Kemkes-Matthes B, Plusczyk T, Lasch H G
Zentrum für Innere Medizin, Universität Giessen, Germany.
Thromb Res. 1992 Jan 1;65(1):85-94. doi: 10.1016/0049-3848(92)90228-3.
Pulmonary cancer patients are known to have an elevated risk to suffer from thromboembolic complications. Because hereditary deficiencies of coagulation inhibitors antithrombin III, protein C and protein S are known to cause thromboembolic events it was the aim of our study to search for acquired alterations of these proteins in pulmonary cancer patients. We could demonstrate antithrombin III and protein C to be within the normal range in patients suffering from pulmonary carcinoma. In contrast, in patients suffering from metastatic pulmonary carcinoma bound protein S was increased, while free protein S was significantly reduced. In some patients the decrease of free protein S was comparable to the diminution observed in hereditary protein S deficient patients. A high positive correlation was observed between C4b-binding protein and bound protein S, indicating C4b-binding protein to be a regulatory protein for the shift from free and anticoagulatory active to bound and anticoagulatory inactive protein S. In conclusion, the decrease of free protein S is one source for thromboembolic complications in pulmonary cancer patients. For interpretation of altered free protein S levels it is useful to measure C4b-binding protein.
众所周知,肺癌患者发生血栓栓塞并发症的风险较高。由于已知凝血抑制剂抗凝血酶III、蛋白C和蛋白S的遗传性缺陷会导致血栓栓塞事件,我们研究的目的是探寻肺癌患者中这些蛋白质的获得性改变。我们能够证明,肺癌患者的抗凝血酶III和蛋白C处于正常范围内。相比之下,转移性肺癌患者的结合蛋白S增加,而游离蛋白S显著减少。在一些患者中,游离蛋白S的降低与遗传性蛋白S缺乏患者中观察到的减少相当。观察到C4b结合蛋白与结合蛋白S之间存在高度正相关,表明C4b结合蛋白是游离且具有抗凝活性的蛋白S转变为结合且无抗凝活性的蛋白S的调节蛋白。总之,游离蛋白S的降低是肺癌患者血栓栓塞并发症的一个来源。为了解释游离蛋白S水平的改变,检测C4b结合蛋白是有用的。