Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2009
Liver HCV-antigens and steatosis in chronic hepatitis C: role of different genotypes.
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Grassi A, Cipriano V, Quarneti C, Bianchini F, Susca M, Zauli D, Lenzi M, Bianchi G, Bianchi F B, Ballardini G
Аннотация
BACKGROUND: HCV infection is frequently associated with liver steatosis.
AIMS AND METHODS: We studied 126 frozen liver HCV positive specimens (genotype-3=27) without any features of metabolic syndrome, searching for a correlation between the number of HCV infected hepatocytes and the presence, amount and distribution of steatosis in relation to different genotypes.
RESULTS: Mean steatosis score was higher in genotype-3 with respect to non-3 (1.11 vs 0.66, p=0.022). HCV-antigens were detected by an immunoperoxidase technique in 91/126 (72.2%) cases. A significant correlation between the number of HCV-antigen positive cells and the degree of liver steatosis was observed in genotype-3 (p=0.01) but not in non-3 patients, matched for sex and age. Steatotic cells usually outnumbered HCV-infected cells. Steatosis was observed both in HCV-antigen positive and negative hepatocytes, and HCV-antigens were detected in both hepatocytes with and without steatosis: while no lobular codistribution was found in genotype non-3, in genotype-3 steatosis and HCV-antigens were usually found in the same areas.
CONCLUSION: Our data support the role of HCV-antigen liver expression in the pathogenesis of steatosis in genotype-3, however, since the presence of HCV-antigens is not directly related to steatosis within single hepatocytes, an indirect mechanism might be operative too.
AIMS AND METHODS: We studied 126 frozen liver HCV positive specimens (genotype-3=27) without any features of metabolic syndrome, searching for a correlation between the number of HCV infected hepatocytes and the presence, amount and distribution of steatosis in relation to different genotypes.
RESULTS: Mean steatosis score was higher in genotype-3 with respect to non-3 (1.11 vs 0.66, p=0.022). HCV-antigens were detected by an immunoperoxidase technique in 91/126 (72.2%) cases. A significant correlation between the number of HCV-antigen positive cells and the degree of liver steatosis was observed in genotype-3 (p=0.01) but not in non-3 patients, matched for sex and age. Steatotic cells usually outnumbered HCV-infected cells. Steatosis was observed both in HCV-antigen positive and negative hepatocytes, and HCV-antigens were detected in both hepatocytes with and without steatosis: while no lobular codistribution was found in genotype non-3, in genotype-3 steatosis and HCV-antigens were usually found in the same areas.
CONCLUSION: Our data support the role of HCV-antigen liver expression in the pathogenesis of steatosis in genotype-3, however, since the presence of HCV-antigens is not directly related to steatosis within single hepatocytes, an indirect mechanism might be operative too.