Gout results from the precipitation of urate crystals in the tissues and the subsequent inflammatory response. Acute gout usually causes an exquisitely painful distal monoarthritis, but it also can cause joint destruction, subcutaneous deposits (tophi), and renal calculi and damage. Gout affects -0.5-1% of the population of Western countries.
The pathophysiology of gout is understood poorly. While a prerequisite, hyperuricemia does not inevitably lead to gout. Uric acid, the end product of purine metabolism, is relatively insoluble compared to its hypoxanthine and xanthine precursors, and normal serum urate levels approach the limit of solubility. In most patients with gout, hyperuricemia arises from underexcretion rather than overproduction of urate. Urate tends to crystallize in colder or more acidic conditions. Neutrophils ingesting urate crystals secrete inflammatory mediators that lower the local pH and lead to further urate precipitation.
The aims of treatment are to decrease the symptoms of an acute attack, decrease the risk of recurrent attacks, and lower serum urate levels. Therapy of gout focuses on colchicine, allopurinol, and the uricosuric agents—probenecid, sulfinpyrazone, and benzbromarone.
Several tNSAIDs reportedly are effective in the treatment of acute gout. The specific COX-2 inhibitor etoricoxib has been shown to be effective in gout. When effective, NSAIDs should be given at relatively high doses for 3-4 days and then tapered for a total of 7-10 days. Indomethacin, naproxen, sulindac, and celecoxib all have been found to be effective, although the first three are the only NSAIDs that are FDA-approved for the treatment of gout. Aspirin is not used because it can inhibit urate excretion at low doses, and through its uricosuric actions increase the risk of renal calculi at higher doses. In addition, aspirin can inhibit the actions of uricosuric agents. Likewise, apazone should not be used in acute gout because of the concern that its uricosuric effects may promote nephrolithiasis.
Recurrent attacks of gout can be prevented with the use of colchicine (e.g., 0.6 mg daily or on alternate days). Indomethacin (25 mg/day) also has been used. These agents are used early in the course of uricosuric therapy when mobilization of urate is associated with a temporary increase in the risk of acute gouty arthritis.
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