73 copies/mL (4.04-9.11 copies/mL), 3.58 IU/mL (1.17-5.10 IU/mL), and 1.71 Paul Ehrlich (PE) IU/mL (−0.64 to 2.63 PE IU/mL), respectively. For the prediction of VR (HBV DNA

< 60 copies/mL at 24 months) in HBeAg(+) LY294002 purchase patients, baseline alanine aminotransferase (P = 0.013), HBV DNA (P = 0.040), and qHBsAg levels (P = 0.033) were significant. For the prediction of VR, the area under the curve for the baseline log qHBsAg level was 0.823 (P < 0.001); a cutoff level of 3.98 IU/mL (9550 IU/mL on a nonlogarithmic scale) yielded the highest predictive value with a sensitivity of 86.8% and a specificity of 78.9%. As for SR (HBeAg loss at 24 months), the reduction of qHBeAg was significantly greater in the SR(+) group versus the SR(−) group. The sensitivity and specificity were 75.0% and 89.8%, respectively, with a decline of 1.00 PE IU/mL at 6 months. With ETV therapy, the correlation between HBV DNA and qHBsAg peaked at 6 months in HBeAg(+) patients. Conclusion: Both qHBsAg and qHBeAg decreased significantly with ETV therapy. The baseline qHBsAg levels and the on-treatment decline of qHBeAg in HBeAg(+) patients were proven to be highly useful in predicting VR and SR, respectively. The determination of qHBsAg and qHBeAg can help us to select the appropriate strategy for the management of patients with CHB. However, the dynamic interplay between qHBsAg,

qHBeAg, and HBV DNA during antiviral therapy remains to be elucidated. (Hepatology 2011;) Chronic infection with hepatitis B virus (HBV) is a worldwide health problem, with more than 400 million people thought to www.selleckchem.com/products/rxdx-106-cep-40783.html be infected. Moreover, these patients are at increased risk for disease progression to cirrhosis and hepatocellular carcinoma.1 Large cohort studies have shown that elevated levels of HBV DNA are closely associated with the development of cirrhosis and hepatocellular carcinoma, and reducing HBV DNA to undetectable levels is one of the primary goals in patients receiving antiviral therapy.2,

3 The current gold standard in monitoring viral loads is real-time 上海皓元 polymerase chain reaction (PCR), which offers high sensitivity and accuracy.4 Data from these assays reflect the disease status and are employed by most clinical studies.2, 3 The shortcomings of PCR, however, are its relatively high cost and unavailability in some areas. Moreover, viral activity can still be monitored in patients with undetectable HBV DNA through the measurement of hepatitis B surface antigen (HBsAg) and/or hepatitis B e antigen (HBeAg) titers. HBsAg has long served as a qualitative serological marker for the diagnosis of HBV. Recent advances in the development of HBsAg assays with a quantitative, analytical approach have led to the exploration of its potential role in monitoring disease and therapy outcome. Since 2004, when Deguchi et al.