Zurborn K H, Bernsmeier R, Schamerowski F, Stöhr A, Bruhn H D
Onkologie. 1982 Aug;5(4):186-90. doi: 10.1159/000214997.
Thromboembolic and haemorrhagic complications are not rarely seen in the course of malignant diseases. The underlying coagulation disorders were investigated by means of coagulation analysis in 61 patients with solid tumors and 60 control persons as well as 51 patients with leukemia and 50 control persons. As a cause for the thrombotic diathesis in patients with solid tumors and leukemias can be demonstrated a hypercoagulability (shortened PTT and raised factor VIII activity). In addition we found a raised level of fibrinogen, a hypofibrinolysis (prolonged euglobulin lysis time) and in increased platelet aggregation in patients with solid tumors. Predominantly bleeding complications in leukemias are caused by thrombopenia. Another reason, however, may be an activated fibrinolysis or a clot instability because of the reduction of factor XIII. Pathogenetic mechanisms, underlying the tumor induced coagulation disorders, as for example the release of tumor cell thromboplastins from malignant cells are discussed.
血栓栓塞和出血并发症在恶性疾病病程中并不少见。通过凝血分析对61例实体瘤患者和60例对照者以及51例白血病患者和50例对照者的潜在凝血障碍进行了研究。实体瘤和白血病患者血栓形成素质的原因可表现为高凝状态(部分凝血活酶时间缩短和因子VIII活性升高)。此外,我们发现实体瘤患者纤维蛋白原水平升高、纤维蛋白溶解功能减退(优球蛋白溶解时间延长)以及血小板聚集增加。白血病患者主要的出血并发症是由血小板减少引起的。然而,另一个原因可能是由于因子XIII减少导致的纤维蛋白溶解激活或凝块不稳定。本文讨论了肿瘤诱导凝血障碍的发病机制,例如恶性细胞释放肿瘤细胞凝血活酶。