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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. Attacks of gout usually come on suddenly, stop after five to 10 days, and can keep recurring.

Description

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 bloodstream, is formed as the body breaks down waste products, mainly those containing purine, a substance that is produced by the body and 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. As a result, it builds up in the blood stream, a condition known as hyperuricemia. Some people are more susceptible to gout because of inherited genes. Being overweight and eating a rich diet also increases susceptibility. 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.

Hyperuricemia doesn't always cause gout. However, over the course of years, sharp urate crystals build up in the synovial fluid of the joints. Often, some precipitating event, such as an infection, surgery, 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 (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 patient 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 cause kidney stones, also called renal calculi or uroliths.

Gout affects an estimated one million Americans. Men are more commonly affected than women by a ratio of 4 to 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. When estrogen levels fall during menopause, urate crystals can begin to accumulate 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.

Diagnosis

Usually, physicians can diagnose gout based on the physical examination and medical history (a person'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 (for example, Aleve), ibuprofen (for example, Advil), or indomethacin (for example, Indocin). In some cases, these drugs can aggravate a peptic ulcer or existing kidney disease and cannot be used. Doctors sometimes also use colchicine (for example, 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 (for example, Deltasone) and adrenocorticotropic hormone (for example, 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. Uricosuric drugs, such as probenecid (for example, Benemid) and sulfinpyrazone (for example, Anturane), lower the levels of urate in the blood by increasing its removal from the body (excretion) through urine. These drugs may promote the formation of kidney stones, and they may not work for all persons, especially those with kidney disease. Allopurinol (Zyloprim), for example, 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 treat gout. The potential side effects of allopurinol include rash, a skin condition known as dermatitis, and liver dysfunction. Once people begin taking these medications, they must take them for life or the attacks of gout will continue to return.

Alternative treatment

The alternative medicine approach to gout focuses on correcting hyperuricemia by losing weight 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 quickly resolve pain.

Prognosis

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

Health care team roles

Family practitioners or internists, nurse practitioners, and physician assistants commonly make a diagnosis of and treat gout. Nurses also provide patient education and monitor the patient's progress after treatment is begun.

Prevention

For centuries, gout has been known as a "rich man's disease" or a disease of overindulgence in food and drink. While this view is perhaps a little over-stated 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. All people are advised 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.

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 friction between the joints.

Tophi—Stone-like deposits of uric acid crystals that may build up in the joints, ligaments, and tendons, and lead to permanent joint deformity and decreased motion.

Urate crystals—Crystals formed by high levels of uric acid in the blood.

Resources

BOOKS

Cederbaum, Stephen D. "Diseases of the Urea Cycle." In Harrison's Principles of Internal Medicine. 14th ed. Edited by Anthony S. Fauci, et al. New York: McGraw-Hill, 1998.

Hershfield, Michael S. "Gout and Uric Acid Metabolism." In Harrison's Principles of Internal Medicine. 14th ed. Edited by Anthony S. Fauci, et al. New York: McGraw-Hill, 1998.

Porter, Roy, and George S. Rosseau. Gout: The Patrician Malady New Haven, CT: Yale University Press, 1998.

Ruddy, Shaun, et al., eds. Kelley's Textbook of Rheumatology. 6th ed. Philadelphia, Saunders, 2001.

Schneiter, Jodi. Gout Hater's Cookbook: Recipes Lower in Purines. 3rd ed. Palm Coast, FL: Reachment Publications, 2000.

Smythe, Charley J., and Michael V. Holers. Gout, Hyperuricemia, and Other Crystal-Associated Arthropathies. New York: Marcel Dekker, 1998.

Wortmann, Robert L. "Gout and Other Disorders of Purine Metabolism." In Cecil Textbook of Medicine. 21st ed. Edited by Lee Goldman and Claude J. Bennett. Philadelphia: W.B. Saunders, 2000.

PERIODICALS

Agudelo C.A., and C.M. Wise. "Gout: Diagnosis, Pathogenesis, and Clinical Manifestations." Current Opinion in Rheumatology 13, no. 3 (2001): 234-239.

Bynum B. "Irregular Gout." Lancet 356, no. 9233 (2000): 948-951.

Hill, J. "Gout: Its Causes, Symptoms and Treatment." Nursing Times 95, no. 47 (1999): 48-50.

Li-Yu J, et al. "Treatment of Chronic Gout. Can We Determine When Urate Stores Are Depleted Enough to Prevent Attacks of Gout?" Journal of Rheumatology 28. no. 3 (2001): 577-580.

Mikulecky M., and J. Rovensky. "Gout Attacks and Lunar Cycle. Medical Hypotheses 55, no. 1 (2000): 24-25.

Schlesinger N., and H.R. Schumacher. "Gout: Can Management Be Improved?" Current Opinion in Rheumatology 13, no. 3 (2001): 240-244.

ORGANIZATIONS

American College of Foot and Ankle Surgeons. 515 Busse Highway, Park Ridge, Illinois 60068-3150. (888) 843-3338. mail@acfas.org. 〈http://www.acfas.org/index.html〉.

American College of Rheumatology. 1800 Century Place, Suite 250, Atlanta, GA, 30345. (404) 633-3777. acr@rheumatology.org. 〈http://www.rheumatology.org〉.

American Podiatric Medical Association. 9312 Old Georgetown Road, Bethesda, MD 20814-1698. (800) 366-8227. (301) 571-9200. askapma@apma.org. 〈http://www.apma.org/〉.

OTHER

"Gout." Merck Manual. 〈http://www.merck.com/pubs/mmanual/section5/chapter55/55a.htm〉 (August 9, 2001).

Pittman, Joel R., and Michael H. Bross. "Diagnosis and Management of Gout." American Family Physician. April 1, 1999. 〈http://www.aafp.org/afp/990401ap/1799.html〉 (August 9, 2001).

Gout

© Ariel Skelley/CORBIS. Reproduced by permission.


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