58%) in only 1 case. Conclusions: The increased frequency of AA changes in S gene unrelated to LMV resistance suggests enhanced immune escape; further studies are needed to clarify whether this is related to Nuc pressure or natural history of the disease. In “a” determinant, immune escape variants other than the common sG1 45R were detected, suggesting a different pattern in our area. Study funded by Instituto de Salud Carlos III, grant PI 11/01973,

cofinanced by the European R428 price Regional Development Fund (ERDF). Disclosures: Rafael Esteban – Speaking and Teaching: MSD, BMS, Novartis, Gilead, Glaxo, MSD, BMS, Novartis, Gilead, Glaxo, Janssen Maria Buti – Advisory Committees or Review Panels: Boerhinger Inghelm, Boer-hinger Inghelm; Speaking and Teaching: MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen, MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen The following people have nothing to disclose: David Tabernero, Francisco Rodriguez-Frias, Rosario Casillas, Josep Gregori, Irene Belmonte Mula, Maria Homs, Maria Blasi, Josep Quer, Leonardo

Nieto, Silvia Camos, Andrea Caballero, Carolina Gonzalez Background: The role of quantitative hepatitis B surface antigen (HBsAg) after hepatitis B e-antigen (HBeAg) seroclearance is not well defined Aim: To determine the role of HBsAg levels in predicting significant viremia and hepatitis flares after HBeAg seroclearance, and to describe the trend of HBsAg levels and its correlation with HBV DNA in a longitudinal study. Methods: 228 chronic hepatitis B patients with spontaneous HBeAg seroclearance were Y 27632 included, with a minimum of 5 years follow-up after seroclearance. Patients were followed up regularly at 3-6 monthly intervals with routine liver biochemistry and hepatitis B serology. Levels of HBV DNA and HBsAg were measured at yearly intervals for up to 5 years after HBeAg seroclearance. Results: The median age at the time of seroclearance was 38 years (range, 14-77), with a similar male:female ratio (51%:49%). Of the 228 patients, 218 (95.6%) had evidence of seroconversion with detectable anti-HBe, with the remaining 1 0 (4.4%) patients remaining anti-HBe negative. The median log HBsAg and HBV DNA level

after HBeAg seroclearance was 3.52 IU/mL and 4.13 IU/mL Fenbendazole respectively, with no significant correlation (p=0.572). There was a gradual but significant decline in HBV DNA with increasing time from HBeAg seroclearance. The HBV DNA at HBeAg seroclearance was 4.13 log IU/mL, compared with 3.12 log IU/mL after 5 years (p<0.001). In contrast, the level of HBsAg remained consistent throughout each time-point after HBeAg seroclearance in non-treated patients. At the time of HBeAg seroconversion, the median HBsAg level was 3.52 log IU/mL, and this was comparable to the level of 3.50 log IU/mL (p=0.991) at 5 years. Hepatitis B flares occurred in 103 (45.2%) patients. Patients who developed hepatitic flares compared with those without hepatitic flares were older (39 vs 35 years, p=0.