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from Part VIII - Major Human Diseases Past and Present
Published online by Cambridge University Press: 28 March 2008
Gout is a chronic, intermittently symptomatic disease. It is manifested primarily by small numbers of acutely painful swollen joints that result from an inflammatory reaction to the precipitation of crystals of monosodium urate.
Etiology
The predisposing metabolic factor for primary gout is an abnormally high or rapidly changing concentration of uric acid in the blood. Hyperuricemia may result from an accelerated synthesis of uric acid, or decreased excretory capacity for uric acid in otherwise normal kidneys as a result of unidentified but probably heritable causes. Hyperuricemia leading to secondary gout occurs particularly (1) in diseases of the blood-forming tissues that increase the availability of precursors of uric acid; (2) in kidney failure, which limits the excretion of uric acid; or (3) as a result of medications that either accelerate the breakdown of purine-rich cells (e.g., antineoplastic drugs) or interfere with the renal excretory mechanism (e.g., some diuretics). Dissolved in the serum, uric acid is harmless. However, because of unidentified local circumstances it may leak from capillaries and crystallize. The crystals of monosodium urate elicit the inflammatory reaction, which is the gouty attack, and the microscopic identification of the crystals in synovial fluid confirms the diagnosis. Why this inflammation occurs predominantly in joints, and why much more commonly in some joints (such as those of the feet or in the knee) than in others (such as the hip or those of the vertebral column) are unexplained characteristics.
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