Soluble Thrombomodulin and Fibrinolysis in Behçet’s Disease

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Abstract
Behçet’s disease is a chronic relapsing systemic vasculitis in which recurrent urogenital ulceration is a prominent feature. The precise reason underlying the thrombotic tendency in Behçet’s disease is unknown, but endothelial injury/dysfunction and hypofibrinolysis are believed to be the most important pathogenetic mechanisms. Thrombomodulin (TM) belongs to the natural anticoagulant system and plays a crucial role in the regulation of blood coagulation in vivo. Consequently, quantitative and/or qualitative impairment of TM could possibly play a pathogenetic role in thrombotic events in patients with Behçet’s disease. This study explores whether, in Behçet’s disease, any alterations involving tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1), thrombin-antithrombin III complex (TAT) and TM concentrations occur. The study group comprised 20 patients with Behçet’s disease (10 females, 10 males) and 28 healthy volunteers (19 females, 9 males). TM, TAT concentrations, PAI-1 antigen and activity and t-PA activity were notably increased in patients with Behçet’s disease, while t-PA antigen was not different from the normal group. It is concluded that endothelial cell injury, evidenced by increased TM concentration and activated intravascular coagulation which was reflected by increased TAT levels and alterations of t-PA/PAI-1 binding kinetics, may account for the pathogenesis of thrombotic tendency in Behçet’s disease.

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