Information For Healthcare Professionals
Gout Treatment

Case Studies

Case Study:

A 48-Year-Old Male With a Second Gout Attack

Patient History and Presentation

A 48-year-old overweight male with controlled hypertension and controlled hyperlipidemia presents with his second attack of gout. Symptoms that he described as severe began the day before. His first attack occurred approximately 9 months ago. This attack was managed with anti-inflammatory drugs. At that time, dietary modifications and physical activity were recommended for weight reduction.

Diagnostic Workup

Physical examination and laboratory results were unremarkable.

Medical Considerations

Compliance with recommended lifestyle modifications is often less than ideal. The patient has experienced 2 gout attacks within a 9-month period. Uric acid lowering therapy was considered previously, but not pursued.

Discussion

Sixty-two percent of gout patients will have a second attack within 1 year and 78% within 2 years.1

Furthermore, gout is a chronic disease that can progress and have debilitating sequelae.1,2 Even during asymptomatic periods, silent deposition of monosodium urate crystals may occur in joints not previously affected by gout attacks.3

Lifestyle modifications and episodic treatment may not be adequate for treating chronic gout.4,5 For example, a diet totally restricted in purine content may lower the mean serum uric acid concentration by about 1 mg/dL.1

Gout should be considered a chronic disease that requires chronic therapy. Gout should be managed like any other chronic disease, such as hypertension or hypertriglyceridemia, that may require lifelong treatment.2

Long-term control of hyperuricemia should target a serum uric acid level less than 6.0 mg/dL, with the goal to:

  • Increase dissolution of crystals1,4
  • Reduce risk of recurrent gout attacks6
  • Reduce tophaceous deposits1

References

  1. Wortmann RL, Kelley WN. Gout and hyperuricemia. In: Harris ED Jr, Budd RC, Genovese MC, et al, eds. Kelley’s Textbook of Rheumatology. 7th ed. Philadelphia, Pa: Elsevier Saunders; 2005:1402-1429.
  2. Gibson T. Clinical features of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1919-1928.
  3. McLean L. The pathogenesis of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1903-1918.
  4. Emmerson BT. The management of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1929-1936.
  5. Roberts LJ II, Morrow JD. Analgesic-antipyretic and anti-inflammatory agents and drugs employed in the treatment of gout. In: Hardman JG, Limbird LE, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 10th ed. New York: McGraw-Hill;2001:687-731.
  6. Shoji A, Yamanaka H, Kamatani N. A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis Rheum. 2004;51:321-325.

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Case Study:

A 63-Year-Old Female With Increasing Left Knee Pain

Patient History and Presentation

A 63-year-old Asian female presents with pain and restricted mobility in her left knee. Her symptoms began approximately 3 months prior and progressively worsened, leading her to seek medical attention. The patient has a history of well-controlled diabetes mellitus and hyperuricemia with chronic gout. Gout was diagnosed by aspiration of fluid from the first MTP joint of her left foot during her first attack 10 years previously. She experienced several attacks since that time, all in the great toe. She was prescribed symptomatic treatment for her acute pain.

Diagnostic Workup

Physical examination and laboratory results were unremarkable, except serum uric acid was 7.4 mg/dL. An MRI of the knee was obtained. A large tophus in the medial femoral condyle was revealed along with associated bony erosions.

Medical Considerations

The patient had never experienced a gout attack in her left knee, but based on the presence of the tophus, she had “silent” deposition of urate crystals within this joint.

Discussion

Gout is a chronic disease that can progress.1,2 Even during asymptomatic periods, silent deposition of monosodium urate crystals may occur in joints not previously affected by gout attacks. In fact, crystals have been demonstrated in asymptomatic joints.3

References:

  1. Wortmann RL, Kelley WN. Gout and hyperuricemia. In: Harris ED Jr, Budd RC, Genovese MC, et al, eds. Kelley’s Textbook of Rheumatology. 7th ed. Philadelphia, Pa: Elsevier Saunders; 2005:1402-1429.
  2. Gibson T. Clinical features of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1919-1928.
  3. McLean L. The pathogenesis of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1903-1918.

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Case Study:

Chronic Gout in a Patient With Chronic Kidney Disease

Patient History and Presentation

A 65-year-old male with well-controlled type 2 diabetes, chronic kidney disease, and chronic gout began to experience increasingly frequent gout attacks. Initially, the patient responded well to symptomatic treatment. However, his attacks continued to worsen.

Diagnostic Workup

Of note, the patient’s creatinine clearance was 30 mL/min/1.73 m2 (stage 3 kidney disease)1 and his serum uric acid was 10 mg/dL.

Medical Considerations

Due to compromised renal function, there must be careful consideration of therapeutic options for this patient.

Discussion

Gout is a chronic disease that can progress and have debilitating sequelae.2,3 Even during asymptomatic periods, silent deposition of monosodium urate crystals may occur in joints not previously affected by gout attacks.4

Lifestyle modifications and episodic treatment may not be adequate for treating chronic gout.5,6 For example, a purine-restrictive diet may lower the mean serum uric acid concentration by about 1 mg/dL.2

Gout should be considered a chronic disease that requires chronic therapy. Gout should be managed like any other chronic disease, such as diabetes or renal dysfunction, that may require lifelong treatment.2,3 Long-term control of hyperuricemia should target a serum uric acid level less than 6.0 mg/dL, with the goal to:

  • Increase dissolution of crystals2,5
  • Reduce risk of recurrent gout attacks7
  • Reduce tophaceous deposits2

Because two thirds of uric acid is renally excreted,8 levels may further increase as renal function deteriorates.2 Combined with the treatment challenges typically associated with renal dysfunction, the effective management of gout could be particularly difficult.

References:

  1. Eknoyan G, Levin NW. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis. 2002;39:S1-S266.
  2. Wortmann RL, Kelley WN. Gout and hyperuricemia. In: Harris ED Jr, Budd RC, Genovese MC, et al, eds. Kelley’s Textbook of Rheumatology. 7th ed. Philadelphia, Pa: Elsevier Saunders; 2005:1402-1429.
  3. Gibson T. Clinical features of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1919-1928.
  4. McLean L. The pathogenesis of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1903-1918.
  5. Emmerson BT. The management of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1929-1936.
  6. Roberts LJ II, Morrow JD. Analgesic-antipyretic and anti-inflammatory agents and drugs employed in the treatment of gout. In: Hardman JG, Limbird LE, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 10th ed. New York: McGraw-Hill; 2001:687-731.
  7. Shoji A,Yamanaka H, Kamatani N. A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis Rheum. 2004;51:321-325.
  8. Hawkins DW, Rahn DW. Gout and hyperuricemia. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 5th ed. New York: McGraw-Hill; 2002:1659-1664.

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Case Study:

A 49-Year-Old Male With a History of Chronic Gout

Patient History and Presentation

A 49-year-old male presents with pain, swelling, and redness in the first MTP of his right foot. He has a long history of of controlled hypertension, controlled hyperlipidemia, and hyperuricemia with chronic gout. The patient had been well until 2 days ago, when he began to experience what he described as the beginnings of a gout attack.

Diagnostic Workup

Vital signs and physical examination were normal, except for the first MTP of his right foot, which was swollen, warm, tender, and red. Motion was severely restricted due to intense pain. Laboratory results, including serum uric acid, were also normal.

Medical Considerations

The patient’s laboratory workup was unremarkable (serum uric acid level was normal), but his presentation was consistent with a gout attack.

Discussion

Serum uric acid may not be elevated at the time of an attack.1,2 This observation is not completely understood, but increased urinary excretion of uric acid may result in lower uric acid levels during a gout attack.2 One study demonstrated that the acute inflammatory process may play a role in this phenomenon, and serum uric acid increased after the attack.3 Therefore, an assessment of hyperuricemia during the intercritical period may be more appropriate.

References:

  1. Wortmann RL, Kelley WN. Gout and hyperuricemia. In: Harris ED Jr, Budd RC, Genovese MC, et al, eds. Kelley’s Textbook of Rheumatology. 7th ed. Philadelphia, Pa: Elsevier Saunders; 2005:1402-1429.
  2. Gibson T. Clinical features of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003:1919-1928.
  3. Urano W, Yamanaka H, Tsutani H, et al. The inflammatory process in the mechanism of decreased serum uric acid concentrations during acute gouty arthritis. J Rheumatol. 2002;29:1950-1953.

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