View clinical trials related to Early Allograft Dysfunction.
Filter by:Ischemia-reperfusion injury (IRI) is unavoidably typical of solid organ transplantation. Post-reperfusion syndrome (PRS), characterized by hemodynamic instability at reperfusion of the implanted graft, is a possible complication of liver transplantation. For sure, IRI plays a fundamental role in the multifactorial pathogenesis of PRS. IRI and PRS are associated with a higher risk of early allograft dysfunction (EAD) and, consequently, graft failure. Liver grafts from both extended criteria donors (ECD) and donation after circulatory death (DCD) are particularly susceptible to IRI and, accordingly, are at higher risk of PRS, EAD and graft failure. Anyway, in the present scenario of organ shortage, such donors greatly contribute to enlarge the organ pool. So, various strategies have been developed for the purpose of a safer use of this kind of grafts. Among them, ex vivo hypothermic oxygenated perfusion (HOPE) reduces IRI and is beneficial for high-risk liver grafts. The pathogenesis of IRI is an extremely complex downstream inflammation process, involving many different cytokines, chemokines and growth factors. In particular, tumor necrosis factor-alfa (TNF-alfa), interleukin-6 (IL-6), IL-8 and endothelin-1 (ET-1) are crucial in the development of IRI in liver transplantation. In experimental models, cytokine filtration during ex vivo lung perfusion (EVLP) was proved to be safe and effective in reducing inflammatory response and, thus, pulmonary edema development. Since - in liver transplantation, IRI and PRS are associated with a higher risk of EAD and graft failure - liver grafts from ECD and DCD are particularly susceptible to IRI and are at higher risk of PRS, EAD and graft failure - HOPE of high-risk liver grafts reduces IRI - in solid organ transplantation, various cytokines, chemokines and growth factors are involved in the pathogenesis of IRI - in experimental models of EVLP, cytokine filtration was proved to reduce inflammatory response and subsequent organ damage, our hypothesis is that cytokine filtration during HOPE of high-risk liver grafts may potentiate the beneficial effects of HOPE, further reducing IRI and, consequently, further decreasing the incidence of PRS and EAD. So, the aim of this study is to verify the feasibility and safety of cytokine filtration during end-ischemic HOPE of liver grafts.
Liver transplantation is currently the treatment of choice for end-stage liver cirrhosis of different origin, as well as for a number of inborn metabolism disorders and liver tumors. The need to perform a liver transplantation is high and amounts to 10 - 20 patients per 1 million population per year. Experimental and clinical evidence demonstrate the harmful short and long-term effects of ischemia-reperfusion injury (IRI) of the donor organ on the outcome of the intervention performed. Severe manifestations of IRI of the liver transplant (LT) is one of the main reasons for the increased length of hospitalization, the high cost of treating patients during the post- surgery period, the development of persistent early allograft dysfunction or loss, frequent crises of acute rejection, acute renal and multiple organ failure, and mortality of the operated patients. This pilot clinical study is designed to evaluate the efficacy and safety of Reparixin, which is a new, potent and specific inhibitor of chemokine CXCL8 (Interleukin-8), as an agent to prevent early allograft dysfunction caused by ischemia-reperfusion injury in patients undergoing orthotopic liver transplantation.
The primary aim is to determine the accuracy of CAP in the quantification of liver steatosis using liver biopsies as reference. Secondarily, investigators will correlate transient elastography (TE) and CAP results, analyze possible associations between CAP/TE and post-liver transplant (LT) clinical outcomes, and evaluate the change in CAP after LT. The study aims to include as many donors as needed to achieve at least 120 transplanted liver allografts.
The purpose of this study is to determine whether the Tacrolimus added to histidine-tryptophan-ketoglutarate (HTK) solution given through intraportal and intraarterial infusion during back-table procedure is capable of reducing the degree of early allograft liver dysfunction, as assessed by postoperative levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), during first 7 postoperative days and by serum and histochemical markers of liver injury and inflammation.