Anders O, Nagel H R, Ernst B, Konrad H, Zgola M
Klinik für Innere Medizin, Bereiches Medizin der Wilhelm-Pieck-Universität Rostock.
Folia Haematol Int Mag Klin Morphol Blutforsch. 1988;115(5):769-80.
In 64 patients affected with acute leukaemia (51 patients with acute non-lymphatic leukaemia and 13 patients with acute lymphatic leukaemia) extensive investigations of blood coagulation were made during cytostatic therapy. The following conspicuous changes of haemostatasis could be observed in making the diagnosis: Lowered quick value and shortened PTT, increased fibrinogen, fibrinopeptide, A, alpha 1-antitrypsin and alpha 2-macroglobulin, diminished plasminogen and plasma fibrininectin. According to TAD (VP) protocol the induction therapy leads to hypercoagulability which can be recognized by an increase of fibrinopeptide A, coagulating factors and shortening of PTT. During the therapy with L-asparaginasis procoagulatoric as well as thromboprotective coagulating proteins are diminished. A dense laboratory control enables those disturbances of haemotasis caused by disease or therapy to be separated and contributes to preventing complications during the cytostatic induction therapy.
对64例急性白血病患者（51例急性非淋巴细胞白血病患者和13例急性淋巴细胞白血病患者）在进行细胞抑制治疗期间进行了广泛的血液凝固研究。在诊断过程中可观察到以下明显的止血变化：快速值降低和部分凝血活酶时间缩短，纤维蛋白原、纤维蛋白肽A、α1-抗胰蛋白酶和α2-巨球蛋白增加，纤溶酶原和血浆纤维连接蛋白减少。根据TAD（VP）方案，诱导治疗会导致高凝状态，这可通过纤维蛋白肽A增加、凝血因子增加和部分凝血活酶时间缩短来识别。在使用L-天冬酰胺酶治疗期间，促凝血以及血栓保护凝血蛋白减少。严密的实验室监测能够区分由疾病或治疗引起的那些止血障碍，并有助于预防细胞抑制诱导治疗期间的并发症。
