Turkish Journal of Medical Sciences




Aim: The precise pathogenetic mechanisms causing thrombotic complications in Behçet´s disease (BD) are still not known. To explain the pathogenesis with coagulation induction or a defective fibrinolysis superimposed on endothelial dysfunction, various hemostatic parameters were studied. Thrombin activatable fibrinolysis inhibitor (TAFI), downregulating plasmin generation and fibrinolysis, is a novel risk factor for thrombotic disorders. We studied plasma TAFI levels in BD in comparison with healthy controls. Materials and Methods: Twenty-three patients with BD (mean age: 38.3 ± 10.83, M/F: 5/18) diagnosed according to the criteria of the International Study Group and 20 healthy volunteers (mean age: 38.05 ± 6.29, M/F: 9/11) were enrolled in this study. Patients with liver or renal disease, diabetes mellitus, coronary artery disease, hemophilia, antiphospholipid antibody positivity or using oral contraceptive drugs were excluded from the study. Plasma TAFI levels were determined by using an ELISA test. Results: The mean TAFI antigen levels were 8.40 ± 1.81µg/ml in BD patients and 7.30 ± 0.64 µg/ml in healthy volunteers. A statistically significant difference was found between TAFI antigen levels of these two groups (P = 0.01). Conclusions: TAFI antigen levels were found to be increased in BD, regardless of thrombotic events. To clarify the exact role of TAFI in thrombotic complications of the disease, future studies including more patients with and without thrombosis are needed.


Behçet’s disease, TAFI, fibrinolysis, coagulation

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