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Gout
From WikiSM
Contents
Other Names
- Gouty Arthritis
- Monosodium Urate Cystal Arthropathy
- Crystal Arthropathy
- Tophus or tophi
- Podagra
- Hyperuricemia
- Tophaceous Gout
Background
- This page refers to gout, a monosodium urate crystal (MSU) arthropathy
- Most commonly affects Knee Joint, 1st Metatarsalphalangeal Joint, although gout can occur in any joint
History
- First documented in ancient Egypt[1]
Epidemiology
- Prevalence
- 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
- 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
- Morbid Obesity
- Hypertension
- Chronic Kidney Disease
- Cardiovascular disease
- Diabetes Mellitus
- Hyperlipidemia, Hypertriglyceridemia
- Hyperuricemia
- Genetic[12][13]
- SLC2A9 (Glut-9 transporter)
- SLC22A11 (OAT1 transporter)
- SLC22A12 (URAT1 transporter)
- Hypoxanthine-guanine phosphoribosyltransferase (HPRT) enzyme deficiency
Differential Diagnosis
- Cellulitis
- Pseudogout
- Osteoarthritis
- Psoriatic arthritis
- Reactive arthritis
- Rheumatoid arthritis
- Sarcoidosis
- Septic Arthritis
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
- 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
- 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
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
- Vitamin C: No effect on uric acid levels[35]
- Acupuncture: low quality evidence it helps with pain, lowers uric acid level[36]
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
- https://www.sportsmedreview.com/blog/overview-of-gout/
- Sports Medicine Review Foot Pain: https://www.sportsmedreview.com/by-joint/foot/
- Sports Medicine Review Knee Pain: https://www.sportsmedreview.com/by-joint/knee/
References
- ↑ Nuki G, Simkin PA. A concise history of gout and hyperuricemia and their treatment. Arthritis Res Ther. 2006;8(suppl 1):S1.
- ↑ Dalbeth N, Merriman TR, Stamp LK. Gout. Lancet. 2016;388(10055):2039–2052.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot? J Foot Ankle Res. 2011;4(1):13.
- ↑ Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987;82(3):421–426.
- ↑ Schumacher HR Jr. The pathogenesis of gout. Cleve Clin J Med. 2008;75(suppl 5):S2–S4.
- ↑ 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.
- ↑ Krishnan E, Baker JF, Furst DE, Schumacher HR. Gout and the risk of acute myocardial infarction. Arthritis Rheum. 2006;54(8):2688–2696.
- ↑ 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.
- ↑ Reginato AM, Mount DB, Yang I, Choi HK. The genetics of hyperuricaemia and gout. Nat Rev Rheumatol. 2012;8(10):610–621.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Tausche AK, Jansen TL, Schröder HE, et al. Gout—current diagnosis and treatment. Dtsch Arztebl Int. 2009;106(34-35):549–555.
- ↑ Perez-Ruiz F, Dalbeth N, Urresola A, et al. Imaging of gout: findings and utility. Arthritis Res Ther. 2009;11(3):232.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Schlesinger N, Detry MA, Holland BK, et al. Local ice therapy during bouts of acute gouty arthritis. J Rheumatol. 2002;29(2):331–334.
- ↑ 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
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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
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24 March 2023 05:49:30
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