МЕХАНИЗМЫ ТРОМБО-ВОСПАЛЕНИЯ У ПАЦИЕНТОВ С СИСТЕМНОЙ КРАСНОЙ ВОЛЧАНКОЙ

Abstract

Introduction. Systemic lupus erythematosus (SLE) is a systemic autoimmune inflammatory disease. According to different authors, the incidence of thrombotic complications in this disease is higher than the average in the population and can be up to 40%. Aim. The aim of the present review is to provide an overview of mechanisms of thrombosis in patients with systemic lupus erythematosus. Material and methods. Analytical review of foreign and native publications in PubMed and eLibrary.ru between 1985-2020. Results and discussion. SLE represents a model of inflammation-induced thrombosis. The hypercoagulability state which characterizes SLE seems to be associated with inflammation-driven alterations of the thrombotic balance. Tissue-nonspecific autoantibodies, as well as cytokines and acute phase proteins induce a proinflammatory endothelial cell phenotype. Platelets are activated following endothelial dysfunction; they participate in inflammatory and thrombotic events occurring in an injured area. One of the possible initiators of the thrombosis process is considered to be an interaction of antiphospholipid antibodies with phospholipids of platelet membranes, endothelium and phospholipid-linked plasma proteins. Local unbalanced thrombin generation leading to hypercoagulability is another source central for thrombosis. Patients with systemic lupus erythematosus show multidirectional disorders of the coagulation system, with predominance of hypercoagulation especially in patients with II-III degree of disease activity. Conclusion. The mechanism of thrombo-inflammation in systemic lupus erythematosus is multifactorial, involving all components of the hemostatic system. Chronic endothelial dysfunction, platelet activation, hypercoagulation, suppression of fibrinolysis reflects an interplay between thrombosis and inflammation. Persisting autoimmune inflammation plays a key role in these abnormalities.