Chapter 36

A systematic search of the medical literature was performed on July 14, 2005, and again on February 16, 2007. The search, limited to human subjects and English language journals, included MEDLINER® (1999 to February 2007), the Cochrane Database of Systemic Reviews, ACP Journal Club, and Database of Abstracts of Reviews of Effectiveness. Search terms included gout and gouty arthritis. Selected review articles and clinical trials were examined. Pertinent references of the identified articles were also examined. Additionally, the American College of Rheumatology website, www.rheumatology.org was reviewed for information.

Gout is a disease characterized by deposition of monosodium urate crystals in the joints and tendons. It is the most common form of inflammatory arthritis in men more than 40 years of age.1 Historically, gout was limited to affluent members of society; however, the incidence and prevalence of gout continue to increase in all social classes, probably because of growing waistlines, increased longevity, and changing dietary patterns.2,3

Men are affected with gout approximately 7 to 9 times more commonly than women, except in older age groups where approximately half of newly diagnosed cases will be in women.3,4 The incidence of gout increases with age, with annual incidence ranging from one per 1000 for men aged 40 to 44 years to 1.8 per 1000 for those aged 55 to 64 years.5 The lowest rates of gout are observed in younger women, in which there are approximately 0.8 cases per 10000 patient-years.6

Gout results from physiologic disturbances of urate metabolism which lead to hyperuricemia. Normal uric acid levels are near the limits of urate solubility because of a delicate balance that exists between the amount of urate produced and excreted.7 Hyperuricemia is defined as a serum urate level of >7 mg/dL in men or >6 mg/dL in women.4 In the hyperuricemic state, uric acid salts form crystals and are deposited in and around the joints and soft tissue. Hyperuricemia can result in four distinct clinical stages: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout (intervals between attacks), and chronic tophaceous gout.

Serum urate levels are the single most important risk factor for the development of gout; however, hyperuricemia and gout are not always concurrently present, and most patients with hyperuricemia remain asymptomatic.4 The risk of gout increases in a parallel manner with serum urate levels. The 5-year cumulative risk of gout in patients with serum urate <7 mg/dL is 0.6%, compared to a risk of 30.5% with urate levels >10 mg/dL.8

Two distinct mechanisms can lead to hyperuricemia: decreased uric acid clearance or overproduction of uric acid. Several conditions (Table 36-1) are associated with either mechanism.5,9,10 The vast majority (80–90%) of patients with gout have a relative deficit in the renal excretion of uric acid for an unknown reason (primary idiopathic hyperuricemia).4

Table 36-1. Causes of Hyperuricemia

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