Hepatic stellate cell activation in liver transplant patients with hepatitis C recurrence and in non-transplanted patients with chronic hepatitis C

✍ Scribed by Laura Cisneros; Maria-Carlota Londoño; Carmen Blasco; Ramón Bataller; Rosa Miquel; Miquel Bruguera; Pere Ginès; Antoni Rimola

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 406 KB
• Volume: 13
• Category: Article
• ISSN: 1527-6465
• DOI: 10.1002/lt.21178

✦ Synopsis

The pathogenic mechanisms of accelerated graft fibrosis in hepatitis C recurrence after liver transplantation (LT) are not well established. The aim of the study was to assess whether a greater activation of hepatic stellate cells (HSC), the major collagen-producing cells in the liver, can occur in these patients as compared to non-LT patients with chronic hepatitis C. We determined the amount of activated HSC by computer-based morphometric analysis of ␣-smooth muscle actin (␣SMA)-positive cells and the hepatic TGF␤ 1 expression by immunohistochemistry in 46 LT patients with hepatitis C recurrence, 35 non-LT patients with chronic hepatitis C, and 16 controls. Hepatic ␣SMA and TGF␤ 1 expression was higher in LT patients with hepatitis C recurrence than in controls and was correlated with fibrosis stage and progression rate. No significant difference in ␣SMA and TGF␤ 1 expression was observed between LT and non-LT patients with hepatitis C, with the exception of a higher transforming growth factor ␤-1 (TGF␤ 1 ) expression in non-LT patients in the early stages of fibrosis. LT patients receiving cyclosporine (CsA) or tacrolimus (FK) had a similar fibrosis progression rate and ␣SMA and TGF␤ 1 expression. In conclusion, the accelerated fibrosis observed in LT patients with hepatitis C recurrence does not seem to be related to a greater amount of activated HSC and TGF␤ 1 expression in the grafts of these patients as compared to non-LT patients with chronic hepatitis C. In LT patients, the amount of activated HSC and TGF␤ 1 expression correlated with fibrosis stage and progression, without any apparent influence of the type of calcineurin inhibitor administered.