Gout: Diagnosis and Treatment  

Diagnosis

Signs and symptoms consistent with acute monoarticular arthritis suggest gout. However, definitive diagnosis requires demonstration of urate crystals in joint or tophus aspirate.

Elevated serum uric acid level is present in most cases.

Synovial fluid aspirate reveals negatively birefringent, needle–shaped crystals, or tophi aspirate reveals urate crystals.

A 24–hour urine uric acid collection may help distinguish overproduction from underexcretion (>800 mg of uric acid/24 hours indicates overproduction).

Early in the disease, x–rays of the joints may appear normal. As the disease progresses, punched–out erosions with a rim of cortical bone may appear.

Treatment

Treatment of asymptomatic hyperuricemia is usually not indicated, aside from the dietary adjustments noted below in Nutritional Considerations. Anti–inflammatory agents for acute attacks and prophylaxis for patients with high risks of recurrence are the cornerstones of therapy.

The treatment of choice for acute attacks in otherwise healthy adults is bed rest and nonsteroidal anti–inflammatory drugs (NSAIDs); indomethacin is often used.

Corticosteroids are reserved for severe disease or in patients who cannot take NSAIDs (eg, patients with renal failure). Monoarticular disease may be treated with intra–articular steroid administration. Polyarticular gout may be treated with oral or IV steroids.

Due to the high incidence of side effects, colchicine is now used less commonly than in the past.

Prophylactic medications to reduce the risk of further attacks include allopurinol, which inhibits xanthine oxidase and decreases urate production, and probenicid, which decreases renal uric acid reabsorption.

Surgery is reserved for severe cases, including joint deformities, intractable pain, and nerve compression due to tophi.