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严重乙肝相关肝病发病机理和治疗(英文版)
HBV-associated Severe Liver Diseases: Progress on Pathogenesis and Treatment Yuming Wang Institute for Infectious Diseases of PLA Southwest Hospital Third Military Medical University Chongqing, P. R. China The Progress of Pathogenesis Viral Factors Evidence for the role of viral factors Long-term follow-up studies demonstrated the close relationship between disease severity and viral factors NA has been showed to be effective in prevention and treatment of hepatitis exacerbation HBV mutation and genotypes are closely related to disease severity Immune suppressed ALF: overwhelming viral replication and immune paralysis HBV mutation and genotyping is closely related to disease severity Precore (G1896A) mutation /core-promoter (G1762T/G1764A) mutations PreS2 mutations HBV genotypes Fig. Frequencies of Precore/C-promoter mutations compared between pts. with FH and self-limited acute hepatitis who were infected with HBV/Bj or Ce Outcome of acute hepatitis B virus infection Pts with FH were older (34y) FH was frequent (13%) and associated with Bj and Ce Lack of HBeAg High replication due to precore mutation Pathogenesis of Special Fulminant Hepatitis---- Immunosuppression-induced ALF(Fibrosing Cholastatic Hepatitis, FCH) Why do the pts. in tolerance stage have no FCH manifestations ? Immune tolerance≠ immune paralysis Immune tolerance:virus and host have a relationship of mutually restriction immune paralysis: host loses its restriction to the virus Medical strategy for two categories of ALF Immune suppression induced ALF - Inhibition of virus Immune mediated ALF - Immune suppression by using steroids - Inhibition of virus, ceasing of Immune mediated liver necrosis The Progress of Treatment Antiviral therapy by NA Hospitalized pts. with HBV-associated hepatic failure in Our Dept. through 1991-2005 Outcome of severe hepatitis patients after LAM treatment Target sequence: 394 bp. located in the Rt region of the polymerase gene in HBV
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