Clinical Variability of the Gouty Diathesis

Abstract

Gouty arthritis with or without tophaceous deposits and uric acid nephrolithiasis are the clinical manifestations of hyperuricemia known collectively as the gouty diathesis. While the pathogenesis of hyperuricemia may involve either a primary (genetic) or secondary abnormality of uric acid metabolism, the incidence and severity of the clinical manifestations have been related to two other factors, the magnitude and the duration of hyperuricemia¹ However, recent investigations into the pathogenesis of gouty arthritis have demonstrated that both soluble and cellular mediators of the inflammatory process are important in the pathogenesis of the articular inflammation associated with monosodium urate (MSU) crystals². The relationship of these factors to those previously shown to be of importance in the pathogenesis of gouty arthritis has not been clarified. However, they introduce new variables which potentially are of significance in determining the eventual clinical manifestations of hyperuricemia. This report concerns an 83 year-old patient who noted the gradual appearance of multiple tophaceous deposits over a period of at least 20 years, yet had never experienced an attack of gouty arthritis.