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| [[File:Tophaceous gout-Rt-great-toe.jpg|thumb|'''Figure 1:Tophaceous gout affecting the right great toe and finger interphalangeal joints'''. Note the asymmetrical swelling and yellow-white discolouration.<ref name="Roddy2011">{{cite journal|last1=Roddy|first1=Edward|title=Revisiting the pathogenesis of podagra: why does gout target the foot?|journal=Journal of Foot and Ankle Research|volume=4|issue=1|year=2011|issn=1757-1146|doi=10.1186/1757-1146-4-13}}</ref>]]
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| __NOTOC__ | | __NOTOC__ |
| | {{Gout}} |
| | {{CMG}} {{AE}} {{Shivam Singla}} |
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| '''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
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| {{Gout}}
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| {{CMG}}; {{AE}} {{CZ}}
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| {{SK}} Urate crystal arthropathy; uric acid crystal deposition in joint; gouty arthritis; podagra | | {{SK}} Urate crystal arthropathy; uric acid crystal deposition in joint; gouty arthritis; podagra |
| == [[Gout overview|Overview]] ==
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| == [[Gout historical perspective|Historical Perspective]] == | | ==[[Gout overview|Overview]]== |
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| == [[Gout pathophysiology|Pathophysiology]]== | | ==[[Gout historical perspective|Historical Perspective]]== |
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| == [[Gout differential diagnosis|Differentiating Gout from other Diseases]] == | | ==[[Gout pathophysiology|Pathophysiology]]== |
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| == [[Gout epidemiology and demographics|Epidemiology and Demographics]] == | | ==[[Gout differential diagnosis|Differentiating Gout from other Diseases]]== |
| | ==[[Gout epidemiology and demographics|Epidemiology and Demographics]]== |
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| == [[Gout risk factors|Risk Factors]] == | | ==[[Gout risk factors|Risk Factors]]== |
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| == [[Gout screening|Screening]] == | | ==[[Gout screening|Screening]]== |
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| == [[Gout natural history, complications and prognosis|Natural History, Complications and Prognosis]] == | | ==[[Gout natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| ==[[Diagnosis]]== | | ==[[Diagnosis]]== |
| | | [[Gout staging|Staging]] | [[Gout history and symptoms|History and Symptoms]] | [[Gout physical examination|Physical Examination]] | [[Gout laboratory tests|Laboratory Findings]] | [[Gout electrocardiogram|Electrocardiogram]] | [[Gout x ray|X Ray]] | [[Gout CT|CT]] | [[Gout MRI|MRI]] | [[Gout echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Gout other imaging findings|Other Imaging Findings]] | [[Gout other diagnostic studies|Other Diagnostic Studies]] |
| The diagnosis of gout is based upon the identification of intracellular monosodium urate (MSU) crystals in the synovial fluid aspirate of an affected joint, under polarizing light microscopy. But when this is not possible, a clinical diagnosis can be deduced with the help of classical clinical features, including the history and physical examination, laboratory findings, and various imaging studies.
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| === Diagnosis of acute gout ===
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| * While the favored approach is to find MSU crystals in the synovial fluid aspirate of an affected joint, in clinical practice a crystal evaluation is routinely not done<ref name="pmid21288096">{{cite journal| author=Neogi T| title=Clinical practice. Gout. | journal=N Engl J Med | year= 2011 | volume= 364 | issue= 5 | pages= 443-52 | pmid=21288096 | doi=10.1056/NEJMcp1001124 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21288096 }} </ref><ref name="pmid15014182">{{cite journal| author=Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G| title=Purine-rich foods, dairy and protein intake, and the risk of gout in men. | journal=N Engl J Med | year= 2004 | volume= 350 | issue= 11 | pages= 1093-103 | pmid=15014182 | doi=10.1056/NEJMoa035700 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15014182 }} </ref>.
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| * When a patient is presenting with classic symptoms of rapid onset (within 24 hours), podagra, swelling, and erythema, supported by the presence of hyperuricemia, a clinical diagnosis of gout can easily be concluded. <ref>http://pubmed.gov/16707533</ref> <ref>http://pubmed.gov/18299687 <ref>http://pubmed.gov/25789770</ref>
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| * When an arthrocentesis is done, synovial fluid should be examined readily under routine light and polarizing light microscopy and looked for negatively birefringent needle-shaped MSU crystals. <ref>http://pubmed.gov/13773775</ref>
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| * In addition, testing for cell counts with differential, gram staining and culture should also be done on the aspirate.
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| * The sensitivity of this technique in demonstrating negatively birefringent intra- and extracellular crystals in patients with gout flares is at least 85 percent, and the specificity for gout is 100 percent. <ref>http://pubmed.gov/856219</ref> <ref>http://pubmed.gov/16462524</ref>. The sensitivity of can be further improved by examination of the sediment in a centrifuged specimen. <ref>http://pubmed.gov/10803751</ref>
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| {| class="wikitable" align="right"
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| |+ Accuracy of diagnostic criteria for gout among patients who had [[synovial fluid]] analysis | |
| <ref name="pmid19125136">{{cite journal| author=Malik A, Schumacher HR, Dinnella JE, Clayburne GM| title=Clinical diagnostic criteria for gout: comparison with the gold standard of synovial fluid crystal analysis. | journal=J Clin Rheumatol | year= 2009 | volume= 15 | issue= 1 | pages= 22-4 | pmid=19125136 | doi=10.1097/RHU.0b013e3181945b79 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19125136 }} </ref>
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| ! !! Criteria!!Sensitivity !! Specificity
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| | ARA (ACR)||6 of 12 criteria||align="center"| 70% ||align="center"| 79%
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| | Rome||2 of 4 criteria:<br/>• Painful joint swelling, abrupt onset, Clearing in 1-2 weeks initially<br/>• Serum uric acid: >7 in males; >6 in females<br/>• Presence of tophi<br/>• Urate crystals in synovial fluid or tissues||align="center"| 70% ||align="center"| 83%
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| | New York||2 of 5 criteria:<br/>• 2 attacks of painful limb joint swelling<br/>• Abrupt onset and remission in 1—2 weeks initially<br/>• First MTP attack<br/>• Presence of a tophus<br/>• Response to colchicine-major reduction in inflammation within 48 h||align="center"| 67% ||align="center"| 89%
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| |}
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| Several sets of diagnostic criteria exit (see table).<ref name="pmid19125136">{{cite journal| author=Malik A, Schumacher HR, Dinnella JE, Clayburne GM| title=Clinical diagnostic criteria for gout: comparison with the gold standard of synovial fluid crystal analysis. | journal=J Clin Rheumatol | year= 2009 | volume= 15 | issue= 1 | pages= 22-4 | pmid=19125136 | doi=10.1097/RHU.0b013e3181945b79 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19125136 }} </ref>
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| {| class="wikitable" align="right"
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| |+ The serum uric acid level during an attack of gout<ref name="pmid20625017">{{cite journal| author=Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, Janssen M| title=A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. | journal=Arch Intern Med | year= 2010 | volume= 170 | issue= 13 | pages= 1120-6 | pmid=20625017 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20625017 | doi=10.1001/archinternmed.2010.196 }} </ref><ref name="pmid19369457">{{cite journal |author=Schlesinger N, Norquist JM, Watson DJ |title=Serum urate during acute gout |journal=J. Rheumatol. |volume=36 |issue=6 |pages=1287–9 |year=2009 |month=June |pmid=19369457 |doi=10.3899/jrheum.080938 |url=http://www.jrheum.org/cgi/pmidlookup?view=long&pmid=19369457 |issn=}}</ref>
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| ! !! Sensitivity !! Specificity
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| | > 5.88 mg/dl<ref name="pmid20625017"/>|| align="center"|95%|| align="center"|53%
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| | ≥ 6 mg/dl<ref name="pmid19369457"/>||align="center"| 86% ||align="center"| ?
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| | ≥ 8 mg/dl<ref name="pmid19369457"/>|| align="center"|68% || align="center"|?
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| A [[clinical prediction rule]] ([http://www.umcn.nl/Research/Departments/eerstelijnsgeneeskunde/Pages/Jichtcalculator.aspx online link]) found that the following predicted urate crystals by aspiration:<ref name="pmid20625017">{{cite journal| author=Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, Janssen M| title=A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. | journal=Arch Intern Med | year= 2010 | volume= 170 | issue= 13 | pages= 1120-6 | pmid=20625017 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20625017 | doi=10.1001/archinternmed.2010.196 }} </ref>
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| * Male
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| * Onset within one day
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| * Joint redness
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| * First metatarsaophalangeal joint
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| * Previous arthritis attack per patient
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| * History of hypertension or 1 or more [[cardiovascular disease]]s
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| * Serum [[uric acid]] level > 5.88 mg/dl
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| However, among patients with high scores, 20% did not have crystals. Only one of 381 patients had bacterial arthritis.
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| === Diagnosis of intercritical and tophaceous gout ===
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| * In patients where a diagnosis of gout wasn’t ascertained during an acute flare, a synovial fluid analysis identifying urate crystals from the previously affected joints would allow a late establishment of the disease.
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| * Urate crystals are present in synovial fluid of all untreated gouty patients and in approximately 70 percent of those under urate-lowering therapy. 8624633 10577299 444319
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| * For tophaceous gout, demonstration of urate crystals in aspirates of tophi provides an easy way to confirm the diagnosis 10834006
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| === Clinical diagnosis “rule” for acute gout ===
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| * In patients with acute gout where a diagnosis couldn’t be confirmed due to a negative synovial fluid analysis for MSU crystals, a clinical diagnostic approach can be implemented. 20625017
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| * This approach utilizes a set of clinical parameters with a scoring value. The parameters are derived from history, clinical presentation, and the laboratory findings. 25231179
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| * This approach has been shown to improve the accuracy of diagnosis without joint fluid analysis of a gout flare in primary care practice settings 20625017
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| * The model uses seven variables to calculate a total score to distinguish three levels of risk for gout. These are:
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| *# Male sex (2 points)
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| *# Previous patient-reported arthritis flare (2 points)
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| *# Onset within one day (0.5 points)
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| *# Joint redness (1 point)
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| *# First metatarsal phalangeal joint involvement (2.5 points)
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| *# Hypertension or at least one cardiovascular disease (1.5 points)
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| *# Serum urate level greater than 5.88 mg/dL (3.5 points)
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| * Based upon the total score, patients can be identified as having low (≤4 points), intermediate (>4 to <8 points), or high (≥8 points) probability of having acute gout.
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| * In patients with an intermediate score (>4 but <8 points), a preliminary diagnosis of gout may be made for the purpose of clinical management based upon a prevalent clinical features favoring gout.
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| * This diagnostic approach is not recommended for patients presenting with oligoarticular and polyarticular arthritis, as it was developed studying patients with monoarthritis seen by family physicians.
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| ==[[Treatment]]== | | ==[[Treatment]]== |
| [[Clinical practice guideline]]s address treatment.<ref name="pmid23024029">{{cite journal| author=Khanna D, Khanna PP, Fitzgerald JD, Singh MK, Bae S, Neogi T et al.| title=2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis. | journal=Arthritis Care Res (Hoboken) | year= 2012 | volume= 64 | issue= 10 | pages= 1447-61 | pmid=23024029 | doi=10.1002/acr.21773 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23024029 }} </ref><ref name="pmid23024028">{{cite journal| author=Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T et al.| title=2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. | journal=Arthritis Care Res (Hoboken) | year= 2012 | volume= 64 | issue= 10 | pages= 1431-46 | pmid=23024028 | doi=10.1002/acr.21772 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23024028 }} </ref><ref name="pmid16707532">{{cite journal |author=Zhang W, Doherty M, Bardin T, ''et al'' |title=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) |journal=Ann. Rheum. Dis. |volume=65 |issue=10 |pages=1312–24 |year=2006 |month=October |pmid=16707532 |doi=10.1136/ard.2006.055269 |url=http://ard.bmj.com/cgi/pmidlookup?view=long&pmid=16707532 |issn=}}</ref> However, trials comparing [[glucocorticoid]]s ([[glucocorticoid|steroids]]) and [[non-steroidal anti-inflammatory agent]]s (NSAIDs) were not published till after the guidelines. | | [[Gout medical therapy|Medical Therapy]] | [[Gout surgery|Surgery]] | [[Gout primary prevention|Primary Prevention]] | [[Gout secondary prevention|Secondary Prevention]] | [[Gout cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Gout future or investigational therapies|Future or Investigational Therapies]] |
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| A nurse-led protocol with treatment goal of 6 mg/dL was beneficial<ref name="pmid30343856">{{cite journal| author=Doherty M, Jenkins W, Richardson H, Sarmanova A, Abhishek A, Ashton D et al.| title=Efficacy and cost-effectiveness of nurse-led care involving education and engagement of patients and a treat-to-target urate-lowering strategy versus usual care for gout: a randomised controlled trial. | journal=Lancet | year= 2018 | volume= 392 | issue= 10156 | pages= 1403-1412 | pmid=30343856 | doi=10.1016/S0140-6736(18)32158-5 | pmc=6196879 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30343856 }} </ref>.
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| Regarding [[medication]]s, if there are no mitigating factors in choosing a drug, [[glucocorticoid]]s, [[non-steroidal anti-inflammatory agent]]s (NSAIDs), and [[colchicine]] all work; however, [[colchicine]] consistently causes [[drug toxicity]].
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| A combination treatment is ice four times a day with oral prednisone 30 mg orally tapered over 6 days (30 mg for two days, 20 mg for two days, 10 mg for two days) and colchicine 0.6 mg/day.<ref name="pmid11838852">{{cite journal |author=Schlesinger N, Detry MA, Holland BK, ''et al'' |title=Local ice therapy during bouts of acute gouty arthritis |journal=J. Rheumatol. |volume=29 |issue=2 |pages=331–4 |year=2002 |pmid=11838852 |doi=}}</ref> An advantage of this regimen is the reduced toxicity from the low dose of colchicine and that the colchicine helps prevent flares if allopurinol is later started. Colchicine has been combined with NSAIDs<ref name="pmid15570646">{{cite journal |author=Borstad GC, Bryant LR, Abel MP, Scroggie DA, Harris MD, Alloway JA |title=Colchicine for prophylaxis of acute flares when initiating allopurinol for chronic gouty arthritis |journal=J. Rheumatol. |volume=31 |issue=12 |pages=2429–32 |year=2004 |month=December |pmid=15570646 |doi= |url=http://www.jrheum.com/subscribers/04/12/2429.html |issn=}}</ref> that are not metabolized by the CYP3A4 [[isoenzyme]] of [[cytochrome P-450]] ([[naproxen]] is not metabolized by CYP3A4). Combining [[glucocorticoid]]s with NSAIDs increased the risk for gastrointestinal [[drug toxicity]]<ref name="pmid1892140">{{cite journal |author=Fries JF, Williams CA, Bloch DA, Michel BA |title=Nonsteroidal anti-inflammatory drug-associated gastropathy: incidence and risk factor models |journal=Am. J. Med. |volume=91 |issue=3 |pages=213–22 |year=1991 |month=September |pmid=1892140 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0002-9343(91)90118-H |issn=}}</ref>
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| ===Local ice===
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| Ice packs, applied for 30 minutes 4 times per day, can help according to a [[randomized controlled trial]] without allocation concealment.<ref name="pmid11838852">{{cite journal |author=Schlesinger N, Detry MA, Holland BK, ''et al'' |title=Local ice therapy during bouts of acute gouty arthritis |journal=J. Rheumatol. |volume=29 |issue=2 |pages=331–4 |year=2002 |pmid=11838852 |doi=}}</ref> In this trial, ice reduced the [[pain measurement|visual pain analog score]] by an additional 33 mm beyond the reduction provided by a combination of [[glucocorticoid]]s and [[colchicine]].
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| ===Non-steroidal anti-inflammatory agents===
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| [[Non-steroidal anti-inflammatory agent]]s (NSAIDs) are better than placebo according to a [[randomized controlled trial]] of 30 total patients.<ref>García de la Torre, Ignacio. (1987) Estudio doble-ciego paralelo, comparativo con tenoxicam vs placebo en artritis gotosa aguda (A comparative, double-blind, parallel study with tenoxicam vs placebo in acute gouty arthritis). ''Invet Med Int '14:'''92–7 [[http://bases.bireme.br/cgi-bin/wxislind.exe/iah/online/?IsisScript=iah/iah.xis&src=google&base=LILACS&lang=p&nextAction=lnk&exprSearch=62234&indexSearch=ID Abstract in Spanish]]</ref> According to a summary of this trial, "the knee was affected in 14 cases and the great toe in only two cases. After 24 h, 67% of tenoxicam group had ≥50% reduction in pain compared with 26% of placebo group (P<0.05). However, at the end of the treatment (4 days), there was no significant difference between the groups."<ref name="pmid16632483">{{cite journal |author=Sutaria S, Katbamna R, Underwood M |title=Effectiveness of interventions for the treatment of acute and prevention of recurrent gout--a systematic review |journal=Rheumatology (Oxford) |volume=45 |issue=11 |pages=1422–31 |year=2006 |month=November |pmid=16632483 |doi=10.1093/rheumatology/kel071 |url=http://rheumatology.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=16632483 |issn=}}</ref>
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| ===Glucocorticoids===
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| {| class="wikitable" align="right"
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| |+ Comparison of NSAID and steroids for acute gout
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| ! rowspan="2"| !!rowspan="2"| Patients!!colspan="2"|Interventions !! rowspan="2"|Results
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| ! [[Glucocorticoid|Steroid]]||[[Non-steroidal anti-inflammatory agent|NSAID]]
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| | Janssens et al 2008<ref name="pmid18514729">{{cite journal |author=Janssens HJ, Janssen M, van de Lisdonk EH, van Riel PL, van Weel C |title=Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial |journal=Lancet |volume=371 |issue=9627 |pages=1854–60 |year=2008 |month=May |pmid=18514729 |doi=10.1016/S0140-6736(08)60799-0 |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(08)60799-0 |issn=}}</ref>
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| ||120 total patients with [[uric acid]] crystals on [[arthrocentesis]]
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| ||[[Prednisolone]] 35 mg once daily for 5 days
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| ||[[Naproxen]] 500 mg twice daily for 5 days
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| ||NSAID trended better (88% versus 80% response; p=0.3)<br/>No differences in rates of [[drug toxicity]].
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| | Man et al 2007<ref name="pmid17276548">{{cite journal |author=Man CY, Cheung IT, Cameron PA, Rainer TH |title=Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial |journal=Annals of emergency medicine |volume=49 |issue=5 |pages=670–7 |year=2007 |pmid=17276548 |doi=10.1016/j.annemergmed.2006.11.014}}</ref>
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| ||90 total patients with clinical diagnosis of gout†
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| ||Initially [[prednisolone]] 30 mg<br/>Followed by prednisolone 30 mg daily for 5 days and as needed [[acetaminophen]]
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| ||Initially [[diclofenac]] 75 mg with [[indomethacin]] 50 mg<br/>Followed by indomethacin 50 mg every 8 hrs for 2 days then 25 mg every 8 hrs for 3 days and as needed [[acetaminophen]].
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| ||Steroids faster reduction in pain.<br/>Steroids used more [[acetaminophen]].<br/>More adverse effects from [[indomethacin]].<br/>
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| [[Indomethacin]] trended to more relapses at 2 weeks (11% vs 17%).
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| |- | |
| |colspan="5"|Notes:<br/>
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| † Clinical diagnosis of gout was "pain and warmth in a joint, and presented within 3 days of the onset of pain and also had 1 or more of the following: metatarsal-phalangeal joint involvement; knee or ankle joint involvement and aspirate containing crystals; or typical gouty arthritis, with either gouty tophi present or previous joint aspiration confirming the diagnosis of gout." Seven patients allowed arthrocentesis and all were positive for gout.
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| |}
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| [[Randomized controlled trial]]s find similar benefit from [[non-steroidal anti-inflammatory agent]]s and oral [[glucocorticoid]]s. In the first trial the reduction in [[pain measurement|visual analog scale]] after 5 days was 44.7 with [[prednisolone]] and 46.0 with [[naproxen]].<ref name="pmid17276548">{{cite journal |author=Man CY, Cheung IT, Cameron PA, Rainer TH |title=Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute gout-like arthritis: a double-blind, randomized, controlled trial |journal=Annals of emergency medicine |volume=49 |issue=5 |pages=670–7 |year=2007 |pmid=17276548 |doi=10.1016/j.annemergmed.2006.11.014}}</ref> Less [[adverse drug reaction]]s occurred in the [[glucocorticoid]]s group; however, the NSAID group received a high dose (50 mg every 8 hours for 2 days, followed by 25 mg every 8 hours for 3 days)<ref name="pmid8664664">{{cite journal |author=Henry D, Lim LL, Garcia Rodriguez LA, ''et al'' |title=Variability in risk of gastrointestinal complications with individual non-steroidal anti-inflammatory drugs: results of a collaborative meta-analysis |journal=BMJ |volume=312 |issue=7046 |pages=1563–6 |year=1996 |month=June |pmid=8664664 |pmc=2351326 |doi= |url=http://bmj.com/cgi/pmidlookup?view=long&pmid=8664664 |issn=}}</ref>.
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| In the second [[randomized controlled trial]] statistically equal effect resulted from prednisolone 35 mg orally per day or naproxen 500 mg orally twice per day; however there was an insignificant 8% improvement in the NSAID group.<ref name="pmid18514729">{{cite journal |author=Janssens HJ, Janssen M, van de Lisdonk EH, van Riel PL, van Weel C |title=Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial |journal=Lancet |volume=371 |issue=9627 |pages=1854–60 |year=2008 |month=May |pmid=18514729 |doi=10.1016/S0140-6736(08)60799-0 |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(08)60799-0 |issn=}}</ref> There were no significant differences in [[drug toxicity]].
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| ===Colchicine===
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| [[Colchicine]] is better than placebo according to a [[systematic review]] by the [[Cochrane Collaboration]]<ref name="pmid17054279">{{cite journal |author=Schlesinger N, Schumacher R, Catton M, Maxwell L |title=Colchicine for acute gout |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD006190 |year=2006 |pmid=17054279 |doi=10.1002/14651858.CD006190 |url=http://dx.doi.org/10.1002/14651858.CD006190 |issn=}}</ref> that found a single [[randomized controlled trial]] of 43 patients<ref name="pmid3314832">{{cite journal |author=Ahern MJ, Reid C, Gordon TP, McCredie M, Brooks PM, Jones M |title=Does colchicine work? The results of the first controlled study in acute gout |journal=Aust N Z J Med |volume=17 |issue=3 |pages=301–4 |year=1987 |month=June |pmid=3314832 |doi=10.1111/j.1445-5994.1987.tb01232.x |url= |issn=}} [http://www.medicine.ox.ac.uk/bandolier/booth/gout/colchrct.html Summary at Bandolier]</ref>. In this study, colchicine 1 mg orally, followed by 0.5 mg every two hours led to a 50% reduction in pain in about 70% of patients compared to about 35% of patients who received placebo. However, all patients had [[drug toxicity]] from colchicine and in 90% of the patients toxicity occurred before 50% reduction in pain.
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| Regarding the best dose, 1.2 mg followed by 0.6 mg in 1 hour may be as effective as higher dose.<ref name="pmid20131255">{{cite journal| author=Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW| title=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. | journal=Arthritis Rheum | year= 2010 | volume= 62 | issue= 4 | pages= 1060-8 | pmid=20131255
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| | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&retmode=ref&cmd=prlinks&id=20131255 | doi=10.1002/art.27327 }} </ref>
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| To avoid [[drug toxicity]], lower doses of colchicine (0.6 per day) have been used in combination with [[glucocorticoid]]s.<ref name="pmid11838852">{{cite journal |author=Schlesinger N, Detry MA, Holland BK, ''et al'' |title=Local ice therapy during bouts of acute gouty arthritis |journal=J. Rheumatol. |volume=29 |issue=2 |pages=331–4 |year=2002 |month=February |pmid=11838852 |doi= |url=http://www.jrheum.com/subscribers/02/02/331.html |issn=}}</ref> The UK National Library for Health recommends 0.5 mg two to four times a day.<ref>CKS (2007) Gout - Management (Topic Review). Clinical Knowledge Summaries. http://cks.library.nhs.uk/gout/management [Accessed: Date]</ref>
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| ===Anti-cytokines===
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| The [[monoclonal antibody]] against [[interleukin]]-1 beta, [[canakinumab]], may help according to a [[randomized controlled trial]].<ref name="pmid20533546">{{cite journal| author=So A, De Meulemeester M, Pikhlak A, Yücel AE, Richard D, Murphy V et al.| title=Canakinumab for the treatment of acute flares in difficult-to-treat gouty arthritis: Results of a multicenter, phase II, dose-ranging study. | journal=Arthritis Rheum | year= 2010 | volume= 62 | issue= 10 | pages= 3064-76 | pmid=20533546 | doi=10.1002/art.27600 | pmc= | url= }} </ref>
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| ==Prognosis==
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| ===Acute flares===
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| Without treatment, one third of flares improve within 2 days.<ref name="pmid3314832">{{cite journal |author=Ahern MJ, Reid C, Gordon TP, McCredie M, Brooks PM, Jones M |title=Does colchicine work? The results of the first controlled study in acute gout |journal=Aust N Z J Med |volume=17 |issue=3 |pages=301–4 |year=1987 |month=June |pmid=3314832 |doi=10.1111/j.1445-5994.1987.tb01232.x |url= |issn=}}</ref>
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| ==Case Studies==
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| :[[Gout case study one|Case #1]]
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| ==Related Chapter==
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| * [[Pseudogout]]
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| ==External Links==
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| * {{cite web | title=Answers and Questions on Gout| url=http://www.niams.nih.gov/Health_Info/Gout/default.asp | publisher= U.S. [[National Institutes of Health]]—[[National Institute of Arthritis and Musculoskeletal and Skin Diseases]] |date=September 28th, 2007 | accessdate=2007-08-28}}
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| * {{cite web | title=Coffee Consumption and Reduced Gout Risk | url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17530645 | work= Drinking coffee reduces risk of gout in middle age men | publisher= U.S. [[National Institutes of Health]] | accessdate=2007-05-25}}
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| ==References==
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| {{Reflist|2}}
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| {{Diseases of the musculoskeletal system and connective tissue}}
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| [[Category:Arthritis]]
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| [[Category:Rheumatology]]
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| [[Category:Disease]]
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| [[Category:Primary care]]
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| {{WH}}
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| {{WS}}
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| [[ar:نقرس]]
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| [[bg:Подагра]]
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| [[cs:Dna]]
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| [[da:Gigt]]
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| [[de:Gicht]]
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| [[es:Gota (enfermedad)]]
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| [[eo:Podagro]]
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| [[fa:نقرس]]
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| [[fr:Arthrite goutteuse]]
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| [[io:Kiragro]]
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| [[id:Gout]]
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| [[it:Gotta]]
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| [[he:שיגדון]]
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| [[lb:Giicht]]
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| [[ms:Gout]]
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| [[nl:Jicht]]
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| [[ja:痛風]]
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| [[no:Urinsyregikt]]
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| [[pl:Dna moczanowa]]
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| [[pt:Gota (doença)]]
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| [[ru:Подагра]]
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| [[sk:Dna]]
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| [[sr:Гихт]]
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| [[fi:Kihti]]
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| [[sv:Gikt]]
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| [[te:గౌటు]]
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| [[tr:Gut hastalığı]]
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| [[zh:痛风]]
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