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Pathophysiology of gouty arthritis

Michael A Becker, MD
Section Editor
Nicola Dalbeth, MBChB, MD, FRACP
Deputy Editor
Paul L Romain, MD


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: Pharmacologic urate-lowering therapy and treatment of tophi" 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)

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Literature review current through: Nov 2017. | This topic last updated: Feb 08, 2017.
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