Gout

A recurrent acute or chronic arthritis of peripheral joints that results from deposition in and about the joints and tendons of monosodium urate crystals from supersaturated hyperuricemic body fluids.

Gout most often manifests in middle-aged men and postmenopausal women. Gout correlates with hyperuricemia (usually serum urate levels > 7 mg/dL [> 420 µmol/L]), which represents an imbalance between endogenous urate production and renal urate excretion. Most cases of primary and secondary hyperuricemia are characterized by a defect in renal handling of urate. Hyperuricemia may be exacerbated by drugs commonly used by elderly patients (eg, thiazide diuretics and salicylates, even in small doses).

Symptoms, Signs, and Diagnosis

Acute gouty arthritis is characterized by acute onset of inflammatory arthritis, possibly after trauma, illness, or surgery. The metatarsophalangeal joint of the great toe is the typical site of acute pain (podagra). Monarticular or polyarticular pain may also affect the ankle, knee, wrist, elbow, small joints of the hands or feet, or bursae (especially the bursa of olecranon).

Fever (up to 39° C [102.2° F]) often develops. Tenderness is usually so exquisite that the patient cannot move the affected joint or tolerate the weight of bedclothes. Inflammation often extends beyond the joint, suggesting cellulitis in some cases. A history of recurrent acute episodes of arthritis, especially involving the great toe, suggests gout.

Acute gouty arthritis may be accompanied by blood leukocytosis and an elevated ESR. An elevated serum urate level supports the diagnosis but is neither specific nor sensitive. The definitive finding is urate crystals in synovial fluid. If possible, synovial fluid should be analyzed in acute monarticular or oligoarticular arthritis. Microcrystalline disease is important to differentiate from infection. In acute gouty arthritis, the synovial fluid shows typical inflammatory changes with a WBC count of 5,000 to 50,000/µL. In 90% of cases, urate crystals can be seen free in the fluid or engulfed by phagocytes. When viewed with a polarizing microscope, they are negatively birefringent.

Chronic gouty arthritis may cause morning stiffness and achy joints, mimicking rheumatoid arthritis and other chronic polyarticular arthritides. It occurs primarily in patients who have tophaceous gout. Such patients often have x-ray evidence of monosodium urate deposits (tophi) in soft tissue or bone adjacent to the joints. The number of tophi increases with the severity of hyperuricemia. Tophi are commonly found in bursae, the articular cartilage, and bone. Tophi may be confused with rheumatoid nodules when they appear in the bursa of olecranon or over the extensor surface of the forearm.

Treatment

Acute gouty arthritis, if untreated, resolves in a few days to weeks. Treatment begins with an NSAID at the usual dosage (see Table 51-1). Relief occurs in 24 hours, and symptoms usually resolve in 3 days, after which the NSAID can be discontinued. If taken at the first sign of a gouty attack, colchicine 0.5 to 1.0 mg daily or bid may prevent the full-blown attack. Alternatively, colchicine relieves acute symptoms when given 1 to 2 mg diluted in 0.9% sodium chloride and injected IV over 3 to 5 minutes to avoid extravasation. However, severe local and systemic reactions may occur. Oral colchicine 0.5 mg q 2 h following an initial 1-mg dose also may be given until relief is obtained or gastrointestinal toxicity supervenes. However, because almost all patients must take colchicine until gastrointestinal toxicity occurs, this treatment is used less frequently than in the past. Systemic corticosteroids (prednisone 40 mg/day or equivalent tapered over 5 to 10 days) are effective in treating acute gout, particularly if polyarticular.

Acute gout of the large joints can be treated by withdrawing synovial fluid and injecting a long-lasting corticosteroid (eg, triamcinolone 20 to 40 mg). This treatment is especially effective in patients who cannot take oral drugs nor tolerate NSAIDs or colchicine.

Uricosuric drugs and allopurinol should be avoided during the acute attack. Long-term colchicine 0.5 mg bid may lower the incidence of recurrent acute gouty arthritis.

Chronic gouty arthritis may require measures to lower serum urate levels. Such measures may be useful if tophi or renal calculi are present or if long-term colchicine administration does not control acute attacks.

Allopurinol blocks the metabolic pathway of urate production, inhibiting xanthine oxidase. Because allopurinol does not produce its effect through the kidney and reduces the renal urate load, it is indicated in patients with renal calculi. The initial dosage of 100 mg bid may be increased gradually to 600 mg/day if necessary.

Alternatives to allopurinol are the uricosuric drugs. Probenecid (maintenance dosage ranges from 500 mg to 1.5 g po q 12 h) or sulfinpyrazone (100 to 400 mg/day po bid in divided doses) effectively keeps serum urate levels <= 6.5 mg/dL (<= 390 µmol/L).