Fruchter Oren, Blich Miry, Jacob Giris
Recanati Autonomic Dysfunction Center, Department of Internal Medicine C, Rambam Medical Center, Haifa, Israel.
Am J Med Sci. 2002 May;323(5):279-80. doi: 10.1097/00000441-200205000-00010.
Because platelets play a major role in most thrombotic events, it is not surprising that all cases of myocardial infarctions in patients with idiopathic thrombocytopenic purpura (ITP) have been reported to occur only when platelets counts begin to rise. We report on a 69-year-old man with ITP who had acute myocardial infarction while he was severely thrombocytopenic (2000/microL). We hypothesize that the pathogenesis of myocardial infarction in thrombocytopenic patients with ITP may result from endothelial damage induced by autoantibodies directed against antigens present on both platelets and coronary endothelial cells.
由于血小板在大多数血栓形成事件中起主要作用，特发性血小板减少性紫癜（ITP）患者的所有心肌梗死病例据报道仅在血小板计数开始上升时才会发生，这并不奇怪。我们报告了一名69岁的ITP男性患者，他在严重血小板减少（2000/微升）时发生了急性心肌梗死。我们推测，ITP血小板减少患者发生心肌梗死的发病机制可能是针对血小板和冠状动脉内皮细胞上存在的抗原的自身抗体诱导的内皮损伤所致。
