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The formation of uric acid crystals in the joints leads to inflammation
The formation of uric acid crystals in the joints leads to inflammation


• Disorder with a heterogeneous group of clinical presentations resulting from tissue deposition of monosodium urate crystals  

ICD-9 codes

• 274.0 Gouty arthropathy
• 274.1 Gouty nephropathy
• 274.8 Gout with other specified manifestations
• 274.9 Gout, unspecified Types
• Gouty arthritis (acute)
• Chronic tophaceous gout
• “Saturnine gout” — linked to lead intoxication


• Estimated prevalence 1.4%-2%
• Male-to-female ratio approximately 4:1
• Age of onset typically 40-60 years in men, seven years later (on average) in women — rare after menopause

Causes and risk factors

• Urate underexcretion (more common than overproduction) may be primary or associated with such conditions as renal impairment, hypertension, hypothyroidism, or various medications (e.g., aspirin).
• Urate overproduction may be primary or associated with
     — Dietary factors: excessive intake of purines, fructose, or alcohol
     — Lymphoma/myeloproliferative disorders, psoriasis, high cell-turnover disorders
     — Medications: cytotoxic agents or vitamin B12
     — Hypoxanthine-guanine phosphoribo- syltransferase deficiency (Lesch-Nyhan syndrome)
     — Metabolic conditions: obesity or hypertriglyceridemia
• Hyperuricemia most important risk factor
     — Age at onset of first attack inversely related to serum uric acid level
     — Majority of patients with elevated serum uric acid levels, however, will not develop clinical gout.
• Documented risk factors in males
     — Obesity, weight gain, and hypertension (metabolic factors)
     — High intake of alcohol (especially beer), sugars, meats, and seafood
     — Diuretic use (may not be independent of other risk factors, such as hypertension and congestive heart failure)
     — High intake of dairy products and coffee (more than four cups daily) may be protective.
• History of organ transplantation (especially heart or kidney)/use of cyclosporine
• Risk factors for chronic tophaceous gout include diuretic use in renal insufficiency/congestive heart failure (especially in women) and long history of disease or alcohol abuse.

Complications and associated conditions

• Progressive kidney failure
• Joint erosion/destruction (chronic tophaceous gout)
• Risk for development of type 2 diabetes, hypertriglyceridemia, and cardiovascular disease


• Common triggers for acute event include
     — Infection, acidosis (metabolic)
     — Initiation of chemotherapy, starting/stopping allopurinol, diuretic therapy
     — Trauma, surgery, or use of IV contrast media
     — Alcohol use
• Acute attack typically self-limited, with spontaneous resolution in 3-14 days
     — Sudden onset of extreme pain, tenderness, and joint inflammation
     — Often begins at night or early morning, with pain and other symptoms increasing for 24-48 hours
     — 90% of initial attacks are monoarticular, most commonly the first metatarsophalangeal.
• Subsequent attacks are typically longer, involve more joints, and may not resolve without medical therapy.
• Recurrent attacks lead to accumulating crystal deposits in joints (chronic tophaceous gout), which become stiff and swollen.

Physical exam

• Affected joint typically swollen, red, and extremely tender
• Skin may resemble cellulitis, with desquamation over inflamed area.
• Characteristics of tophi include
     — Overlying skin is pulled taut.
     — Visible/palpable soft-tissue masses or asymptomatic intradermal/subcutaneous nodules
     — Typically contain whitish or yellowish deposits

Making the diagnosis

• Demonstration of urate crystals in synovial fluid analysis or in tophus by polarized light microscopy
• Presumptive diagnosis can be made based on presence of hyperuricemia, documentation of risk factors, and suggestive findings on history and physical exam.
• Rule out
     — Septic arthritis
     — Calcium pyrophosphate dihydrate deposition disease (“pseudogout”)
     — Rheumatoid/psoriatic arthritis
     — Erosive osteoarthritis or sarcoid arthropathy
     — Bacterial cellulitis


• Synovial fluid analysis/culture needed to exclude septic arthritis if patient is febrile and has leukocytosis
• Serum uric acid ( >6.8 mg/dL [404 µmol/L] is sufficient for crystal precipitation; level often normal during acute attack).
• X-ray may help confirm.
• 24-hour urine uric acid level as adjunctive test for
     — Identifying/excluding overproducers of urate
     — Patients being considered for uricosuric therapy
• Blood culture to rule out infection


• Risk of recurrence after initial attack 60% within one year and >90% within 10 years

Treatment of acute attack

• Oral nonsteroidal anti-inflammatory drugs (NSAIDs) at maximum dose for one to two weeks (drugs of choice for symptomatic relief)
• Colchicine effective but slower to work than NSAIDs
• Corticosteroids, especially in patients with contraindications to NSAIDs
• Rest, ice packs, joint elevation (“Bed cage” may keep bedclothes off inflamed joint.)
• Avoid alcohol; ensure adequate fluid intake (>2 L water daily).
• Allopurinol should not be started or discontinued during acute attack (avoid sudden changes in serum urate levels).
• Consider discontinuation of diuretics.

For complete references, see www.ebscohost.com/dynamed.
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