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Wikipedia - Gout

Gout
Classification and external resources

A 1799 cartoon depicting gout.
ICD-10 M10.
ICD-9 274.00 274.1 274.8 274.9
OMIM 138900 300323
DiseasesDB 29031
MedlinePlus 000422
eMedicine emerg/221 med/924 med/1112 oph/506 orthoped/124 radio/313
MeSH D006073

Gout (also known as podagra) is a medical condition characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. It is caused by elevated levels of uric acid in the blood. The uric acid crystallizes and is deposited in joints, tendons, and surrounding tissues. Gout affects around 1% of the Western population at some point in their lives.

Treatment with non-steroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms. Once the acute attack has subsided, levels of uric acid are usually lowered via lifestyle changes and long-term prevention with allopurinol or probenicid. Gout was historically known as "the disease of kings" or "rich man's disease".

Contents

[edit] Signs and symptoms

Gout presenting in the metatarsal-phalangeal joint of the big toe. Note the slight redness of the skin overlying the joint.
Tophi of the knee.

Gout can present in a number of different ways, although the most usual is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint).[1] The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases.[2] Other joints such as the heels, knees, wrists, and fingers may also be affected.[2] Joint pain usually begins over 2–4 hours and during the nighttime.[2] Other symptoms that may occur along with the joint pain include fatigue and fever.[2]

Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology including hard, non-painful deposits of uric acid crystal known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[3] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys resulting in stone formation. This may result in urate nephropathy.[4]

[edit] Cause

Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons including dietary, genetic, or underexcretion of urate, the salts of uric acid.[1] About 10% of people with hyperuricemia develop gout.[5]

[edit] Lifestyle

About 12% of gout is attributed to dietary causes.[1] This includes a strong association with the consumption of alcohol, sugar, meat, and seafood.[3] The intake of dairy products, purine rich vegetables, and the total protein intake do not affect the occurrence.[6][7] Coffee consumption and physical fitness appears to decrease the risk.[8][9]

[edit] 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.[2] Other conditions which are commonly complicated by gout include: polycythaemia, obesity, diabetes, Lesch-Nyhan syndrome, hypertension, renal failure, hemolytic anemia and solid organ transplants.[10] A body mass index greater than or equal to 35 increases a male's risk of gout three-fold.[7] Chronic lead exposure and lead contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.[11]

[edit] Medication

Diuretics have been associated with attacks of gout however a low dose of hydrochlorothiazide (HCTZ) does not seem to increase the risk.[12] Other medicines that have been associated include niacin and aspirin (acetylsalicylic acid).[3] Cyclosporine is also associated with gout, particularly when used in combination with hydrochlorothiazide.[13]

[edit] Pathophysiology

Uric acid

Gout occurs when crystals of uric acid, in the form of monosodium urate, precipitate in joints, on tendons, and in the surrounding tissues.[3] These crystals may then trigger a local immune mediated inflammatory reaction.[3] The triggers for precipitation are not well understood. While uric acid may crystallize at normal levels it is more likely as levels increase.[3][14] Other factors believed to be important in triggering an acute episode of arthritis include: cool temperatures, rapid changes in uric acid levels, and acidosis.[15][16] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.[1]

[edit] Diagnosis

Spiked rods of uric acid (MSU) crystals photographed under a microscope with polarized light from a synovial fluid sample. Formation of uric acid crystals in the joints are associated with gout.

[edit] Synovial fluid

A definitive diagnosis of gout is based upon the identification of monosodium urate (MSU) crystals in synovial fluid or a tophus.[2] Under polarized light microscopy they have a needle-like morphology and strong negative birefringence. This test is difficult to perform and often requires a trained observer.[17]

[edit] Blood tests

Hyperuricemia is a classic feature of gout, however gout occurs nearly half of the time without hyperuricemia and most people with raised uric acid levels never develop gout.[2][18] Thus the diagnostic utility of measuring a uric acid level is limited.[2] 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.[19] Other blood tests commonly performed are white blood cell count, electrolytes, renal 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.[20][21]

[edit] Differential diagnosis

An important differential diagnosis in gout is septic arthritis.[2] This should be considered in those with signs of infection or those who do not improve with treatment.[2] To help with diganosis in synovial fluid gram stain and culture may be performed.[2] Other conditions which present similarly include pseudogout and rheumatoid arthritis.[2] Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma,[22] or other neoplasms.[23]

[edit] Prevention

Both lifestyle changes and medication can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of food high in purines such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption and avoiding obesity.[1] A low-calorie diet in obese men decreased uric acid levels by 100 µmol/L (1.7 mg/dL).[12] Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45% compared to 250 mg per day.[24] Coffee but not tea consumption is associated with a lower risk of gout.[25] 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.[26]

[edit] Treatment

The initial aim of treatment is to settle the symptoms of an acute attack.[27] Repeated attacks can be prevented by different drugs used to reduce the serum uric acid levels,[27] but are not recommended until after a second attack of gout,[1] unless destructive joint changes, tophi, or urate nephropathy exists[4] as it is not until this point that medications have been found to be cost effective.[1] Ice applied for 20 to 30 minutes several times a day decreases pain.[1][28] Options for acute treatment include application of nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and steroids.[1]

[edit] NSAIDs

NSAIDs are the usual first-line treatment for gout, and no agent is significantly more or less effective than any other.[1] Improvement may be seen within 4 hours.[1] They however are not recommended in those with certain other health problems such as gastrointestinal bleeding, renal failure, or heart failure.[29] While indomethacin has historically been the most commonly used NSAID, an alternative like ibuprofen may be preferred due to its better side-effect profile in the absence of superior effectivenes.[12] For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.[30]

[edit] Colchicine

Colchicine is an alternative for those unable to tolerate NSAIDs.[1] Its side-effects (primarily gastrointestinal upset) limit its usage.[31][32] Gastrointestinal upset, however, depends on the dose and the risk can be decreased by using smaller yet still effective doses.[12] Colchicine may interact with other commonly prescribed drugs such as atorvastatin and erythromycin among others.[32]

[edit] Steroids

Glucocorticoids have been found to be as effective as NSAIDs[33] and may be used if contraindications exist for NSAIDs.[1] They also lead to improvement when injected into the joint, however the risk of a joint infection must be excluded as they worsen this condition.[1]

[edit] Prophylaxis

A number of medications are useful for preventing further episodes of gout including: allopurinol, probenecid, and febuxostat. They are not started until one to two weeks after an acute attack has resolved, due to theoretical concerns of worsening the attack.[1] If these medications are being used chronically at the time of the attack they should not be.[2] Urate lowering measures should be increased until serum uric acid levels are below 360 µmol/L (6.0 mg/dL).[1]

Allopurinol blocks uric acid production and is the most commonly used hypourecemic agent.[1] Long term therapy is safe and well tolerated, and can be used in people with renal impairment or urate stones. Hypersensitivity occurs in a small number of people.[1] Probenecid is effective for treating hyperuricemia but has been found to be less effective than allopurinol.[1] Febuxostat, a non-purine inhibitor of xanthine oxidase, may be an alternative to allopurinol. It is approved in both Europe[34] and the United States.[35]

[edit] Epidemiology

Gout affects around 1% of the Western population at some point in their lifetime and is becoming more common.[1] Rates of gout have approximately doubled between 1990 and 2010.[3] 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.[7] A number of factors have been found to influence rates of gout including: age, race, and the season of the year. In men over the age of 30 and women over the age of 50 prevalence is 2%.[29] In the United States, gout is twice as likely in African American males as it is in European-Americans.[36] Rates are high among the peoples of the Pacific Islands and the Maori of New Zealand, but rare in Australian aborigines despite a higher mean concentration of serum uric acid in the latter group.[37] Some studies have 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.[38]

[edit] History

Anton van Leeuwenhoek described the microscopic appearance of uric acid crystals in 1679.[39]

The word gout was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin word gutta, meaning "a drop" (of liquid).[39] Gout has however been known since antiquity. Historically it has been referred to as "the disease of kings"[40] or "rich man's disease".[41] The first documented description is from Egypt in 2,600 BC. The Greek physician Hippocrates around 400 BC, also commented on it.[39] 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.[42]

The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.[39] In 1848 English physician Alfred Baring Garrod realized that this excess uric acid in the blood was the cause of gout.[43]

[edit] In other animals

Gout is rare in most other animals due to their ability to produce the enzyme uricase which breaks down uric acid.[44] Humans have lost this ability.[44] The Tyrannosaurus rex specimen known as "Sue" however is believed to have suffered from gout.[45]

[edit] Research

A number of new medications are under study for treating gout including: anakinra, canakinumab, and rilonacept.[46]

[edit] See also

Search Wiktionary Look up gout in Wiktionary, the free dictionary.

[edit] References

  1. ^ a b c d e f g h i j k l m n o p q r s t Chen LX, Schumacher HR (October 2008). "Gout: an evidence-based review". J Clin Rheumatol 14 (5 Suppl): S55–62. doi:10.1097/RHU.0b013e3181896921. PMID 18830092. 
  2. ^ a b c d e f g h i j k l m Schlesinger N (March 2010). "Diagnosing and treating gout: a review to aid primary care physicians". Postgrad Med 122 (2): 157–61. doi:10.3810/pgm.2010.03.2133. PMID 20203467. 
  3. ^ a b c d e f g Terkeltaub R (January 2010). "Update on gout: new therapeutic strategies and options". Nat Rev Rheumatol 6 (1): 30–8. doi:10.1038/nrrheum.2009.236. PMID 20046204. 
  4. ^ a b Tausche AK, Jansen TL, Schröder HE, Bornstein SR, Aringer M, Müller-Ladner U (August 2009). "Gout--current diagnosis and treatment". Dtsch Arztebl Int 106 (34-35): 549–55. doi:10.3238/arztebl.2009.0549. PMID 19795010. 
  5. ^ Vitart V, Rudan I, Hayward C, et al. (April 2008). "SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout". Nat. Genet. 40 (4): 437–42. doi:10.1038/ng.106. PMID 18327257. 
  6. ^ Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G (March 2004). "Purine-rich foods, dairy and protein intake, and the risk of gout in men". N. Engl. J. Med. 350 (11): 1093–103. doi:10.1056/NEJMoa035700. PMID 15014182. 
  7. ^ a b c Weaver AL (July 2008). "Epidemiology of gout". Cleve Clin J Med 75 Suppl 5: S9–12. PMID 18819329. 
  8. ^ Hak AE, Choi HK (March 2008). "Lifestyle and gout". Curr Opin Rheumatol 20 (2): 179–86. doi:10.1097/BOR.0b013e3282f524a2. PMID 18349748. 
  9. ^ Williams PT (May 2008). "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. PMID 18469274. 
  10. ^ Stamp L, Searle M, O'Donnell J, Chapman P (2005). "Gout in solid organ transplantation: a challenging clinical problem". Drugs 65 (18): 2593–611. PMID 16392875. 
  11. ^ Loghman-Adham M (September 1997). "Renal effects of environmental and occupational lead exposure". Environ. Health Perspect. (Brogan & Partners) 105 (9): 928–38. doi:10.2307/3433873. PMID 9300927. 
  12. ^ a b c d Laubscher T, Dumont Z, Regier L, Jensen B (December 2009). "Taking the stress out of managing gout". Can Fam Physician 55 (12): 1209–12. PMID 20008601. 
  13. ^ Firestein, MD, Gary S.; Budd, MD, Ralph C.; Harris Jr., MD, Edward D. et al., eds (2008). "Chapter 87: Gout and Hyperuricemia". KELLEY'S Textbook of Rheumatology (8th ed.). Elsevier. ISBN 978-1-4160-4842-8. 
  14. ^ Virsaladze DK, Tetradze LO, Dzhavashvili LV, Esaliia NG, Tananashvili DE (May 2007). "[Levels of uric acid in serum in patients with metabolic syndrome] [Levels of uric acid in serum in patients with metabolic syndrome]" (in Russian). Georgian Med News (146): 35–7. PMID 17595458. 
  15. ^ Moyer RA, John DS (April 2003). "Acute gout precipitated by total parenteral nutrition". The Journal of rheumatology 30 (4): 849–50. PMID 12672211. 
  16. ^ Halabe A, Sperling O (1994). "Uric acid nephrolithiasis". Mineral and electrolyte metabolism 20 (6): 424–31. PMID 7783706. 
  17. ^ Schlesinger N (December 2007). "Diagnosis of gout". Minerva Med. 98 (6): 759–67. PMID 18299687. 
  18. ^ Sturrock R (2000). "Gout. Easy to misdiagnose". BMJ 320 (7228): 132–33. doi:10.1136/bmj.320.7228.132. PMID 10634714. PMC 1128728. http://bmj.bmjjournals.com/cgi/content/full/320/7228/132. 
  19. ^ Sachs L, Batra KL, Zimmermann B (November 2009). "Medical implications of hyperuricemia". Med Health R I 92 (11): 353–55. PMID 19999892. 
  20. ^ "Gout: Differential Diagnoses & Workup - eMedicine Rheumatology". http://emedicine.medscape.com/article/329958-diagnosis. 
  21. ^ "Gout and Pseudogout: Differential Diagnoses & Workup - eMedicine Emergency Medicine". http://emedicine.medscape.com/article/808628-diagnosis. 
  22. ^ Jordan DR, Belliveau MJ, Brownstein S, McEachren T, Kyrollos M (2008). "Medial canthal tophus". Ophthal Plast Reconstr Surg 24 (5): 403–4. doi:10.1097/IOP.0b013e3181837a31. PMID 18806664. 
  23. ^ Sano K, Kohakura Y, Kimura K, Ozeki S (March 2009). "Atypical Triggering at the Wrist due to Intratendinous Infiltration of Tophaceous Gout". Hand (N Y) 4 (1): 78–80. doi:10.1007/s11552-008-9120-4. PMID 18780009. 
  24. ^ Choi HK, Gao X, Curhan G (March 2009). "Vitamin C intake and the risk of gout in men: a prospective study". Arch. Intern. Med. 169 (5): 502–7. doi:10.1001/archinternmed.2008.606. PMID 19273781. 
  25. ^ Choi HK, Curhan G (June 2007). "Coffee, tea, and caffeine consumption and serum uric acid level: the third national health and nutrition examination survey". Arthritis Rheum. 57 (5): 816–21. doi:10.1002/art.22762. PMID 17530681. 
  26. ^ Abrams B (February 2005). "Gout is an indicator of sleep apnea". Sleep 28 (2): 275. PMID 16171252. 
  27. ^ a b Zhang W, Doherty M, Bardin T, et al. (October 2006). "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. doi:10.1136/ard.2006.055269. PMID 16707532. 
  28. ^ Schlesinger N et al. (2002). "Local ice therapy during bouts of acute gouty arthritis". J. Rheumatol. 29 (2): 331–4. doi:10.1093/rheumatology/29.5.331. PMID 11838852. 
  29. ^ a b Winzenberg T, Buchbinder R (July 2009). "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. PMID 19607767. 
  30. ^ Clinical Knowledge Summaries. "Gout - Management -- What treatment is recommended in acute gout?". National Library for Health. http://cks.library.nhs.uk/gout/management/detailed_answers/managing_acute_gout/treatment. Retrieved 2008-10-26. 
  31. ^ Gout~Medication at eMedicine
  32. ^ a b "Information for Healthcare Professionals: New Safety Information for Colchicine (marketed as Colcrys)". U.S. Food and Drug Administration. http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/ucm174315.htm. 
  33. ^ Man CY, Cheung IT, Cameron PA, Rainer TH (2007). "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. doi:10.1016/j.annemergmed.2006.11.014. PMID 17276548. 
  34. ^ "Adenuric (febuxostat) receives marketing authorisation in the European Union" (PDF). http://www.ipsen.com/articles/mediacentre/pressreleases/20080505___autorisation_adenuric_eu_10.pdf. Retrieved 2008-05-28. 
  35. ^ "FDA Okays New Treatment for Gout-Related Hyperuricemia". http://www.medpagetoday.com/ProductAlert/Prescriptions/12902. Retrieved 2009-05-25. 
  36. ^ Rheumatology Therapeutics Medical Center. "What Are the Risk Factors for Gout?". http://www.arthritisconsult.com/gout.html#risk. Retrieved 2007-01-26. 
  37. ^ Roberts-Thomson RA, Roberts-Thomson PJ (May 1999). "Rheumatic disease and the Australian aborigine". Ann. Rheum. Dis. 58 (5): 266–70. doi:10.1136/ard.58.5.266. PMID 10225809. PMC 1752880. http://ard.bmjjournals.com/cgi/content/full/58/5/266. 
  38. ^ Fam AG (May 2000). "What is new about crystals other than monosodium urate?". Curr Opin Rheumatol 12 (3): 228–34. doi:10.1097/00002281-200005000-00013. PMID 10803754. 
  39. ^ a b c d Pillinger, MH; Rosenthal P, Abeles AM (2007). "Hyperuricemia and gout: new insights into pathogenesis and treatment". Bulletin of the NYU Hospital for Joint Diseases 65 (3): 215–221. PMID 17922673. http://www.nyuhjdbulletin.org/Permalink.aspx?permalinkId=0c3ec9d1-8cc8-49d5-850d-4c5a55cb0669. 
  40. ^ Kubitz possibly has gout."The Disease Of Kings - Forbes.com". Forbes. http://www.forbes.com/2003/04/01/cx_cd_0401feat.html. 
  41. ^ "Rich Man's Disease - definition of Rich Man's Disease in the Medical dictionary - by the Free Online Medical Dictionary, Thesaurus and Encyclopedia.". http://medical-dictionary.thefreedictionary.com/Rich+Man%27s+Disease. 
  42. ^ "LacusCurtius • Celsus — On Medicine — Book IV". http://penelope.uchicago.edu/Thayer/E/Roman/Texts/Celsus/4*.html. 
  43. ^ Storey GD (October 2001). "Alfred Baring Garrod (1819-1907)". Rheumatology (Oxford, England) 40 (10): 1189–90. doi:10.1093/rheumatology/40.10.1189. PMID 11600751. http://rheumatology.oxfordjournals.org/cgi/content/full/40/10/1189. 
  44. ^ a b Agudelo CA, Wise CM (May 2001). "Gout: diagnosis, pathogenesis, and clinical manifestations". Curr Opin Rheumatol 13 (3): 234–9. doi:10.1097/00002281-200105000-00015. PMID 11333355. 
  45. ^ Rothschild, BM; Tanke D, Carpenter K (1997). "Tyrannosaurs suffered from gout". Nature 387 (6631): 357. doi:10.1038/387357a0. PMID 9163417. http://www.nature.com/nature/journal/v387/n6631/abs/387357a0.html. 
  46. ^ "New therapeutic options for gout here and on the horizon - The Journal of Musculoskeletal Medicine". http://www.musculoskeletalnetwork.com/gout/content/article/1145622/1533314. 

[edit] External links

Search Wikimedia Commons Wikimedia Commons has media related to: Gout
v • d • e
Antigout preparations (M04)
Uricosurics
Xanthine oxidase inhibitors
Mitotic inhibitors
Other

M: JNT

anat(h/c,u,t,l)/phys

proc, drug(M4)
v • d • e
Musculoskeletal disorders: Arthropathies (M00–M19, 711–719)
Arthritis
(monoarthritis/
polyarthritis)
Noninfectious
Noninflammatory
Other

M: JNT

anat(h/c,u,t,l)/phys

proc, drug(M4)
v • d • e
Inborn error of purine-pyrimidine metabolism (E79, 277.2)
Purine metabolism
Anabolism
Catabolism
Pyrimidine metabolism
Anabolism
Catabolism

M: MET

mt, a/u/y/n/h, r/g/c/p/i, f/s/l/o, m, e, t

au/y/n/h, rgcp/i, f/s/l/o, m, epon

meds(A16, C10),intm(a/u/y/n/h, r/g/c/p/i, f/s/o, e, t)
Retrieved from "http://en.wikipedia.org/wiki/Gout"

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Gout".

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