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Impact of precore and core promoter mutations on hepatic histology in patients with chronic hepatitis B
Author(s) -
YUAN H.J.,
YUEN M.F.,
KAHO WONG D.,
SUM S.M.,
SABLON E.,
OILIN NG I.,
LAI C.L.
Publication year - 2005
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2005.02563.x
Subject(s) - hepatitis b virus , medicine , antigen , hepatitis b , hepatitis , virology , fibrosis , promoter , virus , immunology , pathology , biology , gene expression , gene , biochemistry
Summary Background:  The details of liver histology of patients with precore and core promoter mutations are still not clear. Aim:  To determine the role of precore and core promoter mutations in liver histology in Chinese patients with chronic hepatitis B. Patients and methods:  Intrahepatic hepatitis B virus DNA (by COBAS Amplicor hepatitis B virus Monitor test) and precore and core promoter mutations (by a line probe assay) were measured in 54 chronic hepatitis B patients. Expression of hepatitis B core antigen, hepatitis B e antigen and hepatitis B surface antigen was determined by immunohistological staining. Histological activity index was scored according to Knodell's criteria. Results:  Compared with patients without core promoter mutations, patients with core promoter mutations had more severe intrahepatic inflammation and fibrosis, and more cytoplasmic expression of hepatitis B core antigen ( P  = 0.028). No such differences were found in patients with and without precore mutations. Logistic regression showed that core promoter mutations were independently associated with cytoplasmic expression of hepatitis B core antigen ( P  = 0.026). Intrahepatic hepatitis B virus DNA levels correlated with serum hepatitis B virus DNA levels ( r  = 0.71, P  < 0.001) and the percentage of hepatitis B core antigen‐positive hepatocytes ( r  = 0.37, P  = 0.047), but had no correlation with serum alanine aminotransferase levels nor the degree of inflammation and fibrosis. Conclusions:  Patients with core promoter mutations had more severe inflammation and fibrosis, and more frequent cytoplasmic expression of hepatitis B core antigen. This suggested that core promoter mutations might cause more serious liver disease.

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