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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.
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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
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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
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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.
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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
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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
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