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

  1. Explain the pathophysiologic mechanisms underlying gout and hyperuricemia.

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

  3. Assess the signs and symptoms of an acute gout attack.

  4. List the treatment goals for a patient with gout.

  5. Develop a pharmacotherapeutic plan for a patient with acute gouty arthritis that includes individualized drug selection and monitoring for efficacy and safety.

  6. Identify patients for whom prophylactic urate-lowering therapy for gout and hyperuricemia is warranted.

  7. Formulate appropriate educational information for a patient on lifestyle modifications to help prevent gouty arthritis attacks.

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


Image not available. Gout is an inflammatory condition of the arthritis-type that results from deposition of uric acid crystals in joint spaces or surrounding tissues, leading to an inflammatory reaction that causes intense pain, erythema, and joint swelling. It is associated with hyperuricemia, defined as a SUA level of 6.8 mg/dL (404 μmol/L) or greater, but not all patients with hyperuricemia demonstrate symptoms.1 Four organizations publish guidelines that provide recommendations for the diagnosis and/or management of gout.2-9 There is much similarity in the recommendations, and this chapter focuses primarily on the consensus expert panel recommendations of the American College of Rheumatology (ACR).5,6 However, the American College of Physicians (ACP) guideline includes updated clinical trial data and some distinct and controversial differences.8-10


Gout is the most common inflammatory arthritis in men, with a male:female incidence of about 4:1; it affects over 3% of US adults.1,11 The National Health and Nutrition Examination Survey (NHANES) 2007–2008 estimated the prevalence of gout among US adults to be 8.3 million.12 The incidence increases with age and is rising in part due to a larger number of patients with risk factors for gout.13 There is also a significant economic cost and humanistic burden associated with gout, which increases with worsening disease severity.14

In order to lessen the incidence and disease severity of gout, it is important to be mindful of risk factors and pharmacologic agents that can influence the disease. Dietary risk factors involve ingestion of animal purines, fructose, and alcohol (especially beer). Patients experiencing frequent attacks and those with poorly controlled advanced disease should be educated to avoid sweetbreads (organ meats such as thymus and pancreas), liver, and kidney meat; high-fructose corn syrup; and alcohol use.5 Other risk factors include male sex, obesity, hypertension, dyslipidemia, and the metabolic syndrome.11 Gout also occurs frequently in patients with type 2 diabetes mellitus, chronic kidney disease (CKD), and coronary artery disease.15 Prospective data indicate that gout is an independent risk factor for coronary heart disease,16 and the cardiovascular impact ...

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