Anti-TNFα agents curb platelet activation in patients with rheumatoid arthritis

摘要: Background Cardiovascular disease is important in rheumatoid arthritis (RA). Tissue factor (TF) expressed upon platelet activation and initiates coagulation. Anti-tumour necrosis factor-α (TNFα) agents seem to decrease RA-associated cardiovascular events. We investigated whether (1) TNFα activates human platelets (2) pharmacological blockade modulates the platelet-leucocyte reciprocal RA. Design The expression of receptors has been assessed by flow cytometry immunogold electron microscopy. Platelet leucocyte also presence antibodies against 1 2 infliximab. TF expression, binding fibrinogen phosphatidylserine exposure, cytometry, activity coagulation time endogenous thrombin generation. Markers have 161 subjects: 42 patients with RA, 12 osteoarthritis, 37 age-matched sex-matched chronic stable angina 70 healthy subjects. Results elicited TF, which turn prompted generation clot formation. Inhibition TNFα-induced restricted ability activate leucocytes induce TF. inhibition did not influence induced collagen, ADP or receptor activating peptide-6. Platelets RA were more activated than those controls. Activation was reduced treated inhibitors. Conclusions TNFα-dependent pathways control Further studies will verify protective effect inhibitors on events involves their modulate function.