| 抄録 |
HBV infection is endemic in Asian countries including Taiwan, and most Asian HBV carriers acquire the virus early in life. The pathogenesis of HBV infection is mainly immune mediated, causing a wide spectrum of liver disease, including inactive carrier state, chronic hepatitis, cirrhosis and HCC. HBV factors including HBV DNA level, genotype and naturally occurring mutants predictive of clinical outcomes have been identified. Recent studies from Taiwan further showed that qHBsAg is helpful in the management of CHB. For example, combination of HBsAg≤1000 IU/mL and HBV-DNA≤ 2000 IU/mL can identify minimal risk HBV carriers. In addition, in HBeAg-negative carriers with normal ALT, the lower the baseline HBsAg level, the higher the chance of spontaneous HBsAg seroclearance, and an HBsAg≤10-100 IU/mL is an appropriate cut-off for predicting HBsAg loss over time. In contrast, among HBeAg-negative patients with low viral loads, HBsAg≥1000 IU/mL increases HCC risk. As to the treatment of chronic hepatitis B, our data indicated that basal core promoter mutation is associated with higher HBeAg seroconversion and combined response rates at 6 months off therapy in HBeAg-positive CHB patients treated with peginterferon alpha-2a. In addition, genetic variants in HLA-DPA1 region may also affect treatment-induced HBeAg seroconversion. Among HBeAg-positive CHB patients treated with entercavir, a higher baseline qHBsAg level is associated with a sub-optimal 2-year virologic response, and a significant on-treatment decline of HBV-DNA but not qHBsAg level at month 6 could predict HBeAg loss at 2 years of therapy. |
