Takahashi H, Tatewaki W, Wada K, Shibata A
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Am J Hematol. 1989 Dec;32(4):255-7. doi: 10.1002/ajh.2830320404.
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-alpha 2-antiplasmin complex (PAP) in ten patients with acute TTP. Plasma TAT [mean 6.7 +/- (SD) 3.7 micrograms/liter] as well as PAP (2.1 +/- 1.2 mg/liter) were elevated in patients with TTP as compared with healthy subjects (TAT of 1.7 +/- 0.3 microgram/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.
血栓性血小板减少性紫癜（TTP）被认为主要由内皮细胞损伤或原发性血小板凝集引起。凝血筛查通常显示正常或仅有微小变化，但许多TTP患者的纤维蛋白原/纤维蛋白降解产物（FDP）会有适度升高。为了评估TTP患者体内的凝血酶生成情况，我们检测了10例急性TTP患者血浆中凝血酶 - 抗凝血酶III复合物（TAT）水平以及纤溶酶 - α2 - 抗纤溶酶复合物（PAP）水平。与健康受试者（TAT为1.7±0.3微克/升，PAP为0.2±0.1毫克/升；n = 10）相比，TTP患者的血浆TAT[平均6.7±（标准差）3.7微克/升]以及PAP（2.1±1.2毫克/升）均升高。这些发现表明，尽管大多数患者没有消耗性凝血病的迹象，但TTP患者体内实际上会生成大量的凝血酶和纤溶酶。
