Subject(s)
Embolism/etiology , Hepatic Artery , Massive Hepatic Necrosis/etiology , Organ Transplantation/adverse effects , Adult , Embolism/diagnostic imaging , Embolism/physiopathology , Embolism/therapy , Hepatic Artery/diagnostic imaging , Hepatic Artery/physiopathology , Hepatic Encephalopathy/etiology , Humans , Male , Massive Hepatic Necrosis/diagnostic imaging , Massive Hepatic Necrosis/physiopathology , Thrombectomy , Treatment Outcome , Vascular PatencyABSTRACT
Aim: the number of intestinal IgA+ lymphocytes are decreased in acute liver necrosis and the mechanism remains poorly understood. The purpose of this study was to observe the role of lymphocyte homing and apoptosis associated with decreased intestinal IgA positive lymphocytes in acute liver necrosis. Methods: the acute liver necrosis mouse model and LTßR pre-treatment were used to assess intestinal mucosal addressin cell adhesion molecule-1 (MAdCAM - 1) expression, cell apoptosis, IgA+ cells and secretory immunoglobulin A (SIgA). Results: MAdCAM - 1 mRNA and protein expression decreased significantly in the acute necrosis group; 0.57 ± 0.032 fold vs. baseline (p < 0.05) and 0.45 ± 0.072 fold vs. baseline (p < 0.05), respectively. LTßR pre-treatment could significantly improve the decline of MAdCAM - 1 mRNA and protein expression in the intestinal mucosa (1.83 ± 0.064 fold vs. baseline, p < 0.05 and 1.75 ± 0.046 fold vs. baseline, p < 0.05, respectively) and partially restore the decline in IgA+ lymphocytes and SIgA levels. There were increased rates of enterocyte apoptosis in both the acute liver necrosis and LTßR pre-treatment group; 0.79% vs. control (p < 0.05) and 0.77% vs. control (p < 0.05), respectively). Conclusion: our results suggest that the dysfunction of lymphocyte homing and apoptosis are both involved with decreased intestinal IgA+ lymphocytes in acute liver necrosis. LTßR pre-treatment can partially restore IgA+ cells and SIgA by increasing MAdCAM - 1 expression, rather than inhibiting lymphocyte apoptosis
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Subject(s)
Animals , Mice , Massive Hepatic Necrosis/physiopathology , Lymphocyte Depletion/methods , Immunoglobulin A/isolation & purification , Cell Death/physiology , Lymphocyte Count/methods , Intestinal Mucosa/physiopathology , Immunologic Tests/methods , Disease Models, AnimalABSTRACT
AIMS: To determine the frequency of extramedullary haematopoiesis (EMH) in massive hepatic necrosis (MHN). METHODS AND RESULTS: Explanted livers of 11 adult patients transplanted consecutively for MHN were examined histologically and immunohistochemically for the presence of EMH. The aetiology of the liver damage was unknown in seven cases and drug induced in four. The presence of stem cell markers (CD34, c-kit), erythroid precursors (glycophorin A), myeloid precursors (myeloperoxidase) and megakaryocyte precursors (CD31) was investigated by immunohistochemistry. Erythroid, myeloid and megakaryocyte precursors were observed in all cases. Morphologically, haematopoietic blast cells were clustered in areas of collapse, separating islands of regenerating ductules and scattered between ductules, in a similar distribution to immunohistochemically identified c-kit-positive putative stem cells. No CD34+ cells other than endothelial cells were seen. All 11 patients were anaemic at the time of transplantation. CONCLUSIONS: EMH is a frequent finding in patients undergoing liver transplantation for MHN. This may be a consequence of the anaemia associated with this condition. Alternatively, the possibility that intrahepatic haematopoiesis is linked with hepatopoiesis is an additional, intriguing possibility that deserves further study.
