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  • Caused by deposition of uric acid crystals and usually associated with hyperuricemia.
  • Usually begins as an intermittent, acute monoarthritis, especially of the first metatarsophalangeal joint.
  • Over time, attacks become more frequent, less intense, and involve more joints.
  • Diagnosed by demonstrating uric acid crystals in joint fluid.
  • Extra-articular manifestations include tophi and renal stones.
  • Arthritis responds to nonsteroidal anti-inflammatory drugs or colchicine.

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The underlying basis for gout is an increased total body urate pool. This is generally manifested as hyperuricemia, which is defined as a serum urate concentration more than 6.8 mg/dL. The concentration of 6.8mg/dL is important because fluids with urate content greater than that are supersaturated with urate, a condition that favors urate crystal precipitation.

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At least 10% of asymptomatic Americans manifest hyperuricemia on at least one occasion during adulthood. Hyperuricemia may be even more common in Europe and in countries in the Far East.

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The likelihood of developing symptomatic gout and the age at which that occurs correlates with the duration and magnitude of hyperuricemia. In one study, persons with urate levels between 7.0 and 8.0 mL/dL had a cumulative incidence of gouty arthritis of 3%, while those with urate levels >9.0 mL/dL had a 5-year cumulative incidence of 22%. However, hyperuricemia alone is not sufficient for the diagnosis of gout, and asymptomatic hyperuricemia in the absence of gout is not a disease. It appears that clinical gout develops in fewer than 1 in 4 hyperuricemic persons at any point.

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Gout presents predominantly in men with a peak age of onset in the fifth decade. The incidence of gout in women approaches that of men only after they have reached age 65 years. The onset of disease in men prior to adulthood or in women before menopause is quite rare and is almost always due to an inborn error of metabolism or congenital condition. The prevalence of self-reported gout is estimated to be 13.6 per 1000 men and 6.4 per 1000 women.

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Hyperuricemia can result from increased urate production, decreased uric acid excretion by the kidneys, or a combination of the two mechanisms. Less than 5% of patients with gout are hyperuricemic because of urate overproduction. These persons can be recognized because they excrete more than 800 mg of uric acid in their urine during a 24-hour period. Those who excrete less uric acid than 800 mg are hyperuricemic because of impaired renal excretion. Defining individuals as “over-producers” or “underexcreters” is helpful in predicting whether the hyperuricemia is associated with a variety of acquired or genetic disorders (Table 44–1) and may be useful in some cases in determining the most appropriate treatment.

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Table 44–1. Classification of Hyperuricemia.

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