117例急性白血病患者纤溶抑制物研究

目的 探讨急性白血病(AL)患者凝血酶激活的纤溶抑制物(TAFI)、纤溶酶原激活剂抑制物(PAI)、α2抗纤溶酶(α2:-PI)等纤溶抑制物的变化及其临床意义.方法 采用ELISA法测定117例AL患者和50名正常对照的PAI-1抗原(PAI-1:Ag)含量、TAFI抗原含量;采用发色底物法测定PAI活性、α2-PI活性、TAFI活性.结果 ①AL患者的α2-PI活性水平明显低于对照组,其中急性淋巴细胞白血病患者(96.8±21.2)%]较对照组(129.1±13.1)%]下降更明显;②急性髓系白血病患者PAI-1:Ag含量(37.8±9.2)μg/L]高于对照组(33.8±4.9)μg/L];③急性早幼粒细胞白血病患者PAI-1:Ag含量(37.8±9.0)μg/L]高于对照组,TAFI活性水平(13.3±4.8)mg/L]低于对照组(16.9±2.6)mg/L],急性单核细胞白血病患者PAI-1:Ag含量(39.9±11.6)μg/L]高于对照组;④复发/难治组的PAI-1:Ag含量(39.6±11.6)μg/L]高于对照组;⑤明显出血组TAFI活性水平(13.2±5.3)mg/L]低于对照组及无出血组(17.0±4.6)mg/L];⑥TAFI活性与出血程度呈显著负相关,r=-0.276(P《0.05).结论 α2-PI及TAFI活性降低是AL出血的原因之一,且TAFI活性与卅血程度呈显著负相关.

Study of fibrinolysis inhibitors in 117 acute leukemia patients

OBJECTIVE: To explore the clinical significance of fibrinolysis inhibitors including thrombin activatable fibrinolysis inhibitor(TAFI), plasminogen activator inhibitor (PAI) and alpha2-plasmin inhibitor (alpha2-PI) in acute leukemia (AL). METHODS: PAI-1 antigen and TAFI antigen were investigated by enzyme-linked immunosorbent assay and PAI activity, alpha2-PI activity, TAFI activity by chrimato-substrate assay in 117 AL patients and 50 normal controls. RESULTS: 1) alpha2-PI activities in AL patients were reduced, especially in ALL patients (96.8 +/- 21.2)%]; 2) PAI-1 antigens in AML patients (37.8 +/- 9.2) microg/L] were significantly higher than that in normal controls (33.8 +/- 4.9) microg/L]; 3) PAI-1 antigens in APL (37.8 +/- 9.0) microg/L] and AML-M5 patients (39.9 +/- 11.6) microg/L] were higher and TAFI activities in APL patients (13.3 +/- 4.8) mg/L] were lower than that in normal controls (16.9 +/- 2.6) mg/L]; 4) PAI-1 antigens of relapsed/refractory patients (39.6 +/- 11.6) microg/L) were significantly elevated; 5) TAFI activities in bleeding patients (13.2 +/- 5.3) mg/L] were significantly lower than that in normal control as well as non-bleeding patients (17.0 +/- 4.6) mg/L); 6) The severity of bleeding was negatively correlated with TAFI activity (r = - 0.276, P <0.05). CONCLUSIONS: Hyperfibrinolysis caused partially by decrease of alpha2-PI and TAFI activity takes part in the pathogenesis of bleeding in AL.