METHODS: We wanted to study the outcomes of Entacavir therapy in this subset of patients. Study was conducted between April 2007 to April 2008. We enrolled 30 CHB patients who had Non response to 12-24 weeks of 10 mg ADV therapy. Non response and suboptimal response was defined as non dimunition of at least one log of HBVDNA from baseline after 12 weeks of therapy and Persistence of 3 log10 after 24 weeks of therapy respectively.They were switched to 1mg entacavir before breakfast daily for at least 12 months.They had serial ALT CBC and HBVDNA measured every 12 weeks. Results: Out of 30 patients 20 male and 10 were female. Only 8 patients were HBeAg(+).Mean HBVDNA level prior to ADV exposure was 6.5 log copies/ml.Mean duration of exposure to ADV was 26 weeks.5 patients lost to F/U.We did intention to treat analysis. 15 out 30 (50%) patient has, undetectable level of HBVDNA after 12 weeks of therapy labelled as group 1.6 out of 30 (20%) had HBVDNA level reduced by a mean of 3 log 10 copies/ml labelled as group 2.on week 24 treatment analysis all 15 patients from group 1 was HBVDNA undetectable, 2 additional patients from group 2 had undetectable HBVDNA. Conclusion: Entacavir therapy results in rapid suppression of HBVDNA levels in majority of patients with primary nonresponse or partial non response to ADV therapy. Background: Except for serum ALT level, baseline factors predictive of therapeutic response to lamivudine in patients with HBeAg-positive chronic hepatitis B remain largely unknown. We thus studied the influence of pre-therapy viral factors on end-of-treatment responses to lamivudine therapy. Methods: A total of 116 treatment-naïve HBeAg carriers who had pre-therapy serum ALT level> 5xULN and received lamivudine for 18 months reimbursed by the National Health Insurance were prospectively enrolled. HBeAg seroclearance and combined HBeAg seroclearance, ALT normalization as well as undetectable HBV DNA at the end of therapy were defined as primary and secondary endpoint, respectively. The pre-therapy viral factors including viral load, genotype, precore stop codon (PC)/ basal core promoter (BCP) status, and pre-S deletion were determined to correlate with therapeutic endpoints. Results: The frequency of patients with detectable PC mutation (G1896A), BCP mutation (A1762T/G1764A), and pre-S deletion at baseline was 22.4%, 21.6%, and 12.1%, respectively. After completing 18-month lamivudine therapy, overall HBeAg seroclearance rate was 56.0%. Patients with HBeAg seroclearance had a higher prevalence of baseline PC mutation than those without (30.8% vs, 11.8%, P= .015). By multivariate analysis, the odds ratio of patients with PC mutation to develop HBeAg seroclearance was 3.33 (P= .024). In addition, the presence of PC mutation also correlated with the combined response. Conclusions: For HBeAg-positive chronic hepatitis B patients with serum ALT> 5xULN, PC mutation could predict a higher HBeAg seroclearance rate at the end of 18-month lamivudine therapy.