Gout: Rapid Evidence Review


Am Fam Physician. 2020 Nov 1;102(9):533-538.

  Patient information: Handouts on this topic are available at https://familydoctor.org/condition/gout/ and https://familydoctor.org/low-purine-diet/.

Author disclosure: No relevant financial affiliations.

Gout is caused by monosodium urate crystal deposition in joints and tissues. Risk factors include male sex; obesity; hypertension; alcohol intake; diuretic use; a diet rich in meat and seafood; chronic kidney disease; a diet heavy in fructose-rich food and beverages; being a member of certain ethnic groups, including Taiwanese, Pacific Islander, and New Zealand Maori; and living in high-income countries. Gout is characterized by swelling, pain, or tenderness in a peripheral joint or bursa, including the development of a tophus. Diagnosis of gout can be made using several validated clinical prediction rules. Arthrocentesis should be performed when suspicion for an underlying septic joint is present; synovial fluid or tophus analysis should be performed if the diagnosis is uncertain. Colchicine, nonsteroidal anti-inflammatory drugs, and corticosteroids relieve pain in adults with acute gout episodes. Indications for long-term urate-lowering therapy include chronic kidney disease, two or more flare-ups per year, urolithiasis, the presence of tophus, chronic gouty arthritis, and joint damage. Allopurinol and febuxostat are used to prevent flare-ups, although febuxostat is associated with an increase in all-cause and cardiovascular mortality and is therefore not routinely recommended.

Gout, caused by monosodium urate crystal deposition in joints and tissues, is commonly encountered in primary care. This article provides a review of patient-oriented evidence to guide the diagnosis and management of gout.

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Clinical recommendationEvidence ratingComments

Lifestyle modifications to prevent recurrent gout include reducing the consumption of high-fructose soft drinks, fruit juices, fruits, and purine-rich foods (e.g., anchovies, sardines, scallops, mussels, bacon, beef, liver, turkey, veal, venison).14


Systematic review of mostly observational studies

A validated clinical prediction rule (Table 3) should be used to determine the likelihood of gout based on the presence of typical signs and symptoms and the uric acid level.17


Limited quality, patient-oriented evidence, individual validation trial

Nonsteroidal anti-inflammatory drugs and corticosteroids are equally effective for the treatment of acute gout, with no significant difference in pain relief or adverse effects.34


Limited quality, patient-oriented evidence, individual randomized controlled trial

In acute gout, low-dose colchicine (1.2 mg followed by 0.6 mg in 1 hour) is as effective as high-dose colchicine (1.2 mg followed by 0.6 mg every hour for 6 hours) with fewer adverse effects.35


Limited-quality, patient-oriented evidence, individual randomized controlled trial

Allopurinol is the preferred first-line urate-lowering therapy to prevent recurrent gout. It is as effective as febuxostat (Uloric) in preventing gout flare-ups; however, febuxostat increases all-cause and cardiovascular mortality.41,42


Good-quality, patient-oriented evidence, individual randomized controlled trial

The allopurinol hypersensitivity assay, or HLA-B*58:01 test, should be considered in select patients (Korean adults with stage 3 or higher chronic kidney disease and all adults of Han or Thai descent) before initiating allopurinol therapy.44


Expert opinion, consensus guideline

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.

The Authors

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KARL T. CLEBAK, MD, FAAFP, is the residency program director and an assistant professor in the Department of Family and Community Medicine at Penn State Health Milton S. Hershey (Pa.) Medical Center....

ASHLEY MORRISON, MD, is the director of geriatric medicine and an assistant professor in the Department of Family and Community Medicine at Penn State Health Milton S. Hershey Medical Center.

JASON R. CROAD, DO, is an assistant professor in the Department of Family and Community Medicine at Penn State Health Milton S. Hershey Medical Center.

Address correspondence to Karl T. Clebak, MD, FAAFP, Penn State College of Medicine, 121 Nyes Rd., Harrisburg, PA 17111 (email: kclebak@pennstatehealth.psu.edu). Reprints are not available from the authors.

Author disclosure: No relevant financial affiliations.


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