positive patints received nucleoside analogues (7 LAM and 7 ETV), and 12 (55%) of anti-HBc and/or anti-HBs-positive patients received nucleoside analogues (8 LAM and 4 ETV). Mean duration of treatment for 14.2 months in HBsAg-positive patients, and for 4.1 months in anti-HBc and/or anti-HBs-positive patients, the resistance virus occurred to 3 (75%) of 4 HBsAg-positive patients treated with LAM for collagenosis disease more than two years. Conclusion: When HB carriers of collagenaous disease undergoing immunosuppressive therapy required the nucleoside analogues more than two years, we recommended treatment to prevent HBV reactivation with ETV. Background: Adefovir dipivoxil is used for the initial treatment of chronic hepatitis B or rescue treatment of lamivudine-resistant chronic hepatitis B, and exhibits excellent antiviral activity. However, the presence of resistance to adefovir dipivoxil was more frequently in lamivudine-resistant chronic hepatitis B patients than in lamivudine-naïve patients during adefovir dipivoxil monotherapy. But the rate of adefovir resistance related mutations is little known in lamivudine-resistant patients before adefovir dipivoxil treatment. The aim of this study was to investigate the rate of adefovir resistance-related mutations in polymerase gene of hepatitis B virus in lamivudine-resistant patients not treated with adefovir dipivoxil. Methods: The existence of adefovir resistance-related mutations was examined in 240 lamivudine-resistant chronic hepatitis B patients with breakthrough hepatitis and 100 antiviral-naïve chronic hepatitis B patients. Both polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) and directly sequencing of PCR product were used to detect resistant viruses. Results: rtA181T mutants were detected in only two sera of lamivudine-resistant patients, while none in the antiviral-naïve chronic hepatitis B patients. There was no rtN236T detected in the two groups. Conclusion: Our results suggest that the rtA181 mutant virus were present in a few lamivudine-resistant chronic hepatitis B patients before they have been treated with adefovir dipivoxil, but the rtN236T mutant was not detected in any of the two groups. The rate of adefovir resistance-related mutations in polymerase gene of hepatitis B virus was low in such lamivudine-resistant patients before adefovir dipivoxil treatment. Objective: In this study, we tried to detect and identify the special protein of HBV related chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. To find new opinion on the developing of chronic liver disease. Methods: The sera of health adult, HBV related chronic hepatitis, liver cirrhosis and hepatocellular carcinoma were respectively detected by surface enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS). The arrays of every group were analysised by clustering analysis and to establish disease predictive model. Then the sample was eluted with different pH Tris, trypsinization on-chip, mass determination and peptide database comparison. Results: