The most serious manifestations of Kawasaki disease (KD), also called mucocutaneous lymph node syndrome, are myocardial infarction and the development of aneurysms, especially of the coronary arteries.1,2 Mortality in this disease is due to cardiac disease, mainly from myocardial infarction secondary to coronary artery thromboses.2 It is known that the blood platelet is involved in many types of arterial occlusive disease.3,4 The pathologic changes in the heart in children who have died of KD suggest that platelets are involved in this vasculitic-thrombotic process. In addition, thrombocytosis (platelet counts greater than 500 000/mm3 [500 × 109/L]) characteristically develops in patients with KD in the second to third week of the illness. During this period of time, aneurysms make their appearance. With regard to the platelet, is this a cause and effect relationship?
The poor, defenseless platelet is being watched, counted, analyzed,