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001 TREATMENT OF LIVER FIBROSIS: FROM BENCH TO BEDSIDE
D. Schuppan.Department of Medicine I, University of Erlangen-Nuerberg, Germany
Antifibrotic therapies should preferentially be targeted to the activated hepatic mesenchymal cells. Those cells resemble wound healing myofibroblasts and synthesise an excess of matrix proteins. They derive from quiescent hepatic stellate cells and (myo-) fibroblasts. Several fibrogenic cytokines and other mediators trigger or mitigate their activation. Although various agents have been shown to inhibit hepatic stellate cell/myofibroblast proliferation and collagen synthesis in vitro, only few of them are effective in suitable animal models in vivo, and finally in man. Useful animal models are rat secondary biliary cirrhosis or the speed of reversion of fibrosis after withdrawal of a hepatotoxin like thioacetamide.
The interferons (IFNγ>αβ) have proven antiproliferative and fibrosuppressive activity on mesenchymal cells in culture. Retrospective data suggest that IFNα therapy for hepatitis C can halt or even reverse fibrosis. However, this has to be confirmed by randomised prospective studies. Strategies to inhibit the key profibrogenic cytokine TGF-β and the associated connective tissue growth factor, eg by soluble decoy receptors, are evolving, but results are not yet convincing. IL-10 has little if any antifibrotic effect and hepatocyte growth factor, an epithelial mitogen, enhances hepatocyte regeneration with the inherent risk of promoting the development …