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Upon completion of the chapter, the reader will be able to:

  1. Recognize major risk factors for developing gout in a given person.

  2. Develop a pharmacotherapeutic plan for a patient with acute gouty arthritis or uric acid nephropathy that includes individualized drug selection and monitoring for efficacy and safety.

  3. Identify patients for whom maintenance therapy for gout and hyperuricemia is warranted.

  4. Select an appropriate drug to reduce serum uric acid (SUA) levels in patients with gout, and outline a plan for monitoring efficacy and toxicity.

  5. Educate patients on appropriate lifestyle modifications to help prevent gouty arthritis attacks.

  6. Identify patients at risk for tumor lysis syndrome and develop a rational plan to prevent this syndrome.




  • Image not available. Gout results from deposition of uric acid crystals in joint spaces, leading to an inflammatory reaction that causes intense pain, erythema, and joint swelling.

  • Image not available. Some drugs can cause hyperuricemia and gout, such as thiazide diuretics, niacin, pyrazinamide, cyclosporine, and, occasionally, low-dose aspirin.

  • Image not available. Long-term consequences of gout and hyperuricemia include joint destruction, tophi, and nephrolithiasis.

  • Image not available. Treatment of gout involves: (a) acute relief of a gouty arthritis attack, and (b) in some patients, long-term maintenance treatment to prevent future attacks.

  • Image not available. Nonsteroidal anti-inflammatory drugs, colchicine, or corticosteroids are used for acute attacks. Selection depends on several patient factors, especially renal function.

  • Image not available. Asymptomatic hyperuricemia usually does not require treatment.

  • Image not available. Patients with recurrent attacks, evidence of tophi or joint destruction, or uric acid nephrolithiasis are candidates for maintenance therapy with allopurinol, febuxostat, probenecid, or pegloticase to lower SUA levels.

  • Image not available. Tumor lysis syndrome (TLS) is a metabolic disorder caused by rapid cell destruction (usually during chemotherapy treatment for cancer) and is associated with several electrolyte disturbances, notably hyperuricemia.




Gout is the most common inflammatory arthritis in the United States and western Europe.1 The annual incidence is approximately 62 cases per 100,000 persons in the United States.2 The incidence increases with age and appears to be rising, probably because of a larger number of patients with risk factors for gout.3




Gout is caused by an abnormality in uric acid metabolism. Uric acid is a waste product of the breakdown of purines contained in the DNA of degraded body cells and dietary protein. Uric acid is water soluble and excreted primarily by the kidneys, although some is broken down by colonic bacteria and excreted via the GI tract.4,5


The solubility of uric acid depends on concentration and temperature. At high serum concentrations, lower body temperature causes the precipitation of monosodium urate (MSU) crystals. Collections of these crystals (called microtophi) can form in joint spaces in the distal extremities.


Image not available. Gout results from deposition of uric acid crystals in joint spaces, leading to an inflammatory reaction that causes intense pain, erythema, and joint swelling. Free ...

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