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Pathophysiology of gouty arthritis


Gout refers to disease that occurs in response to the presence of crystals of monosodium urate (MSU) in joints, bones, and soft tissues. Both acute arthritis and chronic arthropathy (tophaceous gout) are considered under the rubric of gout.

The mechanisms of crystal deposition, crystal-induced inflammation, and destructive lesions of joints and bones associated with macroscopic collections of MSU (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".)


Hyperuricemia can be caused by impaired renal excretion, overproduction of uric acid, and/or by overconsumption of purine-rich foods that are metabolized to urate. Detailed discussions of the causes of hyperuricemia and of the normal mechanisms of urate handling are presented separately. (See "Asymptomatic hyperuricemia" and "Uric acid balance".)

A causative relationship among hyperuricemia, deposition of urate crystals, and gout was proposed by Garrod in 1859 and later [1]. However, injection of solutions of uric acid into blood or joints failed to reproduce the clinical features of the disease, casting doubt on the association. Freudweiler noted in 1899 that injection of tophaceous material caused inflammation [2,3].

The identification of monosodium urate (MSU) crystals within phagocytes when synovial fluid was examined using compensated polarized microscopy was an important advance in understanding the pathogenesis of gout [4]. This was followed by the observation that injection of MSU crystals into normal joints produced acute gout attacks, reestablishing the connection between urate crystals and gout [5,6]. The outline of the pathophysiology of gout is as follows: a period of hyperuricemia leads to MSU crystal deposition, reaction to which can result in acute and/or chronic inflammation.


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Literature review current through: Mar 2014. | This topic last updated: Jan 22, 2013.
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