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{{short description|Medical condition that results in recurrent pain and swelling of joints}}{{Redirect|Podagra|the moth genus|Podagra (moth)}}{{pp-semi|small=yes}}{{Good article}}

HASLAM>FIRST=FIONADATE=1996LOCATION=LIVERPOOLPAGE=143EDITION=1. PUBL., | synonyms = Podagraɡt}}GOUT {{!, Definition of Gout by Lexico >url= accessdate=20 October 2019 |language=en}}| field = RheumatologyJoint pain, joint effusion>swelling, and rednessmenopause>post-menopausal women| causes = Uric acid| risks = Diet high in meat or beer, being overweightSeptic arthritis>Joint infection, rheumatoid arthritis, pseudogout, othersNEOGI >FIRST1=T JOURNAL=ANNALS OF INTERNAL MEDICINE VOLUME=165 PAGES=ITC1-16 PMID=27380294, Review, | prevention = Weight loss, vitamin C, not drinking alcohol, allopurinolnon-steroidal anti-inflammatory drug>NSAIDs, glucocorticoid, colchicineQASEEMLAST2=HARRISLAST3=FORCIEALAST4=CLINICAL GUIDELINES COMMITTEE OF THE AMERICAN COLLEGE OFTITLE=MANAGEMENT OF ACUTE AND RECURRENT GOUT: A CLINICAL PRACTICE GUIDELINE FROM THE AMERICAN COLLEGE OF PHYSICIANSDATE=3 JANUARY 2017ISSUE=1PMID=27802508, 10.7326/m16-0570, | frequency = 1–2% (developed world)}}Gout is a form of inflammatory arthritis characterized by recurrent attacks of a red, tender, hot, and swollen joint.JOURNAL, Hui, M, Carr, A, Cameron, S, Davenport, G, Doherty, M, Forrester, H, Jenkins, W, Jordan, KM, Mallen, CD, McDonald, TM, Nuki, G, Pywell, A, Zhang, W, Roddy, E, British Society for Rheumatology Standards, Audit and Guidelines Working, Group., The British Society for Rheumatology Guideline for the Management of Gout, Rheumatology (Oxford, England), 56, 7, e1–e20, 26 May 2017, 10.1093/rheumatology/kex156, 28549177, Pain typically comes on rapidly, reaching maximal intensity in less than 12 hours. The joint at the base of the big toe is affected in about half of cases.JOURNAL, Schlesinger N, Diagnosing and treating gout: a review to aid primary care physicians, Postgrad Med, 122, 2, 157–61, March 2010, 20203467, 10.3810/pgm.2010.03.2133, It may also result in tophi, kidney stones, or kidney damage.Gout is due to persistently elevated levels of uric acid in the blood. This occurs from a combination of diet, other health problems, and genetic factors. At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout. Gout occurs more commonly in those who regularly eat meat or seafood, drink beer, or are overweight.JOURNAL, 27452679, 2016, Beyl Jr, R. N., Update on Importance of Diet in Gout, The American Journal of Medicine, 129, 11, 1153–1158, Hughes, L, Morgan, S, 10.1016/j.amjmed.2016.06.040, Diagnosis of gout may be confirmed by the presence of crystals in the joint fluid or in a deposit outside the joint. Blood uric acid levels may be normal during an attack.Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms.JOURNAL, 27802478, 2017, Shekelle, P. G, Management of Gout: A Systematic Review in Support of an American College of Physicians Clinical Practice Guideline, Annals of Internal Medicine, 166, 1, 37–51, Newberry, S. J, Fitzgerald, J. D, Motala, A, O'Hanlon, C. E, Tariq, A, Okunogbe, A, Han, D, Shanman, R, 10.7326/M16-0461, Once the acute attack subsides, levels of uric acid can be lowered via lifestyle changes and in those with frequent attacks, allopurinol or probenecid provides long-term prevention.JOURNAL, Richette P, Bardin T, Gout, Lancet, 375, 9711, 318–28, January 2010, 19692116, 10.1016/S0140-6736(09)60883-7, Taking vitamin C and eating a diet high in low-fat dairy products may be preventive.WEB, Questions and Answers about Gout,weblink National Institute of Arthritis and Musculoskeletal and Skin Diseases, 2 February 2016, June 2015, live,weblink" title="">weblink 15 January 2016, JOURNAL, Roddy, E, Choi, HK, Epidemiology of gout., Rheumatic Diseases Clinics of North America, May 2014, 40, 2, 155–75, 10.1016/j.rdc.2014.01.001, 24703341, 4119792, Gout affects about 1 to 2% of the Western population at some point in their lives. It has become more common in recent decades. This is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy, and changes in diet. Older males are most commonly affected. Gout was historically known as "the disease of kings" or "rich man's disease".WEB,weblink Rich Man's Disease – definition of Rich Man's Disease in the Medical dictionary, Free Online Medical Dictionary, Thesaurus and Encyclopedia, It has been recognized at least since the time of the ancient Egyptians.

Signs and symptoms

missing image!
- Gout2010.JPG -
upright=1.4|alt=side view of a foot showing a red patch of skin over the joint at the base of the big toe|Gout presenting as slight redness in the metatarsal-phalangeal joint of the big toe
Gout can present in multiple ways, although the most common is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint). The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases. Other joints, such as the heels, knees, wrists, and fingers, may also be affected. Joint pain usually begins during the night and peaks within 24 hours of onset. This is mainly due to lower body temperature. Other symptoms may rarely occur along with the joint pain, including fatigue and a high fever.JOURNAL, Eggebeen AT, Gout: an update, Am Fam Physician, 76, 6, 801–8, 2007, 17910294, Long-standing elevated uric acid levels (hyperuricemia) may result in other symptoms, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.


The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout. This can occur because of diet, genetic predisposition, or underexcretion of urate, the salts of uric acid. Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lifetimes.JOURNAL, Vitart V, Rudan I, Hayward C, etal, SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout, Nat. Genet., 40, 4, 437–42, April 2008, 18327257, 10.1038/ng.106, The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 Î¼mol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 Î¼mol/l (9 mg/dL), the risk is 4.5% per year.


Dietary causes account for about 12% of gout,JOURNAL, Chen LX, Schumacher HR, Gout: an evidence-based review, J Clin Rheumatol, 14, 5 Suppl, S55–62, October 2008, 18830092, 10.1097/RHU.0b013e3181896921, and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood. Among foods richest in purines yielding high amounts of uric acid are dried anchovies, shrimp, organ meat, dried mushrooms, seaweed, and beer yeast.JOURNAL, Kaneko, Kiyoko, Aoyagi, Yasuo, Fukuuchi, Tomoko, Inazawa, Katsunori, Yamaoka, Noriko, Total Purine and Purine Base Content of Common Foodstuffs for Facilitating Nutritional Therapy for Gout and Hyperuricemia, Biological and Pharmaceutical Bulletin, 2014, 37, 5, 709–721, 10.1248/bpb.b13-00967, 24553148, Chicken and potatoes also appear related.JOURNAL, Major, Tanya J, Topless, Ruth K, Dalbeth, Nicola, Merriman, Tony R, Evaluation of the diet wide contribution to serum urate levels: meta-analysis of population based cohorts, BMJ, 363, 10 October 2018, k3951, 10.1136/bmj.k3951, 30305269, 6174725, Other triggers include physical trauma and surgery.Studies in the early 2000s found that other dietary factors are not relevant.JOURNAL, Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G, Purine-rich foods, dairy and protein intake, and the risk of gout in men, N. Engl. J. Med., 350, 11, 1093–103, March 2004, 15014182, 10.1056/NEJMoa035700, live, Specifically, moderate consumption of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) are not associated with gout.JOURNAL, Singh, JA, Reddy, SG, Kundukulam, J, Risk factors for gout and prevention: a systematic review of the literature, Current Opinion in Rheumatology, March 2011, 23, 2, 192–202, 21285714, 10.1097/BOR.0b013e3283438e13, 4104583, Neither is total consumption of protein. Alcohol consumption is strongly associated with increased risk, with wine presenting somewhat less of a risk than beer or spirits.JOURNAL, Roddy, E., Mallen, C. D., Doherty, M., Gout, BMJ, 1 October 2013, 347, oct01 3, f5648, 10.1136/bmj.f5648, 24473446, Eating skim milk powder enriched with glycomacropeptide (GMP) and G600 milk fat extract may reduce pain but may result in diarrhea and nausea.JOURNAL, Moi, John HY, Sriranganathan, Melonie K, Edwards, Christopher J, Buchbinder, Rachelle, 2013-05-31, Lifestyle interventions for chronic gout, Cochrane Database of Systematic Reviews, 5, CD010039, 10.1002/14651858.cd010039.pub2, 23728699, 1465-1858, The eating or drinking of coffee, vitamin C, and dairy products, as well as physical fitness, appear to decrease the risk.JOURNAL, Hak AE, Choi HK, Lifestyle and gout, Curr Opin Rheumatol, 20, 2, 179–86, March 2008, 18349748, 10.1097/BOR.0b013e3282f524a2, JOURNAL, Williams PT, Effects of diet, physical activity and performance, and body weight on incident gout in ostensibly healthy, vigorously active men, Am. J. Clin. Nutr., 87, 5, 1480–7, May 2008, 18469274, 4090353, 10.1093/ajcn/87.5.1480, JOURNAL, Choi HK, A prescription for lifestyle change in patients with hyperuricemia and gout, Curr Opin Rheumatol, 22, 2, 165–72, March 2010, 20035225, 10.1097/BOR.0b013e328335ef38, JOURNAL, Park, Kyu Yong, Kim, Hyun Jung, Ahn, Hyeong Sik, Kim, Sun Hee, Park, Eun Ji, Yim, Shin-Young, Jun, Jae-Bum, Effects of coffee consumption on serum uric acid: systematic review and meta-analysis, Seminars in Arthritis and Rheumatism, April 2016, 45, 5, 580–586, 10.1016/j.semarthrit.2016.01.003, 26905267, Vitamin C supplements do not appear to have a significant effect in people who already have established gout. Peanuts, brown bread, and fruit also appear protective. This is believed to be partly due to their effect in reducing insulin resistance.


Gout is partly genetic, contributing to about 60% of variability in uric acid level. The SLC2A9, SLC22A12, and ABCG2 genes have been found to be commonly associated with gout and variations in them can approximately double the risk.JOURNAL, Merriman, TR, Dalbeth, N, The genetic basis of hyperuricaemia and gout, Joint, Bone, Spine : Revue du Rhumatisme, 2011, 78, 1, 35–40, 20472486, 10.1016/j.jbspin.2010.02.027, JOURNAL, Reginato AM, Mount DB, Yang I, Choi HK, The genetics of hyperuricaemia and gout, Nature Reviews Rheumatology, 2012, 22945592, 10.1038/nrrheum.2012.144, 8, 10, 610–21, 3645862, Loss-of-function mutations in SLC2A9 and SLC22A12 causes low blood uric acid levels by reducing urate absorption and unopposed urate secretion. The rare genetic disorders familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.

Medical conditions

Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in nearly 75% of cases. Other conditions commonly complicated by gout include lead poisoning, kidney failure, hemolytic anemia, psoriasis, solid organ transplants, and myeloproliferative disorders such as polycythemia.JOURNAL, Stamp L, Searle M, O'Donnell J, Chapman P, Gout in solid organ transplantation: a challenging clinical problem, Drugs, 65, 18, 2593–611, 2005, 16392875, 10.2165/00003495-200565180-00004, A body mass index greater than or equal to 35 increases male risk of gout threefold. Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.JOURNAL, Loghman-Adham M, Renal effects of environmental and occupational lead exposure, Environ. Health Perspect., 105, 9, 928–38, September 1997, 9300927, 1470371, 10.2307/3433873, 3433873,


Diuretics have been associated with attacks of gout, but a low dose of hydrochlorothiazide does not seem to increase risk. Other medications that increase the risk include niacin, aspirin (acetylsalicylic acid), ACE inhibitors, angiotensin receptor blockers, beta blockers, ritonavir, and pyrazinamide. The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout, the former more so when used in combination with hydrochlorothiazide.BOOK, Gary S., Firestein, MD, Ralph C., Budd, MD, Edward D., Harris Jr., MD, Iain B., McInnes PhD, FRCP, Shaun, Ruddy, MD, John S., Sergent, MD, Kelley's Textbook of Rheumatology, 8th, 2008, Elsevier, 978-1-4160-4842-8, Chapter 87: Gout and Hyperuricemia,


missing image!
- Harnsäure Ketoform.svg|thumb|upright=1.4|alt=structure of organic compound: 7,9-dihydro-1H-purine-2,6,8(3H)-trione| Chemical structure of uric aciduric acidGout is a disorder of purine metabolism, and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating and forming deposits (tophi) in joints, on tendons, and in the surrounding tissues. Microscopic tophi may be walled off by a ring of proteins, which blocks interaction of the crystals with cells and therefore avoids inflammation.JOURNAL, Liu-Bryan, Ru, Terkeltaub, Robert, 2006, Evil humors take their Toll as innate immunity makes gouty joints TREM-ble, Arthritis & Rheumatism, 54, 2, 383–386, 10.1002/art.21634, 16447213, Naked crystals may break out of walled-off tophi due to minor physical damage to the joint, medical or surgical stress, or rapid changes in uric acid levels. When they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages, which is initiated by the NLRP3 inflammasome protein complex. Activation of the NLRP3 inflammasome recruits the enzyme caspase 1, which converts pro-interleukin 1β into active interleukin 1β, one of the key proteins in the inflammatory cascade.JOURNAL, Dalbeth, N, Merriman, TR, Stamp, LK, Gout, Lancet, April 2016, 388, 10055, 2039–52, 10.1016/S0140-6736(16)00346-9, 27112094, Review, An evolutionary loss of urate oxidase (uricase), which breaks down uric acid, in humans and higher primates has made this condition common.The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.JOURNAL, Virsaladze DK, Tetradze LO, Dzhavashvili LV, Esaliia NG, Tananashvili DE, [Levels of uric acid in serum in patients with metabolic syndrome], Russian, Georgian Med News, 146, 35–7, 2007, 17595458, Levels of uric acid in serum in patients with metabolic syndrome, Other triggers believed to be important in acute episodes of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration and extracellular matrix proteins.JOURNAL, Moyer RA, John DS, Acute gout precipitated by total parenteral nutrition, The Journal of Rheumatology, 30, 4, 849–50, 2003, 12672211, JOURNAL, Halabe A, Sperling O, Uric acid nephrolithiasis, Mineral and Electrolyte Metabolism, 20, 6, 424–31, 1994, 7783706, The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected. Rapid changes in uric acid may occur due to factors including trauma, surgery, chemotherapy and diuretics. The starting or increasing of urate-lowering medications can lead to an acute attack of gout with febuxostat of a particularly high risk.WEB, Gout,weblink NICE, 22 August 2019,weblinkweblink 22 August 2019, Calcium channel blockers and losartan are associated with a lower risk of gout compared to other medications for hypertension.JOURNAL, Choi HK, Soriano LC, Zhang Y, Rodríguez LA, Antihypertensive drugs and risk of incident gout among patients with hypertension: population based case-control study, BMJ, 2012, 344, d8190, 22240117, 10.1136/bmj.d8190, 3257215,


File:Gichtfuss im Roentgenbild 002.png
File:Fluorescent uric acid.JPG|thumb|upright=1.4|alt=numerous multi-colored needle-shaped crystals against a purple background|Microscope photograph of spiked rods of uric acid crystals found in a synovial fluid sample illuminated with polarized light. Formation of uric acid crystals in the joints is associated with gout.]]Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic acute arthritis of the base of the great toe (known as podagra). Synovial fluid analysis should be done if the diagnosis is in doubt.JOURNAL, Qaseem, A, McLean, RM, Starkey, M, Forciea, MA, Clinical Guidelines Committee of the American College of, Physicians., Diagnosis of Acute Gout: A Clinical Practice Guideline From the American College of Physicians, Annals of Internal Medicine, 3 January 2017, 166, 1, 52–57, 27802479, 10.7326/m16-0569, Plain X-rays are usually normal and are not useful for confirming a diagnosis of early gout. They may show signs of chronic gout such as bone erosion.

Synovial fluid

A definitive diagnosis of gout is based upon the identification of monosodium urate crystals in synovial fluid or a tophus. All synovial fluid samples obtained from undiagnosed inflamed joints by arthrocentesis should be examined for these crystals. Under polarized light microscopy, they have a needle-like morphology and strong negative birefringence. This test is difficult to perform and requires a trained observer.JOURNAL, Schlesinger N, Diagnosis of gout, Minerva Med., 98, 6, 759–67, 2007, 18299687, The fluid must be examined relatively soon after aspiration, as temperature and pH affect solubility.

Blood tests

Hyperuricemia is a classic feature of gout, but nearly half of the time gout occurs without hyperuricemia and most people with raised uric acid levels never develop gout.JOURNAL, Sturrock R, Gout. Easy to misdiagnose, British Medical Journal, BMJ, 320, 7228, 132–33, 2000, 10634714, 10.1136/bmj.320.7228.132, 1128728, Thus, the diagnostic utility of measuring uric acid levels is limited. Hyperuricemia is defined as a plasma urate level greater than 420 μmol/l (7.0 mg/dl) in males and 360 μmol/l (6.0 mg/dl) in females.JOURNAL, Sachs L, Batra KL, Zimmermann B, Medical implications of hyperuricemia, Med Health R I, 92, 11, 353–55, 2009, 19999892, Other blood tests commonly performed are white blood cell count, electrolytes, kidney function and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection.JOURNAL,weblink Gout: Differential Diagnoses & Workup – eMedicine Rheumatology, Medscape, live,weblink" title="">weblink 2010-07-25, 2019-01-17, JOURNAL,weblink Gout and Pseudogout: Differential Diagnoses & Workup – eMedicine Emergency Medicine, Medscape, live,weblink" title="">weblink 2010-03-11, 2019-01-17, A white blood cell count as high as 40.0×109/l (40,000/mm3) has been documented.

Differential diagnosis

The most important differential diagnosis in gout is septic arthritis. This should be considered in those with signs of infection or those who do not improve with treatment. To help with diagnosis, a synovial fluid Gram stain and culture may be performed. Other conditions that can look similar include pseudogout, rheumatoid arthritis, psoriatic arthritis, and reactive arthritis. Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinomaJOURNAL, Jordan DR, Belliveau MJ, Brownstein S, McEachren T, Kyrollos M, Medial canthal tophus, Ophthal Plast Reconstr Surg, 24, 5, 403–4, 2008, 18806664, 10.1097/IOP.0b013e3181837a31, or other neoplasms.JOURNAL, Sano K, Kohakura Y, Kimura K, Ozeki S, Atypical Triggering at the Wrist due to Intratendinous Infiltration of Tophaceous Gout, Hand (N Y), 4, 1, 78–80, March 2009, 18780009, 10.1007/s11552-008-9120-4, 2654956,


Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of purine-rich foods of animal origin such as meat and seafood, alcohol, and fructose (especially high fructose corn syrup). Eating dairy products, vitamin C, coffee, and cherries may help prevent gout attacks, as does losing weight.JOURNAL, Bitik, B, Öztürk, MA, An old disease with new insights: Update on diagnosis and treatment of gout, European Journal of Rheumatology, June 2014, 1, 2, 72–77, 27708879, 10.5152/eurjrheumatol.2014.021, 5042282, Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.JOURNAL, 2654686, 2009, Abrams, B, Sleep Apnea as a Cause of Gout Flares, The Medscape Journal of Medicine, 11, 1, 3, 19295924,


A number of medications are useful for preventing further episodes of gout, including allopurinol, probenecid, febuxostat, benzbromarone, and colchicine.JOURNAL, Dalbeth, N, Merriman, TR, Stamp, LK, Gout, Lancet, 22 October 2016, 388, 10055, 2039–2052, 27112094, 10.1016/s0140-6736(16)00346-9, JOURNAL, Kydd, Alison SR, Seth, Rakhi, Buchbinder, Rachelle, Edwards, Christopher J, Bombardier, Claire, 2014-11-14, Uricosuric medications for chronic gout, Cochrane Database of Systematic Reviews, 11, CD010457, 10.1002/14651858.cd010457.pub2, 25392987, 1465-1858, Long term medications are not recommended until a person has had two attacks of gout, unless destructive joint changes, tophi, or urate nephropathy exist.JOURNAL, Tausche AK, Jansen TL, Schröder HE, Bornstein SR, Aringer M, Müller-Ladner U, Gout—current diagnosis and treatment, Dtsch Arztebl Int, 106, 34–35, 549–55, August 2009, 19795010, 2754667, 10.3238/arztebl.2009.0549, It is not until this point that medications are cost-effective. They are not usually started until one to two weeks after an acute flare has resolved, due to theoretical concerns of worsening the attack. They are often used in combination with either an NSAID or colchicine for the first three to six months.Urate-lowering measures should be increased until serum uric acid levels are below 300–360 Âµmol/l (5.0–6.0 mg/dl) and continue indefinitely.JOURNAL, Ruoff, G, Edwards, NL, Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL?, Postgraduate Medicine, September 2016, 128, 7, 706–15, 27558643, 10.1080/00325481.2016.1221732, If these medications are in chronic use at the time of an attack, it is recommended that they be continued. Levels that cannot be brought below 6.0 mg/dl while attacks continue indicates refractory gout.JOURNAL, Ali, S, Lally, EV, Treatment failure gout, Medicine and Health, Rhode Island, November 2009, 92, 11, 369–71, 19999896, While historically it is not recommended to start allopurinol during an acute attack of gout, this practice appears acceptable.JOURNAL, Robinson, PC, Stamp, LK, The management of gout: Much has changed, Australian Family Physician, May 2016, 45, 5, 299–302, 27166465, Allopurinol blocks uric acid production, and is the most commonly used agent. Long term therapy is safe and well tolerated, and can be used in people with renal impairment or urate stones, although hypersensitivity occurs in a small number of individuals.Febuxostat is only recommended in those who cannot tolerate allopurinol.WEB, Febuxostat for the management of hyperuricaemia in people with gout Guidance and guidelines,weblink, 28 March 2017, 17 December 2008, live,weblink 28 March 2017, There are concerns about more deaths with febuxostat compared to allopurinol.WEB, Drug Safety and Availability – FDA adds Boxed Warning for increased risk of death with gout medicine Uloric (febuxostat),weblink FDA, 26 February 2019, en, 21 February 2019, Febuxostat may also increase the rate of gout flares during early treatment.JOURNAL, Tayar, Jean H, Lopez-Olivo, Maria Angeles, Suarez-Almazor, Maria E, 2012-11-14, Febuxostat for treating chronic gout, Cochrane Database of Systematic Reviews, 11, CD008653, 10.1002/14651858.cd008653.pub2, 23152264, 4058893, 1465-1858, However, there is tentative evidence that febuxostat may bring down urate levels more than allopurinol.JOURNAL, Seth, Rakhi, Kydd, Alison SR, Buchbinder, Rachelle, Bombardier, Claire, Edwards, Christopher J, 2014-10-14, Allopurinol for chronic gout, Cochrane Database of Systematic Reviews, 10, CD006077, 10.1002/14651858.cd006077.pub3, 25314636, 1465-1858, Probenecid appears to be less effective than allopurinol and is a second line agent. Probenecid may be used if undersecretion of uric acid is present (24-hour urine uric acid less than 800 mg).BOOK, Elizabeth D Agabegi, Agabegi, Steven S., Step-Up to Medicine (Step-Up Series), Lippincott Williams & Wilkins, Hagerstwon, MD, 2008, 251, 978-0-7817-7153-5,weblink It is, however, not recommended if a person has a history of kidney stones. Pegloticase is an option for the 3% of people who are intolerant to other medications.WEB,weblink FDA approves new drug for gout, FDA, September 14, 2010, live,weblink" title="">weblink September 17, 2010, It is a third line agent. Pegloticase is given as an intravenous infusion every two weeks, and reduces uric acid levels.JOURNAL, Sundy JS, Baraf HS, Yood RA, Edwards NL, Gutierrez-Urena SR, Treadwell EL, Vázquez-Mellado J, White WB, Lipsky PE, Horowitz Z, Huang W, Maroli AN, Waltrip RW, Hamburger SA, Becker MA, Efficacy and tolerability of pegloticase for the treatment of chronic gout in patients refractory to conventional treatment: two randomized controlled trials, JAMA: The Journal of the American Medical Association, Aug 17, 2011, 306, 7, 711–20, 21846852, 10.1001/jama.2011.1169, Pegloticase is useful decreasing tophi but has a high rate of side effects and many people develop resistance to it.JOURNAL, Sriranganathan, MK, Vinik, O, Bombardier, C, Edwards, CJ, Interventions for tophi in gout, The Cochrane Database of Systematic Reviews, Oct 20, 2014, 10, 10, CD010069, 25330136, 10.1002/14651858.CD010069.pub2, Potential side effects include kidney stones, anemia and joint pain.JOURNAL, Anderson, Amy, Singh, Jasvinder A, 2010-03-17, Pegloticase for chronic gout, Cochrane Database of Systematic Reviews, 3, CD008335, 10.1002/14651858.cd008335.pub2, 20238366, 6599816, 1465-1858, In 2016 it was withdrawn from the European market.WEB, Krystexxa,weblink, 28 March 2017, en, live,weblink" title="">weblink 28 March 2017, JOURNAL, Pegloticase: withdrawal of its EU marketing authorisation is welcome, Prescrire International, March 2017, 26, 180, 71, Lesinurad reduces blood uric acid levels by preventing uric acid absorption in the kidneys.WEB, Zurampic,weblink, 14 October 2018, 1 January 2018, It was approved in the United States for use together with allopurinol, among those who were unable to reach their uric acid level targets.WEB, Drug Trial Snapshot: Zurampic,weblink US Food and Drug Administration, 14 October 2018, 22 December 2015, Side effects include kidney problems and kidney stones.WEB, Zurampic,weblink European Medicines Agency, 14 October 2018, 18 February 2016,


The initial aim of treatment is to settle the symptoms of an acute attack.JOURNAL, Zhang W, Doherty M, Bardin T, etal, EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT), Ann. Rheum. Dis., 65, 10, 1312–24, October 2006, 16707532, 1798308, 10.1136/ard.2006.055269, Repeated attacks can be prevented by medications that reduce serum uric acid levels. Tentative evidence supports the application of ice for 20 to 30 minutes several times a day to decrease pain.JOURNAL, Moi, JH, Sriranganathan, MK, Edwards, CJ, Buchbinder, R, Lifestyle interventions for acute gout, The Cochrane Database of Systematic Reviews, 4 November 2013, 11, 11, CD010519, 24186771, 10.1002/14651858.CD010519.pub2, Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and steroids. While steroids and NSAIDs work equally well, steroids may be safer.JOURNAL, Billy, CA, Lim, RT, Ruospo, M, Palmer, SC, Strippoli, GFM, Corticosteroid or Nonsteroidal Antiinflammatory Drugs for the Treatment of Acute Gout: A Systematic Review of Randomized Controlled Trials, The Journal of Rheumatology, 45, 1, 128–136, 1 August 2017, 10.3899/jrheum.170137, 28765243, Options for prevention include allopurinol, febuxostat, and probenecid. Lowering uric acid levels can cure the disease. Treatment of associated health problems is also important. Lifestyle interventions have been poorly studied. It is unclear whether dietary supplements have an effect in people with gout.JOURNAL, Andrés, M, Sivera, F, Falzon, L, Buchbinder, R, Carmona, L, Dietary supplements for chronic gout, The Cochrane Database of Systematic Reviews, Oct 7, 2014, 10, 10, CD010156, 25287939, 10.1002/14651858.CD010156.pub2,


NSAIDs are the usual first-line treatment for gout. No specific agent is significantly more or less effective than any other. Improvement may be seen within four hours and treatment is recommended for one to two weeks. They are not recommended for those with certain other health problems, such as gastrointestinal bleeding, kidney failure, or heart failure. While indometacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.JOURNAL, Laubscher T, Dumont Z, Regier L, Jensen B, Taking the stress out of managing gout, Can Fam Physician, 55, 12, 1209–12, December 2009, 20008601, 2793228, For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.JOURNAL, Cronstein, BN, Terkeltaub, R, The inflammatory process of gout and its treatment, Arthritis Research & Therapy, 2006, 8 Suppl 1, S3, 16820042, 10.1186/ar1908, 3226108, There is some evidence that COX-2 inhibitors may work as well as nonselective NSAIDs for acute gout attack with fewer side effects.JOURNAL, van Durme, CM, Wechalekar, MD, Landewé, RB, Nonsteroidal anti-inflammatory drugs for treatment of acute gout, JAMA, 9 June 2015, 313, 22, 2276–7, 26057289, 10.1001/jama.2015.1881, JOURNAL, van Durme, CM, Wechalekar, MD, Buchbinder, R, Schlesinger, N, van der Heijde, D, Landewé, RB, Non-steroidal anti-inflammatory drugs for acute gout, The Cochrane Database of Systematic Reviews, 16 September 2014, 9, 9, CD010120, 25225849, 10.1002/14651858.CD010120.pub2,


Colchicine is an alternative for those unable to tolerate NSAIDs. At high doses, side effects (primarily gastrointestinal upset) limit its usage.WEB, Information for Healthcare Professionals: New Safety Information for Colchicine (marketed as Colcrys),weblink U.S. Food and Drug Administration, live,weblink" title="">weblink 2009-10-18, At lower doses, which are still effective, it is well tolerated.JOURNAL, van Echteld, I, Wechalekar, MD, Schlesinger, N, Buchbinder, R, Aletaha, D, Colchicine for acute gout, The Cochrane Database of Systematic Reviews, Aug 15, 2014, 8, 8, CD006190, 25123076, 10.1002/14651858.CD006190.pub2, Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.


Glucocorticoids have been found to be as effective as NSAIDsJOURNAL, Man CY, Cheung IT, Cameron PA, Rainer TH, Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial, Annals of Emergency Medicine, 49, 5, 670–7, 2007, 17276548, 10.1016/j.annemergmed.2006.11.014,weblink JOURNAL, van Durme, CM, Wechalekar, MD, Buchbinder, R, Schlesinger, N, van der Heijde, D, Landewé, RB, Non-steroidal anti-inflammatory drugs for acute gout, The Cochrane Database of Systematic Reviews, Sep 16, 2014, 9, 9, CD010120, 25225849, 10.1002/14651858.CD010120.pub2, and may be used if contraindications exist for NSAIDs.JOURNAL, Wechalekar, Mihir D, Vinik, Ophir, Schlesinger, Naomi, Buchbinder, Rachelle, 2013-04-30, Intra-articular glucocorticoids for acute gout, Cochrane Database of Systematic Reviews, 4, CD009920, 10.1002/14651858.cd009920.pub2, 23633379, 1465-1858, They also lead to improvement when injected into the joint. A joint infection must be excluded, however, as steroids worsen this condition. There were no short-term adverse effects reported.JOURNAL, Janssens, Hein J, Lucassen, Peter LBJ, Van de Laar, Floris A, Janssen, Matthijs, Van de Lisdonk, Eloy H, 2008-04-23, Systemic corticosteroids for acute gout, Cochrane Database of Systematic Reviews, 2, CD005521, 10.1002/14651858.cd005521.pub2, 18425920, 1465-1858,weblink


Interleukin-1 inhibitors, such as canakinumab, showed moderate effectiveness for pain relief and reduction of joint swelling, but have increased risk of adverse events, such as back pain, headache, and increased blood pressure.JOURNAL, 25177840, 2014, Sivera, F, Interleukin-1 inhibitors for acute gout, Cochrane Database of Systematic Reviews, 9, CD009993, Wechalekar, M. D, Andrés, M, Buchbinder, R, Carmona, L, 10.1002/14651858.CD009993.pub2, They, however, may work less well than usual doses of NSAIDS. The high cost of this class of drugs may also discourage their use for treating gout.


Without treatment, an acute attack of gout usually resolves in five to seven days; however, 60% of people have a second attack within one year. Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and kidney and cardiovascular disease and thus are at increased risk of death.JOURNAL, Kim SY, De Vera MA, Choi HK, Gout and mortality, Clin. Exp. Rheumatol., 26, 5 Suppl 51, S115–9, 2008, 19026153, It is unclear whether medications that lower urate affect cardiovascular disease risks.JOURNAL, Zhang, T, Pope, JE, Cardiovascular effects of urate-lowering therapies in patients with chronic gout: a systematic review and meta-analysis, Rheumatology (Oxford, England), 56, 7, 1144–1153, 30 March 2017, 10.1093/rheumatology/kex065, 28379501, This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi. These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons. With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people and occur due to low urine pH promoting the precipitation of uric acid. Other forms of chronic kidney dysfunction may occur.File:Case 30-top.jpg|Gouty tophi presenting as nodules on the finger and helix of the earImage:ChronicGout.jpg|Tophus of the kneeImage:Case 30-bottom.jpg|Tophii on the toe and ankleImage:Tophigout.JPG|Gout complicated by ruptured tophi, the exudite of which tested positive for uric acid crystalsImage:GoutCropped2016.jpg|Gout in the joint of the big toe


Gout affects around 1–2% of the Western population at some point in their lifetimes and is becoming more common. Some 5.8 million people were affected in 2013.JOURNAL, Global Burden of Disease Study 2013, Collaborators, Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013, Lancet, 22 August 2015, 386, 9995, 743–800, 26063472, 10.1016/s0140-6736(15)60692-4, 4561509, Rates of gout approximately doubled between 1990 and 2010.JOURNAL, Terkeltaub R, Update on gout: new therapeutic strategies and options, Nature Reviews Rheumatology, 6, 1, 30–8, January 2010, 20046204, 10.1038/nrrheum.2009.236, This rise is believed to be due to increasing life expectancy, changes in diet and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure.JOURNAL, Weaver, AL, Epidemiology of gout, Cleveland Clinic Journal of Medicine, July 2008, 75 Suppl 5, S9–12, 18819329, 10.3949/ccjm.75.Suppl_5.S9, Factors that influence rates of gout, include age, race, and the season of the year. In men over 30 and women over 50, rates are 2%.JOURNAL, Winzenberg T, Buchbinder R, Cochrane Musculoskeletal Group review: acute gout. Steroids or NSAIDs? Let this overview from the Cochrane Group help you decide what's best for your patient, J Fam Pract, 58, 7, E1–4, 2009, 19607767, In the United States, gout is twice as likely in males of African descent than those of European descent.WEB, Rheumatology Therapeutics Medical Center, What Are the Risk Factors for Gout?,weblink 2007-01-26, dead,weblink" title="">weblink 2007-03-25, Rates are high among Pacific Islanders and the Māori, but the disease is rare in aboriginal Australians, despite a higher mean uric acid serum concentration in the latter group.JOURNAL, Roberts-Thomson, R. A, Roberts-Thomson, P J, Rheumatic disease and the Australian Aborigine, Annals of the Rheumatic Diseases, 1 May 1999, 58, 5, 266–270, 10.1136/ard.58.5.266, 10225809, 1752880, It has become common in China, Polynesia, and urban sub-Saharan Africa. Some studies found that attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.JOURNAL, Fam AG, What is new about crystals other than monosodium urate?, Curr Opin Rheumatol, 12, 3, 228–34, May 2000, 10803754, 10.1097/00002281-200005000-00013,


{{also|List of people with gout}}File:Anthonie van Leeuwenhoek (1632-1723). Natuurkundige te Delft Rijksmuseum SK-A-957.jpeg|thumb|alt=A man wearing a long, curly wig and a full robe is sitting, looking out. His left arm rests on a small table, with his left hand holding a box. Behind him is a globe.|Antonie van LeeuwenhoekAntonie van LeeuwenhoekThe term "gout" was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin word gutta, meaning "a drop" (of liquid). According to the Oxford English Dictionary, this is derived from humorism and "the notion of the 'dropping' of a morbid material from the blood in and around the joints".WEB,weblink gout, n.1, Oxford English Dictionary, Second edition, 1989, 18 September 2011, Gout has been known since antiquity. Historically, it was referred to as "the king of diseases and the disease of kings"WEB,weblink The Disease Of Kings -, Forbes, live,weblink 2017-09-01, or "rich man's disease". The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women.JOURNAL, Pillinger, MH, Rosenthal P, Abeles AM, Hyperuricemia and gout: new insights into pathogenesis and treatment, Bulletin of the NYU Hospital for Joint Diseases, 65, 3, 215–221, 2007,weblink 17922673, dead,weblink" title="">weblink 2008-12-16, WEB,weblink The Internet Classics Archive Aphorisms by Hippocrates, July 27, 2010, MIT, live,weblink" title="">weblink July 7, 2010, Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women and associated kidney problems:Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.WEB,weblink On Medicine, A. Cornelius Celsus, Book IV, University of Chicago, In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning and its predilection for older males:Gouty patients are, generally, either old men or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle, or instep. The pain is like that of a dislocation and yet parts feel as if cold water were poured over them. Then follows chills and shivers and a little fever... The night is passed in torture, sleeplessness, turning the part affected and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint and being worse as the fit comes on.WEB,weblink Gout – The Affliction of Kings, h2g2, BBC, December 23, 2012, live,weblink" title="">weblink September 11, 2010, Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679. In 1848, English physician Alfred Baring Garrod identified excess uric acid in the blood as the cause of gout.JOURNAL, Storey GD, Alfred Baring Garrod (1819–1907), Rheumatology (Oxford, England), 40, 10, 1189–90, October 2001, 11600751, 10.1093/rheumatology/40.10.1189,

Other animals

Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid.JOURNAL, Agudelo CA, Wise CM, Gout: diagnosis, pathogenesis, and clinical manifestations, Curr Opin Rheumatol, 13, 3, 234–9, 2001, 11333355, 10.1097/00002281-200105000-00015, Humans and other great apes do not have this ability, thus gout is common. Other animals with uricase include fish, amphibians and most non-primate mammals.JOURNAL, Choi, HK, Mount, DB, Reginato, AM, American College of, Physicians, American Physiological, Society, Pathogenesis of gout, Annals of Internal Medicine, 4 October 2005, 143, 7, 499–516, 16204163, 10.7326/0003-4819-143-7-200510040-00009, The Tyrannosaurus rex specimen known as "Sue" is believed to have suffered from gout.JOURNAL, Rothschild, BM, Tanke D, Carpenter K, Tyrannosaurs suffered from gout, Nature, 387, 6631, 357, 1997, 10.1038/387357a0, 9163417, 1997Natur.387..357R,


A number of new medications are under study for treating gout, including anakinra, canakinumab, and rilonacept.JOURNAL,weblink New therapeutic options for gout here and on the horizon, Journal of Musculoskeletal Medicine, March 8, 2010, Abeles, A. M., Pillinger, M. H., live,weblink" title="">weblink May 20, 2010, Canakinumab may result in better outcomes than a low dose of a steroid, but costs five thousand times more.JOURNAL, Sivera, F, Wechalekar, MD, Andrés, M, Buchbinder, R, Carmona, L, Interleukin-1 inhibitors for acute gout, The Cochrane Database of Systematic Reviews, Sep 1, 2014, 9, 9, CD009993, 25177840, 10.1002/14651858.CD009993.pub2, A recombinant uricase enzyme (rasburicase) is available but its use is limited, as it triggers an immune response. Less antigenic versions are in development.



External links

{hide}Medical resources
| DiseasesDB = 29031
| ICD10 = {{ICD10|M|10||m|05{edih}
| ICD9 = {{ICD9|274.00}} {{ICD9|274.1}} {{ICD9|274.8}} {{ICD9|274.9}}
| ICDO =
| OMIM = 138900
| OMIM_mult = {{OMIM2|300323}}
| MedlinePlus = 000422
| eMedicineSubj = emerg
| eMedicineTopic = 221
| eMedicine_mult = {{eMedicine2|med|924}} {{eMedicine2|med|1112}} {{eMedicine2|oph|506}} {{eMedicine2|orthoped|124}} {{eMedicine2|radio|313}}
| MeshID = D006073
| RP = gout
| WO = gout
}}{{Commons category|Gout}}{{Offline|med}}
  • {{dmoz|Health/Conditions_and_Diseases/Musculoskeletal_Disorders/Arthritis/Gout/}}
  • EB1911, Gout, 12, 289–291,
{{Diseases of the musculoskeletal system and connective tissue}}{{Authority control}}

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