Studies on the Effect of Long‐Term Use of Low Dose Aspirin in Kawasaki Disease

Abstract The inhibitory action of long‐term low dose aspirin (1–2 mg/kg/day for over 10 months) on the cyclooxygenase pathway in platelets and vascular endothe‐lium was evaluated in 10 patients with Kawasaki disease. The results were compared with those obtained after taking aspirin at 5–10 mg/kg/day during the acute phase of the illness. Platelet aggregations induced by adenosinedi‐phosphate (ADP), epinephrine and collagen were inhibited by aspirin doses of 1–2 and 5–10 mg/kg/day, when compared with those of controls (p < 0.05). Platelet synthesis of thromboxane B2 (TXB2) under doses of 1–2 and 5–10 mg/kg/day was 0.57 ± 0.07 and 0.72 ± 0.09 ng/ml platelet‐rich plasma (PRP) /105 platelets, respectively (p > 0.1). These values were significantly lower than those of the control group (22.88± 3.42 ng/ml PRP/105 platelets) (p < 0.05). No differences were found in platelet aggregation and TXB2 productivity between the two aspirin doses. Levels of 6 keto‐prostaglandin F1α (6k‐PGF1α) in platelet‐poor plasma (PPP) did not differ significantly in these 3 sets of data. The results indicate that long‐term administration of low dose aspirin (1–2 mg/kg/day) inhibits platelet aggregation by inhibiting synthesis of thromboxane A2 (TXA2), without interfering with prostacyclin production probably in the endothelium of blood vessels.