Liver transplantation for cryptogenic cirrhosis

M R Charlton, M Kondo, S K Roberts, J L Steers, R A Krom, R H Wiesner – 30 December 2003 – End‐stage liver disease secondary to cryptogenic cirrhosis is the indication for orthotopic liver transplantation (OLT) in 7% to 14% of recipients. However, there are no reports documenting the outcome of OLT for this indication. The aim of this study was to determine (1) survival and (2) the incidence of histological recurrence of cryptogenic cirrhosis after OLT. Between March 1985 and December 1994, 560 OLTs were performed at our institution.

Recurrent nonalcoholic steatohepatitis and cirrhosis after liver transplantation

R M Molloy, R Komorowski, R R Varma – 30 December 2003 – Nonalcoholic steatohepatitis (NASH) may progress to cirrhosis and lead to liver failure. Histologically, NASH is often indistinguishable from liver disease caused by alcohol use; the cause of NASH remains unknown. A subgroup of patients with NASH eventually develops fibrosis and/or cirrhosis, and in many cases, transplantation is performed for end‐ stage liver disease attributed to steatohepatitis in patients who do not consume alcohol.

Interleukin‐2 and interleukin‐12 mediate distinct effector mechanisms of liver allograft rejection

N L Thai, Y Li, F Fu, S Qian, A J Demetris, R J Duquesnoy, J J Fung – 30 December 2003 – Interleukin‐2 (IL‐2), interleukin‐12 (IL‐12) or interleukin‐4 (IL‐4) were administered postoperatively to otherwise spontaneously accepting mouse liver allograft recipients (C57BL/10 → C3H) to test whether TH1 cytokines are critical mediators of rejection in this model.

A new survival trick of hepatitis C virus: Blocking the activation of interferon regulatory factor‐3

Markus H. Heim – 30 December 2003 – Persistent infections with hepatitis C virus (HCV) are likely to depend on viral inhibition of host defenses. We show that the HCV NS3/4A serine protease blocks the phosphorylation and effector action of interferon regulatory factor‐3 (IRF‐3), a key cellular antiviral signaling molecule. Disruption of NS3/4A protease function by mutation or a ketoamide peptidomimetic inhibitor relieved this blockade and restored IRF‐3 phosphorylation after cellular challenge with an unrelated virus.

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