gout
- gout
- Gout is a disease that afflicts mostly men, and mostly middle-aged ones. Women who are affected tend to be post-menopausal.
- Risk factors for gout are obesity, high blood pressure, heart disease and diabetes, but the primary one is a high serum level of uric acid.
- A gout attack consists of painful swelling of the joints of the extremities, especially in the hands, feet and elbows. It can also cause lower back pain.
- More attacks of gout occur in springtime than in any other season.
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gout
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n.
- A disturbance of uric-acid metabolism occurring chiefly in males, characterized by painful inflammation of the joints, especially of the feet and hands, and arthritic attacks resulting from elevated levels of uric acid in the blood and the deposition of urate crystals around the joints. The condition can become chronic and result in deformity.
- A large blob or clot: "and makes it bleed great gouts of blood" (Oscar Wilde).
[Middle English goute, from Old French, drop, gout, from Medieval Latin gutta, from Latin, drop (from the belief that gout was caused by drops of morbid humors).]
goutiness gout'i·ness n.gouty gout'y adj.
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Hereditary metabolic disorder in which excess uric-acid salts, normally excreted in urine, are deposited as needle-sharp crystals in joints, causing attacks of severe inflammation. The most common site is the base of the big toe. One of the oldest diseases in medical literature, gout is far more common in men. Attacks usually do not begin until middle age. They cause heat, redness, and extreme tenderness and pain and often subside in a week or two. Colchicine is used to treat acute attacks. Drugs such as allopurinol inhibit uric-acid synthesis.
For more information on gout, visit Britannica.com.
A hereditary disease due to abnormal purine metabolism. The disease is characterized by increased amounts of blood uric acid (hyperurilcemia), acute and chronic inflammatory arthritis, tophaceous deposits of uric acid crystals, and renal insufficiency. The increase of uric acid is thought to be caused by increased production or decreased excretion of uric acid from the kidney or both. See also Arthritis; Purine.
Primary gout occurs most frequently in middle-aged males and is passed as a familiar or hereditary trait which for some unknown reason does not appear as often in females. Secondary gout refers to the disease when associated with some underlying disorder causing an elevation in uric acid production (for example, myeloproliferative disorders).
The uric acid becomes deposited as urates in soft tissues, especially around the joints, in the cartilages of the ear, along the shafts of long bones, in the kidney, and occasionally on the heart valves. Such deposits, when superficial, can be seen grossly as reddish, inflamed masses called tophi. See also Protein metabolism; Uric acid.
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Painful disease caused by accumulation of crystals of uric acid in the synovial fluid of joints; may be due to excessive synthesis and metabolism of purines, which are metabolized to uric acid, or to impaired excretion of uric acid. Traditionally associated with a rich diet, although there is little evidence for dietary factors in causing the condition. May be exacerbated by alcohol.
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A defect in metabolism resulting in an excessive build up of uric acid crystals in the bloodstream and joints. Crystals may be deposited in the kidneys (where they may contribute to the formation of kidney stones), tendons, and joints. Usually, the first symptom of gout is an intense pain felt in the first joint of the big toe. There are a variety of causes, but the main one is poor excretion of uric acid. High intakes of alcohol or fructose can increase the risk of gout.
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Gout is a metabolic disorder characterized by excessive concentration of uric acid in the blood occasioning the deposition of sodium urate in the joints — particularly the extremities, and notoriously the great toe. Joints become swollen and very painful (‘like walking on my eyeballs’, remarked the Revd Sydney Smith, himself a sufferer). Chalky deposits called tophi (routinely likened to crab's eyes) often form around the joints and under the skin, especially of the ear. Thomas Sydenham, the illustrious clinician and another sufferer, gave the classical description of gout in the 1670s. The parts affected, according to Sydenham, became ‘so exquisitely painful as not to endure the weight of the clothes nor the shaking of the room from a person's walking briskly therein’. By the eighteenth century different kinds of gout were distinguished. The classic swelling of the toes, heels, ankles, and wrists was labelled ‘regular gout’. Then there was ‘irregular gout’ (also called ‘visceral’, ‘metastatic’, or ‘repelled gout’) — gout which, failing to be expelled in the standard way, allegedly rebounded from the extremities to the vital organs — head, brain, liver, heart — where it was judged more ominous. A third type was ‘flying gout’, where the pain flitted, apparently randomly, around the body.
Greek medicine had understood gout as a humoral disease, and the Hippocratic aphorisms inter alia noted that eunuchs do not get gout; nor women, unless their menses be stopped; nor even youths, till they indulged in coitus. Gout, in other words, was a disorder of mature, sexually-active males.
The sixteenth-century iconoclastic Swiss physician Paracelsus repudiated humoral thinking and sought a chemical explanation. Later developments supported Paracelsus' general outlook. In 1776, the Swedish chemist, Karl Scheele, isolated uric acid, and in A Treatise upon Gravel and Gout (1793), Murray Forbes speculated that gout was attended by an excess of uric acid. Four years later, William Hyde Wollaston obtained uric acid from a gouty tophus. And the victory of the theory was assured when, in 1859, Alfred Garrod tendered his classic analysis. In a normal healthy person, he argued, uric acid is excreted in the urine; if that process be interrupted, deposition of uric acid occurs in the form of urate of soda. Not least, Garrod devised an effective clinical test — the thread test — for uric acid. His The Nature and Treatment of Gout and Rheumatic Gout (1859) proved a milestone in the scientific understanding of the disorder.
Gout became one of those body-disfiguring diseases that acquired a distinctive personality, so much so that it could even be regarded as a desirable acquisition. It was widely viewed as exclusive to the upper classes, and therefore a mark of a good breeding, wealth, social status, and cultural superiority. ‘Gout is the distemper of a gentleman’, insisted Lord Chesterfield in the mid eighteenth century, ‘whereas the rheumatism is the distemper of a hackney coachman.’ ‘Gout loves ancestors and genealogy, ’ declared Sydney Smith, ‘it needs five or six generations of gentlemen or noblemen to give it its full vigour’. Hence, like melancholy in the Renaissance or tuberculosis in the Romantic era, gout achieved a social cachet.
More singularly, perhaps, gout assumed an identity, amongst doctors and sufferers alike, as a ‘healthy’ disease which protected sufferers against the depredations of worse diseases. ‘I have so good an opinion of the gout’, remarked the long-suffering Horace Walpole, ‘that when I am told of an infallible cure I laugh the proposal to scorn and declare that I do not desire to be cured … I am serious … I believe the gout a remedy and not a disease.’ For that reason, the apparent incurability of gout paradoxically caused no problems. If gout was indeed truly protective, then a cure might be worse than the disease.
The theory underlying such views was that gout was a healthy response through which a strongly constitutioned body attempted to divest itself of morbid matter by expelling it to the extremities, like the big toe, where it could do no harm. Hence, though a chronic disease, it was at bottom a symptom of basic good health. The poet William Cowper congratulated a friend on becoming gouty, ‘because it seems to promise us that we shall keep you long.’
Gout thus affords a good instance of what Susan Sontag has called ‘disease as metaphor’, one laden with meanings that transcend strict medico-scientific bounds.
Gout is still with us, but rarely in its florid form: an excess of uric acid in the blood can be recognized and controlled by drugs which diminish its excessive formation or enhance its deficient excretion — either of which may account for the excess. The link with affluence has some foundation, since a high protein diet can be a factor; uric acid is a breakdown product of purines, which are essential body constituents — for example of DNA. Purines are abundant in a protein-rich diet, and both ingested and internally synthesized purines contribute to the turnover which produces uric acid; so a high intake combined with subnormal ability of the kidneys to handle the load can cause excess in the blood.
— Roy Porter
Bibliography
- Copeman, W. S. (1964). A short history of the gout and the rheumatic diseases. University of California Press, Berkeley, CA.
- Sontag, S. (1978). Illness as metaphor. Farrar, Straus and Giroux, New York
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gout, condition that manifests itself as recurrent attacks of acute arthritis, which may become chronic and deforming. It results from deposits of uric acid crystals in connective tissue or joints. The presence of increased uric acid (a breakdown product of DNA) in the body distinguishes gout from other forms of arthritis, although hyperuricemia alone, which often occurs in the complete absence of gout, is not thought to be the sole causative factor. About 95% of patients with this disorder are men, usually over 30. Gout is associated with obesity and a hereditary factor in some cases. Diet also has an affect on gout. Consumption of meat and seafood, which are high in purine (from which digestion produces uric acid), increase the risk of gout, and gout is worsened by kidney problems and drinking alcoholic beverages, which slow the excretion of uric acid. Beer, which is higher than other alcoholic beverages in purines, also has been shown to increase the risk of gout.
Gout usually begins with an acute attack of pain, inflammation, extreme tenderness, and redness in the affected joint-often the big toe and sometimes the ankle or knee. After repeated attacks the disease can cause the deposition of sodium urate crystals in the tissues about the joints, causing stiffness and deformity. The aim of treatment is to minimize the formation of uric acid crystals. A high liquid intake that increases daily urine output is usually recommended. An acute attack of gout is usually treated with nonsteroidal anti-inflammatory drugs, such as indomethecine or naproxen, or the corticosteroid prednisone. Colchicine, a preparation of the meadow saffron, used since 1763 for gout, is still used when symptoms are not controlled by other drugs. Allopurinol and other xanthine oxidase inhibitors are used to prevent gout attacks in patients with chronically elevated uric acid levels; they lower uric acid concentrations in the blood by inhibiting the conversion of xanthine to uric acid.
(gowt)
A disorder of metabolism characterized by attacks of painful inflammation in the joints, particularly those of the feet and hands. The inflammation is caused by the deposition of crystals of uric acid in the joints. Gout occurs most often in middle-aged men. The tendency toward developing gout is inherited. Stress, fatigue, or excessive exercise are among the factors that can bring on an attack.
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gout
A cynical view of the world by Ambrose Bierce
n.
A physician's name for the rheumatism of a rich patient.
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a condition characterized by inflammation of the joints and cartilage due to hyperuricemia and consequent deposition of monosodium urate crystals in the joints, often within polymorphonuclear leukocytes. The hyperuricemia results from overproduction of uric acid, which may be due to elevated activity of ATP phosphoribosyltransferase (PRPP synthetase; EC 2.4.2.17), an abnormal amidophosphoribosyltransferase, or deficiency of hypoxanthine phosphoribosyltransferase (EC 2.4.2.8). Allopurinol is useful in treatment.
| gossypol, gonosome, gonane | |
| gp, gp32, gp96 |
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A disorder of uric acid metabolism in which there is hyperuricemia and deposition of urates in and around the joints. Occurs in humans and anthropoid apes. Most animals possess the enzyme uricase that converts uric acid to allantoin. Dalmatian dogs excrete large amounts of uric acid in their urine, but the breed is not affected by gout. A disease called gout occurs in commercial chickens due to feeding of excessive amounts of protein.
- articular g. — caused by gross excesses of protein in the diet. A chronic disease manifested by swelling of the joints which contain a thick white fluid consisting largely of uric acid crystals.
- visceral g. — birds become weak and listless and die. The viscera are covered with a frosting of urea crystals. There is a primary renal disease and a fatal uremia. The high-protein diet exacerbates that original disease.
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n
A disease associated with an inborn error of uric acid metabolism that increases production or interferes with the excretion of uric acid. Excess uric acid is converted to sodium urate crystals that precipitate from the blood and become deposited in joints and other tissues. The great toe is a common site for the accumulation of urate crystals. This condition can be exceedingly painful with swelling of a joint and may be accompanied by chills and fever.
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categories related to 'gout'
- Diseases and Infestations - gout: accumulation of excess uric acid in bloodstream and joints that causes joint destruction, kidney stones, and arthritis
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"Podagra" redirects here. For the moth genus, see Podagra (moth).
| Gout | |
|---|---|
| Classification and external resources | |
 Gout, a 1799 caricature by James Gillray |
|
| 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 when it involves the big toe)[1] is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallizes and the crystals are deposited in joints, tendons, and surrounding tissues.
A clinical diagnosis is confirmed by the visualization of the characteristic crystals in joint fluid. Treatment with nonsteroidal 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 in those with frequent attacks allopurinol or probenecid provide long-term prevention.
Gout has increased in frequency in recent decades affecting approximately one to two percent of the Western population at some point in their lives. The increase is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy and changes in diet. Gout was historically known as "the disease of kings" or "rich man's disease".
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Contents
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Signs and symptoms
Gout can present in a number of ways, although the most usual is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint).[2] The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases.[3] Other joints, such as the heels, knees, wrists and fingers, may also be affected.[3] Joint pain usually begins over 2–4 hours and during the night.[3] The reason for onset at night is due to the lower body temperature then.[1] Other symptoms that may rarely occur along with the joint pain include fatigue and a high fever.[1][3]
Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[4] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.[5]
Cause
Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid.[2] Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%.[6] About 10% of people with hyperuricemia develop gout at some point in their lifetimes.[7] The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/L (7 and 8.9 mg/dL), the risk is 0.5% per year, while in those with a level greater than 535 μmol/L (9 mg/dL), the risk is 4.5% per year.[1]
Lifestyle
Dietary causes account for about 12% of gout,[2] and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.[4][8] Other triggers include physical trauma and surgery.[6] Recent studies have found dietary factors once believed to be associated are, in fact, not; including the intake of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) and total protein.[9][10] The consumption of coffee, vitamin C and dairy products as well as physical fitness appear to decrease the risk.[11][12][13] This is believed to be partly due to their effect in reducing insulin resistance.[13]
Genetics
The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level.[6] Two genes called SLC2A9 and ABCG2 have been found to commonly be associated with gout and variations in them can approximately double the risk.[14] A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.[6]
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.[3] Other conditions that are commonly complicated by gout include: polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants.[6][15] A body mass index greater than or equal to 35 increases a male's risk of gout threefold.[10] Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.[16] Lesch-Nyhan syndrome is often associated with gouty arthritis.
Medication
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk.[17] Other medicines that have been associated include niacin and aspirin (acetylsalicylic acid).[4] The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout,[6] the former particularly when used in combination with hydrochlorothiazide.[18]
Pathophysiology
Gout is a disorder of purine metabolism,[6] and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues.[4] These crystals then trigger a local immune-mediated inflammatory reaction[4] with one of the key proteins in the inflammatory cascade being interleukin 1β.[6] An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates is what has made this condition so common.[6]
The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.[4][19] Other factors believed to be important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis,[20][21] articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate.[6] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.[2] Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.[1] Calcium channel blockers and losartan are associated with a lower risk of gout as compared to other medications for hypertension. [22]
Diagnosis
Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic podagra. Synovial fluid analysis should be done, however, if the diagnosis is in doubt.[1] X-rays, while useful for identifying chronic gout, have little utility in acute attacks.[6]
Synovial fluid
A definitive diagnosis of gout is based upon the identification of monosodium urate (MSU) crystals in synovial fluid or a tophus.[3] All synovial fluid samples obtained from undiagnosed inflamed joints should be examined for these crystals.[6] 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.[23] The fluid must also be examined relatively quickly after aspiration, as temperature and pH affect their solubility.[6]
Blood tests
Hyperuricemia is a classic feature of gout; gout occurs, however, nearly half of the time without hyperuricemia, and most people with raised uric acid levels never develop gout.[3][24] Thus, the diagnostic utility of measuring uric acid level is limited.[3] 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.[25] 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.[26][27] A white blood cell count as high as 40.0×109/L (40,000/mm3) has been documented.[1]
Differential diagnosis
The most important differential diagnosis in gout is septic arthritis.[3][6] This should be considered in those with signs of infection or those who do not improve with treatment.[3] To help with diagnosis, a synovial fluid Gram stain and culture may be performed.[3] Other conditions which present similarly include pseudogout and rheumatoid arthritis.[3] Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma,[28] or other neoplasms.[29]
Prevention
Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of food such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption, and avoiding obesity.[2] A low-calorie diet in obese men decreased uric acid levels by 100 µmol/L (1.7 mg/dL).[17] Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45%.[30] Coffee, but not tea, consumption is associated with a lower risk of gout.[31] 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.[32]
Treatment
The initial aim of treatment is to settle the symptoms of an acute attack.[33] Repeated attacks can be prevented by different drugs used to reduce the serum uric acid levels.[33] Ice applied for 20 to 30 minutes several times a day decreases pain.[2][34] Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids,[2] while options for prevention include allopurinol, febuxostat and probenecid. Lowering uric acid levels can cure the disease.[6] Treatment of comorbidities is also important.[6]
NSAIDs
NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective than any other.[2] Improvement may be seen within 4 hours, and treatment is recommended for 1–2 weeks.[2][6] They are not recommended, however in those with certain other health problems, such as gastrointestinal bleeding, renal failure, or heart failure.[35] While indomethacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.[17] For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.[36]
Colchicine
Colchicine is an alternative for those unable to tolerate NSAIDs.[2] Its side effects (primarily gastrointestinal upset) limit its usage.[37] Gastrointestinal upset, however, depends on the dose, and the risk can be decreased by using smaller yet still effective doses.[17] Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.[37]
Steroids
Glucocorticoids have been found to be as effective as NSAIDs[38] and may be used if contraindications exist for NSAIDs.[2] They also lead to improvement when injected into the joint; a joint infection must be excluded, however, as steroids worsens this condition.[2]
Pegloticase
Pegloticase (Krystexxa) was approved in the USA to treat gout in 2010.[39] It will be an option for the 3% of people who are intolerant to other medications.[39] Pegloticase is administered as an intravenous infusion every two weeks[39] and has been found to reduce uric acid levels in this population.[40]
Prophylaxis
A number of medications are useful for preventing further episodes of gout, including xanthine oxidase inhibitor (including allopurinol and febuxostat) and uricosurics (including probenecid and sulfinpyrazone). They are not usually commenced until one to two weeks after an acute attack has resolved, due to theoretical concerns of worsening the attack,[2] and are often used in combination with either an NSAID or colchicine for the first 3–6 months.[6] They are not recommended until a person has suffered two attacks of gout,[2] unless destructive joint changes, tophi, or urate nephropathy exist,[5] as it is not until this point that medications have been found to be cost effective.[2] Urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/L (5.0-6.0 mg/dL) and are continued indefinitely.[2][6] If these medications are being used chronically at the time of an attack, it is recommended they be continued.[3]
As a rule of thumb, uricosuric drugs are preferred if there is undersecretion of uric acid, in turn indicated if a 24-hour collection of urine results in a uric acid amount of less than 800mg. [41] They are, however, contraindicated if the person has a history of renal stones.[41] In contrast, a 24-hour urine excretion of more than 800mg indicates overproduction, and xanthine oxidase inhibitors are preferred.[41] Overall, probenecid appears to be less effective than allopurinol.[2]
Xanthine oxidase inhibitors (including allopurinol and febuxostat) block uric acid production, and long term therapy is safe and well tolerated, and can be used in people with renal impairment or urate stones, although allopurinol has caused hypersensitivity in a small number of individuals.[2] In such cases, the alternative drug febuxostat has been recommended.[42]
Prognosis
Without treatment, an acute attack of gout will usually resolve in 5 to 7 days. However, 60% of people will have a second attack within one year.[1] Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular disease and thus at increased risk of death.[6][43] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.[43]
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.[6] These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons.[6] With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.[6] Other forms of chronic renal dysfunction may occur.[6]
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Nodules of the finger and helix of the ear representing gouty tophi
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Tophus of the knee
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Tophus of the toe, and over the external malleolus
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Gout complicated by ruptured tophi (exudate tested positive for uric acid crystals)
Epidemiology
Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common.[2][6] Rates of gout have approximately doubled between 1990 and 2010.[4] 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.[10] 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%.[35]
In the United States, gout is twice as likely in African American males as it is in European Americans.[44] Rates are high among the peoples of the Pacific Islands and the Māori of New Zealand, but rare in Australian aborigines, despite a higher mean concentration of serum uric acid in the latter group.[45] It has become common in China, Polynesia, and urban sub-Saharan Africa.[6] Some studies have found attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.[46]
History
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).[47] According to the Oxford English Dictionary, this is derived from humorism and "the notion of the 'dropping' of a morbid material from the blood in and around the joints".[48]
Gout has, however, been known since antiquity. Historically, it has been referred to as "the king of diseases and the disease of kings"[6][49] or "rich man's disease".[50] The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. The Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women.[47][51] 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.[52]
While in 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning, and its predilection for older males:
Gouty patients are, generally, either old men, or men who have so worn themselves out in youth as to have brought on a premature old age - of such dissolute habits none being more common than the premature and excessive indulgence in venery, and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. The pain is like that of a dislocation, and yet parts feel as if cold water were poured over them. Then follows chills and shivers, and a little fever... The night is passed in torture, sleeplessness, turning the part affected, and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint, and being worse as the fit comes on.[53]
The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.[47] In 1848 English physician Alfred Baring Garrod realized that this excess uric acid in the blood was the cause of gout.[54]
In other animals
Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid.[55] Humans and other great apes don't have this ability, and thus gout is common.[1][55] The Tyrannosaurus rex specimen known as "Sue", however, is believed to have suffered from gout.[56]
Research
A number of new medications are under study for treating gout, including anakinra, canakinumab, and rilonacept.[57] A recombinant uricase enzyme (rasburicase) is available; its use, however, is limited, as it triggers an autoimmune response. Less antigenic versions are in development.[1]
References
- ^ a b c d e f g h i j Eggebeen AT (September 2007). "Gout: an update". Am Fam Physician 76 (6): 801–8. PMID 17910294.
- ^ a b c d e f g h i j k l m n o p q r s 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.
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External links
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Wikimedia Commons has media related to: Gout |
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This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
Translations:
Top
Gout
Dansk (Danish)
n. - gigt, podagra, stænk, klat, stråle, cigarsyge
Nederlands (Dutch)
jicht, (bloed)druppel, klonter, straal
Français (French)
n. - (Méd) goutte
Ελληνική (Greek)
n. - (παθολ.) ουρική αρθρίτιδα, ποδάγρα
Português (Portuguese)
n. - gota (f) (Med.)
Русский (Russian)
подагра, капля, пятно, шлюз
Svenska (Swedish)
n. - gikt, droppe
中文（简体）(Chinese (Simplified))
味, 嗜好, 趣味
中文（繁體）(Chinese (Traditional))
n. - 味, 嗜好, 趣味
한국어 (Korean)
n. - (병) 통풍, (피 등의) 응어리
العربيه (Arabic)
(الاسم) النقرس, : داء المفاصل
עברית (Hebrew)
n. - שיגדון, פודגרה, צינית
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