Fibrinolysis abnormalities in systemic lupus erythematosus and their relation to vasculitis.
Fibrinolysis was evaluated in 16 women with SLE, who were divided into three groups of increasing disease severity according to their past history, and in 10 normal subjects. Fibrinolysis parameters assessed were tissue-type plasminogen activator (t-PA) activity in plasma and in euglobulin fractions and rapid plasminogen activator inhibitor activity. All parameters were evaluated before and after venous occlusion to assess endothelial cell t-PA release in response to localized anoxia. Markers of deficient fibrinolysis were persistently undetectable t-PA activity and increased rapid plasminogen activator inhibitor activity after venous occlusion. Defective fibrinolysis was correlated with disease severity; it was noted only in patients with severe or moderate disease and in no patients with mild disease or in controls. Fibrinolysis abnormalities were independent of disease activity, suggesting that vascular endothelium injuries occurring during flare-ups persist during inactive phases of the disease. No correlation was found between fibrinolysis abnormalities and disease duration, corticosteroid administration, or the presence of lupus anticoagulant or anticardiolipin antibodies. These data support the hypothesis of parallelism between the severity of vascular injuries, suggested by deficient fibrinolysis, and the severity of clinical manifestations in SLE.
D000328:Adult; D001799:Blood Sedimentation; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use; D010959:Tissue Plasminogen Activator / Q000493:pharmacokinetics; D014657:Vasculitis / Q000209:etiology*
D010959:Tissue Plasminogen Activator; D011241:Prednisone