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{{Infobox_Disease |
__NOTOC__
  Name          = Gout |
{{Gout}}
  Image          = upper_tophaceous_gout.jpg |
{{CMG}} {{AE}} {{Shivam Singla}}
  Caption        = Tophaceous Gout <br> (Image courtesy of Charlie Goldberg, M.D.)|
  DiseasesDB    = 29031 |
  ICD10          = {{ICD10|M|10||m|05}} |
  ICD9          = {{ICD9|274.0}} {{ICD9|274.1}} {{ICD9|274.8}} {{ICD9|274.9}} |
  ICDO          = |
  OMIM          = 138900 |
  OMIM_mult      = {{OMIM2|300323}} |
  MedlinePlus    = |
  eMedicineSubj  = med |
  eMedicineTopic = 924 |
  eMedicine_mult = {{eMedicine2|orthoped|124}} {{eMedicine2|emerg|221}} {{eMedicine2|med|1112}} {{eMedicine2|oph|506}} {{eMedicine2|radio|313}} |
  MeshID        = D006073 |
}}
{{SI}}
{{CMG}}


'''Associate Editor-In-Chief:''' {{CZ}}
{{SK}} Urate crystal arthropathy; uric acid crystal deposition in joint; gouty arthritis; podagra


{{EH}}
==[[Gout overview|Overview]]==


==Overview==
==[[Gout historical perspective|Historical Perspective]]==


'''Gout''' (also called ''metabolic arthritis'') is a disease due to a [[congenital]] disorder of [[uric acid]] metabolism. In this condition, monosodium urate or uric acid crystals are deposited on the articular [[cartilage]] of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the blood stream. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material.
==[[Gout pathophysiology|Pathophysiology]]==


==History==
==[[Gout differential diagnosis|Differentiating Gout from other Diseases]]==
Writing ca. 30 AD, [[Aulus Cornelius Celsus]] appeared to recognize many of the features of gout, including its link with a urinary solute, late onset in women, linkage with alcohol, and perhaps even prevention by dairy products. [http://penelope.uchicago.edu/Thayer/E/Roman/Texts/Celsus/5*.html]  "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." and "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.  Upon the commencement of pain blood should be let; for when this is carried out at once in the first stages it ensures health, often for a year, sometimes for always. Some also, when they have washed themselves out by drinking asses' milk, evade this disease in perpetuity; some have obtained lifelong security by refraining from wine, mead and venery for a whole year; indeed this course should be adopted especially after the primary attack, even although it has subsided."
==[[Gout epidemiology and demographics|Epidemiology and Demographics]]==


The Roman gladiatorial surgeon [[Galen]] described gout as a discharge of the four [[Four Temperaments|humors]] of the body in unbalanced amounts into the joints. The [[Latin]] term for a drop, as a drop of discharge, is gutta -- the term gout descends from this word.
==[[Gout risk factors|Risk Factors]]==


==Pathogenesis==
==[[Gout screening|Screening]]==


Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. [[Purine metabolism]] gives rise to uric acid, which is normally excreted in the urine. Uric acid is more likely to form into crystals when there is a [[hyperuricaemia]], although it is 10 times more common without clinical gout than with it<ref>{{cite journal | author=Virsaladze D, Tetradze L, Djavashvili L, Esakia N, Tananashvili D. | title=Levels of uric Acid in serum in patients with metabolic syndrome. | journal=Georgian Med News | year=2007 | volume=146 | pages=34&ndash;7 | id=PMID 17595458}}</ref>
==[[Gout natural history, complications and prognosis|Natural History, Complications and Prognosis]]==


Purines can be generated by the body via breakdown of cells in normal cellular turnover, or can be ingested in purine-rich foods such as seafood. the kidneys are responsible for approximately one-third of uric acid excretion, with the gut responsible for the rest. It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.
==[[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]]
There are also different racial propensities to develop gout. Gout is high among the peoples of the Pacific Islands, and the Māori of New Zealand, but rare in the Australian aborigine despite the latter's higher mean concentration of serum uric acid.<!--
==[[Treatment]]==
  --><ref>{{cite journal | author = Roberts-Thomson R, Roberts-Thomson P | title = Rheumatic disease and the Australian aborigine | journal = Ann Rheum Dis | volume = 58 | issue = 5 | pages = 266&ndasgh;70 | year = 1999 | id = PMID 10225809 | url=http://ard.bmjjournals.com/cgi/content/full/58/5/266}}</ref>  In the United States, gout is twice as prevalent in African American males as it is in Caucasians.<!--
[[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]]
  --><ref>{{cite web | author = Rheumatology Therapeutics Medical Center | title = What Are the Risk Factors for Gout? | url=http://www.arthritisconsult.com/gout.html#risk | accessdate = 2007-01-26}}</ref>
 
A seasonal link also may exist, with significantly higher incidence of acute gout attacks occurring in the spring.<ref>{{cite web | author =Schlesinger N, Gowin KM, Baker DG, Beutler AM, Hoffman BI, Schumacher HR Jr. | title = Acute gouty arthritis is seasonal. | url=http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=9489831&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus | accessdate = 2007-09-27}}</ref> <ref>{{cite web | author = Gallerani M, Govoni M, Mucinelli M, Bigoni M, Trotta F, Manfredini R. | title = Seasonal variation in the onset of acute microcrystalline arthritis. | url=http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=10534553&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus| accessdate = 2007-09-27}}</ref>
 
Hyperuricemia is considered an aspect of [[metabolic syndrome]], although its prominence has been reduced in recent classifications. This explains the increased prevalence of gout among [[obesity|obese]] individuals.
 
Gout is a form of arthritis that affects mostly men between the ages of 40 and 50. The high levels of uric acid in the blood are caused by protein rich foods. Alcohol intake often causes acute attacks of gout and hereditary factors may contribute to the elevation of uric acid. Typically, persons with gout are obese, predisposed to diabetes and hypertension, and at higher risk of heart disease. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol.<ref>{{cite book|author = Robert S. Ivker, D.O. , et al | title = The Complete Self-Care guide to Holistic Medicine | year = 1999 | pages=186&ndash;8 | id = ISBN0-87477-986-J}}</ref> It is known that [[Lead(II) acetate|lead sugar]] was used to sweeten wine, and that chronic [[lead poisoning]] is a cause of gout,<ref>{{cite journal | author=Lin JL, Huang PT. | title=Body lead stores and urate excretion in men with chronic renal disease | journal=J Rheumatol | year=1994 | volume=21 | issue=4 | pages=705&ndash;9 | id=PMID 8035397}}</ref><ref>{{cite journal | author=Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. | title=Effect of low level lead exposure on hyperuricemia and gout among middle aged and elderly men: the Normative Aging Study | journal=J Rheumatol | year=2000 | volume=27 | issue=7 | pages=1708&ndash;12 | id=PMID 10914856}}</ref> which condition is then known as '''saturnine gout,''' because of its association with alcohol and excess.<ref>{{cite journal | author=Ball GV. | title=Two epidemics of gout | journal=Bull Hist Med | year=1971 | volume=45 | issue=5 | pages=401&ndash;8 | id=PMID 4947583}}</ref>
 
Gout also can develop as co-morbidity of other diseases, including polycythaemia, [[leukaemia]], intake of [[cytotoxic]]s, [[obesity]], [[diabetes]], [[hypertension]], [[renal]] disorders, and [[hemolytic anemia]]. This form of gout is often called secondary gout. [[Diuretic]]s (particularly [[thiazide]] diuretics) have traditionally been blamed for precipitating attacks of gout, but a Dutch case-control study from 2006 appears to cast doubt on this conclusion.<ref>{{cite journal | author = Janssens H, van de Lisdonk E, Janssen M, van den Hoogen H, Verbeek A | title = Gout, not induced by diuretics? A case-control study from primary care | journal = Ann Rheum Dis | volume = 65 | issue = 8 | pages = 1080&ndash;3 | year = 2006 |  id = PMID 16291814 | doi=10.1136/ard.2005.040360}}</ref>
 
==Signs and symptoms==
 
The classic picture is of excruciating, sudden, unexpected, burning [[Pain and nociception|pain]], swelling, redness, warmness and stiffness in the joint. Low-grade fever may also be present. The patient usually suffers from two sources of pain. The crystals inside the joint cause intense pain whenever the affected area is moved. The inflammation of the tissues around the joint also causes the skin to be swollen, tender and sore if it is even slightly touched. For example, a blanket or even the lightest sheet draping over the affected area could cause extreme pain.
 
Gout usually attacks the [[hallux|big toe]] (approximately 75 percent of first attacks); however, it also can affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, and spine. In some cases, the condition may appear in the joints of small toes that have become immobile due to impact injury earlier in life, causing poor blood circulation that leads to gout.
 
Patients with longstanding [[hyperuricemia]] (see below) can have uric acid crystal deposits called ''tophi'' (singular: [[tophus]]) in other tissues such as the [[Helix (ear)|helix of the ear]]. Uric acid stones can form as one kind of [[kidney stone]] in some common occasions.
 
==Diagnosis==
 
[[Hyperuricemia]] is a common feature; however, urate levels are not always raised.<!--
  --><ref>{{cite journal | author = Sturrock R | title = Gout. Easy to misdiagnose | journal = [[British Medical Journal|BMJ]] | volume = 320 | issue = 7228 | pages = 132&ndash;3 | year = 2000 | id = PMID 10634714 | url=http://bmj.bmjjournals.com/cgi/content/full/320/7228/132}}</ref>
Hyperuricemia is defined as a [[blood plasma|plasma]] urate (uric acid) level greater than 420 ''μ''mol/L (7.0 mg/dL) in males (or 380 ''μ''mol/L in females); however, a high [[uric acid]] level does not necessarily mean a person will develop gout. Urate is within the normal range in up to two-thirds of cases.<!--Hypothyroidism as well
  --><ref>{{cite journal | author = Siva C, Velazquez C, Mody A, Brasington R | title = Diagnosing acute monoarthritis in adults: a practical approach for the family physician | journal = Am Fam Pghysician | volume = 68 | issue = 1 | pages = 83&ndash;90 | year = 2003 | id = PMID 12887114}}</ref>
If gout is suspected, the serum urate test should be repeated once the attack has subsided. Other blood tests commonly performed are [[full blood count]], [[electrolyte]]s, [[renal function]] and [[erythrocyte sedimentation rate]] (ESR). This helps to exclude other causes of [[arthritis]], most notably [[septic arthritis]].
 
A definitive [[diagnosis]] of gout is from [[light microscopy]] of fluid aspirated from the joint (this test may be difficult to perform) to demonstrate [[intracellular]] monosodium urate crystals in [[synovial fluid]] [[polymorphonuclear leukocytes]]. The urate crystal is identified by strong negative bi-refringence under polarised microscopy and its needle-like morphology. A trained observer does better in distinguishing them from other crystals.
 
===Pathology===
 
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, CA)
 
<div align="left">
<gallery heights="175" widths="175">
Image:upper_hand_mcp_gout.jpg|Gout of Left MCP Joints: Diffuse redness and swelling over MCP joints caused by inflammation induced by gout. Right hand is normal, for comparison.
Image:upper_wrist_gout.jpg|Gout of the Right Wrist: Note swelling and redness over right wrist area. Left wrist is normal.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:upper_wrist_gout1.jpg|Gout of the Left Wrist: Note swelling and redness over left wrist area.
Image:upper_wrist_gout2.jpg|A normal wrist for comparison.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:upper_tophaceous_gout2.jpg|Tophaceous Gout
Image:upper_gout_toph.jpg|Tophaceous Gout
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:upper_toph_gout.jpg|Tophaceous Gout
Image:extremities_gout.jpg|Gout of the Left Great Toe: Diffuse swelling and redness centered at the left MTP joint.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:extremities_greattoe_gout.jpg|Gout of the Right Great Toe: Diffuse swelling and redness centered at the right MTP joint, but extending over much of the foot.
Image:upper_tophaceous_gout.jpg|Tophaceous Gout
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:extremities_gout_normal.jpg|Gout of the Knee: Image demonstrates redness and swelling caused by acute gouty arthritis.
Image:extremities_gout_inflamed.jpg|Picture demonstrates normal knee for comparison. skin changes seen in both legs are related to burns that patient suffered previously.
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:ChronicGout.jpg|Gout with tophi on elbow and knee.
Image:Gout (no birefringence).jpg|Gout (Needles, no birefringence, monosodium urate) <ref>http://picasaweb.google.com/mcmumbi/USMLEIIImages</ref>
</gallery>
</div>
 
==Treatment==
 
===Acute attacks===
The first line of treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are [[indomethacin]], other [[Non-steroidal anti-inflammatory drug|nonsteroidal anti-inflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAIDs]]), oral [[glucocorticoids]], or intra-articular [[glucocorticoids]] administered via a [[joint injection]].
 
[[Colchicine]] was previously the drug of choice in acute attacks of gout, as it impairs the motility of [[granulocyte]]s and can prevent the inflammatory phenomena that initiate an attack. Colchicine should be taken within the first 12 hours of the attack and usually relieves the pain within 48 hours, although side effects (gastrointestinal upset such as [[diarrhea]] and [[nausea]]) can complicate its use. [[Non-steroidal anti-inflammatory drug|NSAIDs]] are the preferred form of analgesia for patients with gout.
 
A [[randomized controlled trial]] found similar benefit from [[Non-steroidal anti-inflammatory drug|nonsteroidal anti-inflammatory drugs]] and oral [[glucocorticoids]]; however, less [[adverse drug reaction]]s occurred in the [[glucocorticoids]] group.<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> In the [[Non-steroidal anti-inflammatory drug|nonsteroidal anti inflammatory drugs]] group, each patient initially received [[diclofenac]] (75 mg) intramuscularly, [[indomethacin]] 50 mg orally, and [[acetaminophen]] 1 g orally. The patient was received a 5-days of indomethacin (50 mg orally every 8 hours for 2 days, followed by indomethacin 25 mg every 8 hours for 3 days), and acetaminophen 1 g every 6 hours as needed. The [[glucocorticoids]] patients received [[prednisolone]] 30 mg orally, and acetaminophen 1 g orally. The patient was then given prednisolone 30 mg orally once per day for five days.
 
Before medical help is available, some over-the-counter medications can provide temporary relief from pain and swelling. [[Non-steroidal anti-inflammatory drug|NSAIDs]] such as [[ibuprofen]] can reduce the pain and inflammation slightly, although [[aspirin]] should not be used as it can worsen the condition. [[Preparation H]] [[hemorrhoid]]al [[ointment]] can be applied to the swollen skin to reduce the swelling temporarily. Professional medical care is needed for long-term management of gout.
 
Ice may be applied for 20–30 minutes several times a day, and a [[randomized controlled trial]] found that  patients who used ice packs had better relief of pain without side effects.<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>  Keeping the affected area elevated above the level of the heart also may help.
 
Due to swelling around affected joints for prolonged periods, shedding of skin may occur. This is particularly evident when small toes are affected and may promote fungal infection in the web region if dampness occurs, and treatment is similar to that for common [[athlete's foot]].
 
Some sufferers of Gout report an aggravation of the condition in the knees and toes associated with long periods of immobility, such as when sitting at a computer desk for long hours. This can be particularly unfortunate if the sufferer is searching for work as the aggravation can interefere with mobility. Sufferers who notice early swelling or early pain may appear to be able to arrest the aggravation when medical treatment is applied before the condition gets worse. Where this is the case, a medically prescribed anti-inflammatory oral treatment taken with food and bed rest may provide relief within 6-8 hours. 
 
Another possibility is use of [[acetazolamide]], one of the first diuretics discovered. This drug inhibits the action of carbonic anhydrase on the proximal convoluted tubules within the kidneys, which effectively inhibits reabsorption of [[bicarbonate]], thus alkalinizing the urine. After two to three days of usage, the diuretic effects of this drug decline because of increased downstream reabsorption of ions and water by the renal tubules; however, the alkalinization of urine persists, and this basic urine attracts weak acids such as '''uric acid''' and cystine into the urine, thus increasing their urinary excretion.<sup>35</sup>
 
===Chronic joint changes===
For ''extreme'' cases of gout, surgery may be necessary to remove large tophi and correct joint deformity.
 
==Prevention==
 
===Medications===
 
* [[Allopurinol]] and [[azathioprine]] (Imuran) used together present a risk of a potentially fatal [[drug interaction]], a severe risk of allopurinol use which is of importance to transplant patients being treated with azathioprine for [[immunosuppression]].[http://www.medsafe.govt.nz/Profs/PUarticles/azathioprine.htm]
 
* [[Febuxostat]] ((2-[3-cyano-4-isobutoxyphenyl]-4-methylthiazole-5-carboxylic acid) - a non-purine inhibitor of xanthine oxidase seems to be an alternative that is superior to allopurinol; it is currently in [[Clinical trials#Phase III| Phase III trials]].<ref>{{cite journal | author = Becker M, Schumacher H, Wortmann R, MacDonald P, Eustace D, Palo W, Streit J, Joseph-Ridge N | title = Febuxostat compared with allopurinol in patients with hyperuricemia and gout | journal = N Engl J Med | volume = 353 | issue = 23 | pages = 2450&ndash;61 | year = 2005 | id = PMID 16339094}}</ref>
 
* [[Probenecid]], a uricosuric drug that promotes the excretion of uric acid in urine, is also commonly prescribed - often in conjunction with [[colchicine]]. The drug [[fenofibrate]] (which is used in treating [[hyperlipidemia]]) also exerts a beneficial uricosuric effect.<ref>{{cite journal | author = Bardin T | title = Fenofibrate and losartan | journal = Ann Rheum Dis | volume = 62 | issue = 6 | pages = 497&ndash;8 | year = 2003 | id = PMID 12759281 | url=http://ard.bmjjournals.com/cgi/content/full/62/6/497}}</ref>
 
* As arterial hypertension quite often coexists with gout, treating it with [[losartan]], an [[angiotensin II receptor antagonist]], might have an additional beneficial effect on uric acid plasma levels. This way losartan can offset the negative side-effect of [[thiazide]]s (a group of [[diuretic]]s used for [[arterial hypertension|high blood pressure]]) on uric acid metabolism in patients with gout.
 
* It is suspected that in many cases gout may be secondary to untreated [[sleep apnea]], when oxygen-starved cells break down and release purines as a by-product. Treatment for apnea can be effective in lessening incidence of acute gout attacks.<ref>{{cite journal | author = Abrams B | title = Gout is an indicator of sleep apnea | journal = Sleep | volume = 28 | issue = 2 | pages = 275 | year = 2005 | id = PMID 16171252}}</ref>
 
* A study in 2004 suggests that animal flesh sources of purine, such as beef and seafood, greatly increase the risk of developing gout. However, high-purine vegetable sources did not. Dairy products such as milk and cheese significantly reduced the chances of gout. The study followed over 40000 men over a period of 12 years, in which 1300 cases of gout were reported.<ref name="Choi et al 2004">{{cite journal | author = Choi H, Atkinson K, Karlson E, Willett W, Curhan G | title = Purine-rich foods, dairy and protein intake, and the risk of gout in men | journal = N Engl J Med | volume = 350 | issue = 11 | pages = 1093&ndash;103 | year = 2004 | id = PMID 15014182 | url=http://www.nutritionaustralia.org/News_in_Nutrition/Journal_Articles/purine%20rich%20foods.pdf | format=PDF}}</ref>
 
* PEG-uricase, a polyethylene glycol ("PEG") conjugate of recombinant porcine uricase (urate oxidase), which breaks down the uric acid deposits is being studied in [[clinical trial#Phase III|Phase III clinical trials]] for the treatment of severe, treatment-refractory gout in the United States in 2006.[http://www.savientpharma.com/pipeline/puricase.asp Pipeline]
 
*[[Sodium bicarbonate]] (baking soda) is an old remedy,<ref>The British Pharmaceutical Codex.  Published by direction of the Council of the Pharmaceutical Society of Great Britain, 1911. [http://www.henriettesherbal.com/eclectic/bpc1911/sodium.html Sodium]</ref> thought to work by raising blood pH (lowering blood acidity).  However, the added sodium may be inappropriate for some people.
 
*Research from the University of British Columbia suggests long-term coffee consumption is associated with a lower risk of gout.<ref>{{cite journal | author = Hyon K. Choi, Walter Willett, Gary Curhan | title =
Coffee consumption and risk of incident gout in men: A prospective study | journal = Arthritis & Rheumatism | volume = 56 | issue = 6 | pages = 2049&ndash;2055 | year = 2007 | id = PMID 17530645}}</ref> <ref>{{cite journal | author = Choi HK, Curhan G. | title =
Coffee, tea, and caffeine consumption and serum uric acid level: The third national health and nutrition examination survey | journal = Arthritis & Rheumatism | volume = 57 | issue = 5 | pages = 816&ndash;821 | year = 2007 | id = PMID 17530681 }}</ref>
 
===Diet===
 
''See Saag and Choi, 2006, an open-access review article, for detailed references and further information.''<ref>{{cite journal |author=Saag KG, Choi H |title=Epidemiology, risk factors, and lifestyle modifications for gout |journal=Arthritis Res. Ther. |volume=8 Suppl 1 |issue= |pages=S2 |year=2006 |pmid=16820041 |doi=10.1186/ar1907 |url=http://arthritis-research.com/content/8/S1/S2 }}</ref>
 
The serum level of uric acid is the primary risk factor for gout. The serum level is the result of both intake (diet) and output (excretion).
 
====Reduce intake of purines====
 
The solubility threshold for uric acid is approximately 6.7 mg/dl;  above this threshold crystals may form.  Healthy subjects in the Normative Aging Study who had serum levels of uric acid over 9.0 mg/dl suffered a 22% incidence of gout over six years, compared to less than one percent for those with 7.0-8.9 mg/dl. The average uric acid level in men is 5.0 mg/dl, and substitution of a purine-free formula diet reduces this to 3.0 mg/dl. A purine-restricted diet lowers the level nearly as much (1-2 mg/dl).
 
A diet low in purines reduces the serum level of uric acid. Notable sources of dietary purines include:
*beer (high in [[guanosine]]
 
'''Protein''' is a crude proxy for purines;  a more precise proxy is '''muscle'''.  Apart from the notable dietary purines above, the main source of dietary purines is [[DNA]] and [[RNA]], via their bases [[adenine]] and [[guanine]].  All sources of dietary protein supply some purines, but some sources provide far more purines than others.  Meat (particularly dark meat) and seafood are high in purine because [[muscle]] cells are packed with [[mitochondrion|mitochondria]], which have their own DNA and RNA.  In a large prospective study, high consumption of meat and seafood were found associated with an elevated risk of gout onset (41% and 50%, respectively).  High consumption of dairy products, high in protein but very low in DNA and RNA, was associated with a 44% ''decrease'' in the incidence of gout.  Consumption of the more purine-rich vegetables or a high protein diet per se had no significant correlation.
 
Consumption of '''beer''' is associated with a 49% increase in relative risk per daily 12-oz serving.  By contrast, consumption of spirits was associated with only a 15% increase in relative risk, and no association at all was found with consumption of wine.
 
Some '''medical drugs''' are purine-based.  Notable among these are the purine-analog [[antimetabolite]] drugs, sometimes used as [[chemotherapy]] agents.
 
====Increase output of uric acid====
 
Ingestion of 500 mg of [[Vitamin C]] per day has been shown to bring about a 0.5 mg/dl decrease in serum uric acid through increased excretion. Some Gout sufferers have recently found that taking up to 1,000 mg of Vitamin C, combined with a small dosage (approx. 10-15 mg./day) of [[Lithium]] have had very beneficial effects on their uric acid levels.
 
Vitamin C, taken in high doses, can help decrease blood uric acid levels, but should not be taken without a doctor's supervision. Note that there is a small subset of people with gout who will actually get worse with high levels of vitamin C. Also, a single high dose can free up too much uric acid and cause kidney stones. (University of Maryland Medical Center for Integrative Medicine).
 
====Other approaches====
 
Additional dietary recommendations can be made which reduce gout indirectly, by reducing gout risk factors such as [[obesity]], [[hypertension]], [[cardiovascular disease]], [[diabetes]], and [[metabolic syndrome]].
 
'''The following suggestions do not meet with universal approval among medical practitioners.'''
 
Low [[purine]] diet:
* To lower uric acid:
** cherries were reported to reduce uric acid in a small study.<ref>{{cite journal |author=Jacob RA, Spinozzi GM, Simon VA, ''et al'' |title=Consumption of cherries lowers plasma urate in healthy women |journal=J. Nutr. |volume=133 |issue=6 |pages=1826-9 |year=2003 |pmid=12771324 |doi=}}</ref><ref>{{cite journal |author=BLAU LW |title=Cherry diet control for gout and arthritis |journal=Tex. Rep. Biol. Med. |volume=8 |issue=3 |pages=309-11 |year=1950 |pmid=14776685 |doi=}}</ref>
** [[celery]] extracts (celery or celery seed either in capsule form or as a tea) is believed by many to reduce uric acid levels (although these are also [[diuretic]]s). Celery extracts have been reported to act synergistically with anti-inflammatory drugs.<ref>{{cite journal |author=Whitehouse MW, Butters DE |title=Combination anti-inflammatory therapy: synergism in rats of NSAIDs/corticosteroids with some herbal/animal products |journal=Inflammopharmacology |volume=11 |issue=4 |pages=453-64 |year=2003 |pmid=15035799 |doi=10.1163/156856003322699636}}</ref>
** Cheese has been recommended as a low-purine food,<ref>{{cite journal |author=Harris MD, Siegel LB, Alloway JA |title=Gout and hyperuricemia |journal=American family physician |volume=59 |issue=4 |pages=925-34 |year=1999 |pmid=10068714 |doi= |url=http://newcms.aafp.org/afp/990215ap/925.html}}</ref> and dairy products have been found to reduce the risk of gout.
*Food to avoid:
**foods high in [[purine]]s
*** limit food high in protein such as meat, fish, poultry, or [[tofu]] to 8 ounces (226 grams) a day. Avoid entirely during a flare up. Tofu has been proposed as a safe source of protein for gout patients due to its small and transient effect on plasma urate levels.<ref>{{cite journal |author=Yamakita J, Yamamoto T, Moriwaki Y, Takahashi S, Tsutsumi Z, Higashino K |title=Effect of Tofu (bean curd) ingestion and on uric acid metabolism in healthy and gouty subjects |journal=Adv. Exp. Med. Biol. |volume=431 |issue= |pages=839-42 |year=1998 |pmid=9598181 |doi=}}</ref>
***sweetbreads, [[kidney]]s, [[liver]], [[brain]]s, or other offal meats.<ref>{{cite journal |author=Robinson CH |title=The low purine diet |journal=Am. J. Clin. Nutr. |volume=2 |issue=4 |pages=276-7 |year=1954 |pmid=13188851 |doi= |url=http://www.ajcn.org/cgi/reprint/2/4/276}}</ref><ref>{{cite journal |author=Chou P, Soong LN, Lin HY |title=Community-based epidemiological study on hyperuricemia in Pu-Li, Taiwan |journal=J. Formos. Med. Assoc. |volume=92 |issue=7 |pages=597-602 |year=1993 |pmid=7904493 |doi=}}</ref>
***sardines and anchovies <ref>{{cite journal |author=Robinson CH |title=The low purine diet |journal=Am. J. Clin. Nutr. |volume=2 |issue=4 |pages=276-7 |year=1954 |pmid=13188851 |doi= |url=http://www.ajcn.org/cgi/reprint/2/4/276}}</ref>
***[[seafood]] <ref>{{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. |volume=350 |issue=11 |pages=1093-103 |year=2004 |pmid=15014182 |doi=10.1056/NEJMoa035700}}</ref>
***[[alcohol]].<ref>{{cite journal |author=Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G |title=Alcohol intake and risk of incident gout in men: a prospective study |journal=Lancet |volume=363 |issue=9417 |pages=1277-81 |year=2004 |pmid=15094272 |doi=10.1016/S0140-6736(04)16000-5}}</ref> Some claim that this applies especially to beer, on the basis that brewer's yeasts are very rich in purine. Since most modern commercial beer contains only trace amounts of yeast, this claim requires further substantiation. Formerly, port wine was sweetened with litharge, causing [[lead poisoning]], of which gout is a complication.  Ironically, red wines, particularly those produced by traditional methods,<ref>{{cite journal |author=Corder R, Mullen W, Khan NQ, ''et al'' |title=Oenology: red wine procyanidins and vascular health |journal=Nature |volume=444 |issue=7119 |pages=566 |year=2006 |pmid=17136085 |doi=10.1038/444566a}}</ref> contain procyanidins released from grape seeds during wine making, which have been reported to lower serum uric acid levels by an indirect mechanism.<ref>{{cite journal |author=Wang Y, Zhu JX, Kong LD, Yang C, Cheng CH, Zhang X |title=Administration of procyanidins from grape seeds reduces serum uric acid levels and decreases hepatic xanthine dehydrogenase/oxidase activities in oxonate-treated mice |journal=Basic Clin. Pharmacol. Toxicol. |volume=94 |issue=5 |pages=232-7 |year=2004 |pmid=15125693 |doi=10.1111/j.1742-7843.2004.pto940506.x}}</ref> However, withdrawal of urate-lowering therapy is associated with recurrence of acute gouty arthritis.<ref>{{cite journal |author=Perez-Ruiz F, Atxotegi J, Hernando I, Calabozo M, Nolla JM |title=Using serum urate levels to determine the period free of gouty symptoms after withdrawal of long-term urate-lowering therapy: a prospective study |journal=Arthritis Rheum. |volume=55 |issue=5 |pages=786-90 |year=2006 |pmid=17013833 |doi=10.1002/art.22232}}</ref>
***meat extracts, consommés, and gravies<ref>{{cite journal |author=Robinson CH |title=The low purine diet |journal=Am. J. Clin. Nutr. |volume=2 |issue=4 |pages=276-7 |year=1954 |pmid=13188851 |doi= |url=http://www.ajcn.org/cgi/reprint/2/4/276}}</ref>
 
* To avoid [[dehydration]]:
** Drink plenty of liquids, especially [[water]], to dilute and assist excretion of urates;
** Avoid [[diuretic]] foods or medicines like [[aspirin]](aspirin should be avoided from those suffering from gout, unless specified by a trained physician), [[vitamin C]], [[tea]] and alcohol.  The role of diuretics in triggering gout has been disputed.<ref>{{cite journal |author=Janssens HJ, van de Lisdonk EH, Janssen M, van den Hoogen HJ, Verbeek AL |title=Gout, not induced by diuretics? A case-control study from primary care |journal=Ann. Rheum. Dis. |volume=65 |issue=8 |pages=1080-3 |year=2006 |pmid=16291814 |doi=10.1136/ard.2005.040360}}</ref>
 
* Moderate intake of purine-rich vegetables is not associated with increased gout.<!--
  --><ref name="Choi et al 2004"/>
 
==Pathological Findings==
 
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0001.jpg|Kidney: Uric Acid Deposition: Gross, an excellent example of gouty nephropathy with deposits and excavation in pyramids
Image:Gout 0002.jpg|Kidney: Papillary Necrosis: Gross, yellow foci in pyramids, a gout kidney
Image:Gout 0003.jpg|Skin: Tophus: Micro med mag H&E uric acid deposits with giant cells. Easily recognizable as gout or uric acid tophus
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0004.jpg|Bone, synovium: Gout: Gross natural color opened joint with extensive white deposits of uric acid
Image:Gout 0005.jpg|Bone, synovium: Gout: Gross natural color close-up of extensive uric acid deposits
Image:Gout 0006.jpg|Bone, synovium: Gout: Gross natural color section through sternum and clavicle showing very well uric acid deposits in the periarticular tissue
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0007.jpg|Bone: Gout: Gross close-up of elbow with enlargement of proximal radius due to gout
Image:Gout 0008.jpg|Hand: Gout: Gross view of both hand with enlarged joints
Image:Gout 0009.jpg|Kidney: Gout: Gross natural color close-up view of uric acid deposit in medullary pyramid
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0010.jpg|Hand: Gout: Gross natural color
Image:Gout 0011.jpg|Urinary Tract: Staghorn calculi in renal pelvis, Gout
Image:Gout 0012.jpg|Bones-Joints: Gout
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0013.jpg|Bones-Joints: Gout
Image:Gout 0014.jpg|Bones-Joints: Gout
Image:Gout 0015.jpg|Bones-Joints: Gout
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0016.jpg|Bones-Joints: Gout
Image:Gout 0017.jpg|Bones-Joints: Gout
Image:Gout 0018.jpg|Bones-Joints: Gout
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0019.jpg|Bones-Joints: Gout
Image:Gout 0020.jpg|Bones-Joints: Gout
Image:Gout 0021.jpg|Bones-Joints: Gout
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0022.jpg|Bones-Joints: Gout, alcohol fixed tissues, monosodium urate crystals
Image:Gout 0023.jpg|Bones-Joints: Gout, alcohol fixed tissues, monosodium urate crystals
Image:Gout 0024.jpg|Bones-Joints: Gout, alcohol fixed tissues, monosodium urate crystals
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0025.jpg|Bones-Joints: Gout
Image:Gout 0026.jpg|Bones-Joints: Gout
Image:Gout 0027.jpg|Gout; Bursa of Knee
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0028.jpg|Joint: Uric Acid Crystals in Acute Gout
Image:Gout 0029.jpg|Joint: Gout
Image:Gout 0030.jpg|Knee Joint: Gout. Heavy Deposition of Urate Crystals in Articular Cartilage
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0031.jpg|Kidney: Uric Acid Deposition: Gross, infant kidney with excellent uric acid streaks
Image:Gout 0032.jpg|Kidney: Uric Acid Deposition: Gross good example uric acid streaks in medulla (very ischemic kidney)
Image:Gout 0033.jpg|Kidney: Uric Acid Nephropathy: Gross, natural color, an excellent view of hydronephrosis with inflamed pelvis and multiple calculi with deposits in medullary pyramids
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0034.jpg|Kidney: Uric Acid Deposition: Gross natural color close-up and excellent view of opaque material in medullary pyramid of adult kidney
Image:Gout 0035.jpg|Kidney: Uric Acid Infarcts: Gross natural color opened kidney showing marked ischemia with dark red medullary pyramids which contrast sharply with the uric acid deposits
Image:Gout 0036.jpg|Kidney: Uric Acid Infarcts: Gross natural color typical lesion well shown
</gallery>
</div>
 
 
<div align="left">
<gallery heights="175" widths="175">
Image:Gout 0037.jpg|Kidney: Uric Acid In Medulla: Gross natural color cut surface of kidney uric acid easily seen
Image:Gout 0038.jpg|Kidney: Uric Acid Infarcts: Gross natural color close-up outstanding photo of the uric acid streaks in medullary pyramids
Image:Gout 0039.jpg|Skin: Tophus: Micro med mag H&E easily recognized uric acid deposit lesion from elbow
</gallery>
</div>
 
==See also==
* [[Pseudogout]] is a very similar disease, but caused by deposition of [[calcium pyrophosphate]], not uric acid.
 
==References==
{{reflist|2}}
 
==Additional References==
 
* Katzung, Bertram G. ''Basic and Clinical Pharmacology'', 10th edition.  New York: McGraw Hill Medical, 2007. pp. 242
 
==External links==
* {{cite web | title=American College of Rheumatology | url=http://www.rheumatology.org/public/factsheets/gout_new.asp?aud=pat| American College of Rheumatology  |g publisher= |date=March 23, 2007 | accessdate=2007-03-23}}- (ACR Fact Sheet on Gout)
* {{cite web | title=Questions and Answers on Gout from NIAMS| url=http://www.niams.nih.gov/Health_Info/Gout/default.asp | title = Answers and Questions on Gout  | publisher= U.S. [[National Institutes of Health]]—[[National Institute of Arthritis and Musculoskeletal and Skin Diseases]] |date=September 28th, 2007 | accessdate=2007-08-28}}
* {{cite web | title=Diet and gout | url=http://my.webmd.com/hw/health_guide_atoz/ty2036.asp?navbar=hw69013 | work=A-Z Health Guide  | publisher=webMD.com |date=July 01, 2004 | accessdate=2006-09-18}}
* {{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}}
* {{cite web | title=Purine content in food | url=http://www.britishdalmatianclub.org.uk/downloads/Purine%20Table%202003_files/sheet001.htm | publisher=British Dalmatian Club | accessdate=2006-09-18}}
* [http://health.howstuffworks.com/gout-in-depth.htm Gout in Depth - How Stuff Works]
 
{{SIB}}
{{Diseases of the musculoskeletal system and connective tissue}}
 
[[Category:Arthritis]]
[[Category:Rheumatology]]
 
 
 
[[ar:نقرس]]
[[bg:Подагра]]
[[cs:Dna]]
[[da:Gigt]]
[[de:Gicht]]
[[es:Gota (enfermedad)]]
[[eo:Podagro]]
[[fa:نقرس]]
[[fr:Arthrite goutteuse]]
[[io:Kiragro]]
[[id:Gout]]
[[it:Gotta]]
[[he:שיגדון]]
[[lb:Giicht]]
[[ms:Gout]]
[[nl:Jicht]]
[[ja:痛風]]
[[no:Urinsyregikt]]
[[pl:Dna moczanowa]]
[[pt:Gota (doença)]]
[[ru:Подагра]]
[[sk:Dna]]
[[sr:Гихт]]
[[fi:Kihti]]
[[sv:Gikt]]
[[te:గౌటు]]
[[tr:Gut hastalığı]]
[[zh:痛风]]
 
 
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Latest revision as of 19:01, 2 October 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]

Synonyms and keywords: Urate crystal arthropathy; uric acid crystal deposition in joint; gouty arthritis; podagra

Overview

Historical Perspective

Pathophysiology

Differentiating Gout from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

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