Results: Median HBV DNA levels before therapy was 7.64 log10 copies/mL and the median decreases from baseline in HBV DNA were -4.19, -4.31, -5.09, -5.31, and -5.59 log10 copies/mL at 4 (n=39, p<0.001), 12 (n=62, p<0.001), 24 (n=42, p<0.001), 36 (n=22, p<0.001), and 52 (n=15, p =0.053) weeks of follow-up, respectively. At baseline, overall median ALT was 106 IU/L and the proportions of patients with normal ALT were 13%, 48%, 56%, 71%, 67%, and 69% at baseline (n=82), 4 (n=42), 12 (n=63), 24 (n=44), 36 (n=24), and 52 weeks (n=16) after entecavir therapy, respectively. Thirteen cases (15.9%) of HBeAg seroconversion were noted. Background: Hepatitis B virus (HBV) infection is a major risk factor for the progression of liver diseases. Because its clinical course varies, it is difficult to detect the predictive factor for the prognosis of patients with HBV infection. The aim of the present study was to determine the risk factors for the occurrence of HCC. Methods: A total of 620 patients who tested positive for hepatitis B surface antigen and were referred to Chiba University Hospital between February 1985 and March 2008 were included in the study, and their following characteristics were analyzed: age, gender, the status of HBeAg, ALT, HBV-DNA level, and PLT. Result: HCC was detected in 30 cases during the follow-up period (5.4 ± 5.1 years). Multivariate analysis revealed that age [compared with young patients: odds ratio (OR) = 1.07, 95% confidence interval (CI) = 1.03-1.11] and PLT level (compared with patients with low PLT level: OR = 0.99, 95% CI = 0.98-0.99) were the predictive factors for HCC occurrence. In patients with age more than 35 years, the HBV-DNA level (compared with <5.0 log copies/ml: OR = 3.29, 95% CI = 1.40-11.5) and PLT level (OR = 0.99, 95% CI = 0.98-0.99) were the predictive factors for HCC occurrence. Conclusion: Advanced age and low PLT level were the risk factors for HCC occurrence in patients with HBV infection irrespective of the PLT level at baseline. In patients with age more than 35 years, viral load was also a risk factor for HCC. Results: Before treated by LPS, the total MAPK p38 level of PBMCs have no significant difference among the healthy control group, different stage groups with HBV infection, however, after treated with LPS, The phosphorylated MAPK p38 (pTpY180/182) in healthy control group are significant elevate than HBV infected groups(120.0±52 vs 80.2±84.8, p<0.05). In the two groups which HBsAg, HBV DNA are positive, alanine aminotransferase elevate than normal and HBsAg positive, but HBV DNA lower under the detect limited level, after treated by LPS the pTpY180/182 although lower than healthy control yet, but significant elevated than themselves before treated by LPS(86.6±38.6 vs117.8±21.3, 63.3±24.7 vs 93.1±21.8; p<0.05).Otherwise, in the group of both HBsAg and HBV DNA are positive, but ALT is normal, before and after treated by LPS, the level of pTpY180/182 have no significant difference. Conclusion: MAPK p38 is a important signal transduction pathway which involving in inflammation and immune response, especially, MAPK p38 activated up-regulate the IFN-gamma mRNA. According to the result shown, we propose a hypothesis, HBV infection and virus active replication inhibit the MAPK p38 activated, consequent on host immunotolerance and HBV persistence, thus, MAPK p38 may be as a potential therapeutic target to break immnotolerance and establish host anti-viral states. Van der Helm 10 1 Siriraj Hospital, Bangkok, Thailand, 2 Ramathibodi Hospital, Bangkok, Thailand, 3 Phyathai Hospital, Bangkok, Thailand, 4 Singapore General Hospital, Singapore, 5 National University Hospital, Singapore, 6 Changi General Hospital, Singapore, 7 Cheil General Hospital, Korea, 8 Hwasun Jeonnam University Hospital, Korea, 9 St Mary Hospital, Korea, 10 Roche Diagnostics Ltd, Rotkreuz, Switzerland Background/aims: Hepatitis B virus (HBV) surface antigen (HBsAg) is one of the most important markers for diagnosis of acute and HBV infection. High sensitivity of HBsAg assays can reduce the diagnostic window during course of disease. In addition, the presence of HBV mutants may be affected by the performance of the HBsAg kit. Therefore, the technical performance of the Elecsys ® HBsAg II assay was explored, using samples (including recombinant mutants), at multiple sites in three countries. Methods: Nine HBsAg screening centers in Thailand, Korea and Singapore compared the sensitivity of Elecsys ® HBsAg II assay with that of their routine testing procedure -Abbott Architect ® (7 centers), Abbott AxSym ® (1 center) and Bayer Advia ® Centaur HBsAg assays (1 center) using preselected seroconversion panels (n=5), recombinant HBV mutant panels (n=13) and routine clinical practice samples (n=1,863). Results: The sensitivity of Elecsys ® in seroconversion samples was equivalent to the Architect ® assay, but more sensitive than the AxSym ® and Advia ® Centaur assays (26 vs 23 and 24 vs 18 positive bleeds, respectively). There was concordance between the Elecsys ® and Architect assay results with respect to potentially cross-reactive samples (99.74%). The Elecsys ® and Architect ® assays detected all recombinant mutant samples, whilst AxSym ® and Advia ® Centaur failed to detect three and nine samples, respectively. Conclusion: Elecsys ® HBsAg II assay was not only highly sensitive and specific when compared with established HBsAg screening assays, but also reliably detected HBsAg mutants. Therefore, this attractive assay is suitable for HBV diagnosis and assessing safety of blood products. Background: Recent studies have shown a higher rate of adefovir-resistant mutation in lamivudine-resistant chronic hepatitis B (CHB) patients treated with switch-to therapy than those treated with add-on therapy. We compared the clinical efficacy of adefovir monothrapy and lamivudine-adefovir combination therapy in lamivudine-resistant CHB. Methods: A prospective cohort study was performed in 49 patients with lamivudine-adefovir combination therapy and 77 patients with adefovir monotherapy for lamivudine-resistant CHB over 18 months. Result: Biochemical response was achieved in 41 patients (83.7%) treated with combination therapy and in 77 patients (92.8%) treated with monotherapy (p=0.101). Virologic response was observed in 19 patients (38.8%) in combination therapy and in 26 patients (31.3%) in monotherapy (p=0.383) and treatment periods for virologic response was significantly shorter in patients with combination therapy than in monotherapy (8.9±4.8 months vs. 13.9±5.0 month, p=0.001). Cumulative rate of virologic response was significant higher in patients with combination therapy than monotherapy (p=0.033). HBeAg loss was found in 6 patients (16.2%) in combination therapy and 17 patients (20.5%) in monotherapy (p=0.485). Biochemical breakthrough was found in 17 patients (20.5%) with monotherapy significantly more frequent than 3 patients (6.1%) with combination therapy (p=0.026). Genotypic resistance to adefovir was developed in 1 patient (2.0%) in combination therapy and 9 patients (10.8%) in monotherapy Conclusion: To achieve a complete virological response and reduce the risk of adefovir-resistant mutants in lamivudine-resistant CHB patients, adefovir in combination with lamivudine is preferable. Background/Aims: Adefovir dipivoxil (ADV) effectively inhibits both wild-type and lamivudine (LAM)-resistat chonic hepatitis B virus (CHB) replication. The aims of this study were to determine the factorts associated with antiviral effect of ADV in LAM-resistant CHB. Methods: One hundred-eighteen LAM-resistant CHB patient (74.6% HBeAg-positive) were treated with ADV plus LAM (n=96) or ADV monotherapy (n=22) for a mean of 33.0 months. Restriction-fragment mass polymorphism analysis was used for detection YMDD and ADV mutants. Results: Fifty-eight patients (49.2%) achieved complete response(CR) defined as HBV-DNA levels <2000 copies/ml and ALT normalization. Twenty-eight patients (23.7%) achieved initial vilologic response(IVR) defined as HBV-DNA levels <10 4 copies/ml within the first 6 month of treatment. 47 (53.4%) of 88 HBeAg-positive patients exhibited HBeAg loss and 31% seroconverted to anti-HBe Ab. Five (4.23%) patients developed ADV-related mutations. Factors associated with IVR were pretreatment level of ALT (P=0.00), AST (P=0.00), pretreatment HBV DNA level (P=0.03), HBeAg negativity (P=0.01) and HBeAb positivity (P=0.00). Factors associated with CR were IVR (P=0.00), HBeAb positivity (P=0.01), pretreatment level of ALT (P=0.01), AST (P=0.02) and y-Glutamyl Transferase (P=0.04). Age, sex, presence of liver cirrhosis, pretreatment HBV DNA level and the type of YMDD mutants were not related to an CR during ADV treatment. Conclusions: ADV therapy achieved CR in more than 49% of LAM-resistant CHB. Factors associated with CR were IVR, HBeAb positive status, high base line ALT, AST, GGT levels.