Thrombophilia and Thrombosis in Behçet's Disease

Behçet's disease (BD) is a systemic vasculitis of unknown cause, affecting mainly young adults. Vasculopathy has been reported in 16.8-51.5% of cases. Genetic, infectious factors, environmental factors, presence of autoantibodies, endothelial pathologies and hypercoagulability are responsible for the etiopathogenesis of BD. The main involvements responsible for morbidity and mortality in Behçet's disease are ocular, major cardiovascular and neurological involvements. Although there is an increased thrombotic risk in the etiopathogenesis of Behçet's disease, the cellular and molecular mechanisms are not fully understood. Although endothelial dysfunction due to inflammation has been shown to be the primary cause of vascular damage in Behçet's disease, some clinical evidence suggests that hypercoagulable states also contribute to thrombosis. The most common form of vascular involvement in Behçet's disease is deep vein thrombosis in the lower extremities. Arterial occlusion mostly affects the subclavian and pulmonary arteries. Although arterial involvement is rarer than venous involvement in Behçet's disease, morbidity and mortality are higher than venous involvement. Although an increased thrombotic risk is mentioned in the etiopathogenesis of Behçet's disease, it is still controversial whether vasculitis or susceptibility to hypercoagulability plays a role in the pathogenesis of venous thrombosis. In addition, there are very few studies in the literature in which all thrombophilic parameters were analysed. Again, there is no recent study on this subject. The aim of our study is to determine the risk of hypercoagulability in Behçet's disease patients with vascular involvement, which has a highly mortal course.