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
Epidemiology• 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
History• 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
Testing• 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
Prognosis• 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.