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作者对照研究了20例CMPD患者和20例正常人的血小板功能,并观察了其中 13例患者和 8例正常人的血小板超微结构。发现CMPD患者血小板粘附功能与ADP、肾上腺素、胶原、瑞斯脱霉素所诱导的血小板聚集功能均降低,血小板内致密颗粒数减少。由此表明CMPD 患者具有血小板粘附与聚集功能障碍。作者认为这种功能障碍可能是导致患者出血和血栓形成的主要原因;但从本研究结果还看不出血小板功能变化与患者出血和血栓形成的临床表现之间有何平行关系。
The authors compared platelet function in 20 patients with CMPD and 20 normal controls and observed platelet ultrastructure in 13 patients and 8 normal controls. Found that platelet adhesion function in CMPD patients with ADP, epinephrine, collagen, reeseamycin-induced platelet aggregation were reduced, the number of platelets within the dense particles decreased. This shows that CMPD patients with platelet adhesion and aggregation dysfunction. Authors believe that this dysfunction may be the leading cause of bleeding and thrombosis in patients; but the results of this study also do not see any parallel between platelet function changes and clinical manifestations of patients with bleeding and thrombosis.