6 Thursday, April 15, 2004 11 INTOXICATION WITH AMANITA PHALLOIDES: PROGNOSTIC CRITERIA AND INDICATIONS FOR EMERGENCY LIVER TRANSPLANTATION L. Escudie 1 , C. Francoz 1 , J.P. Vinel 2 , D. Sommacale 3 , F. Dondero 3 , J. Belghiti 3 , D. Valla 1 , F. Durand 1 . 1 Hepatology, Hospital Beaujon, Clichy, France; 2 HepatoGastroenterology, Hospital Purpan, Toulouse, France; 3 Digestive Surgery, Hospital Beaujon, Clichy, France Intoxication with the mushroom Amanita phalloides (AP) is a rare cause of acute liver failure, sometimes requiring emergency liver transplantation (LT). The current criteria for LT seem poorly applicable because of the especially rapid course of liver failure. The aims of this study were to identify risk factors after intoxication with AP and to propose criteria for emergency LT. Twenty five patients admitted for intoxication with AP were studied (12 males and 13 females, mean age 49 years). Six out of these 25 patients developed acute liver failure. Three were transplanted (only one survived); one died before transplantation and 2, who were rejected for LT,died. Predictive factors for a poor outcome (death or LT) were female gender (7/7 vs 5/18, p=0.001), a short interval between ingestion and diar- rhea (7h vs 12h, p=0.001), prolonged prothrombin time (p=0.0003), serum transaminases rebound (reflecting an initial collapsus with hepatic ischemia followed by AP toxicity, 4/7 vs 1/18, p=0.01) and encephalopathy (6/7 vs 1/18, p<0.0001). In all those who died or were transplanted, the interval between encephalopathy and death or LT was < 24 hours. In conclusion, encephalopathy may not be mandatory for deciding LT in this indication since it occurs too shortly before death. In the absence of encephalopathy, LT should be strongly considered when (a) first manifestations occur < 8 hours after ingestion, (b) prothrombin time is < 20% of normal within the first 3 days after ingestion and (c) a rebound in transaminases occur, especially in female patients. 12 ACTIVE IMMUNIZATION AFTER LIVER TRANSPLANTATION FOR HBV RELATED LIVER DISEASE: FAILURE TO INDUCE HBV-SPECIFIC HUMORAL AND CELLULAR IMMUNE RESPONSES J. Rosenau 1 , N. Hooman 1 , K. Rifai 1 , T. Solga 1 , H.L. Tillmann 1 , E. Grzegowski 3 , B. Nashan 2 , J. Klempnauer 2 , C. Trautwein 1 , C. Strassburg 1 , H. Wedemeyer 1 , M.P. Manns 1 . 1 Department of Gastroenterology, Hepatology and Endocrinology, Medizinische Hochschule Hannover, Hannover, Germany; 2 Department of Visceral and Transplant Surgery, Medizinische Hochschule Hannover, Hannover, Germany; 3 GlaxoSmithKline Biologicals, Munich, Germany Long-term hepatitis B reinfection prophylaxis after liver transplantation with hepatitis B immunoglobulin (HBIG) and nucleoside analogues pre- vents HBV recurrence, however, it is expensive and inconvenient. There- fore, several clinical trials evaluated humoral immune response against HBsAg, showing conflicting results. Best response was achieved under continuous HBIG administration with an adjuvant containing HBsAg vac- cine. We vaccinated eight patients who had been HBsAg-positive and HBV- DNA-negative before liver transplantation with recombinant HBsAg for- mulated with the adjuvant 3-deacylated monophosphoryl lipid A (MPL) (20 μg HBsAg, 50 μg MPL). Patients received the 1st vaccination after HBIG had been stopped and anti-HBs-titers had dropped below 10 IU/l. Six vaccinations were applied at weeks 0, 2, 4, 12, 16 and 24. In addition to anti-HBs-titers, HBV-specific cellular immune responses were exam- ined by interferon-gamma ELISPOT and flow-cytometry-based assays. A significant humoral immune response was observed only in 1 out of 8 pa- tients (13%) with a maximum anti-HBs-titer of 561 IU/l. In this patient, anti-HBs decline before vaccination was significantly slower than in the other 7 individuals. In addition, the responding patient was the only one who mounted a HBV-Core-Ag-specific T cell response before vaccination. Importantly, in none of the patients a T-cell-response against HBsAg was induced by vaccination. In conclusion, the MPL-HBsAg vaccine failed to induce a significant humoral or cellular immune response in most patients. Our data are in sharp contrast to recent promising studies. It remains to be determined whether the concomitant HBIG application is a crucial factor for a good response to vaccines even without adjuvants. 13 ANALYSIS OF A SUCCESSFUL HCV-SPECIFIC CD8+ T CELL RESPONSE IN PATIENTS WITH RECURRENT HCV-INFECTION AFTER LIVER TRANSPLANTATION (OLTX) N.H. Gruener 1,2 , A. Ulsenheimer 2 , M-C. Jung 1,2 , J.T. Gerlach 1,2 , R. Zachoval 1 , H.M. Diepolder 1,2 , G. Baretton 3 , R. Schauer 4 , G.R. Pape 1,2 , C.A. Schirren 1,2 . 1 Department of Medicine II, University of Munich, Klinikum Grosshadern, Munich, Germany; 2 Institute For Immunology, University of Munich, Munich, Germany; 3 Institute For Pathology, University of Munich, Munich, Germany; 4 Department For Surgery, University of Munich, Klinikum Grosshadern, Munich, Germany Virusspecific CD8+ T cells play a major role in antiviral immune defense. Their significance in the transplant setting is unclear. In the present study we asked whether in the presence of a strong immunosuppressive treatment HCV-specific CD8+ T cells are detectable and whether we could correlate the HCV-specific CD8+ T cell response with treatment outcome in patients who receive IFN-alpha/ribavirin therapy after OLTx. Liver- and blood- derived T cell lines of 15 patients were studied in parallel before, and for 14 patients at the end and after antiviral treatment. Virus-specific IFN- gamma production at a single cell level in response to a panel of previously identified HCV specific epitopes restricted by the HLA class I molecules A2, A3, B7, B35 and B44 of structural (envelope and core) and non- structural HCV-proteins (NS3/4, NS5) was determined by ELISPOT assay. Without treatment in 10/15 (67%) patients a low number of HCV-specific CD8+ T cells were detectable. Six patient achieved a sustained response. In all patients a significant, multispecific and sustained CD8+ T cell response was detectable which was mainly found in the peripheral blood. Non- responders (n=2) and transient responders (n=6; n=4 relapsers and n=2 breakthroughs) showed no, weak or transient HCV-specific CD8+ T cell response. In conclusion our data indicate that despite immunosuppression HCV-specific CD8+ T cells are detectable in patients with recurrent HCV- infection after OLTx and that only those patients who mount a significant, multispecific, and long-lasting HCV-specific CD8+ T cell response could eliminate the virus under antiviral treatment. 14 DONOR AGE DOES NOT INFLUENCE PROGRESSION OF HCV RECURRENCE AFTER LIVER TRANSPLANTATION D.N. Samonakis 1 , C.K. Triantos 1 , U. Thalheimer 1 , A. Quaglia 2 , G. Leandro 1 , G.V. Papatheodoridis 1 , R. Teixeira 1 , M.L. Raimondo 1 , N. Rolando 1 , A.P. Dhillon 1 , D.W. Patch 1 , B.R. Davidson 1 , K. Rolles 1 , A.K. Burroughs 1 . 1 Liver Transplantation and Hepatobiliary Unit/Royal Free Hospital, London, UK; 2 Histopathology Department/Royal Free Hospital, London, UK Background: Increasing donor age has been associated with decreased survival and worse recurrence of HCV after liver transplantation. However it is not clear if early and/or late mortality is affected, and whether donor age is the key factor. Patients/methods: A consecutive series of 196 HCV cirrhotics (36 with concomitant alcoholic aetiology, 59 with pretransplant or incidental HCC- 10 retransplants, only 1 recurrent HCV), transplanted between 1989 and 2003, with cadaveric donors, mean age 41.6 years (13-73). Donor age was examined in a univariate/multivariate model for early/late survival, as well as fibrosis (grade 4 or more, Ishak score) with regular biopsies. Mean follow up 44.7 months (1-155). Results: For donor age <40, 40-60, >60 y, there was no statistical differ- ence in survival except for <40 vs. >60 y (p=0.031). However this was due to early mortality as no significant differences found in 3 month survivors (n=159). Donor age was only significantly lower 1989-1991. It did not in- fluence fibrosis, in terms of time to grade 4 fibrosis. Multivariate models