• Fibrosis
• hepatitis C

A ductular reaction at the periphery of portal tracts appears to be a common stereotypical response to injury that is observed in a number of chronic liver diseases, including viral hepatitis. It consists of a complex of strings of cholangiocytes, small bile ductules, stroma and inflammatory cells, and occurs at the interface between portal tracts and parenchyma.1 These reactive ductules are postulated to arise from hepatic progenitor cells, small bipotential cells capable of proliferation and differentiation into both hepatocytes and cholangiocytes. This alternative pathway of liver regeneration is activated when mature hepatocytes are unable to proliferate sufficiently to replace lost cells.2 Ductules are rarely seen in normal human liver,3 but increase in number in association with the severity of liver injury. Studies in chronic viral hepatitis, haemochromatosis, and alcoholic and non-alcoholic liver disease have shown a close correlation between progenitor cell expansion and the extent of hepatocellular injury, inflammation or fibrosis, although cause and effect has not been determined.4–7

The study of Svegliati-Baroni and colleagues8 in this issue of Gut (see page 108) demonstrates a significant association between reactive ductular cells, hepatic progenitor cells and stage of fibrosis in patients with chronic hepatitis C virus (HCV) infection, further supporting these earlier studies. Interestingly the current study also …