Major Vessel Involvement in Behçet's Disease: An Update
There has been no consistent primary abnormality of the coagulation, anticoagulation, or fibrinolytic systems identified in Behçet's disease patients. Factor V Leiden and HLA-B5 (B51) have been found to be a risk for thrombophlebitis in certain ethnic groups. An association of MEFV mutations with large vessel disease in Turkish Behçet's disease patients and with venous thrombosis in Israelis has been found. A complexity of susceptibility factors likely complicates attempts to expand findings to diverse populations.
Increased levels of von Willebrand factor and thrombomodulin in Behçet's disease patients likely reflect vascular cell injury. High levels of platelet activating factor and P-selectin activation markers on platelets in patients with thrombosis in Behçet's disease support an association of endothelial activation and thrombosis. Mural production of prostacyclin (PGI2) may be disordered.
Pathogenesis of Thrombosis in Behçet's Disease
There has been no consistent primary abnormality of the coagulation, anticoagulation, or fibrinolytic systems identified in Behçet's disease patients. Factor V Leiden and HLA-B5 (B51) have been found to be a risk for thrombophlebitis in certain ethnic groups. An association of MEFV mutations with large vessel disease in Turkish Behçet's disease patients and with venous thrombosis in Israelis has been found. A complexity of susceptibility factors likely complicates attempts to expand findings to diverse populations.
Increased levels of von Willebrand factor and thrombomodulin in Behçet's disease patients likely reflect vascular cell injury. High levels of platelet activating factor and P-selectin activation markers on platelets in patients with thrombosis in Behçet's disease support an association of endothelial activation and thrombosis. Mural production of prostacyclin (PGI2) may be disordered.
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