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  • 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 antiinflammatory 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: (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 <6 mg/dL (or <5 mg/dL if signs of gout persist at a level of 6 mg/dL).
  • Image not available. Uricosuric agents should be avoided for patients with renal impairment [a creatinine clearance below 50 mL/min (0.84 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 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 to 3 L/day), a daytime urine-alkalinizing agent, and 60 to 80 mEq/day (60 to 80 mmol/L) 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 (i.e., weight loss, reduction of alcohol intake, control of blood pressure, glucose, and lipids) should be undertaken as indicated.

After reviewing this chapter, the reader should be able to:

  1. Describe the clinical manifestations of hyperuricemia.

  2. Explain the pathophysiology of gout and hyperuricemia.

  3. Describe comorbidities that are commonly associated with gout.

  4. Differentiate the clinical presentation of the various forms of gout.

  5. Identify the most common anatomic sites affected in acute gouty arthritis.

  6. Determine the likelihood of nephrolithiasis for patients with hyperuricemia based on urinary pH and uric acid excretion rates.

  7. Differentiate the two types of gouty nephropathy based on pathophysiologic mechanisms.

  8. Identify the most common sites of tophaceous gout.

  9. Formulate a plan for treating acute gouty arthritis for a patient who has been symptomatic for more than 36 hours.

  10. Formulate a plan for treating acute gouty arthritis for a patient with recent (<24 hours) onset.

  11. Recommend treatment for acute gouty arthritis for a patient who is unresponsive to colchicine or nonsteroidal antiinflammatory therapy.

  12. Develop a treatment plan for uric acid nephrolithiasis.

  13. Identify patients with gout in whom urate-lowering therapy should be implemented.

  14. Recommend appropriate urate-lowering therapy for an individual taking into consideration patient-specific characteristics (eg. renal function).

  15. Evaluate both the safety and efficacy of response to urate-lowering therapy.

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