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Am Fam Physician. 2020;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/.

This clinical content conforms to AAFP criteria for CME.

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.

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 CSystematic 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 CLimited 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 BLimited 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 BLimited-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 AGood-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 CExpert opinion, consensus guideline

Epidemiology

  • In western high-income countries, the prevalence of gout is 3% to 6% in men and 1% to 3% in women.1 In 2015 and 2016, the incidence of gout was 3.9% among U.S. adults (2.7% in women and 5.2% in men).2

  • Gout is rare before the age of 20; prevalence increases linearly until plateauing after the age of 80.3

  • Risk factors are summarized in Table 1.114

  • Consumption of purine-rich foods is a risk factor for gout. These include some fish (e.g., anchovies, sardines, scallops, mussels) and meats (e.g., bacon, beef, liver, turkey, veal, venison). A patient handout on a low-purine diet is available at https://familydoctor.org/low-purine-diet.

  • Beer is associated with a larger increase in risk of gout compared with wine or hard liquor.14

  • Use of loop or thiazide diuretic or tacrolimus (Prograf) is associated with increased risk of gout.14

  • Consumption of two or more sugar-sweetened soft drinks per day, fruits high in fructose, or any fruit juices is associated with an increased risk of gout in men. Consumption of diet soft drinks does not appear to increase risk.14

Comorbidities
Cardiovascular disease
Diabetes mellitus
Diuretic use (loop and thiazide)
Elevated triglyceride and cholesterol levels
Hyperuricemia
Menopause
Obesity
Renal disease, including renal insufficiency and chronic kidney disease
Demographic factors
Certain ethnic groups, including indigenous Taiwanese, Pacific Islander, and New Zealand Maori
Living in high-income countries (specifically North America and western Europe)
Male sex (incidence 2 to 6 times higher than in females)
Dietary factors
Alcohol consumption
Diet rich in meat
Diet rich in seafood
Fructose-rich food and drink consumption
DiagnosisCharacteristics
Bacterial cellulitisErythema over the surface of a joint can be confused for a gout flare-up; however, the joint is typically nontender without the presence of effusion
Basic calcium phosphate deposition diseaseMilwaukee shoulder syndrome (rapidly progressing crystal arthropathy involving the shoulder and intra-articular deposition of hydroxyapatite crystals)
Calcium pyrophosphate dihydrate deposition disease (“pseudogout”)Calcium pyrophosphate dehydrate in fluid aspirate from joint
OsteoarthritisGradual typical onset, commonly in the hand, knee, hip, or first metatarsophalangeal joint
Psoriatic arthritisCharacteristic skin and nail changes
Reactive arthritisInflammatory polyarthritis in reaction to bacterial infection (commonly Chlamydia trachomatis genitourinary infections or gastrointestinal infections with Campylobacter, Salmonella, Shigella, or Yersinia)
Rheumatoid arthritisSlow onset with symmetric joint involvement, commonly in hands
SarcoidosisLofgren syndrome involving the ankles and erythema nodosum that can appear similar to gout; however, hilar adenopathy and lung involvement are not present in gout
Septic arthritisAssociated fever, elevated white blood cell count, elevated erythrocyte sedimentation rate

Diagnosis

The differential diagnosis of gout is summarized in Table 2.1,15

SIGNS AND SYMPTOMS

  • Swelling, pain, and tenderness in a peripheral joint or bursa, most commonly the first metatarsophalangeal joint (56% to 78% of patients), are symptoms associated with gout. Other joints, including the midfoot (25% to 50%), ankle (18% to 60%), upper limb (13% to 46%), and interphalangeal joints (6% to 25%), may be involved.16

  • Draining of a chalk-like substance from a subcutaneous nodule under transparent skin, often with overlying vascularity, indicates the presence of a tophus.1 Typical locations are the ear, olecranon bursa, and the finger pulps.

  • Several validated clinical prediction rules do not require joint fluid analysis.17,18 One was derived in 338 patients presenting to their primary care physician with monoarthritis suspected to be gout; it was then prospectively validated in another 338 patients17,19 (Table 317 ).

  • The American College of Rheumatology/European League Against Rheumatism 2015 gout classification criteria20 are available in an online tool (https://www.mdcalc.com/acr-eular-gout-classification-criteria).

Clinical variablePoints
Acute onset, with maximal symptoms on day 10.5
Joint erythema1.0
Hypertension or cardiovascular disease1.5
Male sex2.0
Previous episode of arthritis or joint pain2.0
First metatarsophalangeal joint involvement2.5
Serum uric acid > 5.8 mg per dL (0.35 mmol per L)3.5
Total score (0 to 13 points):———
ScoreSuggested action

≥ 8: high riskDiagnose gout
4.5 to 7.5: intermediate riskPerform or refer for joint aspiration and polarized light microscopy analysis of crystals
≤ 4: low riskConsider alternative diagnosis

DIAGNOSTIC TESTING

  • Diagnosis of gout is made clinically unless a septic joint is suspected based on acute onset of a hot, painful, red, tender, swollen joint with systemic symptoms such as fever or elevated white blood cell count.21

  • Synovial fluid or tophus analysis demonstrating monosodium urate crystals by polarized light microscopy is the definitive test for gout but is recommended only when the diagnosis is uncertain (i.e., intermediate risk on acute gout diagnosis tool) or a septic joint is suspected.21

  • If septic arthritis is suspected, blood culture and arthrocentesis with synovial fluid analysis (Gram stain and culture) should be performed.22,23

  • Serum uric acid levels are usually elevated in people with gout; however, they may be lower during an acute episode and therefore should not be measured in this circumstance.24 In a pooled study of two randomized controlled trials (N = 339), 14% of patients had a serum uric acid level of less than 6 mg per dL (0.36 mmol per L) during an acute gout episode.25

  • Ultrasonography and dual-energy computed tomography (CT) aid in the diagnosis of gout, whereas radiography and CT assess structural damage.26

  • In a study of 824 patients, the presence of any one of three ultrasound findings (double contour sign, tophus, and snowstorm appearance) was moderately accurate when synovial fluid analysis was the reference standard (positive likelihood ratio = 4.8; negative likelihood ratio = −0.27).27

  • Radiography of the affected joint is often normal with nonspecific soft tissue swelling.26

  • Conventional CT may be used to visualize and measure tophi and to assess bony erosions.28

  • Dual-energy CT can aid in detection of monosodium urate deposits in patients with gout. A diagnostic study of 40 patients with crystal-proven nontophaceous gout and 41 patients with other rheumatic diseases found that dual-energy CT was 90% sensitive and 83% specific.26,29

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