[Review of current etiopathogenic data of Buerger disease].

Although 75 years have passed since Buerger's disease was described as a separate nosological, its etiology and pathogenesis are not sufficiently elucidated. According to many authors the disease origin is significantly connected to genetic and environmental factors. Exposure of some patients with special genotype, mainly HLA-A9 and HLA-B5, to environmental factors, mainly nicotine, may be the base of etiology and pathogenesis of Buerger's disease. Discovery of antielastin, anticollagen I and III antibodies, antinicotine and antivascular antigen antibodies in blood of patients, allowed to put forward a theory of immunological character of TO. In Buerger's disease, defined in recent years as an inactive collagenosis, immunological complexes, cell toxins developing during phagocytosis, found in smokers, constitute the main agents responsible for vascular wall damage. Disturbance of prostacyclin I2/thromboxane A2 balance and accelerated platelet aggregation cause spasm of arterioles and in effect lead to higher procoagulant readiness. Some adhesive molecules, for example P and L selectins, play an important role in vascular endothelium damage. Prostaglandin treatment induces an improvement of vascular wall (endothelium) status, and simultaneously improvement of tissue perfusion, expressed by a decrease of selectin and vWF concentrations and of the number of desquamated endothelial cells.