《2009EASL慢性乙肝实践指南》内容预览

Approximately one third of the world’s population has serological evidence of past or present infection with HBV and 350 million people are chronically infected. The spectrum of disease and natural history of chronic HBV infection is diverse and variable, ranging from a low viremic inactive carrier state to progressive chronic hepatitis, which may evolve to cirrhosis and hepatocellu-lar carcinoma (HCC). HBV-related end stage liver dis-ease or HCC are responsible for over 1 million deaths per year and currently represent 5–10% of cases of liver transplantation . Host and viral factors, as well as coinfection with other viruses, in particular hepatitis C virus (HCV), hepatitis D virus (HDV), or human immu-nodeficiency viru s (HIV) together with other co-mor-bidities including alcohol abuse and overweight, can affect the natural course of HBV infection as well as the efficacy of antiviral strategies.
CHB may present either as hepatitis B e antigen (HBeAg)-positive or HBeAg-negative CHB. HBeAg-positive CHB is due to so-called ‘‘wild type” HBV. It typically represents the early phase of chronic HBV infection. HBeAg-negative CHB is due to replication of naturally occurring HBV variants with nucleotide substitutions in the precore and/or basic core promoter regions of the genome and represents a later phase of chronic HBV infection. The prevalence of the HBeAg-negative form of the disease has been increasing over the last decade as a result of HBV-infected population aging and represents the majority of cases in many areas, including Europe .
Morbidity and mortality in CHB are linked to persis-tence of viral replication and evolution to cirrhosis or HCC. Longitudinal studies of patients with CHB indi-cate that, after diagnosis, the 5-year cumulative inci-dence of developing cirrhosis ranges from 8 to 20%.The 5-year cumulative incidence of hepatic decompensa-tion is approximately 20% with the 5-year probability of

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