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 chromatography 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.
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 chromatography substrate assay in 117 ALpatients and 50 normal controls. RESULTS: 1) alpha2-PI activities in ALpatients were reduced, especially in ALL patients [(96.8 +/- 21.2)%]; 2) PAI-1 antigens in AMLpatients [(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-M5patients [(39.9 +/- 11.6) microg/L] were higher and TAFI activities in APLpatients [(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 bleedingpatients [(13.2 +/- 5.3) mg/L] were significantly lower than that in normal control as well as non-bleedingpatients (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.