新英格兰医学杂志：乙肝病毒感染药物治疗学

2,23 Although perinatal infection can result in high-level HBV replication without substantial liver injury in the early decades of life, ultimately the risk of progression to cirrhosis and hepatocellular carcinoma is proportional to the level of HBV DNA maintained persistently over time.24,25

Goals of Antiviral Therapy

Because clinical and histologic improvement accompanies reductions in HBV replication, interventions that reduce HBV replication are expected to limit progressive liver disease and improve the natural history of chronic HBV infection. Practically, however, serious outcomes of HBV infection evolve over decades, whereas clinical trials of antiviral therapy are limited to 1 to 2 years and, rarely, up to 5 years. Therefore, surrogate end points that are achievable during time-limited clinical trials are used. These end points are serologic (i.e., HBeAg loss or seroconversion, usually reflecting a transition to inactive HBV carriage, and, more rarely, HBsAg loss or seroconversion, representing serologic recovery), virologic (i.e., a log10 reduction in the HBV DNA level or suppression of HBV DNA to an undetectable level [<10 to 100 IU per milliliter]), biochemical (i.e., normalization of the serum ALT level), and histologic (i.e., improvement in the necroinflammatory grade and stage of fibrosis).5,6 A course of antiviral therapy may lead to responses that are sustained after treatment withdrawal; more commonly, therapy must be continued to maintain responses achieved during therapy.

Antiviral Drugs

Seven drugs are licensed in the United States for the treatment of HBV infection: interferon alfa,26,27,28,29 pegylated interferon alfa-2a,30,31 lamivudine,32,33,34,35,36 adefovir,37,38,39,40,41 entecavir,42,43,44,45,46 telbivudine,47,48,49 and tenofovir50,51 (Table 1 and Table 2).5,6,52 The use of interferon, which requires injections daily or thrice weekly, has been supplanted by long-acting pegy

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