Gout refers to disease that occurs in response to the presence of monosodium urate (MSU) crystals in joints, bones, and soft tissues. It may result in an acute arthritis and a chronic arthropathy (tophaceous gout).
Hyperuricemia (urate concentration exceeding the solubility of urate in extracellular fluid) is a common and necessary pathogenetic factor in the development of gout, but it is insufficient to explain clinical expression of either self-limited attacks of acute gouty arthritis or chronic gouty arthropathy. These clinical manifestations also require MSU crystal formation and deposition in tissues and acute and/or chronic inflammatory responses to the presence of such crystals.
The pathophysiologic mechanisms of MSU crystal deposition, acute crystal-induced inflammation, and chronic destructive lesions of joints and bones associated with collections of MSU crystals (tophi) will be reviewed here. The clinical features, diagnosis, and treatment of acute gout; the prevention of recurrent gout; asymptomatic hyperuricemia; and associated renal diseases are discussed elsewhere. (See "Clinical manifestations and diagnosis of gout" and "Treatment of acute gout" and "Prevention of recurrent gout" and "Asymptomatic hyperuricemia" and "Uric acid nephrolithiasis" and "Uric acid renal diseases".)
A number of complex interacting processes are responsible for the pathophysiology of gouty arthritis. These include:
●Metabolic, genetic, and other factors that result in hyperuricemia (see 'Hyperuricemia and gout' below)