SOME ASPECTS OF COAGULATORY CASCADE IN CASES OF CUTANEOUS VASCULITIS

Abstract

Cutaneous vasculitis comprises a diverse group of disorders that combine segmental inflammation with necrosis of blood vessels. The vascular damage results from immunologic and I or inflammatory mechanisms. Clinical syndromes are based on criteria that include the gross appearance and the histologic alterations of the vascular lesions, the caliber of the affected blood vessels, the frequency of involvement of specific organs, and the presence or absence of laboratory abnormalities. Although all sizes of blood vessels may be involved in the skin, CV predominantly involves postcapillary venules. CV may occur m association with an underlying chronic disease, may be precipitated by infection or drugs, or may develop for unknown reasons. Initially, the pathogenesis of CV is immune complex related, but in its later stages different pathogenic mechanisms may intensify the reaction and lymphocytes may predominate in the infiltrate. Fibrin deposition and intravascular thrombosis are seen m cutaneous vasculitis syndromes, suggesting local endothelial cell activation. Endothelial cells are important regulators of procoagulant and anticoagulant intravascular processes. The procoagulant properties are formed by the production ofTF and synthesise ofvWF and factor V. The anticoagulant properties are formed by expression of heparin-like glycosaminoglycans (that can bind antithrombin Ill which inactivate thrombin) and thrombomodulin (which bind thrombin) and by release of coagulation factor inhibitors such as protein S and TFPI. In addition, vascular endothelial cells have fibrinolytic properties.