GOUT (from medscape)

GOUT (from medscape)

• Gout has 2 clinical phases: (1) a first phase of intermittent acute attacks that spontaneously resolve during 7 to 10 days with asymptomatic periods between attacks, and (2) a second phase of chronic tophaceous gout involving polyarticular attacks with crystal deposition (tophi) in the soft tissues or joints.
• Risk factors include use of thiazide diuretics, cyclosporine, and low-dose aspirin (< 1 g/day); insulin resistance metabolic syndrome; renal insufficiency; hypertension; congestive heart failure; and organ transplantation.
• Increased dietary intake of purines, ethanol, soft drinks, and fructose also increase the risk for gout. Intake of coffee, dairy products, and vitamin C reduces the risk for gout.
• Triggers for gout attacks include alcohol intake, diuretic use, hospitalization, and surgery.
• The diagnostic standard is synovial fluid examination for negatively birefringent monosodium urate crystals under polarizing microscopy.
• Hyperuricemia may not be present in an acute attack and may not be helpful in diagnosis.
• The differential diagnosis of acute gout includes other crystal-induced arthritides, rheumatoid arthritis, and a septic joint.
• The main aim of treatment is rapid pain relief and prevention of disability.
• Options include the use of NSAIDs; colchicine; glucocorticoids; and, sometimes, corticotrophin.
• Adjunctive measures include applying ice and resting the affected joint.
• NSAIDs and colchicine are first-line treatments of acute gout.
• Colchicine, given at 1.2 mg at the start of an attack and repeated at 0.6 mg 1 hour later, is more effective than placebo for pain relief within 24 hours.
• Glucocorticoids and corticotrophins may be used, but the evidence for intramuscular injections is limited.
• A 5-day course of prednisolone has been shown to be equivalent to indomethacin and naproxen.
• 7 to 10 days of treatment of gout may be needed for symptom control.
• Lowering urate levels may prevent acute flares of gout and development of tophi.
• Urate-lowering therapy for hyperuricemia is recommended for those with at least 2 gout attacks per year or tophi, but such therapy should not be initiated during acute attacks.
• Urate-lowering therapy should be started 2 to 4 weeks after flare resolution, with a low initial dose increased for weeks to months.
• The dose should be adjusted to achieve a urate level below 6 mg/dL, which is associated with a reduced risk for acute attacks and tophi.
• Allopurinol, a xanthine oxidase inhibitor, is the most commonly prescribed agent to lower urate levels.
• Febuxostat is another xanthine oxidase inhibitor approved by the FDA in 2009. At daily doses of 80 mg and 120 mg, has been shown to be 2.5 to 3 times more likely to achieve urate levels less than 6 mg/dL at 1 year.
• Uricosuric drugs (probenecid, sulfinpyrazone, and benzbromarone) block renal tubular urate reabsorption.
• Uricase and pegloticase were FDA approved in 2010 for chronic gout refractory to conventional treatments.
• Lifestyle changes such as avoidance of alcohol and diet modification may not be sufficient to control attacks.
• Intake of vitamin C and dairy products have been shown to reduce urate levels.
• For patients starting allopurinol therapy, the use of colchicine at a dose of 0.6 mg twice daily for an average of 5.2 months has been shown to reduce the risk for gout attacks and severity of flares.
• The optimal duration of treatment of tophi is uncertain, and ongoing prophylaxis until resolution of tophi occurs may be necessary.
• The author concluded that patients suspected of having gout should have the diagnosis confirmed by synovial fluid examination, and acute treatment after multiple attacks should be followed by allopurinol for urate lowering, with colchicine prophylaxis to prevent recurrence of attacks.