4.4 Article

Comparative studies on expression of α-smooth muscle actin in hepatic stellate cells in chronic hepatitis B and C

Journal

DIGESTIVE DISEASES AND SCIENCES
Volume 53, Issue 5, Pages 1364-1369

Publisher

SPRINGER
DOI: 10.1007/s10620-007-9997-8

Keywords

alpha-smooth muscle actin; chronic viral hepatitis; hepatic fibrosis; hepatic stellate cells; hepatitis B; hepatitis C; immunohistochemistry

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Background/aims Chronic hepatitis B and hepatitis C are common causes of liver fibrosis and cirrhosis. We performed a comparative study on the expression of alpha-smooth muscle actin (alpha-SMA) in hepatic stellate cells (HSCs), a marker of HSC activation, in patients with chronic hepatitis B and hepatitis C. Patients and methods Using immunohistochemistry and a semi-quantitative scoring method, the expression of alpha-SMA in HSCs was studied in patients with chronic hepatitis B (n = 50) and hepatitis C (n = 50). The HSC activation index was correlated with age, sex, AST, ALT, viral genotype, viral titers, degrees of hepatic steatosis, necroinflammatory grades and fibrotic stages. Results The HSC activation index correlated significantly (P < 0.05) with necroinflmmatory grades and fibrotic stages in chronic hepatitis B or hepatitis C. Besides, the HSC activation index also correlated significantly (P < 0.05) with hepatic steatosis and marginally significantly (P = 0.08) with serum viral titers in chronic hepatitis C. There was no significant difference in biochemical and histological activities between patients with hepatitis B and hepatitis C, but the latter had a significantly higher HSC activation index than the former. Multiple regression analysis in all 100 patients showed that the HSC activation index correlated significantly (P < 0.05) with necroinflammatory grades, fibrotic stages and hepatitis C (versus hepatitis B). Conclusion In chronic viral hepatitis, the HSC activation index correlated significantly and independently with necroinflammation and fibrosis. Additionally, the HSC activation index was significantly higher in patients with chronic hepatitis C. These data may be compatible with the postulation that hepatitis C virus can directly activate HSCs.

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