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Thrombin generation in patients with thrombotic thrombocytopenic purpura
Author(s) -
Takahashi Hoyu,
Tatewaki Wataru,
Wada Ken,
Shibata Akira
Publication year - 1989
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830320404
Subject(s) - thrombotic thrombocytopenic purpura , fibrinogen , medicine , liter , coagulopathy , platelet , fibrin , immunology , thrombin , coagulation , gastroenterology , endocrinology
Thrombotic thrombocytopenic purpura (TTP) is thought to be caused primarily by endothelial cell injury or primary platelet agglutination. A coagulation screen usually shows normal or minimal changes, but a modest elevation of fibrinogen/fibrin degradation products (FDP) is observed in many patients with TTP. To assess the thrombin generation in vivo in TTP, plasma levels of thrombin‐antithrombin III complex (TAT) were measured together with plasmin‐α 2 ‐antiplasmin complex (PAP) in ten patients with acute TTP. Plasma TAT [mean 6.7 ± (SD) 3.7 μg/liter] as well as PAP (2.1 ± 1.2 mg/liter) were elevated in patients wtih TTP as compared with healthy subjects (TAT of 1.7 ± 0.3 μg/liter and PAP of 0.2 ± 0.1 mg/liter; n = 10). These findings indicate that considerable amounts of thrombin and plasmin are actually generated in TTP, although the majority of patients do not show signs of consumption coagulopathy.

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