Thrombotic Events in Inflammatory Rheumatological Diseases

Mechanisms linking inflammation and thrombosis:There are three main natural anticoagulation mechanisms: the tissue factor (TF) inhibitor, the heparin-antithrombin III pathway, and the protein C anticoagulant pathway (2).These mechanisms exert a strong anticoagulant effect under physiological conditions.However, inflammation can disrupt this balance and induce a predisposing state for thrombosis through several different mechanisms.Active inflammation: It is a prothrombotic state characterized by upregulation of tumor necrosis factor-α (TNF-α) and endothelial cell activation.Upregulation of TNF-α is thought to increase serum TF levels, a natural procoagulant mechanism.In addition, endothelial cell activation promotes platelet activation, which is important for thrombus formation (3).In patients with rheumatoid arthritis (RA) and ankylosing spondylitis, inhibition of TNF-α decreased plasminogen activator inhibitor-1 (PAI-1) and Active inflammation is a prothrombotic state characterized by the activation of procoagulant mechanisms and endothelial cells.In fact, the correlation between antiphospholipid antibodies in systemic lupus erythematosus (SLE) and the predisposition to venous and arterial thrombosis is known.Thus, it appears that thrombotic events are associated with disease activity and/or inflammation in many inflammatory rheumatic diseases.The present study is a review of the main pathogenetic features and clinical aspects of thrombosis in inflammatory rheumatic diseases, SLE, rheumatoid arthritis, vasculitis, Sjögren's syndrome, and dermatomyositis/polymyositis, highlighting the appropriate therapeutic approaches in each case.Therefore, it appears that inflammatory rheumatological diseases are associated with an increased thrombotic risk and predisposition to arterial and venous thrombosis, greater than that in the general population.