• thrombin-antithrombin III complex;
  • plasmin-α2-antiplasmin complex;
  • FDP;
  • acquired coagulopathy


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-α2-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.