丁胺卡那霉素对EDTA依赖性凝集血小板的解离及其机制

目的研究丁胺卡那霉素对EDTA抗凝剂依赖的聚集血小板的解离作用和机制,为血常规标本中血小板凝聚提供可靠的解决方法。方法在EDTA依赖的假性血小板减少症(PTCP)患者的EDTA-K2抗凝血样本中,于不同时间段加入不同浓度丁胺卡那霉素进行凝集血小板的解离试验,通过血小板计数和涂片观察解离效果;用流式细胞仪检测血小板膜表面CD41、CD61、CD62p、PAC-1和IgG的表达百分率。结果抽血后1h内加入丁胺卡那霉素对血小板凝集的解离作用明显,血小板计数可恢复到即时检测的水平,血小板CD62p、PAC-1和IgG的表达量被显著抑制,而CD41和CD61未受明显影响。结论PTCP患者血常规样品抽血后1h内加入丁胺卡那霉素能有效解离凝集的血小板,作用机制可能与抑制患者血小板膜表面CD62p、PAC-1和IgG的表达有关;此法有助于解决EDTA所致的血小板计数的假性减少。

Dissociation of EDTA-dependent pseudo platelet aggregation by amikacin and its mechanism

Objective To study the dissociation of EDTA-dependent pseudo platelet aggregation by amikacin and to clarify the potential mechanism.Methods At different time points,two concentrations of amikacin (6.5 mg/ml and 10.0 mg/ml) were respectively added to EDTA-K2 anti-coagulated whole blood samples collected from two subjects with EDTA-dependent pseudothrombocytopenia.The aggregated-platelet dissociation was investigated by platelet count and microscopical examination.CD41,CD61,CD62p,PAC-1,and IgG on the platelets of the two patients and of a normal control were determined by the FCS under various conditions.Results When amikacin (6.5 mg/ml) was added within 1 hour after blood collection,it dissociated the EDTA induced platelet aggregation and the platelet counts returned to the normal level. The expression of CD62p,PAC-1,and PA-IgG on the platelets was decreased,yet the expression of CD41 and CD61 had no change.Conclusion Amikacin supplementation (6.5 mg/ml) within 1 hour after blood sampling may dissociate the aggregated platelets caused by EDTA. The mechanism may be associated that amikacin might inhibit the expression of CD62p,PAC-1,and PA-IgG on platelets. The amikacin supplementation would be an inexpensive,effective,and practical method to solve the platelet aggregation induced by EDTA.