However, further follow-up are required for the evaluation of eff

However, further follow-up are required for the evaluation of efficacy between

two groups. Disclosures: The following people have nothing to disclose: Sangheun Lee, Jun Yong Park, Hana Park, Moon Young Kim, Sang Hoon Ahn, Pumsoo Kim, Kwang-Hyub Han BACKGROUND: Serum HBsAg levels can be used as a surrogate marker for the interaction between the immune system and the hepatitis B virus. We aimed to study the kinetics of HBsAg levels in chronic hepatitis B (CHB) patients who discontinued nucleos(t)ide analogue (NA) therapy. METHODS: We included 94 consecutive patients who stopped NA after at least one year of therapy. Patients could be HBeAg-positive or HBeAg-negative at start-of-therapy, but all were beta-catenin inhibitor HBeAg-negative and had undetectable HBV DNA at time of discontinuation. Relapse was defined as HBV DNA >2,000 IU/mL measured twice 6 months apart within one year, or retreatment after an initial HBV DNA increase. RESULTS: In total, HBsAg decline could be calculated for 69 patients, of whom 26 were relapsers. The on-treatment HBsAg decline was

comparable between relapsers and sustained responders, whereas the post-treatment HBsAg decline was greater in sustained responders compared to relapsers (Figure). After adjustment for start-of-therapy HBeAg-status, cirrhosis, and consolidation therapy duration, post-treatment HBsAg decline remained significantly Selleck 5-Fluoracil associated with absence of relapse (p=0.014). Forty-seven patients had paired on-treatment and post-treatment HBsAg decline data available. Within Methane monooxygenase this group, HBsAg decline increased in sustained responders from −0.09 to −0.17 log IU/mL per year (p=0.009) after NA therapy

cessation, but not in relapsers (−0.03 vs. −0.07 log IU/ mL per year; p=0.85). CONCLUSIONS: After stopping long-term NA therapy in CHB patients, HBsAg decline increased in sustained responders, whereas these levels remained at the same level in relapsers. These results suggest the potential of host-induced immune control and viral clearance in sustained responders after NA therapy cessation. Disclosures: Colina Yim – Advisory Committees or Review Panels: Merck Canada, Gilead, Janssen Jordan J. Feld – Advisory Committees or Review Panels: Idenix, Merck, Janssen, Gilead, AbbVie, Merck, Theravance, Bristol Meiers Squibb; Grant/Research Support: AbbVie, Boehringer Ingelheim, Janssen, Gilead, Merck Robert J. de Knegt – Advisory Committees or Review Panels: MSD, Roche, Norgine, Janssen Cilag; Grant/Research Support: Gilead, MSD, Roche, Janssen Cilag, BMS; Speaking and Teaching: Gilead, MSD, Roche, Janssen Cilag David K. Wong – Grant/Research Support: Gilead, BMS, Vertex, BI Harry L.

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