INTRODUCTION

Gout (monosodium urate crystal deposition disease) is characterized biochemically by extracellular fluid urate saturation. The clinical manifestations include one or more of the following:

• Recurrent attacks of acute inflammatory arthritis
• Chronic arthropathy
• Accumulation of urate crystals in the form of tophaceous deposits
• Uric acid nephrolithiasis
• A chronic nephropathy that in gouty patients is most often due to comorbid states

All patients with gout have hyperuricemia (saturation of serum for urate) at some point in their disease. (See "Uric acid balance".) However, most hyperuricemic individuals never experience a clinical event resulting from urate crystal deposition. Thus, the diagnosis of gout focuses on the fundamental pathophysiologic events defining the clinical state: tissue deposition of urate crystals and the accompanying inflammatory and potentially destructive consequences. Within this framework, hyperuricemia is viewed as a necessary but not sufficient precondition for the development of urate crystal deposition disease and is to be distinguished from gout, the clinical syndrome.

The clinical manifestations and diagnosis of gout will be reviewed here. Issues related to asymptomatic hyperuricemia, the treatment of acute gout, and prevention of recurrent gout are discussed separately. (See "Asymptomatic hyperuricemia" and "Treatment of acute gout" and "Prevention of recurrent gout".)

HISTORICAL PERSPECTIVE

Descriptions of the epidemiology, clinical features, and natural history of gout evolved over more than two millennia of observations and study. The last half of the twentieth century produced confirmation that the pathogenesis of gout involves urate crystal deposition. Pivotal in this progress was the introduction of polarized light microscopy into clinical practice, providing urate crystal identification in synovial fluid as the means to achieve rapid and definitive diagnosis and to resolve the formerly ambiguous relationship between hyperuricemia and gout [1].