Fibrinogen catabolism in systemic lupus erythematosus.
Because there is mounting evidence that localized intravascular coagulation may contribute to tissue injury following a variety of immunologic events, including immune complex diseases, fibrinogen catabolism was studied in patients with systemic lupus erythematosus to determine factors correlating with accelerated coagulation. 125I-fibrinogen half-life in controls was 90.1+/- 11 hours and the mean SLE half-life was 60.5 +/- 12. SLE patients in complete clinical remission had normal half-lives, but patients with symptomatic clinical disease, including renal disease, had significantly reduced fibrinogen survival. Accelerated fibrinogen consumption also correlated with positive tests for anti-DNA antibodies, but not with hypocomplementemia. These observations support the hypothesis that the coagulation system is activated in patients with immune complex diseases. Further studies are required to define the role, if any, that coagulation may play in causing tissue injury.
D000328:Adult; D000906:Antibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000378:metabolism; D003165:Complement System Proteins / Q000032:analysis; D004247:DNA / Q000032:analysis; D005260:Female; D005340:Fibrinogen / Q000378:metabolism*; D006207:Half-Life; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology / Q000378:metabolism*; D008297:Male; D009393:Nephritis / Q000378:metabolism
D000906:Antibodies; D005340:Fibrinogen; D003165:Complement System Proteins; D004247:DNA