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Antibodies to tissue‐type plasminogen activator in plasma from patients with primary antiphospholipid syndrome
Author(s) -
Cugno Massimo,
Dominguez Miguel,
Cabibbe Mara,
Bisiani Giuliana,
Galli Monica,
AnglesCano Edouard,
Agostoni Angelo
Publication year - 2000
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2000.01948.x
Subject(s) - medicine , thrombosis , antibody , plasminogen activator , fibrinolysis , venous thrombosis , t plasminogen activator , gastroenterology , deep vein , fibrin , antiphospholipid syndrome , tissue plasminogen activator , stroke (engine) , immunology , mechanical engineering , engineering
A reduction in fibrinolysis has been described in association with thrombosis in the primary antiphospholipid syndrome (PAPS). In this study, we measured anti‐tissue‐type plasminogen activator (t‐PA) antibodies and anti‐fibrin‐bound t‐PA antibodies as possible causes of hypofibrinolysis in 39 patients with PAPS. We also evaluated the differences in anti t‐PA antibodies between patients without previous thrombosis (20 patients) and patients with previous episodes of thrombosis (19 patients: deep vein thrombosis in nine, ischaemic stroke in six, arterial leg thrombosis in one, hepatic vein thrombosis in one, thrombophlebitis in one and cerebral venous thrombosis in one). Anti‐t‐PA antibodies were measured by an enzyme‐linked immunosorbent assay (ELISA), and anti‐t‐PA fibrin‐bound antibodies were measured by a solid‐phase fibrin immunoassay (SOFIA) in 39 patients with PAPS and in 39 controls matched for gender and age. High levels of IgG anti‐t‐PA were found in three out of 39 patients with PAPS, and all three patients had a history of thrombosis; four other patients, one of whom had a history of thrombotic events, had high titres of antibodies directed against fibrin‐bound t‐PA. In addition, patients with ischaemic stroke had significantly higher levels of IgG anti‐t‐PA than patients without thrombosis ( P = 0·029). In conclusion, our data showed that, in patients with PAPS, the highest levels of anti‐t‐PA antibodies were present in subjects with previous thrombotic events. The discrepancy in the results obtained with two methods of detection of anti‐t‐PA antibodies, ELISA and SOFIA, indicates a different interaction of the antibodies with the t‐PA molecules, which are directly bound to polystyrene plates in ELISA and bound to fibrin as a bridging molecule in SOFIA.