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Gout: therapy and prevention

Gout is a common ailment with increasing prevalence in the United States. Currently, its prevalence is approximately 1% in both sexes and in all age groups. Its incidence among American men over the age of 30 has been reported to

Gout occurs when sodium urate crystals are deposited in the joints, soft tissue, bursae, and tendons. It takes a variety of forms: acute gout is an acute inflammatory arthritis; tophaceous gout, an accumulation of crystalline aggregates; and gouty nephropathy, a type of

MODIFIABLE RISK FACTORS Hypemricemia, defined as a serum urate concentration >7.0 mg/dL, is a primary risk factor for the development of gout, with studies showing a significant dose-response relationship.2 Serum urate concentrations are gender and age dependent: the prevalence of is higher in men than in women and increases with age in both sexes. Urate concentrations rise in

In addition, serum uric acid levels may vary with body weight, cholesterol level, alcohol consumption, lead exposure, and use of diuretics, particularly thiazide diuretics. Diuretics inhibit clearance of uric acid by enhancing its tubular reabsorp-tion.3 Obesity has

Thus, potentially modifiable risk factors for the development in patients with asymptomatic hyper-uricemia include obesity, especially when weight gain takes place during young adulthood; hypertension; hy-pertriglyceridemia; consumption of alcohol, particularly "home brew" distilled in lead-lined containers; and other

Acute gouty arthritis

Acute gout usually manifests itself as a monoarticular acute arthritis, most commonly of the metatarsophatangeal joint, although it may also occur in the ankle, tarsal area, and knee. Involvement of the joints of the upper extremity is less common.

The pain of an acute attack is abrupt in onset and typically occurs during the night, waking the patient from sleep. The affected joint becomes warm, red, and tender. The overlying skin may desquamate during resolution of the inflammation.

The initial attack generally subsides in 3 to 10 days without treatment, usually followed by an asymptomatic intercritical period between acute attacks. Some may never have another attack, but most patients have another within 2 years. If they are untreated

Preliminary criteria for recognition of acute gout

Urate crystals identified in synovial fluid, or

Urate crystals identified in tophi, or Any six of the following:

More than one attack of acute arthritis

Maximal inflammation reached within 1 day

Attack of monoarthritis

Observed joint redness

Painful or swollen first metatarsal phalangeal joint

Unilateral first metatarsal phalangeal joint involvement

Unilateral tarsal joint involvement

Suspected tophi

Hyperuricemia

X-ray changes consistent with asymmetric swelling

X-ray changes consistent with subcortical cysts without erosions

Negative joint fluid culture for bacteria during acute attack of arthritis

Tophaceous gout

Characteristic tophaceous deposits of uric acid crystals may accumulate in the soft tissue, synovial membrane, cartilage, and tendons of untreated patients approximately

10 years or more after the initial acute attack.

The most common site for the deposition of tophi is the helix of the ear, but they may also occur in the olecranon bursa, the ulnar surface of the forearm, the hands and feet, and the

The initial radiographic changes are nonspecific, showing soft-tissue swelling. Eventually, the tophi may cause erosions that appear on x-ray as '~3unched-out" lesions in the margins of the joint. Caldfication of the tophi is common and is also observable on x-ray.

The gold standard for