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Gout is a form of acute arthritis that causes severe pain and swelling in the joints. It most commonly affects the big toe, but may also affect the heel, ankle, hand, wrist, or elbow. It affects the spine often enough to be a factor in back pain. Gout usually comes on suddenly, goes away after 5-10 days, and can keep recurring. Gout is different from other forms of arthritis because it occurs when there are high levels of uric acid circulating in the blood, which can cause urate crystals to settle in the tissues of the joints.


Uric acid, which is found naturally in the blood stream, is formed as the body breaks down waste products, mainly those containing purine, a substance that is produced by the body and is also found in high concentrations in some foods, including brains, liver, sardines, anchovies, and dried peas and beans. Normally, the kidneys filter uric acid out of the blood and excrete it in the urine. Sometimes, however, the body produces too much uric acid or the kidneys aren't efficient enough at filtering it from the blood, and it builds up in the blood stream, a condition known as hyperuricemia. A person's susceptibility to gout may increase because of the inheritance of certain genes or from being overweight and eating a rich diet. In some cases, another disease (such as lymphoma, leukemia, or hemolytic anemia) may be the underlying cause of the uric acid buildup that results in gout. An additional factor is occupational or environmental; it is now known that chronic exposure to high levels of lead decreases the body's excretion of urates, allowing uric acid to accumulate in the blood.
Hyperuricemia doesn't always cause gout. Over the course of years, however, sharp urate crystals build up in the synovial fluid of the joints. Often, some precipitating event, such as an infection, surgery, the stress of hospitalization, a stubbed toe, or even a heavy drinking binge can cause inflammation. White blood cells, mistaking the urate crystals for a foreign invader, flood into the joint and surround the crystals, causing inflammation—in other words, the redness, swelling, and pain that are the hallmarks of a gout attack.

Causes and symptoms

As a result of high levels of uric acid in the blood, needle-like urate crystals gradually accumulate in the joints. Urate crystals may be present in the joint for a long time without causing symptoms. Infection, injury to the joint, surgery, drinking too much, or eating the wrong kinds of foods may suddenly bring on the symptoms, which include pain, tenderness, redness, warmth, and swelling of the joint. In many cases, the gout attack begins in the middle of the night. The pain is often so excruciating that the sufferer cannot bear weight on the joint or tolerate the pressure of bedcovers. The inflamed skin over the joint may be red, shiny, and dry, and the inflammation may be accompanied by a mild fever. These symptoms may go away in about a week and disappear for months or years at a time. However, over the course of time, attacks of gout recur more and more frequently, last longer, and affect more joints. Eventually, stone-like deposits known as tophi may build up in the joints, ligaments, and tendons, leading to permanent joint deformity and decreased motion. (In addition to causing the tophi associated with gout, hyperuricemia can also cause kidney stones, also called renal calculi or uroliths.)
Gout affects an estimated one million Americans; according to the National Institutes of Health, it accounts for about 5% of all cases of arthritis. It occurs more often in men than in women; the sex ratio is about 4:1. Uric-acid levels tend to increase in men at puberty, and, because it takes 20 years of hyperuricemia to cause gout symptoms, men commonly develop gout in their late 30s or early 40s. Women more typically develop gout later in life, starting in their 60s. According to some medical experts, estrogen protects against hyperuricemia, and when estrogen levels fall during menopause, urate crystals can begin to build up in the joints. Excess body weight, regular excessive alcohol intake, the use of blood pressure medications called diuretics, and high levels of certain fatty substances in the blood (serum triglycerides) associated with an increased risk of heart disease can all increase a person's risk of developing gout.
Gout appears to be on the increase in the American population. According to a study published in November 2002, there was a twofold increase in the incidence of gout over the 20 years between 1977 and 1997. It is not yet known whether this increase is the result of improved diagnosis or whether it is associated with risk factors that have not yet been identified.


Usually, physicians can diagnose gout based on the physical examination and medical history (the patient's description of symptoms and other information). Doctors can also administer a test that measures the level of uric acid in the blood. While normal uric acid levels don't necessarily rule out gout and high levels don't confirm it, the presence of hyperuricemia increases the likelihood of gout. The development of a tophus can confirm the diagnosis of gout. The most definitive way to diagnose gout is
Gout, a form of acute arthritis, most commonly occurs in the big toe. It is caused by high levels of uric acid in the blood, in which urate crystals settle in the tissues of the joints and produce severe pain and swelling.
Gout, a form of acute arthritis, most commonly occurs in the big toe. It is caused by high levels of uric acid in the blood, in which urate crystals settle in the tissues of the joints and produce severe pain and swelling.
(Illustration by Electronic Illustrators Group.)
to take a sample of fluid from the joint and test it for urate crystals.


The goals of treatment for gout consist of alleviating pain, avoiding severe attacks in the future, and preventing long-term joint damage. In addition to taking pain medications as prescribed by their doctors, people having gout attacks are encouraged to rest and to increase the amount of fluids that they drink.
Acute attacks of gout can be treated with nonaspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) such as naproxen sodium (Aleve), ibuprofen (Advil), or indomethacin (Indocin). In some cases, these drugs can aggravate a peptic ulcer or existing kidney disease and cannot be used. Doctors sometimes also use colchicine (Colbenemid), especially in cases where nonsteroidal anti-inflammatory drugs cannot be used. Colchicine may cause diarrhea, which tends to go away once the patient stops taking it. Corticosteroids such as prednisone (Deltasone) and adrenocorticotropic hormone (Acthar) may be given orally or may be injected directly into the joint for a more concentrated effect. While all of these drugs have the potential to cause side effects, they are used for only about 48 hours and are not likely to cause major problems. However, aspirin and closely related drugs (salicylates) should be avoided because they can ultimately worsen gout.
Once an acute attack has been successfully treated, doctors try to prevent future attacks of gout and long-term joint damage by lowering uric acid levels in the blood. There are two types of drugs for correcting hyperuricemia. Such uricosuric drugs as probenecid (Benemid) and sulfinpyrazone (Anturane) lower the levels of urate in the blood by increasing its removal from the body (excretion) through the urine. These drugs may promote the formation of kidney stones, however, and they may not work for all patients, especially those with kidney disease. Allopurinol (Zyloprim), a type of drug called a xanthine-oxidase inhibitor, blocks the production of urate in the body, and can dissolve kidney stones as well as treating gout. The potential side effects of allopurinol include rash, a skin condition known as dermatitis, and liver dysfunction. In 2004, the FDA was seeking trial data on a new drug called oxypurinol (Oxyprim) for treating chronic gout. These medications may have to be taken for life to prevent further gout attacks.
New quality of care indicators were released in 2004 to improve care for patients with gout. The aim of the guidelines was to prevent repeat gout attacks and to reduce medication errors associated with intravenous colchicine in hospitals.

Alternative treatment

Alternative approaches to gout focus on correcting hyperuricemia by encouraging weigt loss and limiting the intake of alcohol and purine-rich foods. In addition, consuming garlic (Allium sativum) has been recommended to help prevent gout. Increasing fluid intake, especially by drinking water, is also recommended. During an acute attack, contrast hydrotherapy (alternating three-minute hot compresses with 30-second cold compresses) can help dissolve the crystals and resolve the pain faster.


Gout cannot be cured but usually it can be managed successfully. As tophi dissolve, joint mobility generally improves. (In some cases, however, medicines alone do not dissolve the tophi and they must be removed surgically.) Lowering uric acid in the blood also helps to prevent or improve the kidney problems that may accompany gout.


For centuries, gout has been known as a "rich man's disease" or a disease caused by overindulgence in food and drink. While this view is perhaps a little overstated and oversimplified, lifestyle factors clearly influence a person's risk of developing gout. Since obesity and excessive alcohol intake are associated with hyperuricemia and gout, losing weight and limiting alcohol intake can help ward off gout. Dehydration may also promote the formation of urate crystals, so people taking diuretics or "water pills" may be better off switching to another type of blood pressure medication. Everyone should be sure to drink at least six to eight glasses of water each day. Since purine is broken down in the body into urate, it may also be helpful to avoid foods high in purine, such as organ meats, sardines, anchovies, red meat, gravies, beans, beer, and wine. A 2004 study revealed that eating more low-fat dairy products could reduce risk of developing gout.

Key terms

Allopurinol — A drug that corrects hyperuricemia by inhibiting urate production.
Colchicine — A drug used to treat painful flare-ups of gout.
Corticosteroids — Medications related to a natural body hormone called hydrocortisone, which are used to treat inflammation.
Hyperuricemia — High levels of a waste product called uric acid in the blood.
Probenecid — A drug that corrects hyperuricemia by increasing the urinary excretion of urate.
Purine — A substance found in foods that is broken down into urate and may contribute to hyperuricemia and gout.
Sulfinpyrazone — A drug that corrects hyperuricemia by increasing the urinary excretion of urate.
Synovial fluid — Fluid surrounding the joints which acts as a lubricant, reducing the friction between the joints.
Tophus (plural, tophi) — A chalky deposit of a uric acid compound found in gout. Tophi occur most frequently around joints and in the external ear.
Urate crystals — Crystals formed by high levels of uric acid in the blood.



Parker, James N., M.D., and Philip M. Parker, Ph. D. The 2002 Official Patient's Sourcebook on Gout. San Diego, CA: ICON Health Publications, 2002.


Arromdee, E., C. J. Michet, C. S. Crowson, et al. "Epidemiology of Gout: Is the Incidence Rising?" Journal of Rheumatology 29 (November 2002): 2403-2406.
Coghill, Kim. "FDA Panel Discusses Endpoints for Approval of Gout Products." Bioworld Today (June 3, 2004).
"Dairy-rich Diet May Help Prevent Gout." Tufts University Health & Nutrition Letter (June 2004): 2.
Hsu, C. Y., T. T. Shih, K. M. Huang, et al. "Tophaceous Gout of the Spine: MR Imaging Features." Clinical Radiology 57 (October 2002): 919-925.
Lin, J. L., D. T. Tan, H. H. Ho, and C. C. Yu. "Environmental Lead Exposure and Urate Excretion in the General Population." American Journal of Medicine 113 (November 2002): 563-568.
MacReady, Norma. "New Gout Quality-of-care Standards Take Aim at Medication-related Errors." Internal Medicine News (June 1, 2004): 18.
Perez-Ruiz, F., M. Calabozo, G. G. Erauskin, et al. "Renal Underexcretion of Uric Acid is Present in Patients with Apparent High Urinary Uric Acid Output." Arthritis and Rheumatism 47 (December 15, 2002): 610-613.
Raj, J. M., S. Sudhakar, K. Sems, and R. W. Carlson. "Arthritis in the Intensive Care Unit." Critical Care Clinics 18 (October 2002): 767-780.
Shekarriz, B., and M. L. Stoller. "Uric Acid Nephrolithiasis: Current Concepts and Controversies." Journal of Urology 168, no. 4, Part 1 (October 2002): 1307-1314.


Arthritis Foundation.1300 W. Peachtree St., Atlanta, GA 30309. (800) 283-7800. http://www.arthritis.org.
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). National Institutes of Health (NIH), 1 AMS Circle, Bethesda, MD 20892-3675. 〈www.niams.nih/gov〉.


National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Questions and Answers About Gout. Bethesda, MD: NIAMS, 2002. NIH Publication No. 02-5027. 〈www.niams.nih.gov/hi/topics/gout/gout/htm〉.


a form of arthritis in which uric acid appears in excessive quantities in the blood and may be deposited in the joints and other tissues. During an acute attack there is swelling, inflammation, and extreme pain in a joint, frequently that of the big toe. After several years of attacks, the chronic form of the disease may set in, permanently damaging and deforming joints and destroying cells of the kidney. Most cases occur in men and the first attack rarely occurs before the age of 30.
Causes. The causes of gout include excessive production of uric acid, as an inherited condition or as a side effect of chemotherapy for tumors, and impairment of clearance due to the antihypertensive agenthydrochlorothiazide or to low-dose aspirin.
Acute Gout. This form usually strikes without warning. The affected joint, which in 70 per cent of cases is that of the big toe, becomes swollen, inflamed, and very painful. The first attack may follow an operation, infection, or minor irritation such as tight shoes, or it may have no apparent cause. The patient may have a headache or fever, and often cannot walk because of the pain.

Without treatment, acute attacks of gout usually last a few days or weeks. The symptoms then disappear completely until the next attack. As the disease progresses, the attacks tend to last longer and the intervals between attacks become shorter.

A definite diagnosis of gout is made by identifying needle-shaped sodium urate crystals in the synovial fluid aspirated from an affected joint. The crystals may be seen inside polymorphonuclear leukocytes. Acute gouty arthritis is an example of an acute inflammatory process. Serial serum uric acid levels are also monitored; levels consistently above 8 mg/100 ml are an abnormal finding.
Treatment. An acute attack of gout can be treated successfully with any of several medicines. colchicine has long been used; in most cases it relieves the pain and swelling in 72 hours or less, although it does not affect the high concentration of uric acid. indomethacin is a nonsteroidal antiinflammatory drug that is particularly effective against acute gout and has become the treatment of choice. Aspirin should be avoided during acute attacks. The dietary management of gout is a subject of disagreement among researchers.
Chronic Gout. After a number of acute attacks of gout, the patient who goes without medical treatment may develop symptoms of chronic gout. This seldom occurs less than 10 years after the first acute attack. Joints affected by chronic gout degenerate in the same way as those affected by rheumatoid arthritis and may eventually lose their ability to move.
Treatment. Chronic gout is treated with probenecid, allopurinol, or other medicines that promote urinary excretion of uric acid. Other treatment may also be necessary if the kidney is involved. With appropriate treatment, gout should be well controlled.
Management Between Attacks. If acute gout is recognized at an early stage and treated correctly, the development of the chronic form can generally be prevented. Weight should be kept within normal limits, and increasing daily intake of liquids is beneficial because it encourages urine production.
Gouty arthritis. Deposits of uric acid crystals in the connective tissue have a chemotactic effect and cause exudation of leukocytes into the joint. The inflammation most often affects the metatarsophalangeal joint of the big toe. From Damjanov, 2000.


(gowt), [MIM*138900]
A disorder of purine metabolism, occurring especially in men, characterized by a raised but variable blood uric acid level and severe recurrent acute arthritis of sudden onset resulting from deposition of crystals of sodium urate in connective tissues and articular cartilage; most cases are inherited, resulting from a variety of abnormalities of purine metabolism. The familial aggregation is for the most part galtonian with a threshold of expression determined by the solubility of uric acid. However, gout is also a feature of the Lesch-Nyhan syndrome, an X-linked disorder [MIM*308000].
[L. gutta, drop]


(gout) a group of disorders of purine and pyrimidine metabolism, characterized by typhi causing recurrent paroxysmal attacks of acute inflammatory arthritis usually affecting a single peripheral joint, usually responsive to colchicine, and usually followed by complete remission; hyperuricemia and uric acid urolithiasis are also present in fully developed cases.gout´y
latent gout , masked gout lithemia without the typical features of gout.


1. 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.
2. A large blob or clot: "and makes it bleed great gouts of blood" (Oscar Wilde).

gout′i·ness n.
gout′y adj.


Etymology: L, gutta, drop
a disease associated with an inborn error of uric acid metabolism that increases production or interferes with 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. Men are more often affected than premenopausal women. The great toe is a common site for the accumulation of urate crystals. The condition can cause exceedingly painful swelling of a joint, accompanied by chills and fever. The symptoms are recurrent. Episodes become longer each year. The disorder is disabling and, if untreated, can progress to the development of destructive joint changes, such as tophi. Treatment usually includes administration of colchicine, phenylbutazone, indomethacin, or glucocorticoid drugs and a diet that excludes purine-rich foods such as organ meats. It may include surgical removal of ulcerated tophi. Chronically, probenecid, allopurinol, or colchicine may be used to decrease uric acid levels. Acquired gout is a condition having the signs and symptoms of gout but resulting from another disorder or treatment for a different condition. Diuretic drugs can alter the concentration of uric acid so that uric acid salts precipitate from the blood and are carried to the joints. See also chondrocalcinosis, Lesch-Nyhan syndrome, tophus.
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A metabolic disorder characterised by increased uric acid in the blood and joints, resulting in recurring painful arthritis and renal dysfunction with deposits of uric acid in the urinary tract, which in some cases is caused by either of two X-linked enzymes.
Clinical findings
One-half of cases present with the classic “podagra” which affects the metatarsophalangeal joint; up to 90% suffer podagra at some time during their disease. With time, the attacks become polyarticular. Gouty tophi accumulate on the ears and over joints. Patients with gout are at high risk of forming kidney stones, which, in extreme cases, can cause renal failure.
Risk factors
Alcoholism, hereditary defect of hypoxanthine-guanine phosphoribosyl transferase (HG-PRT), phosphoribosylpyrophosphate synthetase superactivity, obesity, hypertension, renal dysfunction, drugs; family history of gout is present in about half of cases.
Increased uric acid, often ≥ 410 µmol/L–US: 7.0 mg/ml, a level found in a significant minority of men (90% of gout occurs in men).

Crystals in joints, body fluids, tissues.

Acute treatment
Colchicine, NSAIDs, corticosteroids.
Chronic treatment
Diet, allopurinol, sulfinpyrazone, salicylates.


Orthopedics A condition characterized by ↑ uric acid in the blood and joints, resulting in recurring painful arthritis, renal function and deposits of uric acid in the urinary tract, linked to 2 X-linked enzymes Risk factors Hereditary defects of HG-PRT–hypoxanthine-guanine phosphoribosyl transferase, obesity, weight gain, alcohol intake, HTN, renal dysfunction, drugs Lab ↑ uric acid, often ≥ 410 µmol/L–US: 7.0 mg/ml, a level found in a significant minority of ♂–90% of gout occurs in ♂ Diagnosis Crystals in joints, body fluids, tissues; family Hx of gout is present in ±12 of cases;12 present with the classic 'podagra'–1st metatarsophalangeal joint; up to 90% suffer podagra at some time during their disease Acute treatment Colchicine, NSAIDs, corticosteroids Interval Diet Chronic Allopurinol, sulfinpyrazone, salicylates. See Congenital gout, PseudoGout, Saturnine gout.


A disorder of purine metabolism, occurring especially in men, characterized by a raised but variable blood uric acid level and severe recurrent acute arthritis of sudden onset resulting from deposition of crystals of sodium urate in connective tissues and articular cartilage; usually inherited, resulting from a variety of abnormalities of purine metabolism.
[L. gutta, drop]


(gowt) [Fr. goute, fr L. gutta, a drop]
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GOUT: Uric acid crystals and white blood cells in synovial fluid (orig. mag. ×500)
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A form of arthritis marked by the deposition of monosodium urate crystals in joints and other tissues. Any joint may be affected, but gout usually begins in the knee or the first metatarsophalangeal joint of the foot. Synonym: monosodium urate deposition diseasetophus;


Most hyperuricemic people are asymptomatic between acute attacks. When an attack of acute gouty arthritis develops, it usually begins at night with moderate pain that increases in intensity to the point where no body position provides relief. Low-grade fever and joint inflammation (hot, exquisitely tender, dusky-red or cyanotic joints) may be present. See: illustration


Colchicine, nonsteroidal anti-inflammatory agents, or corticosteroids are used to treat acute gouty attacks. Long-term therapy aims at preventing hyperuricemia by giving uricosuric drugs such as probenecid, or xanthine oxidase inhibitors such as allopurinol. Patients with gout have a tendency to form uric acid kidney stones. The diet should be well balanced and devoid of purine-rich foods, e.g., anchovies, sardines, liver, kidneys, sweetbreads, lentils, beer, wine, and other alcoholic beverages, because these raise urate levels. Fluid intake should be encouraged.

Patient care

During the acute phase, bedrest is prescribed for at least the first 24 hr, and affected joints are elevated, immobilized, and protected by a bed cradle. Analgesics are administered, and hot or cold packs applied, depending on which the patient finds most helpful. The patient is taught about these measures. Colchicine, nonsteroidal anti-inflammatory agents, prednisone, or other prescribed drugs are administered. Allopurinol may be prescribed as maintenance therapy after acute attacks to suppress uric acid formation and control uric acid levels, thus preventing future attacks. Patients should be warned to report adverse effects of allopurinol, e.g., drowsiness, dizziness, nausea, vomiting, urinary frequency, dermatitis. A low-purine diet is recommended. The importance of gradual weight reduction is explained if obesity, which places additional stress on painful joints, is a factor. If soft-tissue tophi are present, e.g., near joints in fingers, knees, or feet, the patient should wear soft clothing to cover these areas and should use meticulous skin care and sterile dressings to prevent infection of open lesions.

Surgery may be required to excise or drain infected or ulcerated tophi, to correct joint deformities, or to improve joint function. Even minor surgery may precipitate gouty attacks (usually within 24 to 96 hr after surgery); therefore, the patient should be instructed about this risk and medications administered as prescribed to prevent acute attacks. The goal of chronic management of gout is to maintain serum uric acid levels below 6 mg/dl. At these levels chronic complications of gout are limited.

abarticular gout

Periarticular gout.

chronic gout

A persistent form of gout.

lead gout

Goutlike symptoms associated with lead poisoning. Synonym: saturnine gout

periarticular gout

Gout that involves structures near the joints.
Synonym: abarticular gout

saturnine gout

Lead gout.

tophaceous gout

Gout marked by the development of tophi (deposits of sodium urate) in the joints and in the external ear.


An acute inflammatory joint disorder (ARTHRITIS) caused by deposition of monosodium urate monohydrate crystals around joints, tendons and other tissues, especially the near joint of the big toe. This occurs when there is excess uric acid in the body, probably as a result of a genetic abnormality. There is excruciating pain and inflammation. Treatment is by non-steroidal anti-inflammatory drugs (NSAIDS), such as indomethacin (indometacin) or naproxen, used early and throughout the attack. Colchicine is also effective. Gout can be prevented by the use of allopurinol which lowers the levels of uric acid in the blood. See also GOUTY TOPHI.


; podagra metabolic disorder, caused by inability to metabolize purines or as a side-effect of drugs (e.g. diuretics) and strongly associated with inflammatory arthropathy of peripheral joints; characterized by raised serum urate levels, birefringent urate crystals in the synovial fluid of affected joints, and ultimately gouty tophus formation; radiographs show marked 'punched-out' marginal erosions within affected joints, with later chronic and marked degenerative arthritis; acute monoarticular gout is treated with high-dose non-steroidal anti-inflammatory drugs (not aspirin), colchicine ± intra-articular injection of corticosteroid; patients with hyperuricaemia and tophus formation require allopurinol or a uricosuric agent

gout (gaut),

n a type of arthritis, which affects primarily males, that is triggered by increased uric acid in serum and joints. The uric acid forms crystals. A common symptom is intense pain and swelling of the metatarsophalangeal joint of the big toe. Also called
rich man's disease.
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(gowt) [MIM*138900]
A disorder of purine metabolism, occurring especially in men, characterized by a raised but variable blood uric acid level and severe recurrent acute arthritis of sudden onset resulting from deposition of crystals of sodium urate in connective tissues and articular cartilage.
[L. gutta, drop]


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. It can be exceedingly painful, with swelling of a joint and may be accompanied by chills and fever.


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 gout
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 gout
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.

Patient discussion about gout

Q. Is gout hereditary? My Mother has gout for a few years now. Is it hereditary? Does this mean I too will get it in the future?

A. most likely, yes!

If other members of your family have had gout, you’re more likely to develop it also, yet, just because someone in the family suffers from gout does not mean everyone in that family will have the disease. This risk varies from person to person.

for further reading , you can visit my blog :

Q. How is gout treated? After a lot of tests, my Doctor concluded that I have gout. What treatment should I expect? Is gout curable?

A. There are basically three types of treatment for gout arthritis : corticosteroids, anti-inflammatory drugs (NSAID- ibuprofen, diclofenac, naproxen), and medication that lowers uric acid levels, such as allopurinol (Zylopric) or probenecid, also may be prescribed to help prevent a gout attack.

Colchicine is used to treat acute gout attack and usually begins working within few hours of taking it. Low doses of colchicine are also used to prevent attacks. These drugs are recommended for people who have had multiple attacks of gout, kidney stones due to uric acid, or tophi.

The goal of lowering the blood uric acid is to slowly dissolve deposits of uric acid in the joint.

Q. what is the connection between gout and drinking cokes? There was an article in your magazine earlier this year about how drinking cokes could affect gout....can I get a copy of that artical?

A. 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.
This is because soft drinks contain large quantities of high-fructose corn syrup (HFCS), a common sweetener in soft drinks, which results in Hyperuricemia in blood.
Hyperuricemia, in turn predispose the body for gout.
(taken from : http://en.wikipedia.org/wiki/Gout )

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