Coagulation disorders in cancer. I. Clinical and laboratory studies

Coagulation disorders in cancer. I. Clinical and laboratory studies
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癌症中的凝血障碍。

DOI:
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发表时间:
1967
期刊:
影响因子:
6.2
通讯作者:
L. Zuckerman
L. Zuckerman
中科院分区:
医学1区
文献类型:
--
作者:
S. Miller;J. Sánchez;Tadeusz Stefanski;L. Zuckerman

文献摘要

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对50例播散性恶性肿瘤患者的止血和凝血机制进行了综合研究。在大多数患者中发现了显著的实验室异常。最常见的模式是“高凝状态”。这包括出血时间短、硅胶凝固时间和部分凝血活酶时间缩短、肝素耐受性增加、因子I、II、V、VIII、IX和XI的血浆水平显著升高以及凝血活酶生成加速。血小板计数升高,接受化疗药物的患者除外。7例患者由于维生素K依赖性凝血因子抑制而导致凝血酶原时间延长。用免疫学和其他技术检测了6例患者的纤维蛋白溶解。数据表明,癌症患者的止血水平发生了变化,凝血因子及其抑制剂的水平均升高,导致相反止血力之间的平衡更容易受到干扰。临床血栓形成或出血可能遵循。
A comprehensive study of the hemostatic and coagulation mechanisms in 50 patients with disseminated malignancy was carried out. Significant laboratory abnormalities were found in the majority of patients. The most common pattern was the “hypercoagulable state.” This included short bleeding time, decreased silicone coagulation time and partial thromboplastin time, increased tolerance to heparin, marked elevation of plasma levels of factors I, II, V, VIII, IX and XI and acceleration of thromboplastin generation. There was elevation of platelet counts, except in patients receiving chemotherapeutic drugs. Seven patients had prolonged prothrombin time due to depression of vitamin‐K‐dependent clotting factors. Fibrinolysis was detected in six patients by immunologic and other techniques. The data suggest that patients with cancer have an alteration in the hemostatic level of control with increased levels of both clotting factors and their inhibitors, resulting in a more easily disturbed balance between opposing hemostatic forces. Clinical thrombosis or bleeding may follow.