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目的 探讨急性早幼粒细胞白血病 (APL)患者用全反维甲酸 (ATRA)和砷剂 (AS2 O3)治疗期间细胞组织因子 (TF)表达及血浆止凝血分子标志物含量变化。方法 用ELISA法检测血浆TF、组织因子途径抑制物 (TFPI)、凝血酶 抗凝血酶复合物 (TAT)、纤溶酶 抗纤溶酶复合物 (PAP)、尿激酶型纤溶酶原激活物 (u PA)、尿激酶型纤溶酶原激活物受体 (u PAR)和细胞裂解液TF含量 ;RT PCR法检测细胞TFmRNA转录水平。结果 治疗前 ,患者血浆TF[(98 3± 19 8)ng/L、(89 6± 15 2 )ng/L]、TFPI[(94 4± 37 0 )mg/L、(93 5± 36 4)mg/L]、TAT [(2 1 9± 9 6 ) μg/L、(18 2± 9 7) μg/L]、PAP[(0 73± 0 2 6 )mg/L、(0 6 3± 0 33)mg/L]、u PA[(0 6 3± 0 2 3) μg/L、(0 5 7± 0 0 1) μg/L]、u PAR[(0 41± 0 14) μg/L、(0 47± 0 16 ) μg/L]水平与正常对照组相比为高 ,差异有显著性或极显著意义(P <0 0 5~ 0 0 1)。骨髓分离的单个核细胞TFmRNA转录、裂解液TF水平 [(6 80 2 4± 45 6 6 1)pg/10 7、(36 8 0 2± 15 1 2 )pg/10 7]与对照组相比均显著升高 ;经ATRA、AS2 O3 治疗后显著下降。结论 APL患者TF表达增高、凝血系统激活、纤溶亢进 ,但随病情好转可逐渐改善。ATRA及AS2 O3 均能抑制早幼粒细胞TFmR
Objective To investigate the changes of tissue factor (TF) expression and plasma coagulation molecular markers in patients with acute promyelocytic leukemia (APL) treated with all-trans-retinoic acid (ATRA) and arsenic (AS2O3). Methods ELISA was used to detect plasma TF, tissue factor pathway inhibitor (TFPI), thrombin antithrombin complex (TAT), plasmin antiplasmin complex (PAP), urokinase-type plasminogen activation (u PA), urokinase-type plasminogen activator receptor (u PAR) and cell lysate TF content; RT PCR method to detect the TF mRNA transcription level. Results Before treatment, patients had plasma TF [(98 3 ± 19 8) ng/L, (89 6 ± 15 2) ng/L], TFPI [(94 4 ± 37 0) mg/L, (93 5± 36 4). ) mg/L], TAT [(2 1 9± 9 6 ) μg/L, (18 2± 9 7) μg/L], PAP [(0 73 ± 0 2 6 ) mg/L, (0 6 3) ± 0 33) mg/L], u PA [(0.63 ± 0 2 3) μg/L, (0 5 7 ± 0 0 1) μg/L], u PAR [(0 41 ± 0 14) μg] The level of /L and (0 47 ± 0 16) μg/L] was higher than that of the normal control group, and the difference was significant or extremely significant (P <0 05 to 0 0 1). Mononuclear cell TF mRNA transcription, lysate TF levels [(6 80 2 4 ± 45 6 61) pg/10 7 (36 8 0 2 ± 15 1 2) pg/10 7] isolated from bone marrow compared with controls Both increased significantly; they were significantly decreased after treatment with ATRA and AS2O3. Conclusions The expression of TF in patients with APL is increased, the coagulation system is activated, and fibrinolysis is hyperactive, but it can be gradually improved with the improvement of the disease. Both ATRA and AS2 O3 can inhibit promyelocytic TFmR