Upon completion of the chapter, the reader will be able to:
Explain the pathophysiologic mechanisms underlying gout and hyperuricemia.
Recognize major risk factors for developing gout in a given person.
Assess the signs and symptoms of an acute gout attack.
List the treatment goals for a patient with gout.
Develop a pharmacotherapeutic plan for a patient with acute gouty arthritis that includes individualized drug selection and monitoring for efficacy and safety.
Identify patients for whom prophylactic urate lowering therapy for gout and hyperuricemia is warranted.
Select an appropriate drug to reduce serum uric acid (SUA) levels in patients with gout, and outline a plan for monitoring efficacy and toxicity.
Formulate appropriate educational information for a patient on lifestyle modifications to help prevent gouty arthritis attacks.
Gout is an inflammatory condition of the arthritis-type that results from deposition of uric acid crystals in joint spaces, 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 There are presently three published guidelines that provide clinical recommendations for management of patients with gout.2,3,4,5,6,7 This chapter will focus primarily on recommendations of the American College of Rheumatology (ACR).5,6,7
EPIDEMIOLOGY AND ETIOLOGY
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.1,8 The National Health and Nutrition Examination Survey (NHANES) 2007–2008 estimated the prevalence of gout among US adults to be 8.3 million.9 Furthermore, the annual US incidence is approximately 62 cases per 100,000 persons and rising.1 The incidence increases with age and is rising in part due to a larger number of patients with risk factors for gout.10
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 gastrointestinal (GI) tract.11
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. Larger tophi may take 10 years or longer to develop.
Free urate crystals can activate several proinflammatory mediators, including tumor necrosis factor α (TNF-α), interleukin 1 (IL-1), and IL-8. Activation of these mediators signals chemotactic movement of neutrophils into ...