Effect of prostaglandin E-1 on Wisconsin University and histidine-tryptophan-ketoglutarate preservation solutions on preservation injury of the perfused liver.

BACKGROUND: The aim of this study was to investigate the effects of prostaglandin E-1 (PGE-1) on preservation injury in livers perfused with the University of Wisconsin (UW) or histidine-tryptophan-ketoglutarate (HTK) solutions. MATERIALS AND METHODS: Five groups each including six rats included. Ringer's lactate RL (group 1), HTK (group 2), HTK + PGE-1 (group 3), UW (group 4), or UW PGE-1 (group 5). Liver tissue and preservation fluid samples were obtained from the perfused lives for pathological and biochemical examinations respectively at 0, 6 and 12 hours. RESULTS: Upon biochemical examination, aspartate aminotrasnferase and alanine aminotransferase values were highest among the group with RL solution and lowest with PGE-1. Liver structure was found to be damaged immediately after RL solution, whereas it was preserved in the other four groups. Fewer cellular changes were reported at the end of 12 hours in the groups administered PGE-1 compared with the other groups. CONCLUSIONS: PGE-1 when applied before preservation protected liver functions, decreased pathologic injury, and delayed changes that occur under cold ischemic conditions.

Role of postreperfusion subcapsular wedge biopsies in predicting initially poor graft function after liver transplantation.

Preservation injury is a major contributing factor to primary allograft failure or poor initial graft function after an orthotopic liver transplant (OLT). We examined the histopathological findings from postreperfusion wedge biopsy specimens in relation to early graft function during the first postoperative week among OLT patients at our center. We reanalyzed subcapsular postreperfusion biopsy specimens from 88 patients to histologically grade the lesions. Grafts were grouped as good function, initial poor function (an alanine aminotransferase or aspartate aminotransferase level >1500 IU/L during week 1), or primary nonfunction (death or retransplantation). Only 1 patient experienced primary nonfunction; the remaining patients fell into the other 2 groups: ie, good function or initial poor function. When patients were compared using numerous morphologic and clinical features, no statistical relation was observed regarding clinical data on bile duct complications, donor type, graft volume, patient age, or type of stent. Histological features of neutrophilic infiltration of the subcapsular region, hepatocellular ballooning, and macro/microvesicular steatosis were not related to initial poor graft function; in contrast, there were prominent sinusoidal neutrophilic infiltrations and hepatocellular necrosis. Preservation-reperfusion injury (grade 2 or grade 3 neutrophilic infiltration) occurred in 78.6% of initial poor function patients and in 39.7% of good function patients. Subcapsular neutrophilic infiltration, a sign of surgical hepatitis, did not provide prognostic information about graft survival. Similar to other studies, we observed neutrophilic infiltration and necrosis away from the capsule to predict subsequent graft function.

Relevant histopathologic findings that distinguish acute cellular rejection from cholangitis in hepatic allograft biopsy specimens.

BACKGROUND AND AIM: Histopathologic differential diagnosis of acute cellular rejection (ACR) and cholangitis continue to pose important problems following liver transplantation. The purpose of the present study was to evaluate the histopathologic features of ACR versus cholangitis. METHODS: The following variables were evaluated among 36 hepatic allograft biopsy specimens, consisting of 21 with ACR (group 1) and 15 with cholangitis (group 2) for ductal neutrophilic infiltration, presence/density of portal eosinophilia, centrilobular necrosis, central/portal vein endothelialitis, pericentral inflammation, hepatocyte ballooning, hepatocanalicular/ductular cholestasis, hepatocyte apoptosis, lobular inflammation, ductular proliferation, periductal fibrosis/edema, ductular epithelial damage, and portal inflammation. Only the first biopsy samples of the ACR group were included in this study. RESULTS: The incidences of ductal neutrophilic infiltration (93.3% vs 19%), hepatocanalicular cholestasis (86.7% vs 47.6%), ductular cholestasis (60% vs 0%), ductular proliferation (93.3% vs 4.8%), and periductal fibrosis/edema (93.3% vs 19%) were significantly greater in group 2 than group 1 (P < .05). In contrasts the incidences of portal eosinophilia (mean +/- SD, 3.37 +/- 3.9 vs 0.73 +/- 0.8), dense portal eosinophilia (mean +/- SD, 0.33 +/- 0.31 vs 0.11 +/- 0.16), central vein endothelialitis (0% vs 57.1%), portal vein endothelialitis (20% vs 95.2%), apoptosis (40% vs 71.4%), and necroinflammation (0% vs 90.5%) were significantly higher in group 1 (P < .05). The other parenchymal histopathologic changes and features of portal inflammation were similar in the 2 groups. CONCLUSION: In the differential diagnosis, ductal changes (cholestasis, neutrophilic infiltration, proliferation, and periductal fibrosis/edema) favor cholangitis, whereas the presence and density of portal eosinophilia favor ACR. Portal inflammation is not a distinctive morphological finding.