Plasma tetranectin levels and disease activity in patients with rheumatoid arthritis.
OBJECTIVE
We investigated alterations of levels of plasma tetranectin, a new regulator of plasminogen activation, in patients with rheumatoid arthritis (RA) in relation to disease activity and other fibrinolytic variables.


METHODS
Tetranectin (TN), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor (PAI-1) were quantitatively assessed (ELISA) in plasma of 41 patients with RA and 30 healthy subjects, alpha 2-Antiplasmin activity was assessed by the amidolytic method. Disease activity was determined as a composite Stoke Index, which measures inflammatory processes in RA. Patients were divided into 3 groups according to Stoke Index score of disease activity: A, minimal-mild, 1-7: B. moderate. 8-11: C. severe. 12-17.


RESULTS
Plasma TN in patients was significantly lower compared to that of healthy subjects [9.11 (4.97-13.49) mg/l, 12.05 (9.50-13.60) mg/l, median (range), respectively; p = 0.0001]. TN decreases with the increase of disease activity from group to group. A significant negative correlation between TN and Stoke Index. C-reactive protein and erythrocyte sedimentation rate was found (rs = -0.49, p = 0.0012; rs = -0.44, p = 0.0044; rs = -0.37, p = 0.016, respectively). alpha 2-Antiplasmin activity was elevated in patients compared to healthy subjects [105.0% (53.0-146.0), 70.6% (48.2-124.0), median (range), respectively; p = 0.0001], showing a negative correlation with Stoke Index (rs = -0.38, p = 0.0139). The close positive correlation of TN with alpha 2-antiplasmin (rs = 0.66, p = 0.0001) and the absence of correlation with t-PA and PAI-1 were explained by the involvement of TN and alpha 2-antiplasmin in localized rather than in systemic fibrinolysis.


CONCLUSIONS
Our findings suggest TN plays a role in the pathophysiology of RA and point to the usefulness of TN assessment as a specific fibrinolytic marker in the evaluation of disease activity in patients with RA. The role of TN in the intraarticular regulation of fibrinolysis, important for the expansion of pannus, tissue remodeling and angiogenesis, is discussed.
Kamper
E F
EF
Department of Experimental Physiology, Medical School, University of Athens, Greece.
Kopeikina
L T
LT
Koutsoukos
V
V
Stavridis
J
J
D000328:Adult; D000368:Aged; D000933:Antifibrinolytic Agents / Q000378:metabolism; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D014408:Biomarkers, Tumor / Q000097:blood*; D001798:Blood Proteins / Q000378:metabolism*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D006801:Humans; D037181:Lectins, C-Type; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012720:Severity of Illness Index; D010959:Tissue Plasminogen Activator / Q000097:blood; D000979:alpha-2-Antiplasmin / Q000378:metabolism
D000933:Antifibrinolytic Agents; D014408:Biomarkers, Tumor; D001798:Blood Proteins; D037181:Lectins, C-Type; D017395:Plasminogen Activator Inhibitor 1; D000979:alpha-2-Antiplasmin; C048648:tetranectin; D010959:Tissue Plasminogen Activator