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目的：观察髓性白血病及正常人骨髓单个核细胞及血浆中ｕＰＡ、ｔＰＡ、ＰＡＩ的表达情况并探讨其临床意义。方法：用ＥＬＩＳＡ 法测定２０ 例急性髓性白血病及１５ 例正常人骨髓单个核细胞及血浆中ｕＰＡ、ｔＰＡ、ＰＡＩ－１、ＰＡＩ－２ 抗原表达，同时用发色底物法测定血浆中ｔＰＡ、ｕＰＡ 和ＰＡＩ－１ 的活性。结果：骨髓中ｔＰＡ 浓度白血病低于正常人（ Ｐ＜ ０．０１），血浆中相反。ｕＰＡ 浓度骨髓及血浆中白血病均高于正常人（ Ｐ＜ ０．００１）。ＰＡＩ－１ 抗原测定两者骨髓及血浆均无差别。ＰＡＩ－２ 正常人骨髓中高于白血病（ Ｐ＜ ０．０１），血浆中相反。急性髓性白血病ｕＰＡ、ｔＰＡ和ＰＡＩ－１ 血浆活性均高于正常人。结论：急性髓性白血病骨髓中ｕＰＡ 表达增高，说明白血病细胞主要表达ｕＰＡ 为主，不产生ｔＰＡ。ｔＰＡ 的释放是由于血管内皮细胞受到白血病细胞损伤引起。在急性髓性白血病患者的出血机制与ｕＰＡ、ｔＰＡ 过度表达导致纤溶亢进有关，而且白血病早期浸润可能与ｕＰＡ、ＰＡＩ的表达有关。
Objective: To observe the expression of uPA, tPA and PAI in myeloid leukemia and normal human bone marrow mononuclear cells and plasma and to explore its clinical significance. Methods: The expression of uPA, tPA, PAI-1 and PAI-2 in 20 cases of acute myelogenous leukemia and 15 cases of normal human bone marrow mononuclear cells were measured by ELISA. Plasma tPA, uPA and PAI-1 activity. Results: The tPA concentration in bone marrow leukemia was lower than that in normal people (P <0.01), and the plasma level was opposite. UPA concentrations in bone marrow and plasma leukemia were higher than normal (P <0.001). PAI-1 antigen determination of both bone marrow and plasma no difference. PAI-2 normal bone marrow higher than leukemia (P <0.01), the plasma opposite. Plasma levels of uPA, tPA and PAI-1 in acute myeloid leukemia were higher than those in normal people. Conclusion: The expression of uPA in bone marrow of patients with acute myeloid leukemia increased, indicating that the main expression of leukemia cells uPA, do not produce tPA. The release of tPA is due to the damage of vascular endothelial cells by leukemia cells. In acute myeloid leukemia patients with bleeding mechanism and uPA, tPA overexpression leads to fibrinolysis, and early leukemia may be related to the expression of uPA, PAI.