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  • Caused by deposition of monosodium urate crystals due to longstanding hyperuricemia.

  • Usually begins as an intermittent, acute mono- or oligoarthritis, especially of the first metatarsophalangeal joint.

  • Flares typically become more frequent and involve more joints over time, in the absence of treatment.

  • Diagnosed by evaluating joint fluid for monosodium urate crystals using polarized light microscopy.

  • Extra-articular manifestations include subcutaneous tophi and renal stones.

  • Flares of arthritis respond to anti-inflammatory drugs such as nonsteroidal anti-inflammatory drugs, colchicine, or glucocorticoids.

General Considerations

Gout affects approximately 4% (9.2 million) of the US general population. Hyperuricemia affects an even greater proportion of the US general population, at about 20% (46 million). Both the prevalence and incidence of gout and hyperuricemia have increased in recent decades in the United States and other Western nations, mirroring trends in the rise of obesity and metabolic syndrome. The prevalence of gout increases with age and is higher among men than women. Gout among premenopausal women is particularly rare because of the uricosuric effect of estrogen.

Chronic hyperuricemia is a prerequisite condition for gout. Sustained serum urate concentrations greater than 6.8 mg/dL favor the precipitation of monosodium urate crystals in and around joints, leading to gout. The likelihood of developing symptomatic gout and the age of onset correlate with the duration and magnitude of hyperuricemia. In one study, persons with serum urate levels between 7.0 and 8.0 mL/dL had a 5-year cumulative incidence of gouty arthritis of 3%, compared to 22% among those with serum urate levels greater than 9.0 mL/dL. However, hyperuricemia alone is not sufficient for the development of gout. It appears that clinical gout develops in fewer than one in four hyperuricemic persons at any point.

Hyperuricemia can result from increased urate production, decreased urate excretion, or a combination of the two mechanisms (Table 40–1). Urate is a by-product of the purine degradation pathway, but overproduction of urate through this mechanism is usually a minor contributor to elevations of serum urate concentrations. 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 urate in their urine during a 24-hour period.

Table 40–1.Classification of hyperuricemia.

Underexcretion of urate is the primary ...

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