Hepatic alpha-smooth muscle actin expression in hepatitis C patients before and after interferon therapy

Background/Aims: The mechanism of hepatic fibrogenesis with chronic viral h epatitis is not well understood. Persistent activation of hepatic stellate cells is felt to play a role in the development of fibrogenesis and progres sion to cirrhosis. Methodology: We determined the expression of hepatic alpha -smooth muscle a ctin, a marker of hepatic stellate cell activation, in 29 patients with chr onic hepatitis C and varying degrees of Liver injury and fibrosis. In addit ion to a baseline evaluation, we assessed the effect of interferon therapy on alpha -smooth muscle actin expression in 11 patients, including 6 with a sustained response to therapy. Specimens were evaluated by light microscop y for grade of inflammation and stage of fibrosis. Expression of alpha -smo oth muscle actin was assessed semiquantitatively by immunohistochemical sta ining. Results: At baseline, all patients had alpha -smooth muscle actin expressed within the liver without; an obvious correlation with the severity of live r injury. However, among sustained responders, a reduction in hepatic necro inflammatory activity was associated with a trend towards a decrease in alp ha -smooth muscle actin expression. This however did not reach statistical significance. Conclusions: Hepatic alpha -smooth muscle actin expression, a s a marker of hepatic stellate cell activation appears reversible and tends to correlate with necroinflammatory activity.