Platelets and vascular disease in gout

Abstract

Vascular complications appear to have more than a coincidental occurrence in primary gout. The presence in gout of hypertension, renal disease, diabetes mellitus, and hyperlipidemia (accepted factors of risk for arterial lesions) may influence onset of atheromas. However, additional data are presented from patients with primary gout, and secondary hyperuricemia, to support the thesis that an elevated serum uric acid level is an increased risk for arterial disease. New data are presented that hyperactive platelet populations occur in at least 51 % of the patients with primary gout. The activation status of the platelet population may relate to the serum uric acid level. It is proposed that the platelet may be a prime reactant linking hyperuricemia (a documented thrombotic risk factor) with the greater incidence of arterial disease in primary gout. Uricosuric drugs can be separated into two classes: those which produce only an indirect inhibitory potential on platelet surface activation by lowering the level of serum uric acid and those which, in addition, possess a direct inhibitory action on platelet surface activation. Halofenate and allopurinol were found to be potent direct inhibitors of platelet activation in both ex vivo and in vivo studies.