Gout is a familial metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium urate in joints and cartilage. Formation of uric acid calculi in the kidneys may also occur. Gout is usually associated with high serum levels of uric acid, a poorly soluble substance that is the major end product of purine metabolism.
The treatment of gout is aimed at relieving the acute gouty attack and preventing recurrent gouty episodes and urate lithiasis. Urate crystals are initially phagocytosed by synoviocytes, which then release prostaglandins, lysosomal enzymes, and interleukin-1. Attracted by these chemotactic mediators, polymorphonuclear leukocytes migrate into the joint space and amplify the ongoing inflammatory process. In the later phases of the attack, increased numbers of mononuclear phagocytes (macrophages) appear, ingest the urate crystals, and release more inflammatory mediators.
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