NAFLD recurrence is common in the first 5 years postliver transplantation and is associated with features of the metabolic syndrome. Although NAFLD recurrence was not associated with higher mortality in our cohort, cardiovascular mortality and morbidity were common, suggesting that the metabolic syndrome is an important link to NAFLD recurrence and cardiovascular deaths posttransplantation.

Patients with clinical acute alcoholic hepatitis (AAH) are not considered suitable candidates for orthotopic liver transplantation (OLT). The histological correlates of AAH are often seen in the explanted liver at the time of transplantation. The importance of these findings remains inconclusive regarding their role as a prognostic marker for patient or allograft health. Our aim was to examine the explanted liver of patients with purely alcoholic liver disease (ALD) for findings of histologic AAH and to correlate these to patient and graft outcomes. We compared patients with and without histological AAH with patients transplanted for non-ALD. Of 1,097 liver transplant recipients, 148 had ALD and 125 were non-ALD control patients with similar demographics. Thirty-two of 148 ALD patients had histologic AAH, and 116 had bland alcoholic cirrhosis (BAC). Twenty-eight percent of the ALD patients reported Ͻ6 months abstinence, and 54% reported Ͻ12 months abstinence. There was a statistically significant relationship between the presence of histologic AAH and abstinence durations Ͻ12 months (P ϭ 0.009), but not Ͻ6 months. Overall, posttransplantation patient and graft survival between the ALD and non-ALD groups was not significantly different (P ϭ 0.53). Furthermore, patient and graft survival between ALD patients with histologic AAH and BAC were similar (P ϭ 0.13 and P ϭ 0.11, respectively). The rate of posttransplantation relapse among ALD patients was 16%; however, there was no increase in graft loss, nor was there decreased survival compared with controls. The patients with histologic AAH and those with BAC had no differences in posttransplantation relapse (P ϭ 0.13). In multivariate analysis, patient and graft survival was not influenced by pretransplantation abstinence or posttransplantation relapse. In conclusion, histological alcoholic hepatitis in the explant did not predict worse outcome regarding relapse, and allograft or patient survival for liver transplant recipients. Caution should be exercised when liver histology is used to discriminate among suitable candidates for OLT concerning alcoholic patients. Liver Transpl 13:1728Transpl 13: -1735Transpl 13: , 2007. © 2007 AASLD.Received May 18, 2007; accepted July 17, 2007. Acute alcoholic hepatitis (AAH) refers to both a clinical syndrome and a set of histological liver biopsy appearances. The syndrome of AAH always arises after sustained consumption of alcohol. Its clinical manifestations cover a wide spectrum, ranging from asymptomatic jaundice to a fatal combination of fever, jaundice, coagulopathy, and leukocytosis.1 The histological counterpart of AAH is characterized by polymorphonuclear infiltrates, centrilobular hepatocyte swelling and degeneration, macrovesicular and microvesicular steatosis, Mallory bodies, and pericentral-perisinusoidal fibrosis.2 Typically, patients with life-threatening clinical AAH are managed medically; they are not considered suitAbbreviations: AAH, acute alcoholic hepatitis; OLT, orthotopic liver transplantation; ALD, alcoh...

No abstract

Although most patients with alcoholic liver disease experience positive outcomes following liver transplantation, data on the outcome after liver transplantation in patients with severe alcoholic hepatitis are limited. Furthermore, predicting which patients with severe alcoholic hepatitis will maintain sobriety after transplantation is especially difficult. We review the arguments in favour and against extending liver transplantation to selected patients with severe alcoholic hepatitis. In conclusion, we propose that liver transplantation should be a rescue option for occasional patients with severe alcoholic hepatitis who meet the following criteria: those with severe alcoholic hepatitis that has failed medical management, who fulfil all other standard criteria for transplantation, including a thorough psychosocial assessment, yet who are unlikely to survive a mandatory 6-month abstinence period.

Bacterial superantigens (SAgs) are potent T-cell stimuli that have been implicated in the pathophysiology of autoimmune and inflammatory disease. We used Staphylococcus aureus enterotoxin B (SEB) as a model SAg to assess the effects of SAg exposure on gut form and cellularity. BALB/c, SCID (lacking T cells) and T-cell-reconstituted SCID mice were treated with SEB (5 or 100 μg intraperitoneally), and segments of the mid-jejunum were removed 4, 12, or 48 h later and processed for histochemical or immunocytochemical analysis of gut morphology and major histocompatibility complex class II (MHC II) expression and the enumeration of CD3+ T cells and goblet cells. Control mice received saline only. SEB treatment of BALB/c mice caused a time- and dose-dependent enteropathy that was characterized by reduced villus height, increased crypt depth, and a significant increase in MHC II expression. An increase in the number of CD3+ T cells was observed 48 h after exposure to 100 μg of SEB. Enteric structural alterations were not apparent in SEB-treated SCID mice compared to saline-treated SCID mice. In contrast, SEB challenge of SCID mice reconstituted with a mixed lymphocyte population or purified murine CD4+ T cells resulted in enteric histopathological changes reminiscent of those observed in SEB-treated BALB/c mice. These findings implicate CD4+ T cells in this SEB-induced enteropathy. Our results show that SAg immune activation causes significant changes in jejunal villus-crypt architecture and cellularity that are likely to impact on normal physiological processes. We speculate that the elevated MHC II expression and increased number of T cells could allow for enhanced immune responsiveness to other SAgs or environmental antigens.