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For the chapter in the Wells Handbook, please go to Chapter 1. Gout and Hyperuricemia.



  • Image not available. In the absence of a history of gout, asymptomatic hyperuricemia may not require treatment.

  • Image not available. Acute gouty arthritis may be treated effectively with short courses of high-dose nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or colchicine.

  • Image not available. Low-dose colchicine is highly effective at relieving acute attacks of gout; dose titration leads to more adverse effects but does not improve efficacy.

  • Image not available. Treatment with urate-lowering drugs to reduce risk of recurrent attacks of gouty arthritis is considered cost-effective for patients having two or more attacks of gout per year.

  • Image not available. Xanthine oxidase inhibitors are efficacious for the prophylaxis of recurrent gout attacks in both underexcreters and overproducers of uric acid. Either allopurinol or febuxostat should be initiated in patients with one of the following indications for urate-lowering therapy (ULT): (a) two or more gout attacks per year, (b) the presence of one or more tophus, (c) chronic kidney disease (stage 2 or worse), or (d) a history of urolithiasis. The dose of the xanthine oxidase inhibitor should be titrated to a goal serum urate concentration of less than 6 mg/dL (less than 357 μmol/L) (or less than 5 mg/dL [less than 297 μmol/L] if signs of gout persist at a level of 6 mg/dL [357 μmol/L]).

  • Image not available. Uricosuric agents should be avoided for patients with renal impairment (a creatinine clearance below 50 mL/min [0.83 mL/s]), a history of renal calculi, or overproduction of uric acid.

  • Image not available. Low-dose colchicine, NSAID, or corticosteroid therapy should be administered during the first 3 to 6 months of urate-lowering therapy (ULT) to minimize the risk of acute gout attacks that may occur during this initiation period.

  • Image not available. Uric acid nephrolithiasis should be treated with adequate hydration (2-3 L/day), a daytime urine-alkalinizing agent, and 60 to 80 mEq/day (mmol/day) of potassium bicarbonate or potassium citrate.

  • Image not available. Patients with hyperuricemia or gout should undergo comprehensive evaluation for signs and symptoms of cardiovascular disease, and aggressive management of cardiovascular risk factors (ie, weight loss, reduction of alcohol intake, control of blood pressure, glucose, and lipids) should be undertaken as indicated.

The term gout describes a heterogeneous clinical spectrum of diseases including elevated serum urate concentration (hyperuricemia), recurrent attacks of acute arthritis associated with monosodium urate (MSU) crystals in synovial fluid leukocytes, deposits of monosodium urate crystals (tophi) in tissues in and around joints, interstitial renal disease, and uric acid nephrolithiasis.1

The underlying metabolic disorder of gout is hyperuricemia, defined physiochemically as serum that is supersaturated with monosodium urate. At 37°C (98.6°F), serum urate concentrations above (or around) 7 mg/dL (416 μmol/L) begin to exceed the limit of solubility for monosodium urate.1 For determination of the risk of gout, hyperuricemia is defined statistically as serum urate concentrations greater than two standard deviations above the population means for age- and sex-matched healthy populations, ...

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