课件：肝病实验室指标.ppt

* all HBV genotypes appear to have a similar seroconversion rate when treated with the oral antiviral agents, and this rate appears to be unaffected by race and similar in patients with or without cirrhosis. Serum HBV DNA becomes undetectable prior to seroconversion. Measuring HBeAg and anti-HBe after the patient becomes serum HBV DNA-undetectable is important such that the time of seroconversion can be documented and antiviral treatment eventually can be discontinued. In patients treated with adefovir, seroconversion continues to increase in a stepwise fashion as long as patients remain on treatment.[19] Long-term data regarding seroconversion are not available for any of the other oral antiviral agents. It is generally recommended that antiviral therapy be continued for 6 months after seroconversion has occurred. Discontinuation of treatment less than 6 months after seroconversion has been associated with an increased risk of seroreverting to an active state and reappearance of HBV DNA and HBeAg.[25] Once patients seroconvert e antigen, they can then seroconvert HBsAg and develop anti-HBs. As a result, once HBeAg seroconversion has occurred, it is useful to begin measuring HBsAg and anti-HBs. * This scenario is unlikely because the patient remains serum HBV DNA-undetectable. A flare in serum ALT occurs when patients with chronic HBeAg-positive active HBV infection spontaneously seroconvert from active to inactive HBV. This is associated with HBeAg loss and appearance of anti-HBe antibody. The flare in serum ALT typically occurs shortly after seroconversion. When e-antigen seroconversion occurs in response to HBV treatment, a flare in serum ALT may also occur. This was first noted when patients with HBeAg-positive active HBV infection were treated with interferon.[27] During interferon therapy, the flare in serum ALT may be high, and if the patient has cirrhosis, hepatic decompensation may occur. It is for this reason that interferon therapy is not often used in p