title: Diagnosis, treatment, and prevention of gout.
abstract: Gout is characterized by painful joint inflammation, most commonly in the first metatarsophalangeal joint, resulting from precipitation of monosodium urate crystals in a joint space. Gout is typically diagnosed using clinical criteria from the American College of Rheumatology. Diagnosis may be confirmed by identification of monosodium urate crystals in synovial fluid of the affected joint. Acute gout may be treated with nonsteroidal anti-inflammatory drugs, corticosteroids, or colchicine. To reduce the likelihood of recurrent flares, patients should limit their consumption of certain purine-rich foods (e.g., organ meats, shellfish) and avoid alcoholic drinks (especially beer) and beverages sweetened with high-fructose corn syrup. Consumption of vegetables and low-fat or nonfat dairy products should be encouraged. The use of loop and thiazide diuretics can increase uric acid levels, whereas the use of the angiotensin receptor blocker losartan increases urinary excretion of uric acid. Reduction of uric acid levels is key to avoiding gout flares. Allopurinol and febuxostat are first-line medications for the prevention of recurrent gout, and colchicine and/or probenecid are reserved for patients who cannot tolerate first-line agents or in whom first-line agents are ineffective. Patients receiving urate-lowering medications should be treated concurrently with nonsteroidal anti-inflammatory drugs, colchicine, or low-dose corticosteroids to prevent flares. Treatment should continue for at least three months after uric acid levels fall below the target goal in those without tophi, and for six months in those with a history of tophi.
authors.affiliation: Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Barry L
authors.initials: BL
authors.lastname: Hainer
authors.affiliation: Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Eric
authors.initials: E
authors.lastname: Matheson
authors.affiliation: Medical University of South Carolina, Charleston, SC, USA.
authors.forename: R Travis
authors.initials: RT
authors.lastname: Wilkes
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D003937:Diagnosis, Differential; D004035:Diet Therapy / Q000379:methods; D019468:Disease Management; D005938:Glucocorticoids / Q000627:therapeutic use; D006073:Gout / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D006074:Gout Suppressants / Q000627:therapeutic use; D006801:Humans; D062072:Patient Acuity; D012307:Risk Factors; D055502:Secondary Prevention / Q000379:methods; D014527:Uric Acid / Q000378:metabolism*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D005938:Glucocorticoids; D006074:Gout Suppressants; D014527:Uric Acid