The latest article in our Clinical Practice series, “Gout,” comes from Dr. Tuhina Neogi from Boston University School of Medicine and School of Public Health.
Gout is a type of inflammatory arthritis induced by the deposition of monosodium urate crystals in synovial fluid and other tissues. It is associated with hyperuricemia, which is defined as a serum uric acid level of 6.8 mg per deciliter (404 micromoles per liter) or higher, the limit of urate solubility at physiological temperature and pH.
• What are the two clinical phases of gout?
Gout has two clinical phases. The first phase is characterized by intermittent acute attacks that spontaneously resolve, typically over 7 to 10 days, with asymptomatic periods between attacks. The second phase is notable for inadequately treated hyperuricemia with a transition to chronic tophaceous gout, which is often characterized by polyarticular attacks, symptoms between attacks, and crystal deposition (tophi) in soft tissues or joints.
• What are the risk factors for developing gout?
Factors that are associated with hyperuricemia and gout include the use of thiazide diuretics, cyclosporine, and low-dose aspirin, as well as insulin resistance, the metabolic syndrome, obesity, renal insufficiency, hypertension, congestive heart failure, and organ transplantation. The risk of incident gout is increased in persons with an increased intake of dietary purines (particularly meat and seafood), ethanol (particularly beer and spirits), soft drinks, and fructose and is decreased in those with an increased intake of coffee, dairy products, and vitamin C (which lower urate levels).
Morning Report Questions
Q: How should acute gout be managed?
A: NSAIDs and colchicine (at a dose of 1.2 mg at the onset of a flare, followed by 0.6 mg 1 hour later) are first-line agents for acute attacks. When the use of NSAIDs or colchicine is poorly tolerated or contraindicated, glucocorticoids or ACTH may be used.
Q: What urate lowering treatment is recommended?
A: Urate-lowering therapy should not be initiated during acute attacks but rather started 2 to 4 weeks after flare resolution. The most commonly drug used to lower urate levels is allopurinol, which is effective in decreasing flares and tophi, particularly among patients with target urate levels. Febuxostat was approved for the treatment of hyperuricemia in gout in 2009. Because rapid lowering of urate levels is associated with gout flares, the general recommendation is to use colchicine at a dose of 0.6 mg once or twice daily for flare prophylaxis.
Table 2. Pharmacologic Options for Hyperuricemia Therapy in Gout.