Coagulation and complement in antiphospholipid syndrome

Coagulation activation and depressed fibrinolysis are recognised thrombogenic pathways of primary and systemic lupus erythematosus related antiphospholipid syndrome (APS), though their relation with antiphospholipid antibodies (aPL) is uncertain [1–3]: once generated, thrombin interacts with thrombomodulin to accelerate almost 1000 fold the activation of thrombin activatable fibrinolysis inhibitor (TAFI) activity that depresses fibrinolysis by removing the C-terminal lysine residues from fibrin and prevent the binding of plasminogen and tissue plasminogen activator to the fibrin clot [4].