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目的：探讨慢性粒细胞白血病（ＣＭＬ）患者血小板膜糖蛋白Ⅳ（ＧＰⅣ）再分布和胞内凝血酶敏感蛋白（ＴＳＰ）释放及血浆中β－血小板球蛋白（β－ＴＧ）和血小板第４因子（ＰＦ４）对其的影响作用。方法：应用１２５Ｉ分别标记血小板ＧＰⅠｂ、ＧＰⅡｂ／Ⅲａ、ＧＰⅣ和ＴＳＰ单克隆抗体并结合放射免疫法检测ＣＭＬ患者血小板膜上相应的结合位点，同时观察β－ＴＧ和ＰＦ４的抑制作用。结果：（１）ＣＭＬ患者未活化和诱导活化（凝血酶１Ｕ／ｍｌ）血小板膜ＧＰⅣ分布和再分布分别为３６０８０±１７０１０、４４３２０±３２３１０抗体结合分子数／血小板，明显高于相应对照组（Ｐ＜０．０１），而血小板膜ＧＰⅠｂ和ＧＰⅡｂ／Ⅲａ则无异常分布；（２）ＣＭＬ患者血小板胞内ＴＳＰ释放并未伴随血小板膜ＧＰⅣ再分布而发生相应的增多；（３）ＣＭＬ患者血浆中β－ＴＧ和ＰＦ４含量增高（Ｐ＜０．０５），体外实验发现β－ＴＧ和ＰＦ４明显地抑制血小板胞内ＴＳＰ释放。结论：ＣＭＬ患者血小板膜ＧＰⅣ再分布增多，可能成为判断血小板功能异常指标之一；而血小板胞内ＴＳＰ释放障碍或结合下降，则受血浆中β－ＴＧ和ＰＦ４的影响。
Objective: To investigate the redistribution of platelet membrane glycoprotein IV (GPIV) and the release of intracellular thrombospondin-sensitive protein (TSP) in patients with chronic myeloid leukemia (CML), and the relationship between plasma β-thromboglobulin (β-TG) and platelet factor 4 (PF4) Effect on it. METHODS: 125I-labeled platelet GPIb, GPIIb/IIIa, GPIV and TSP monoclonal antibodies were combined with radioimmunoassay to detect the corresponding binding sites on platelet membrane of CML patients. The inhibitory effects of β-TG and PF4 were also observed. RESULTS: (1) The distribution and redistribution of platelet membrane GPIV in non-activated and induced activation (thrombin 1 U/ml) of CML patients were respectively 36080±17010, 44320±32310 antibody binding molecules/platelets, which was significantly higher than that of the corresponding control group (P <0.01), but there was no abnormal distribution of platelet membrane GPIb and GPIIb/IIIa; (2) The release of intracellular TSP in platelets of CML patients did not accompany the increase of platelet membrane GPIV redistribution; (3) plasma in CML patients The levels of β-TG and PF4 were increased (P<0.05). In vitro experiments showed that β-TG and PF4 significantly inhibited intracellular TSP release from platelets. Conclusion: The redistribution of platelet membrane GPIV in patients with CML may be one of the indicators of abnormal platelet function. However, the release of TSP from platelets or the decrease of binding of TSP may be affected by plasma β-TG and PF4.