Thromboangiitis obliterans (TAO) or Buerger's disease is associated with both distal ulcers in the extremities and the possibility of amputation. The only treatment that has been shown to be effective in TAO is complete abstention from smoking. In spite of this, the disease progresses in up to 30 percent of cases and finally results in limb amputation. Only a few pharmacological and surgical options are available to date to improve healing ulcers in TAO. The efficacy of prostaglandin analogues is controversial. This paper summarizes the current evidence for medical treatment with bosentan in chronic ulcers in TAO patients. These available data up to date allow us to conclude that the beneficial effects of bosentan on improving endothelial function, inflammatory processes, and selective vasodilatation of damaged vessels result in a clinical enhancement regarding healing and preventive digital ulcers in such patients. In any case, these promising findings have to be confirmed with larger randomised trials. 1. Introduction Thromboangiitis obliterans (TAO) or Buerger’s disease is a thrombotic, occlusive, and nonatherosclerotic segmental vasculitis that affects small- and medium-sized arteries and veins which may involve distal vessel of upper and lower extremities. As a vasculitis, it is characterized by inflammation and fibrinoid necrosis of blood vessel walls. Classically, various mechanisms have been implicated in its etiopathogenesis including cell-mediated inflammation, immune complex-mediated inflammation, and autoantibody-mediated inflammation [1]. Recently, novel pathways have been described in physiopathology of the disease, though not completely well known. The endothelin-1 (ET-1) has been associated in these etiological processes, which can induce to endothelial cell activation causing complications such as vessel occlusion and tissue destruction [2]. ET-1 is a potent vasoconstrictor peptide, which exerts its action by targeting two transmembrane receptors (ETA and ETB). ET-1 facilitates the proliferation of vascular smooth muscle cells, promotes monocytes via activation of the ETA, and contributes to matrix remodelling leading to the abnormal thickening of vessel walls [1–3]. Raised levels of ET-1 have been described in different kind of systemic vasculitis as mixed cryoglobulinemia, secondary Raynaud’s phenomenon [2], acute phase of Henoch-Sch？lein purpura, early stages of giant cell arteritis [1], Takayasu’s arteritis, and Buerger’s disease [3]. This finding supports that ET-1 may act as marker of vascular damage [2, 3]. Other nonvasculitic
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