Arthritis is linked to local and systemic activation of coagulation and fibrinolysis pathways.

摘要: Summary. Background: Activation of coagulation and fibrinolysis play a role in the pathophysiology experimental arthritis. Objective: To determine extent activation fibrinolytic pathways different joint diseases humans to ascertain factors that may influence fibrin deposition within joint. Methods: Plasma from normal subjects (controls, n= 21) plasma synovial fluid samples patients with rheumatoid arthritis (RA; n = 64), osteoarthritis (OA; n = 29), spondyloarthropathy (SpA; n = 22) crystal (CA; n = 25) were analyzed for levels TF (tissue factor) tissue factor pathway inhibitor (TFPI) activities, thrombin–antithrombin III (TAT) complexes, F1 + 2 (thrombin fragment), d-dimer thrombin-activated (TAFI) antigenic levels. The measurements by pairwise correlation each other as well standard parameters inflammation [C-reactive protein (CRP), leukocyte count]. Inter-group comparisons performed look disease-specific differences. Results: Compared healthy controls, had higher TAT, d-dimers their plasma. In fluid, activity, d-dimers, TAFI significantly inflammatory arthritides than OA. highest RA patients. plasma, activity was correlated TAT CRP, TFPI, TAT. CRP levels, count, addition, Conclusions: Activation cascades circulation is evident both degenerative diseases. Within joint, mechanisms leading TF-mediated subsequent most likely explanation observed findings. link between (CRP increase) weak, non-TF-mediated mechanism could explain these characterized arthritides. Although linked inflammation, increased amounts particularly RA, why formation so prominent this condition compared