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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 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 serum uric acid (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.2–8 There is much similarity in the recommendations, and this chapter focuses primarily on the American College of Rheumatology (ACR) guideline for the management of gout.5 However, the American College of Physicians (ACP) guideline includes some distinct and controversial differences.7,8


The National Health and Nutrition Examination Survey (NHANES) 2019 estimates that gout affected about 9.2 million adults (3.9%) in 2015–2016, with gout occurring two to six times more frequently in men than women.9,10 The incidence increases due to unhealthy dietary habits, lack of exercise, and obesity.10 There is also a significant economic cost and humanistic burden associated with gout that increases with worsening disease severity.11

Dietary risk factors for developing gout include ingestion of purines, fructose, and alcohol. 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 and obesity.12 Trauma and surgery may also trigger acute gout attacks by increasing SUA.13 Uric acid excretion is reduced in patients with chronic kidney disease (CKD), putting them at risk for hyperuricemia. Gout involves multiple organ systems and is associated with cardiovascular disease (CVD), type 2 diabetes mellitus (T2DM), CKD, and metabolic syndrome. There is an association between high SUA and endothelial dysfunction, which can promote atherosclerosis.14 Prospective data indicate that gout is an independent risk factor for coronary heart disease,15 and the cardiovascular impact of urate-lowering therapy continues to be ...

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