抗凝剂依赖假性血小板减少症凝集血小板解离及机理研究

目的对丁胺卡那霉素解离EDTA抗凝剂依赖的聚集血小板的作用进行研究,并初步探讨其解离机制,为临床提供准确的血小板计数。方法两名确诊因EDTA依赖的假性血小板减少症(ETCP)患者的EDTA-K2抗凝血中,在不同时间段,加入不同浓度丁胺卡那霉素进行血小板凝集的解离试验,通过血小板及其它细胞计数和涂片观察丁胺卡那霉素对血小板凝集后的解离效果。另外,两名患者的EDTA-K2抗凝血标本在三种不同状态(不加丁胺卡那霉素、即时加入丁胺卡那霉素、2 h后加入丁胺卡那霉素)下,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1 h内加入6.5 mg/ml和10 mg/ml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,而在1.5 h以后加入对血小板凝集解离作用不明显。解离效果与药物浓度无明显的相关性。在两名患者的抗凝血中即时加入丁胺卡那霉素可抑制CD62p、PAC-1和IgG的表达;2 h后加入丁胺卡那霉素对CD62p、PAC-1和IgG的抑制不如前者明显;丁胺卡那霉素对血小板CD41和CD61表达无明显变化。RBC、WBC和Hb等数值无明显的影响。结论抽血后放置1 h内加入6.5 mg/ml丁胺卡那霉素能有效解离EDTA抗凝剂依赖性血小板凝集,且不影响其它血细胞的计数,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。

STUDY ON DISSOCIATION OF AMIKACIN TO EDTA-DEPENDENT PSEUDO PLATELET AGGREGATION AND TO ITS MECHANISM

Objective To study on dissociation of amikacin to EDTA-dependent pseudo platelet(ETCP) aggregation and to explore its mechanism.Methods The different concentrations of amikacin were added into the bloods with EDTA-K2 in order to investigate the aggregated platelet dissociation using the platelet count and microscopically examination during different time after drawing bloods which were from two patients with ETCP.CD41,CD61,CD62p,PAC-1 and IgG on the platelet of two patients with ETCP and a normal control we...