The risk of venous thromboembolism in RA

RA is associated with a markedly increased risk of venous thromboembolism (VTE), reflecting a complex interplay between chronic inflammation, immune dysregulation and haemostatic imbalance. Large population-based studies consistently demonstrate a 50-100% excess risk of deep vein thrombosis and pulmonary embolism in RA, with the highest incidence early after diagnosis and during flares. Mechanistically, inflammatory cytokines, endothelial dysfunction, platelet activation, impaired fibrinolysis and autoantibody-driven immune responses promote a state of chronic immunothrombosis. RA-specific factors such as disease activity, seropositivity, disability and treatment exposures further modify thrombotic risk; some targeted therapies may amplify the risk in a subset of patients. Despite these insights, current VTE risk stratification and prevention strategies are extrapolated from the general population and fail to incorporate RA-specific factors. Improved understanding of the reason(s) behind the increased VTE risks reported with certain immune-modulatory drugs, and development of integrated clinical and biomarker-based stratification tools, are therefore both essential to enable effective thromboprophylaxis in RA.