Median survival was 26 months in the TIPS group (n=65) vs. 27 months without TIPS (n=65), p=1.00. Median follow up was 12 months. Rate of infection did not differ between the 2 groups. Main complications of TIPS (recurrent encephalopathy 34%, stent dysfunction 24.5%, strangulated umbilical hernia 9%, congestive heart failure

7.5%) did not affect patient survival. Conclusion : in this series, TIPS with covered stents appears to improve the natural history of Child-Pugh B cirrhosis with recurrent decompensation. Conversely, decreasing portosystemic pressure gradient does not alter the progression of Child-Pugh C cirrhosis with prolonged decompensation. Earlier implementation of a tips should be discussed for some child-pugh B patients with recurrent ascites or gastrointestinal bleeding. Disclosures: Xavier Adhoute – Speaking and selleck kinase inhibitor Teaching: bayer Marc Bourlière – Advisory Committees or Review Panels: Schering-Plough, Bohringer inghelmein, Schering-Plough, Bohringer inghelmein; Board Membership: Bristol-Myers Squibb, Gilead, Idenix; Consulting: Roche, Novartis, Tibotec, Abott, glaxo smith kline, Merck, Bristol-Myers Squibb, Novartis, Tibotec, Abott, glaxo smith kline; Speaking and Teaching: Gilead, Roche, Merck, Bristol-Myers Squibb Selleck Y27632 The following people have nothing to disclose: Paul

Castellani, Guillaume Penaranda, Olivier Monnet, Herve Perrier, Bernard L. Pol, Cyril Muller, Arthur Laquiere, Valerie Oules, Patrick Beaurain, Christian Boustiere, Olivier Bayle “
“Interleukin-22 (IL-22) plays a key role in promoting antimicrobial immunity and tissue repair at barrier surfaces by binding to the receptors IL-22R1, which is generally thought to be expressed exclusively in epithelial cells, and IL-10R2. Our laboratory previously demonstrated medchemexpress that IL-22 plays an important role in ameliorating liver injury in many rodent models by targeting hepatocytes that express high levels of IL-22R1 and IL-10R2. Recently, we have identified high expression levels of IL-22R1 and IL-10R2 in

liver progenitor cells and hepatic stellate cells (HSCs). Overexpression of IL-22 in vivo or treatment with IL-22 in vitro promotes proliferation of liver progenitor cells via a signal transducer and activator of transcription 3 (STAT3)-dependent mechanism. IL-22 treatment also prevents HSC apoptosis in vitro and in vivo. Surprisingly, overexpression of IL-22, via either gene targeting or exogenous administration of adenovirus expressing IL-22, reduces liver fibrosis and accelerates the resolution of liver fibrosis during recovery. The anti-fibrotic effects of IL-22 are mediated via the activation of STAT3 in HSCs and subsequent induction of suppressor of cytokine signaling 3, which induces HSC senescence. Taken together, the hepatoprotective, mitogenic, and anti-fibrotic effects of IL-22 are beneficial in ameliorating alcoholic liver injury.