Further detailed modeling of intrahepatic and serum kinetics will

Further detailed modeling of intrahepatic and serum kinetics will shed light on the modes of action of HBV antivirals and help to design more efficient drug cocktails. Disclosures: Kazuaki Chayama – Consulting: Abbvie; Grant/Research Support: Metformin supplier Dainippon Sumitomo, Chugai, Mitsubishi Tanabe, DAIICHI SANKYO, Toray, BMS, MSD; Speaking and Teaching: Chugai, Mitsubishi Tanabe, DAIICHI SANKYO, KYORIN, Nihon Medi-Physics, BMS, Dainippon Sumitomo, MSD, ASKA, Astellas, AstraZeneca, Eisai, Olympus, GlaxoSmithKline, ZERIA, Bayer, Minophagen, JANSSEN, JIMRO, TSUMURA, Otsuka, Taiho, Nippon Kayaku, Nippon Shinyaku, Takeda, AJINOMOTO,

Meiji Seika, Toray Alan S. Perelson – Consulting: Achillion Pharmaceuticals, Merck, Roche, Santaris Pharma, Gilead; Grant/Research Support: Roche, Novartis; Stock Shareholder: Pfizer, Merck, Glaxo Harel Dahari – Consulting: Roche TCRC, Inc The following people have nothing to disclose: Regorafenib ic50 Tje Lin Chung, Yuji Ishida, Michio Imamura, Nobuhiko Hiraga, Susan L. Uprichard Background and Aims: It remains unclear the incidence of HBV reactivation and role of quantification of HBsAg (qHBsAg) in HBV reactivation after stopping entecavir treatment. This study investigated the incidence of HBV reactivation and the role qHBsAg level in HBV reactivation after stopping entecavir treatment. Patients and Methods: From 2008 to 201 1, a total

of 126 chronic hepatitis B patients (40 HBeAg-positive, 86 HBeAg-negative at baseline) received entecavir treatment (treatment duration: median: 156 weeks, range: 78-274 weeks) and have stopped the treatment at least 12 months were recruited. The criteria of stopping entecavir therapy met the recommendations of APASL 2012. qHBsAg levels were determined at baseline, month 12 of treatment and at the end of treatment. HBV DNA levels were determined at baseline, every 6 month during treatment and after stopping 上海皓元 treatment. Results: Of the 86 HBeAg-negative patients, the cumulative incidence of viro-logical relapse (HBV DNA>2000 IU/mL) at month 6, 12, 18 and 24 was 12.8%, 46.5%, 57.2%, and 57.2%

respectively, and clinical relapse (ALT>80 U/L and HBV DNA>2000 IU/mL) was 6.8%, 31%, 46.4%, and 46.4% respectively, after stopping entecavir treatment. Cox regression analysis showed that older age [increased per one year; hazard ratio (HR):1.03, 95% confidence interval (CI): 1.006-1.061], qHBsAg level at the end of treatment (increased per one log IU/ml; HR: 2.02, 95% CI: 1.30-3.15) and prior adefovir experience (HR: 2.78, 95% CI: 1.15-6.71) were independent factors for virological relapse. Older age (HR: 1.05, 95% CI: 1.02-1.09), male (HR: 7.56, 95% CI: 1.52-37.53), prior adefovir experience (HR: 8.28, 95% CI: 2.73-25.15) and qHBsAg level at the end of treatment (HR: 2.92, 95% CI: 1.59-5.38) were independent factors for clinical relapse.

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