Enhancement of platelet function has been reported as one of the factors of vascular disorders in patients with gout. Thus, we studied (1) platelet function in patients with gout but no complications; (2) PRP additive tests in healthy subjects and (3)therapeutic effects of antiplatelets in patients with gout and hyperuricemia. In study 1, no significant difference was seen between control and patients with gout in the ADP aggregation, PF4 or β-TG, but collagen aggregation was significantly higher in the gouty patients. In study 2, platelet aggregation was measured by adding uric acids, allopurinol, oxipurinol, sulfinpyrazone, ticlopidine and aspirin to PRP in healthy subject. As a result, aggregation of ADP and collagen was significantly inhibited by aspirin, but no platelet function were significantly inhibited by other drugs. In study 3, the patienth with gout and hyperuricemia were divided into a non - treated serum uric acid group and a treated group before platelet function was measured using ticlopidine. No significant changes were noted in the TXB2, PF4 or β-TG levels in either group, but platelet aggregation was markedly decreased in both groups after in the presence of ticlopidine. Our findings revealed a higher enhancement of platelet function in the patients with gout and hyperuricemia. Nonetheless, this enhancement of platelet functions was not considerd to be associated with serum uric acid. On the other hand, the platelet aggregation in the patients with gout and hyperuricemia was significantly inhibited by ticlopidine.
