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Chapter 102: Gout

Heidi S. Chumley; Mindy A. Smith

PATIENT STORY

A 91-year-old woman arrives by ambulance to the emergency department because she was experiencing severe pain in her right middle finger (Figure 102-1). History reveals that she has had swelling of her finger for approximately 1 year. Palpation of the distal interphalangeal joint demonstrated firmness rather than fluctuance. A radiograph of the finger was ordered (Figure 102-2). The radiograph and physical examination are consistent with acute gouty arthritis superimposed on tophaceous gout. The diagnosis was confirmed by an aspirate of the finger that demonstrated negatively birefringent, needle-like crystals, both intracellularly and extracellularly. She was given 1.2 mg of colchicine followed by a second dose of 0.6 mg after 1 hour. Her pain was markedly decreased in 4 hours. Her serum uric acid level was determined to be 10.7 mg/dL. Colchicine was used in this case because the risk of using nonsteroidal anti-inflammatory drugs (NSAIDs) was considered to be high because of her previous history of gastric bleeding secondary to NSAIDs.

FIGURE 102-1

Acute gouty arthritis superimposed on tophaceous gout. (Reproduced with permission from Geiderman JM. An elderly woman with a warm, painful finger, West J Med. 2000;172(1):51-52.)

A photo shows swelling of the middle finger along with bony enlargement of its distal interphalangeal joint. The swelling shows white spots underneath the skin.
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FIGURE 102-2

This X-ray of the finger in Figure 102-1 shows several tophi (monosodium urate [MSU] deposits) in the soft tissue over the third distal interphalangeal joint. Note the typical punched-out lesions under the tophi. This is subchondral bone destruction. (Reproduced with permission from Geiderman JM. An elderly woman with a warm, painful finger, West J Med. 2000;172(1):51-52.)

An x-ray image of fingers shows subchondral bone destruction.
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INTRODUCTION

Gout is an inflammatory crystalline arthritis. Elevated uric acid leads to deposition of monosodium urate (MSU) crystals in the joints resulting in a red, hot, swollen joint. Gout typically begins as a monoarthritis, but can become polyarthritic. Treatment of acute episodes includes NSAIDs, colchicine, or intraarticular steroids. Chronic therapy includes lowering the uric acid level using dietary modifications and urate-lowering drugs.

EPIDEMIOLOGY

  • One-year prevalence of gout in many different countries is approximately 5 per 1000.1

  • Incidence of gout is approximately 1–2 per 1000 person years.1

  • Gout is four times more common in men than women until age 65; after age 65, gout is three times more common in men than women.2

  • Gout usually begins after the age of 30 in men and after menopause in women.

  • Several polymorphisms that regulate uric acid levels have been associated with increases in risk and severity of gout.2

ETIOLOGY AND PATHOPHYSIOLOGY

  • Defective uric acid metabolism with inefficient renal urate excretion leads to underexcretion of uric acid and an elevated serum uric acid level.

  • Overproduction of uric acid, instead of underexcretion, occurs in approximately 10% of patients ...

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