Abstract
Gout is defined as the deposition of urate crystals, clinically expressed by acute arthritis or tophi. It is well accepted that hyperuricemia, or at least an abnormally high total uric acid pool, is a critical precursor to the deposition phenomenon and that urate crystals, once precipitated in the joint, give rise to an intense phlogistic reaction. The mechanism of urate deposition remains enigmatic and controversial. Garrod (1876) was one of the first to recognize that gouty arthritis was caused by the precipitation of sodium urate crystals in the joints or neighboring tissues:
“Gouty inflammation is invariably attended with the deposition of urate of soda... This fact I wish to impress forcibly upon my readers because in the constancy of such deposition lies the clue that has long been wanting; the occurrence of the deposit is at once pathognomonic and separates gout from every other disease which at first sight might appear allied to it.”
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Katz, W.A. (1978). Role of Proteoglycans in the Development of Gouty Arthritis. In: Kelley, W.N., Weiner, I.M. (eds) Uric Acid. Handbook of Experimental Pharmacology, vol 51. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66867-8_14
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DOI: https://doi.org/10.1007/978-3-642-66867-8_14
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