α-SMA Overexpression Associated With Increased Liver Fibrosis in Infants With Biliary Atresia

Objective: The mechanisms responsible for increased collagen production and hepatic fibrosis in biliary atresia (BA) remain largely unknown. We evaluated alpha-smooth muscle actin (alpha-SMA) expression in liver and the porta hepatis in infants with BA. Methods: Immunohistochemical staining for alpha-SMA and CD68 in the BA liver and porta hepatis was performed. A semiquantitative 3-grade staging system was employed to estimate liver fibrosis. The densities of CD68 in BA liver and the levels of direct bilirubin were assessed in relation to alpha-SMA expression. Results: alpha-SMA was found to be overexpressed in epithelial cells and in periductular collagen fibers. The expression in infants with BA was higher than that in the control group (P<0.05). The amount of alpha-SMA in BA was positively correlated with liver fibrosis scores (r=0.549, P=0.022). The levels of alpha-SMA in the liver of BA were negatively related with improvements in direct bilirubin levels, 3 months postoperatively (r=-0.653, P=0.029). The correlation between the alpha-SMA and CD-68 expression was not significantly different (r=0.444, P=0.057). Conclusions: The expression of alpha-SMA in BA liver is higher than that in control group. alpha-SMA expression is negatively correlated with the reduction of direct bilirubin, 3 months postoperatively, probably due to fibrosis or cirrhosis affecting the entire biliary system.