HBsAg decline was compared between treatment arms and between responders and nonresponders. Response was defined as HBeAg loss with HBV DNA < 10,000 copies/mL at 26 weeks after treatment (week 78); 43 of 221 (19%) patients achieved a response. One year of PEG-IFN with or without lamivudine resulted in a significant decline in serum HBsAg, which was sustained after treatment (decline 0.9 log IU/mL at week 78, P < 0.001). Patients

treated with combination therapy experienced a more pronounced on-treatment decline, but relapsed subsequently. Responders experienced a significantly Pexidartinib clinical trial more pronounced decline in serum HBsAg compared to nonresponders (decline at week 52: 3.3 versus 0.7 log IU/mL, P < 0.001). Patients who achieved no decline at week 12 had a 97% probability of nonresponse through posttreatment follow-up and no chance of HBsAg loss. In a representative subset of 149 patients similar results were found for prediction through long-term (mean 3.0 years) follow-up. Conclusion: PEG-IFN induces a significant decline in serum HBsAg in HBeAg-positive patients. Patients who experience no decline from baseline at week 12 have little chance of achieving a sustained response and no chance of HBsAg loss and should be advised to discontinue therapy with

PEG-IFN. (HEPATOLOGY 2010) Chronic hepatitis B (CHB) is a major health problem, affecting more than 350 million people worldwide. Prolonged infection with the hepatitis B virus (HBV) may ultimately Epothilone B (EPO906, Patupilone) result in severe liver-related morbidity and mortality, AZD6244 manufacturer and treatment of CHB is therefore indicated in patients with persistent liver inflammation.1-4 The ideal outcome of treatment of CHB would be complete eradication of HBV, but this is only scarcely, if ever, achieved, for HBV covalently closed circular DNA (cccDNA) persists in host hepatocytes.5 Therefore, the main goal of therapy is to halt the progression of liver inflammation to fibrosis, cirrhosis

or hepatocellular carcinoma.6, 7 Current treatment options for CHB consist of nucleo(s)tide analogues and (pegylated) interferons (PEG-IFN). Antiviral treatment with nucleo(s)tide analogues aims at inhibiting viral polymerase activity,8 and the most recently approved nucleo(s)tide analogues can effectively maintain suppression of HBV DNA levels for prolonged periods of time in the vast majority of patients.9-11 Nevertheless, PEG-IFN remains an important first-line treatment option for CHB, especially in hepatitis B e antigen (HBeAg)-positive disease, because a long-term off-treatment sustained response can be achieved in about 25% of patients after a finite treatment course.12-14 Response to IFN-based therapy in these patients is accompanied by high rates of hepatitis B surface antigen (HBsAg) seroconversion,15 a reduced incidence of hepatocellular carcinoma, and prolonged survival.