Premium
Increased levels of vascular endothelial cell markers in thrombotic thrombocytopenic purpura
Author(s) -
Wada Hideo,
Kaneko Toshihiro,
Ohiwa Michiaki,
Tanigawa Motoaki,
Hayashi Tatsuya,
Tamaki Shigehisa,
Minami Nobuyuki,
Deguchi Katsumi,
Suzuki Koji,
Nakano Takeshi,
Shirakawa Shigeru
Publication year - 1993
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.2830440206
Subject(s) - thrombomodulin , thrombotic thrombocytopenic purpura , von willebrand factor , endothelial stem cell , plasminogen activator , medicine , platelet , pathogenesis , tissue factor , plasmin , plasminogen activator inhibitor 1 , immunology , endothelium , tissue plasminogen activator , coagulation , thrombin , biology , in vitro , enzyme , biochemistry
We found that patients with thrombotic thrombocytopenic purpura (TTP) have significantly elevated plasma thrombin antithrombin III complex (TAT) and FDP‐D‐dimer levels, while the plasmin‐α2 plasmin inhibitor complex (PIC) level was only slightly increased. The tissue‐type plasminogen activator (t‐PA) level was increased, but it was well correlated with the plasminogen activator inhibitor‐1 (PAl‐l) level. These findings suggest that hypercoagulable and hypofibrinolytic states coexist in these patients, in contrast to patients with disseminated intravascular coagulation, who exhibit coexisting hypercoagulable and hyperfibrinolytic states. Levels of vascular endothelial cell markers, such as PAl‐l, thrombomodulin (TM), and t‐PA, were increased at the onset of TTP, but the level of von Willebrand factor (vWF) antigen was not increased. The outcome in TTP patients was correlated with plasma t‐PA and TM levels but not with TAT or PIC. These results suggest that vascular endothelial cell markers, such as TM and t‐PA, are released from injured or stimulated endothelial cells, reflecting the degree of vascular endothelial damage, and that the main factor in the pathogenesis of TTP is vascular endothelial cell injury. © 1993 Wiley‐Liss, Inc.