Circulating thrombomodulin as a novel endothelial cell marker: Comparison of its behavior with von willebrand factor and tissue‐type plasminogen activator
Circulating thrombomodulin as a novel endothelial cell marker: Comparison of its behavior with von willebrand factor and tissue‐type plasminogen activator
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循环血栓调节蛋白作为一种新型内皮细胞标志物：其与冯维勒布兰德因子和组织型纤溶酶原激活剂的行为比较
DOI：
10.1002/ajh.2830410107
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发表时间：
1992
影响因子：
12.8
通讯作者：
A. Shibata
中科院分区：
文献类型：
--
作者：
Hoyu Takahashi;S. Ito;M. Hanano;K. Wada;H. Niwano;Y. Seki;A. Shibata
Circulating thrombomodulin is a novel endothelial cell marker, which may reflect the endothelial injury. Plasma levels of thrombomodulin were quantitated by an enzymelinked immunosorbent assay (ELISA) in patients with hematological malignancies, liver disease, diabetes mellitus, collagen disease, thrombotic disease, and disseminated intravascular coagulation (DIC), and the thrombomodulin values were compared with those of von Willebrand factor antigen (vWf:Ag) and tissue‐type plasminogen activator (t‐PA) which are released from stimulated or damaged endothelial cells. The mean plasma concentrations of thrombomodulin in these disease states were elevated as compared with healthy subjects. A relatively high mean thrombomodulin level was observed in DIC, liver disease, and collagen disease. Abnormally high thrombomodulin values (> normal mean value + 3 SD) were found in 32.3% of patients with hematological malignancies, 57.7% of patients with liver disease, 39.3% of patients with diabetes mellitus, 30.0% of patients with collagen disease, 23.1% of patients with thrombotic disease, and 69.0% of patients with DIC. Plasma concentrations of both vWf:Ag and t‐PA were also elevated in these patients. On the whole, the plasma thrombomodulin concentration was positively correlated with vWf:Ag (r = 0.441, P < 0.001) and t‐PA (r = 0.398, P < 0.001). These findings indicate that the elevation of plasma thrombomodulin is frequently seen in a variety of diseases and circulating thrombomodulin is possibly useful for evaluating the endothelial damage in selected disease states. © 1992 Wiley‐Liss, Inc.
