Moderate hyperhomocysteinemia is common in chronic alcoholics, mainly in those with liver damage, suggesting that, although folate deficiencies may have a contributory role, liver impairment, through changes in methionine metabolism, is the most important mechanism for the elevated plasma Hcy found in these patients.

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. Liver Transpl 13:1017Transpl 13: -1027Transpl 13: , 2007.Received December 7, 2006; accepted February 26, 2007. Hepatitis C recurrence is one of the most important problems in patients with liver transplantation (LT) for hepatitis C virus (HCV)-related liver disease. At present, liver disease caused by HCV is the leading indication for LT in Western countries. 1 The recurrence of HCV infection occurs almost universally and is followed by chronic hepatitis in the graft in most patients. 2,3 It is important to note that, whereas the course of chronic hepatitis C in immune competent subjects is often indolent, the graft lesion in LT patients with hepatitis C recurrence progresses very rapidly in a substantial proportion of cases, with a probability of cirrhosis in up to 30 to 40% of patients at 5 yr after transplantation. 4 Consequently, hepatitis C recurrence has been shown to have a negative impact on survival of patients receiving a liver transplant for HCV-related liver disease. 5

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Infusion of tumor lysate-pulsed dendritic cells induces a strong cell-mediated antitumor immune reaction in patients with advanced cancer and has some clinical activity.