Abstract
Venous thromboembolic disease remains a major cause of mortality and morbidity despite advances in diagnosis and therapy. The presence of chronic autoimmune inflammatory rheumatic disease represents a certain risk factor for the development of thromboembolic disease depending on the type of disease, activity, therapy and a combination of other risk factors.
The presumed major pathogenetic mechanisms include the persistence of an accelerated inflammatory response associated with the development of endothelial dysfunction, the presence of specific / non-specific prothrombogenic autoantibodies and other endogenous and exogenous causes. Antiphospholipid syndrome (APS) is characterized by the presence of thrombosis or pregnancy complications associated with fetal loss and the presence of antiphospholipid antibodies.
APS occurs as primary or secondary, when it accompanies other autoimmune diseases. The immunomodulatory and anti-inflammatory properties of immunosuppressive therapy affect some prothrombogenic mechanisms to some extent, however, their administration may in itself pose a risk of developing a thrombotic condition in patients with chronic inflammatory rheumatic disease.