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Gout

Gout

Definition

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 lower back pain. Gout is often a recurring condition. An attack usually comes on suddenly and goes away after 510 days. Gout occurs when there are high levels of uric acid circulating in the blood, and the acid crystallizes and settles in the body. According to the National Institutes of Health (NIH), gout accounts for about 5% of all cases of arthritis reported in the United States.

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.

Description

Uric acid is formed in the bloodstream when the body breaks down waste products, mainly those containing purines. Purines can be produced naturally by the body, and they can be ingested from such high-purine foods as meat. Normally, the kidneys filter uric acid particles out of the blood and excrete it into the urine. If the body produces too much uric acid or the kidneys aren't able to filter enough of it out, there is a buildup of uric acid in the bloodstream. This condition is known as hyperuricemia.

Uric acid does not tend to remain dissolved in the bloodstream. Over the course of years, or even decades, hyperuricemia may cause deposits of crystallized uric acid throughout the body. Joints, tendons, ear tips, and kidneys are favored sites. When the immune system becomes alerted to the urate crystals, it mounts an inflammatory response that includes the pain, redness, swelling, and damage to joint tissue that are the hallmarks of an acute gout attack.

The body's uric acid production tends to increase in males during puberty. Therefore, it should come as no surprise that nine out of ten of those suffering from gout are men. Since it can take up to 20 years of hyperuricemia to have gout symptoms, men don't commonly develop gout until reaching their late 30s or early 40s. If a woman does develop gout, typically, it will be later in her life. According to some medical experts, this is because estrogen protects against hyperuricemia. It is not until estrogen levels begin to fall during menopause that urate crystals can begin to accumulate.

Hyperuricemia does not necessarily lead to gout. The tendency to accumulate urate crystals may be due to genetic factors, excess weight, or overindulgence in the wrong kinds of food. In addition, regular use of alcohol to excess, the use of diuretics, and the existence of high levels of cholesterol and triglycerides in the blood can increase the risk of developing the disease. In some cases, an underlying disease such as lymphoma, leukemia , or hemolytic anemia may also lead to gout.

Causes & symptoms

An acute episode of gout often starts without warning. The needle-like urate crystals may be present in the joints for a long time without causing symptoms. Then, there may be a triggering event such as a stubbed toe, an infection, surgery, stress, fatigue , or even a heavy drinking binge. Patients in intensive care units (ICUs) may have an acute flare-up of gout. In addition, it is now known that chronic occupational exposure to lead leads to decreased excretion of urates and an increased risk of developing gout.

In many cases, the gout attack begins in the middle of the night. There is intense pain, which usually involves only one joint. Often it is the first joint of the big toe. The inflamed skin over the joint is warm, shiny, and red or purplish, and the pain is often so excruciating that the sufferer cannot tolerate the pressure of bedcovers. The inflammation may be accompanied by a fever .

Acute symptoms of gout usually resolve in about a week, and then disappear altogether for months or years at a time. Eventually, however, the attacks may occur more frequently, last longer, and do more damage. The urate crystals may eventually settle into hard lumps under the skin around the joints, leading to joint deformity and decreased range of motion. These hard lumps, called tophi, may also develop in the kidneys and other internal organs, under the skin of the ears, or at the elbow. People with gout also face a heightened risk of kidney disease, and almost 20% of people with gout develop kidney stones . As of 2002, however, the relationship between gout and kidney stone formation is still not completely understood.

Diagnosis

Doctors can diagnose gout based on a physical examination and the patient's description of symptoms. In order to detect hyperuricemia, doctors can administer a blood test to measure serum urate levels. However, high urate levels merely point to the possibility of gout. Many people with hyperuricemia don't have urate crystal deposits. Also, it has been shown that up to 30% of gout

sufferers have normal serum urate levels, even at the time of an acute gout attack. The most definitive way to diagnose gout is to take a sample of fluid from an affected joint and test it for the presence of the urate crystals.

Treatment

The symptoms of gout will stop completely a week or so after an acute attack without any intervention. It is important, however, to be diagnosed and treated by a health care practitioner in order to avoid attacks of increasing severity in the future and to prevent permanent damage to the joints, kidneys, and other organs. During an acute attack, treatment should focus on relieving pain and inflammation. On an ongoing basis, the focus is on maintaining normal uric acid levels, repairing tissue damage, and promoting tissue healing.

Diet

Generally, gout is unheard of in vegetarians. It is a condition that responds favorably to improvements in diet and nutrition . Recurrent attacks can be avoided by maintaining a healthy weight and limiting the intake of purinerich foods. A diet high in fiber and low in fat is also recommended. Processed foods should be replaced by complex carbohydrates, such as whole grains. Protein intake should be limited to under 0.8g/kg of body weight per day.

Nutritional supplements

Vitamin E and selenium are recommended to decrease the inflammation and tissue damage caused by the accumulation of urates.

Folic acid has been shown to inhibit xanthine oxidase, the main enzyme in uric acid production. The drug allopurinol (see below) is used for this same purpose in the treatment of gout. The therapeutic use of folic acid for this condition should be prescribed and monitored under the supervision of a heath care practitioner. The recommended dosage range is 400800 micrograms per day.

The amino acids alanine, aspartic acid, glutamic acid, and glycine taken daily improve the kidneys' ability to excrete uric acid. Bromelain , an enzyme found in pineapples, is an effective anti-inflammatory. It can be used as an alternative to NSAIDs and other prescription anti-inflammatory drugs. It should be taken between meals at a dosage of 200300 mg, three times per day.

The bioflavonoid quercetin helps the body absorb bromelain. It also helps decrease uric acid production and prevents the inflammation that leads to the acute symptoms of gout and the resulting tissue destruction. Quercetin should be taken at the same time and dosage as bromelain: 200400 mg, between meals at a three times per day.

Herbs

Dark reddish-blue berries such as cherries, blackberries, hawthorn berries, and elderberries are very good sources of flavonoid compounds that have been found to help lower uric acid levels in the body. Flavonoids are effective in decreasing inflammation and preventing and repairing the destruction of joint tissue. An amount of the fresh, frozen, dried, juiced, or otherwise extracted berries equal to half a pound (about 1 cup) fresh should be consumed daily.

Devil's claw , Harpagophytum procumbens, has been shown to be of benefit. It can be used to reduce uric acid levels and to relieve joint pain.

Gout represents a serious strain on the kidneys. The dried leaves of nettles, Urtica dioica, can be made into a pleasant tea and consumed throughout the day to increase fluid intake and to support kidney functions. However, some people are allergic to nettles.

Therapy

Colchicum is a general homeopathic remedy that can be used for pain relief during a gout attack. It is formulated from the same plant, Autumn crocus, as the drug colchicine, used in the conventional treatment of gout. Gout may be improved by having a constitutional remedy prescribed that is based on the tendency to develop the disease and its symptoms.

During the acute phase of gout, acupuncture can be helpful with pain relief.

Applications of ice or cold water can reduce pain and inflammation during acute attacks.

Allopathic treatment

Standard medical treatment of acute attacks of gout includes nonsteroidal anti-inflammatory drugs (NSAIDs) such as naproxen sodium (Aleve), ibuprofen (Advil), or indomethacin (Indocin). Daily doses until the symptoms have subsided are recommended. Colchicine (Colbenemid), is also used. Corticosteroids such as prednisone (Deltasone, prednisolone, and corticotropin [ACTH]) may be given orally or may be injected directly into the joint for a more concentrated effect. Because these drugs can cause undesirable side effects, they are used for only about 48 hours so as not to cause major problems. Aspirin and other salicylates should be avoided, because they can impair uric acid excretion and may interfere with the actions of other gout medications.

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. Colchicine is the drug of choice to deter recurrence. This medication can be very hard on the vascular system and the kidneys, however, and it is incompatible with a number of antidepressants, tranquilizers, and antihistamines. It should be avoided by pregnant women and the elderly.

There are two types of drugs used for lowering uric acid levels. Sometimes these drugs resolve the problem completely. However, the use of low-level amounts may be required for a lifetime. Uricosuric drugs, such as probenecid (Benemid) and sulfinpyrazone (Anturane), decrease urates in the blood by increasing their excretion. These drugs may also promote the formation of kidney stones, and they are contraindicated for patients with kidney disease. Xanthine oxidase inhibitors block the production of urates in the body. They can dissolve kidney stones as well as treat gout. Allopurinol is the drug most used in this respect. Its adverse effects include reactions with other medications, and the aggravation of existing skin, vascular, kidney, and liver dysfunction.

Expected results

Gout cannot be cured, but it can be managed successfully. Prompt attention to diet and reducing uric acid levels will rectify many of the problems associated with gout. Kidney problems can also be reversed or improved. Tophi can be dissolved or surgically removed, and with the tophi gone, joint mobility generally improves. Gout is generally more severe in those whose initial symptoms appear before age 30. The coexistence of hypertension , diabetes, or kidney disease can make for a much more serious condition.

Prevention

For centuries, gout has been known as the "rich man's disease," a disease of overindulgence in food and drink. While this view is perhaps oversimplified, lifestyle factors clearly influence a person's risk of developing gout. For example, losing weight and limiting alcohol intake can help ward off gout. Since purines are broken down into urates by the body, consumption of foods high in purine should be limited. Foods that are especially high in purines are red meat, organ meats, meat gravies, shellfish, sardines, anchovies, mushrooms, cooked spinach, rhubarb, yeast, asparagus, beer, and wine.

Dehydration promotes the formation of urate crystals, so people taking diuretics, or "water pills," may be better off switching to another type of blood pressure medication. Increased intake of fluids will dilute the urine and encourage excretion of uric acid. Therefore, six to eight glasses of water should be consumed daily, along with plenty of herbal teas and diluted fruit juices.

Consumption of saturated fats impedes uric acid excretion, and consumption of refined carbohydrates, such as sugar and white bread and pasta, increases uric acid production. Both should be seriously limited.

The use of vitamin C should be avoided by people with gout, due to the high levels of acidity.

Resources

BOOKS

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.

PERIODICALS

Arromdee, E., C. J. Michet, C. S. Crowson, et al. "Epidemiology of Gout: Is the Incidence Rising?" Journal of Rheumatology 29 (November 2002): 24032406.

Conos, Juan J., and Robert Kalish. "Gout: Effective Drug Therapy for Acute Attacks and for the Long Term." Consultant (August 1996): 175255.

Emmerson, Bryan T. "The Management of Gout." New England Journal of Medicine (February 15, 1996): 445451.

Hsu, C. Y., T. T. Shih, K. M. Huang, et al. "Tophaceous Gout of the Spine: MR Imaging Features." Clinical Radiology 57 (October 2002): 919925.

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): 563568.

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): 610613.

Raj, J. M., S. Sudhakar, K. Sems, and R. W. Carlson. "Arthritis in the Intensive Care Unit." Critical Care Clinics 18 (October 2002): 767780.

Shekarriz, B., and M. L. Stoller. "Uric Acid Nephrolithiasis: Current Concepts and Controversies." Journal of Urology 168 (October 2002) (4 Pt 1): 13071314.

ORGANIZATIONS

Arthritis Foundation. 1330 W. Peachtree Street, P.O. Box 7669, Atlanta, GA 30357-0669. (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>.

OTHER

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>.

Patience Paradox

Rebecca J. Frey, PhD

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Gout

Gout

Definition

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.

Description

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 inflammationin 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.

Diagnosis

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 to take a sample of fluid from the joint and test it for urate crystals.

Treatment

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.

Prognosis

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.

Prevention

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.

Resources

BOOKS

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.

PERIODICALS

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.

ORGANIZATIONS

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.

OTHER

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.

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gout

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." The Oxford Companion to the Body. . Encyclopedia.com. 30 Apr. 2017 <http://www.encyclopedia.com>.

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"gout." The Oxford Companion to the Body. . Retrieved April 30, 2017 from Encyclopedia.com: http://www.encyclopedia.com/medicine/encyclopedias-almanacs-transcripts-and-maps/gout

gout

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.

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"gout." The Columbia Encyclopedia, 6th ed.. . Encyclopedia.com. 30 Apr. 2017 <http://www.encyclopedia.com>.

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Gout

Gout

What Is Gout?

How Is Gout Diagnosed and Treated?

Resources

Gout (pronounced GOWT) is a painful, inflammatory disease of the joints caused by crystals of uric acid.

KEYWORDS

for searching the Internet and other reference sources

Hyperuricemia

Inflammation

What Is Gout?

Uric (YUR-ik) acid is a waste product made by normal chemical processes in the body, as well as by the breakdown of certain foods, and it is usually eliminated in urine. Sometimes uric acid builds up and forms crystals, like sugar crystals, that collect in joints such as those of the big toe. When that happens, it can cause a painful inflammatory condition known as gout.

Gout is not life-threatening, but it is extremely painful. An attack of gout begins with pain and inflammation (swelling, tenderness, and redness) in a joint. If the condition becomes chronic, that is, if it comes back many times over a long period, it can cause kidney stones and deformities of the joints.

Ninety percent of patients with gout are men over 40. The condition is not contagious. Doctors once believed that gout was caused by eating rich foods and by drinking too much alcohol. But today, factors such as age, a family history of gout, and obesity, among others, are believed to play more important roles.

How Is Gout Diagnosed and Treated?

There are several ways to diagnose gout, including blood tests, testing fluid in the joints for crystals of uric acid, and taking x-rays.

Rich Men AND Rich Food

Members of the privileged classes throughout European history often were diagnosed with gout. Researchers once believed this was due to their frequent consumption of meat, starch, and fortified wine. Current research attributes the susceptibility to age (men over age 40), family history, obesity, and other factors.

Among the more notable names from history who qualify under both theories are:

  • Ambroise Paré (1510-1590), chief surgeon to three kings of France
  • Philip II (1527-1598), king of Spain
  • Thomas Sydenham (1624-1689), English physician, sometimes
  • called the English Hippocrates
  • Benjamin Franklin (1706-1790), American philosopher, diplomat,
  • and statesman
  • Samuel Johnson (1709-1784), English lexicographer and writer.

Treatment often includes weight loss, a lower-protein diet, pain relievers, and medications to reduce the level of uric acid in the blood. Drinking plenty of fluids will help to flush uric acid from the body.

See also

Arthritis

Resources

Book

Porter, Roy, and G. S. Rousseau. The Patrician Malady. New Haven: Yale University Press, 1998.

Organization

Arthritis Foundation, 1330 West Peachtree Street, Atlanta, GA 30309. The Arthritis Foundation provides information on gout. http://www.arthritis.org

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gout

gout (gowt) n. a disease in which a defect in purine metabolism causes an excess of uric acid and its salts (urates) to accumulate in the bloodstream and the joints respectively. It results in attacks of acute gouty arthritis and chronic destruction of the joints and deposits of urates (tophi) in the skin and cartilage, especially of the ears. Treatment with uricosuric drugs or allopurinol can control the disease; acute attacks are treated with anti-inflammatory analgesics. See also podagra.

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gout

gout 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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gout

gout / gout/ • n. 1. a disease in which defective metabolism of uric acid causes arthritis, esp. in the smaller bones of the feet, deposition of chalkstones, and episodes of acute pain. 2. poetic/lit. a drop or spot, esp. of blood, smoke, or flame: gouts of flame and phlegm. DERIVATIVES: gout·i·ness / -tēnis/ n. gout·y adj.

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gout

gout Form of arthritis, featuring an excess of uric acid crystals in the tissues. More common in men, it causes attacks of pain and inflammation in the joints, most often those of the feet or hands. It is treated with anti-inflammatories.

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gout

gout disease orig.
so named from the notion of the dropping of morbid matter from the blood into the joints. XIII. — OF. goute (mod. goutte) drop, gout :- L. gutta drop. Hence gouty XV.

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gout

goutabout, bout, clout, devout, doubt, down-and-out, drought, flout, gout, grout, knout, Kraut, lout, mahout, misdoubt, nowt, out, out-and-out, owt, pout, Prout, right about, rout, scout, shout, snout, spout, sprout, stout, thereabout, thereout, throughout, timeout, tout, trout, way-out, without •layout, payout •buyout • blowout • layabout •gadabout • roundabout • knockabout •walkabout • runabout • turnabout •hereabout • roustabout •handout, standout •readout • hideout • dugout • blackout •checkout •breakout, stakeout, takeout •strikeout •knockout, lockout •walkout •cookout, lookout •workout • sell-out • fallout • pull-out •umlaut • litter lout • spin-out •burnout, turnout •hangout • wipeout •copout, dropout •waterspout • beansprout • clearout •sauerkraut • washout • printout •white-out • shoot-out •cut-out, shut-out

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