Abstract
Background & AimsCardiovascular events represent major cause of non–graft-related death after liver transplant. Evidence suggest that chronic inflammation associated to a remarkable oxidative stress in the presence of endothelial dysfunction and procoagulant environment plays a major role in the promotion of thrombosis. However, the underlying molecular mechanisms are not completely understood. In order to elucidate the mechanisms of post-transplant thrombosis, the aim of the present study was to investigate the role of oxidation-induced structural and functional fibrinogen modifications in liver transplant recipients. MethodsA case-control study was conducted on 40 clinically stable liver transplant recipients and 40 age-, sex-, and risk factor-matched controls. Leukocyte ROS production, lipid peroxidation, glutathione content, plasma antioxidant capacity, fibrinogen oxidation, fibrinogen structural and functional features were compared between patients and controls. ResultsPatients displayed enhanced leukocyte ROS production and an increased plasma lipid peroxidation with a reduced total antioxidant capacity compared to controls. This systemic oxidative stress was associated to fibrinogen oxidation with fibrinogen structural alterations. Thrombin-catalyzed fibrin polymerization and fibrin resistance to plasmin-induced lysis were significantly altered in patients respect to controls. Moreover, steatotic graft and smoking habit were associated to high fibrin degradation rate. ConclusionsROS-induced fibrinogen structural changes might increase the risk of thrombosis in liver transplant recipients.
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