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目的比较急性白血病不同阶段血小板膜糖蛋白CD42a、CD62p、PAC-1表达的差异,探讨应用血小板膜糖蛋白PAC-1、CD62p、CD42a监测血小板的活化状态和预测急性白血病出血的可能性及不同阶段血小板膜糖蛋白表达与血小板聚集、黏附、活化功能之间的联系。方法急性白血病初次确诊未治组28例,急性白血病诱导后早期完全缓解组16例,长期完全缓解组(缓解期达两年以上)10例,正常对照组30例。用流式细胞仪检测微量全血血小板膜糖蛋白PAC-1、CD62p、CD63,二磷酸腺苷(adenosine diphosphate,ADP)激活后检测PAC-1、CD62p、CD42a,观察百分率及平均荧光强度的变化。结果血小板计数、血小板平均体积、血小板压积进行比较,未治组显著低于其他组(P<0.01)。不同阶段血小板膜糖蛋白百分率比较,ADP激活前未治组CD62p、PAC-1表达阳性率均高于其他组(P<0.01);早期完全缓解组CD62p、PAC-1表达阳性率高于长期完全缓解组、对照组(P<0.01)。激活后,未治组及早期完全缓解组CD62p、PAC-1表达阳性率均高于对照组(P<0.01)。CD42a表达阳性率在ADP激活前后各组间比较差异均无显著性(P>0.05)。ADP激活前,未治组CD62p、PAC-1平均荧光强度高于其他组(P<0.01),CD42a平均荧光强度低于其他组(P<0.01);与长期完全缓解组、对照组相比,早期完全缓解组CD62P、PAC-1平均荧光强度较高(P<0.01),CD42a较低(P<0.01)。激活后,未治组CD62p、CD42a平均荧光强度高于其他组(P<0.01),PAC-1低于其他组(P<0.01);与长期完全缓解组、对照组相比,早期完全缓解组CD62P、CD42a平均荧光强度较高(P<0.01),PAC-1较低(P<0.01)。结论急性白血病初诊未治时外周血血小板活化增多,ADP激活后活化功能降低,黏附、聚集功能减低,诱导后早期完全缓解阶段血小板聚集、黏附、活化功能较初诊未治时有所恢复,但仍处于异常状态,长期完全缓解阶段血小板膜糖蛋白表达正常,其血小板功能亦恢复正常。
Objective To compare the expression of platelet membrane glycoproteins CD42a, CD62p and PAC-1 in different stages of acute leukemia and to explore the activation status of platelet glycoproteins PAC-1, CD62p and CD42a and the possibility of predicting the bleeding of acute leukemia and the different stages Platelet membrane glycoprotein expression and platelet aggregation, adhesion, activation of the relationship between. Methods Twenty-eight untreated acute leukemia patients were initially diagnosed as untreated acute leukemia, 16 as early complete remission after acute leukemia induction, 10 as long-term complete remission (remission for more than two years), and 30 as normal control. The changes of percentage and average fluorescence intensity of PAC-1, CD62p and CD42a were detected by flow cytometry after detecting the activation of PAC-1, CD62p, CD63 and adenosine diphosphate (ADP) . Results Platelet count, average platelet volume, and platelet pressure were significantly lower in the untreated group than those in the other groups (P <0.01). The positive rates of CD62p and PAC-1 in untreated group before ADP activation were higher than those in the other groups (P <0.01). The positive rates of CD62p and PAC-1 in early complete remission group were higher than that in long-term complete Remission group and control group (P <0.01). After activation, the positive rates of CD62p and PAC-1 in both untreated group and early complete remission group were higher than those in control group (P <0.01). The positive rate of CD42a expression before and after ADP activation was no significant difference between groups (P> 0.05). Before ADP activation, the average fluorescence intensity of CD62p and PAC-1 in the untreated group was higher than that in the other groups (P <0.01), and the average fluorescence intensity of CD42a was lower than that in the other groups (P <0.01). Compared with the long-term complete remission group and the control group, The average fluorescence intensity of CD62P and PAC-1 in early complete remission group was higher (P <0.01) and CD42a was lower (P <0.01). After activation, the average fluorescence intensity of CD62p and CD42a in the untreated group was higher than that in the other groups (P <0.01), and the PAC-1 was lower than that in the other groups (P <0.01). Compared with the long-term complete remission group and the control group, The average fluorescence intensity of CD62P and CD42a was higher (P <0.01) and PAC-1 was lower (P <0.01). Conclusions The activation of peripheral blood platelets in acute leukemia patients with untreated acute leukemia is increased. The activation of ADP is decreased after activation of ADP, and the adhesion and aggregation functions are decreased. The platelet aggregation, adhesion and activation of early stage of acute leukemia after complete remission are recovered compared with those without initial treatment. In an abnormal state, the long-term complete remission platelet glycoprotein expression is normal, and its platelet function returned to normal.