الفهرس 
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Abstract
gout is a common arthritis caused by deposition of monosodium urate crystals within joints after chronic hyperuricaemia. Gout passes into four stages: asymptomatic hyperuricemia, acute gouty arthritis, intercritical (or interval) gout and chronic tophaceous gout.
The aims of treatment of gout are to alleviate the pain and inflammation associated with acute attack, prevent future attack and decrease uric acid level.
The acute gouty attack may be successfully terminated by any of several drugs. The choice in most situations is among colchicine, a NSAID, a corticosteroid preparation, or ACTH. The timing of therapy initiation is more important than the choice of drug. With any of these agents, the sooner the drug is started, the more rapidly a complete response will be attained.
Guidelines of management of gout recommend that serum urate concentration should be maintained below 6.0 mg/dL to promote crystal dissolution leading to prevention of recurrent gouty attack.
Urate lowering drugs (ULDs), such as allopurinol, benzbromarone, sulfinpyrazone and probencid, were developed in the last century. The two later drugs suffer from lack of efficacy in patients with mild to moderate renal function impairment. Benzbromarone may be considered the most potent ULD ever used in clinical practice. Although rare but severe liver toxicity limits its use.