title: Correlation between clotting and collagen metabolism markers in rheumatoid arthritis.
abstract: Rheumatoid arthritis is a chronic inflammatory disease caused essentially by an immune-mediated mechanism. However, abnormalities of the clotting system have also been incriminated as having an important role in the pathogenesis of this disease. This study aims at assessing the clotting system and collagen metabolism alterations and the relationship between perturbances of the hemostatic pathway and the destructive and fibroproliferative processes in patients with rheumatoid arthritis. The coagulation system was evaluated by measuring thrombin-antithrombin III complex (TAT), prothrombin time (PT), activated partial thromboplastin time (APTT), and antithrombin III (AT-III). The fibrinolysis system was assessed by measuring fibrin degradation products (FDP), fibrinogen (FBG), alpha 2-antiplasmin (alpha 2-PI), D-dimer (DD) and plasmin-alpha 2-antiplasmin complex (PAP). As markers of collagen metabolism, the type III procollagen peptide (PIIIP) and the 7S domain of type IV collagen (7S-collagen) were determined. Blood concentrations of DD, PAP, TAT, PIIIP, and 7S-collagen were significantly higher in rheumatoid arthritis patients compared to controls. Serum levels of PIIIP were significantly correlated with PT, APTT, AT-III, FDP, and DD. 7S-collagen levels were inversely related to AT-III and FBG values. This study demonstrated the occurrence of a subclinical intravascular coagulation in rheumatoid arthritis and suggested the important role of blood coagulation in the alteration of the extracellular matrix metabolism in this disease.
authors.affiliation: Third Department of Internal Medicine, Mie University School of Medicine, Tsu-city, Japan.
authors.forename: E C
authors.initials: EC
authors.lastname: Gabazza
authors.forename: T
authors.initials: T
authors.lastname: Osamu
authors.forename: T
authors.initials: T
authors.lastname: Yamakami
authors.forename: H
authors.initials: H
authors.lastname: Ibata
authors.forename: T
authors.initials: T
authors.lastname: Sato
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Shima
mesh_terms: D000328:Adult; D000933:Antifibrinolytic Agents; D000990:Antithrombin III / Q000378:metabolism; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000150:complications / Q000378:metabolism*; D015415:Biomarkers; D001777:Blood Coagulation / Q000502:physiology*; D003094:Collagen / Q000378:metabolism*; D004211:Disseminated Intravascular Coagulation / Q000209:etiology; D005109:Extracellular Matrix / Q000378:metabolism; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005341:Fibrinolysin / Q000378:metabolism; D005342:Fibrinolysis / Q000502:physiology; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D010447:Peptide Hydrolases / Q000378:metabolism; D011347:Procollagen / Q000378:metabolism; D000979:alpha-2-Antiplasmin / Q000378:metabolism
chemical_list: D000933:Antifibrinolytic Agents; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D011347:Procollagen; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D003094:Collagen; D010447:Peptide Hydrolases; D005341:Fibrinolysin