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| Gout Classification & external resources | |
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| Uric acid | |
| ICD-10 | M10. |
| ICD-9 | 274.0 274.1 274.8 274.9 |
| OMIM | 138900 300323 |
| DiseasesDB | 29031 |
| eMedicine | med/924 orthoped/124 emerg/221 med/1112 oph/506 radio/313 |
| MeSH | D006073 |
Gout (also called metabolic arthritis) is a disease created by a buildup of uric acid. 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.
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Gout is characterized by excruciating, sudden, unexpected, burning pain, as well as swelling, redness, warmness, and stiffness in the affected 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 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 of the ear. Elevated levels of uric acid in the urine can lead to uric acid crystals precipitating in the kidneys or bladder, forming uric acid kidney stones.
A definitive diagnosis of gout is from light microscopy of fluid aspirated from the joints (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 birefringence under polarised microscopy and its needle-like morphology. A trained observer does better in distinguishing them from other crystals.
Hyperuricemia is a common feature, although urate levels are not always raised.Sturrock R (2000). "Gout. Easy to misdiagnose". BMJ 320 (7228): 132–3. PMID 10634714. Hyperuricemia is defined as a plasma urate (uric acid) level greater than 420 μmol/L (7.0 mg/dL) in males (or 380 μmol/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.Siva C, Velazquez C, Mody A, Brasington R (2003). "Diagnosing acute monoarthritis in adults: a practical approach for the family physician". Am Fam Pghysician 68 (1): 83–90. PMID 12887114. 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, electrolytes, renal function, thyroid function tests and erythrocyte sedimentation rate (ESR). This helps to exclude other causes of arthritis, most notably septic arthritis, and to investigate any underlying cause for the hyperuricaemia.
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 hyperuricemia, although it is 10 times more common without clinical gout than with it.Virsaladze D, Tetradze L, Djavashvili L, Esakia N, Tananashvili D. (2007). "Levels of uric Acid in serum in patients with metabolic syndrome.". Georgian Med News 146: 34–7. PMID 17595458.
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.
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.Roberts-Thomson R, Roberts-Thomson P (1999). "Rheumatic disease and the Australian aborigine". Ann Rheum Dis 58 (5): 266&ndasgh;70. PMID 10225809. In the United States, gout is twice as prevalent in African American males as it is in Caucasians.Rheumatology Therapeutics Medical Center. What Are the Risk Factors for Gout?. Retrieved on 2007-01-26.
A seasonal link also may exist, with significantly higher incidence of acute gout attacks occurring in the spring.Schlesinger N, Gowin KM, Baker DG, Beutler AM, Hoffman BI, Schumacher HR Jr.. Acute gouty arthritis is seasonal.. Retrieved on 2007-09-27.Gallerani M, Govoni M, Mucinelli M, Bigoni M, Trotta F, Manfredini R.. Seasonal variation in the onset of acute microcrystalline arthritis.. Retrieved on 2007-09-27.
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 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. When it follows as a consequence of other health conditions such as renal failure, it is often regardless of the person\'s lifestyle.Robert S. Ivker, D.O. , et al (1999). The Complete Self-Care guide to Holistic Medicine, 186–8. ISBN 0874779863. Lin, et al have statistical evidence linking gout to lead poisoning Lin JL, Tan DT, Ho HH, Yu CC 2002 Environmental lead exposure and urate excretion in the general population. Am J Med. 2002 Nov;113(7):563-8. and lead level in the body is significantly correlated with urate excretion and gout.Wright, LF; Saylor, RP; Ceere, FA (1984) Occult lead intoxication in patients with gout and kidney disease. Journal of Rheumatology. 11, no. 4; 517-520. It is known that lead sugar was used to sweeten wine, and that chronic lead poisoning is a cause of gout,Lin JL, Huang PT. (1994). "Body lead stores and urate excretion in men with chronic renal disease". J Rheumatol 21 (4): 705–9. PMID 8035397. Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. (2000). "Effect of low level lead exposure on hyperuricemia and gout among middle aged and elderly men: the Normative Aging Study". J Rheumatol 27 (7): 1708–12. PMID 10914856. which condition is then known as saturnine gout, because of its association with alcohol and excess.Ball GV. (1971). "Two epidemics of gout". Bull Hist Med 45 (5): 401–8. PMID 4947583.
Gout also can develop as co-morbidity of other diseases, including polycythaemia, leukaemia, intake of cytotoxics, obesity, diabetes, hypertension, renal disorders, and hemolytic anemia. This form of gout is often called secondary gout. Diuretics (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.Janssens H, van de Lisdonk E, Janssen M, van den Hoogen H, Verbeek A (2006). "Gout, not induced by diuretics? A case-control study from primary care". Ann Rheum Dis 65 (8): 1080–3. doi:10.1136/ard.2005.040360. PMID 16291814.
Gout with tophi on elbow and knee.
The first line of treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are indomethacin, other nonsteroidal anti-inflammatory drugs (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 granulocytes 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. NSAIDs are the preferred form of analgesia for patients with gout.
A randomized controlled trial found similar benefit from nonsteroidal anti-inflammatory drugs and oral glucocorticoids; however, less adverse drug reactions occurred in the glucocorticoids group.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. In the 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. 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 hemorrhoidal 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 to 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.Schlesinger N, Detry MA, Holland BK, et al (2002). "Local ice therapy during bouts of acute gouty arthritis". J. Rheumatol. 29 (2): 331–4. PMID 11838852. Since gout is caused by crystals, it has been suggested that keeping very well hydrated and heating the affected joint in hot water (rather than cooling with ice) will promote the dissolution and clearance of the urate crytals.rapid response from a GP to BMJ.com. http://www.bmj.com/cgi/eletters/332/7553/1315#135610 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. 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 to 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.35
For extreme cases of gout, surgery may be necessary to remove large tophi and correct joint deformity.
See Saag and Choi, 2006, an open-access review article, for detailed references and further information.Saag KG, Choi H (2006). "Epidemiology, risk factors, and lifestyle modifications for gout". Arthritis Res. Ther. 8 Suppl 1: S2. doi:10.1186/ar1907. PMID 16820041.
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).
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, unless these levels are caused by other health conditions and not as responsive to dietary changes. For notable sources of dietary purines, see "Foods to avoid" section below.
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 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.
Men who consume two or more sugary soft drinks a day have an 85% higher risk of gout compared with those who drink less than one a month. [2]
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.
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.Huang HY, Appel LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller ER 3rd. (2005). "The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial.". Arthritis Rheum. 52 (6): 1143–7. PMID 15934094.
Additional dietary recommendations can be made which reduce gout indirectly, hypertension, cardiovascular disease, diabetes, and metabolic syndrome.
The following suggestions do not meet with universal approval among medical practitioners.
Low purine diet:
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. [3] "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."
The Roman gladiatorial surgeon Galen described gout as a discharge of the four 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.
One of the most famous sufferers of gout was Henry VIII. Others include John Calvin, Charles Spurgeon, Kublai Khan, Nostradamus, Christopher Columbus, John Milton, Queen Anne, Isaac Newton, Gottfried Leibniz, Henry Fielding, Samuel Johnson, Charles IV, Holy Roman Emperor, Charles V, Holy Roman Emperor,Ordi J, Alonso P, de Zulueta J et al. (2006). "The severe gout of Holy Roman Emperor Charles V". N Engl J Med 355 (5): 516–20. PMID 16885558. Pablo Neruda, Alfred Lord Tennyson, George IV, John Hancock, Thomas Jefferson, Jeff Mullis, Karl Marx, William Pitt, 1st Earl of Chatham, Benjamin Disraeli, Kirk Reuter, Peter Paul Rubens, Osbert Sitwell, Lennart Torstenson, Peter Gomes, Alexander Hamilton, George Mason, Benjamin Franklin, Wilkie Collins, Henry James, Frederick the Great, Don Nelson, Jared Leto, Juan Carrasquillo, Pope Clement VIII, David Wells, Joseph Conrad, Curt Schilling , Harry Judd, Guy Debord, and Dmitri VII Czar of Slovakia.
35.) Katzung, Bertram G. Basic and Clinical Pharmacology, 10th edition. New York: McGraw Hill Medical, 2007. pp. 242
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