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Gout

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Other Names

  • Gouty Arthritis
  • Monosodium Urate Cystal Arthropathy
  • Crystal Arthropathy
  • Tophus or tophi
  • Podagra
  • Hyperuricemia
  • Tophaceous Gout

Background

History

  • First documented in ancient Egypt[1]

Epidemiology

  • Prevalence
    • Men (3-6%), Women (1-3%)[2]
    • Roughly 8.3 million people in the US[3]
    • Hyperuricemia, or serum uric acid level greater than 6 mg/dL, seen in 21% of US population
  • Typical age between 40 and 69 years of age

Introduction

  • General
    • Occurs due to monosodium urate crystal deposition in the synovial fluid of joints
  • Food intake
    • Foods high in purine increase risk of developing gout or gout flare
    • Fish (e.g., anchovies, sardines, scallops, mussels)
    • Meats (e.g., bacon, beef, liver, turkey, veal, venison)
    • Paradoxically, purine rich vegetables do not increase uric acid or risk of developing gout[4]
  • Alcohol
    • Beer associated with highest risk, less so with liquor (moderate), wine (low)[5]
  • Affected joints[6]
    • First metatarsophalangeal joint (56% to 78%)
    • Midfoot (25% to 50%)
    • Ankle (18% to 60%)
    • Upper limb (13% to 46%)
    • interphalangeal joints (6% to 25%)
  • Hyperuricemia
    • Defined as serum uric acid level greater than 6 mg/dL
    • Can be relatively benign, only only 22% of men with a serum uric acid greater than 9 mg/dL develop gout over a 5-year period[7]
    • MSU crystals formation, deposition occurs at uric acid levels > 6.8 mg/dL[8]
  • Tophi or tophaceous gout
    • Due to repetitive accumulation of MSU crystals
    • Increased risk of tophi: temperature, mechanical trauma, previous disease, underlying osteoarthritis

Stages of Gout

  • Asymptomatic hyperuricemia
    • Preliminary stage, many will never develop gout
  • Acute gout
    • Abrupt onset, joint is erythematous, warm, swollen, and tender
    • Suspect if acute onset of monoarticular joint pain, maximum intensity occurring within 12 hours
  • Intercritical or interval gout
    • Acute symptoms resolved, low-grade inflammation remains, causing unnoticed damage
    • Persistent hyperuricemia drives MSU crystal deposition, tophi development
    • Leads to erosive changes which can be seen radiographically
  • Chronic gout
    • Persistent arthralgia or repeated episodes of acute gout, usually complicated by tophi formation
    • About 30% of patients develop chronic gout within 5 years[9]
    • Acute gout difficult to recognize in patients with chronic gout, presentation can mimic osteoarthritis

Associated Conditions

  • Gout increases risk of
    • Myocardial Infarction[10]

Risk Factors

  • Non-modifiable risk factors
    • Male gender (2-6x)
    • Increased age (linearly until age 80)[11]
    • Family history
    • Ethnicity: Taiwanese, Pacific Islander, and New Zealand Maori
    • Living in high-income countries
  • Behavioral risk factors
    • Diet rich in red meat, seafood
    • Diet heavy in fructose-rich food and beverages
    • Alcohol consumption
    • Physical inactivity
  • Medications
    • Loop diuretic
    • Tacrolimus, cyclosporine
    • Niacin
    • Aspirin
  • Systemic Illness
  • Genetic[12][13]
    • SLC2A9 (Glut-9 transporter)
    • SLC22A11 (OAT1 transporter)
    • SLC22A12 (URAT1 transporter)
    • Hypoxanthine-guanine phosphoribosyltransferase (HPRT) enzyme deficiency

Differential Diagnosis

Clinical Features

History

  • Key history: onset, timeline, location, previous joint trauma or injury, other arthralgias, dietary intake, alcohol consumption, and medications
  • In acute flares, patients complain of sudden onset joint swelling, pain and tenderness
  • First metatarsophalangeal joint (56% to 78% of patients) most commonly affected
  • Derm: draining of chalk-like substance from a subcutaneous nodule under transparent skin, suggesting tophus
  • Less commonly: ocular, spinal, and visceral manifestations mimicking a tumor or infection

Physical Exam

  • Evaluate affected joint(s) for erythema, swelling, rubor, presence of effusion
  • Tender to palpation with limited range of motion

Evaluation

General

  • Diagnosis can be made clinically
    • Unless suspicious of septic arthritis, which must be excluded with arthrocentesis
    • See ACR/EULAR Criteria below

Arthrocentesis and Synovial Fluid Analysis

  • Arthrocentesis
    • Indicated if moderate or intermediate risk OR need to exclude septic arthritis
  • Monosodium urate crystals
    • Appear negatively birefringent on polarized light microscopy, pathognomonic
    • Note that septic arthritis can coexist with gout, presence of crystals does not exclude SA[14]
    • Optimal timing is during acute gout flare
    • Only seen 70% of the time during intercritical period of acute flare[15]
  • Synovial fluid labs which should routinely be ordered when evaluating for SA
    • Culture and gram stain
    • Culture
    • Cell count
    • Protein and glucose
    • Crystal analysis
    • Synovial lactate

Serology

  • Uric Acid
    • Typically elevated in individuals with gout (> 5.8 mg per dL)
    • Acute gout attack: 14% of patients with low/ normal uric acid[16]
    • Elevated uric acid does not equate to gout as many hyperuricemia patients never develop gout[17]
  • Other
    • Must consider blood cultures, ESR, CRP if septic arthritis a consideration

Radiography

  • Standard evaluation of affected joint
    • Often normal
  • Potential findings in gout
    • Nonspecific soft tissue swelling
    • Chronic: punched-out erosions, interosseous tophi[18]

Ultrasound

  • General
    • Can be used to aid in diagnosis
    • Monitor disease progression/ management with urate lowering therapy
    • Aid in arthrocentesis
  • Double contour sign
    • Hyperechoic signal overlying an anechoic signal
    • Specificity: 96%, although the exact rate varies widely among joints[19]
  • Tophus
    • Heterogeneous, hyperechoic signal with poorly defined contours surrounded by an anechoic signal[20]
  • Snowstorm appearance
  • Diagnostic accuracy
    • Presence of 1/3 (double contour sign, tophus, snowstorm sign) LR+ 4.8, LR- 0.27[21]

CT

  • General
    • Can be used to aid in diagnosis
    • Can be used to evaluate degree of structure damage
  • Findings
    • Tophi
    • Bony erosions
  • Duel Energy CT
    • Can help identify MSU crystals (90% Se, 83% Sp)[22]

MRI

  • General
    • Often cost prohibitive
    • Not required for diagnosis or management
  • Findings
    • Visualize soft tissue, inflammatory changes
    • T2-weighted: tophi (medium-high signal changes), calcifications (low signal changes)

Classification

ACR/EULAR Gout Classification Criteria

  • General
    • From American College of Rheumatology (ACR), European League Against Rheumatism (EULAR) 2015[23]
    • Notably does not require arthrocentesis
  • Points
    • Acute onset, with maximal symptoms on day 1: 0.5
    • Joint erythema: 1.0
    • Hypertension or cardiovascular disease: 1.5
    • Male sex: 2.0
    • Previous episode of arthritis or joint pain: 2.0
    • First metatarsophalangeal joint involvement: 2.5
    • Serum uric acid > 5.8 mg per dL (0.35 mmol per L): 3.5
  • Score
    • ≥ 8: high risk (diagnose gout)
    • 4.5 to 7.5: intermediate risk (needs arthrocentesis, crystal analysis)
    • ≤ 4: low risk (consider alternative diagnosis)

Management

Proposed treatment algorithm (courtesy of AAFP)

Lifestyle Modifications

  • Food avoidance
    • Low-fat
    • Low-purine
    • Fructose-containing soft drinks
  • Recommended foods[24]
    • Skim milk and low-fat yogurt, vegetables, soybeans, vegetable sources of protein, and cherries
  • Dietary Approaches to Stop Hypertension (DASH) Diet
    • 32% lower risk of developing gout (0.68; 95% CI, 0.57 to 0.80)[25]
  • Alcohol avoidance
  • Weight Loss
  • Increased Exercise

Acute Episode

  • NSAIDS
    • First line treatment unless contraindicated
    • Often used meds include naproxen, indomethacin, and sulindac
    • Comparable efficacy other medications at recommended doses[26]
  • Colchicine
    • Ideally started within first 24-36 hours
    • Low-dose (1.2 mg orally followed by 0.6 mg one hour later) as effective as high-dose colchicine (1.2 mg followed by 0.6 mg every hour for six hours)[27]
    • Low dose fewer adverse events (77% in high dose, 36% in low dose)
  • Oral Corticosteroids
    • Oral prednisolone (35 mg QD) is equal to naproxen (500 mg BID), no difference in pain relief or adverse effects[28]
  • Analgesia
    • Ice therapy helps in acute flares[29]
  • Other: Role unknown
    • Interleukin-1 inhibitors (anakinra [Kineret], canakinumab [Ilaris], or rilonacept [Arcalyst])

Chronic Management

  • General
    • ACP, AAFP recommend discuss benefits/ risks before initiating any urate lowering therapy (ULT)[30]
    • Review modifiable risk factors
    • Obtain baseline uric acid level
  • Indications for ULT
    • 3 or more episodes of gout
    • Failure to control uric acid with modification of risk factors
    • Persistent elevation over 6 mg/dL
    • Presence of tophi or uric acid nephrolithiasis
  • Titration
    • ACP does not recommend titrating ULT to 24 hour urine uric acid or serum uric acid
    • British Society for Rheumatology recommends titrating ULT to less than 0.3 mmol per L (5 mg/dL)
    • Reduction to < 5 mg/dL increased tophi reduction[31]
  • Allupurinol
    • First line therapy, dosage varies with severity
  • Febuxostat (Uloric)
    • Noninferior to allopurinol in preventing acute gout episodes[32]
    • However, febuxostat as higher cardiovascular risk and all cause mortality risk
  • Prophylaxis
    • ACR/EULAR recommend prophylaxis while initiating urate-lowering therapy
  • Pegloticase (Krystexxa)
    • Consider when allupurinol, febuxostat fail to control symptoms
    • Proven to lower serum uric acid levels
    • Benefits: quality of life, function, and pain; reduces tophi size in chronic gout[33]
  • Canakinumab [Ilaris]
    • Role not entirely clear
    • One study found it superior to IM steroids, NSAIDS and colchicine for acute gout during first 72 hours[34]

Other

  • Corticosteroid Injection
    • No evidence to recommend for or against
    • Consider in patients whom other medications are contraindicated
  • Complementary Therapies

Rehab and Return to Play

Rehabilitation

  • No definitive guidelines

Return to Play

  • No definitive guidelines

Prognosis and Complications

Prognosis

  • Acute episode
    • Typically self limited, resolution in 1-2 weeks
  • Morbidity and mortality
    • No evidence ULT decreases the risk of cardiovascular events[37]

Complications

  • Degenerative Joint Disease
  • Secondary infections
  • Urate or uric acid nephropathy.
  • Nephrolithiasis
  • Nerve or spinal cord impingement.
  • Fractures in joints with tophaceous gout.

See Also

Internal

External

References

  1. ↑ Nuki G, Simkin PA. A concise history of gout and hyperuricemia and their treatment. Arthritis Res Ther. 2006;8(suppl 1):S1.
  2. ↑ Dalbeth N, Merriman TR, Stamp LK. Gout. Lancet. 2016;388(10055):2039–2052.
  3. ↑ Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. 2011;63(10):3136–3141.
  4. ↑ Zaga L, Theodoratou E, Kyle J, et al. The association of dietary intake of purine-rich vegetables, sugar-sweetened beverages and dairy with plasma urate, in a cross-sectional study. PLoS One. 2012;7(6):e38123.
  5. ↑ Singh JA, Reddy SG, Kundukulam J. Risk factors for gout and prevention: a systematic review of the literature. Curr Opin Rheumatol. 2011;23(2):192–202.
  6. ↑ Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot? J Foot Ankle Res. 2011;4(1):13.
  7. ↑ Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987;82(3):421–426.
  8. ↑ Schumacher HR Jr. The pathogenesis of gout. Cleve Clin J Med. 2008;75(suppl 5):S2–S4.
  9. ↑ Perez-Ruiz F, Calabozo M, Pijoan JI, et al. Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout. Arthritis Rheum. 2002;47(4):356–360.
  10. ↑ Krishnan E, Baker JF, Furst DE, Schumacher HR. Gout and the risk of acute myocardial infarction. Arthritis Rheum. 2006;54(8):2688–2696.
  11. ↑ Kuo CF, Grainge MJ, Mallen C, et al. Rising burden of gout in the UK but continuing suboptimal management: a nationwide population study. Ann Rheum Dis. 2015;74(4):661–667.
  12. ↑ Reginato AM, Mount DB, Yang I, Choi HK. The genetics of hyperuricaemia and gout. Nat Rev Rheumatol. 2012;8(10):610–621.
  13. ↑ Yang Q, Köttgen A, Dehghan A, et al. Multiple genetic loci influence serum urate levels and their relationship with gout and cardiovascular disease risk factors. Circ Cardiovasc Genet. 2010;3(6):523–530.
  14. ↑ Yu KH, Luo SF, Liou LB, et al. Concomitant septic and gouty arthritis—an analysis of 30 cases. Rheumatology (Oxford). 2003;42(9):1062–1066.
  15. ↑ Zhang W, Doherty M, Pascual E, et al. EULAR evidence based recommendations for gout. Part I: diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1301–1311.
  16. ↑ Schlesinger N, Norquist JM, Watson DJ. Serum urate during acute gout [published correction appears in J Rheumatol. 2009;36(8):1851]. J Rheumatol. 2009;36(6):1287–1289.
  17. ↑ Tausche AK, Jansen TL, Schröder HE, et al. Gout—current diagnosis and treatment. Dtsch Arztebl Int. 2009;106(34-35):549–555.
  18. ↑ Perez-Ruiz F, Dalbeth N, Urresola A, et al. Imaging of gout: findings and utility. Arthritis Res Ther. 2009;11(3):232.
  19. ↑ Mathieu S, Pereira B, Couderc M, Soubrier M. Usefulness of ultrasonography in the diagnosis of gout: a meta-analysis. Ann Rheum Dis. 2013;72(10):e23.
  20. ↑ de Ávila Fernandes E, Kubota ES, Sandim GB, et al.Ultrasound features of tophi in chronic tophaceous gout. Skeletal Radiol. 2011;40(3):309–315.
  21. ↑ Ogdie A, Taylor WJ, Neogi T, et al. Performance of ultrasound in the diagnosis of gout in a multicenter study: comparison with monosodium urate monohydrate crystal analysis as the gold standard. Arthritis Rheumatol. 2017;69(2):429–438.
  22. ↑ Bongartz T, Glazebrook KN, Kavros SJ, et al. Dual-energy CT for the diagnosis of gout: an accuracy and diagnostic yield study. Ann Rheum Dis. 2015;74(6):1072–1077.
  23. ↑ Neogi T, Jansen TLTA, Dalbeth N, et al. 2015 gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative [published correction appears in Arthritis Rheumatol. 2016;68(2):515]. Arthritis Rheumatol. 2015;67(10):2557–2568.
  24. ↑ Hui M, Carr A, Cameron S, et al.; British Society for Rheumatology Standards, Audit and Guidelines Working Group.. The British Society for Rheumatology guideline for the management of gout [published correction appears in Rheumatology (Oxford). 2017;56(7):1246]. Rheumatology (Oxford). 2017;56(7):e1–e20.
  25. ↑ Rai SK, Fung TT, Lu N, et al. The Dietary Approaches to Stop Hypertension (DASH) diet, Western diet, and risk of gout in men: prospective cohort study. BMJ. 2017;357:j1794.
  26. ↑ Khanna D, Khanna PP, Fitzgerald JD. 2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res (Hoboken). 2012;64(10):1447–1461.
  27. ↑ Terkeltaub RA, Furst DE, Bennett K, et al. High versus low dosing of oral colchicine for early acute gout flare: twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. 2010;62(4):1060–1068.
  28. ↑ Janssens HJEM, Janssen M, van de Lisdonk EH, et al. Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial. Lancet. 2008;371(9627):1854–1860.
  29. ↑ Schlesinger N, Detry MA, Holland BK, et al. Local ice therapy during bouts of acute gouty arthritis. J Rheumatol. 2002;29(2):331–334.
  30. ↑ American Academy of Family Physicians. Management of acute and recurrent gout; April 2017. Accessed January 29, 2020. https://www.aafp.org/patient-care/clinical-recommendations/all/gout-cpg.html
  31. ↑ Perez-Ruiz F, Calabozo M, Pijoan JI, et al. Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout. Arthritis Rheum. 2002;47(4):356–360.
  32. ↑ White WB, Saag KG, Becker MA, et al.; CARES Investigators. Cardiovascular safety of febuxostat or allopurinol in patients with gout. N Engl J Med. 2018;378(13):1200–1210.
  33. ↑ Strand V, Khanna D, Singh JA, et al. Improved health-related quality of life and physical function in patients with refractory chronic gout following treatment with pegloticase: evidence from phase III randomized controlled trials. J Rheumatol. 2012;39(7):1450–1457.
  34. ↑ Schlesinger N, Alten RE, Bardin T, et al. Canakinumab for acute gouty arthritis in patients with limited treatment options: results from two randomised, multicentre, active-controlled, double-blind trials and their initial extensions. Ann Rheum Dis. 2012;71(11):1839–1848.
  35. ↑ Stamp LK, O'Donnell JL, Frampton C, et al. Clinically insignificant effect of supplemental vitamin C on serum urate in patients with gout: a pilot randomized controlled trial. Arthritis Rheum. 2013;65(6):1636–1642.
  36. ↑ Lee WB, Woo SH, Min BI, et al. Acupuncture for gouty arthritis: a concise report of a systematic and meta-analysis approach. Rheumatology (Oxford). 2013;52(7):1225–1232.
  37. ↑ Zhang T, Pope JE. Cardiovascular effects of urate-lowering therapies in patients with chronic gout: a systematic review and meta-analysis. Rheumatology (Oxford). 2017;56(7):1144–1153.
Created by:
John Kiel on 7 July 2019 05:33:01
Authors:
Last edited:
24 March 2023 05:49:30
Categories:
Knee | Rheumatology | Foot

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