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 5–10 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 400–800 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 200–300 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: 200–400 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): 2403–2406.

Conos, Juan J., and Robert Kalish. "Gout: Effective Drug Therapy for Acute Attacks and for the Long Term." Consultant (August 1996): 1752–55.

Emmerson, Bryan T. "The Management of Gout." New England Journal of Medicine (February 15, 1996): 445–451.

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.

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 (October 2002) (4 Pt 1): 1307–1314.

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

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 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.

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〉.

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,

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.

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 (for example, 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. 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 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. 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.

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 CA, and CM 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. E-mail: [email protected]. <http://www.acfas.org/index.html>.

American College of Rheumatology. 1800 Century Place, Suite 250, Atlanta, GA, 30345. (404) 633-3777. E-mail: [email protected]. <http://www.rheumatology.org>.

American Podiatric Medical Association. 9312 Old Georgetown Road, Bethesda, MD 20814-1698. (800) 366-8227. (301) 571-9200. E-mail: [email protected]. <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).

L. Fleming Fallon, Jr., MD, DrPH

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. [email protected]. 〈http://www.acfas.org/index.html〉.

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

American Podiatric Medical Association. 9312 Old Georgetown Road, Bethesda, MD 20814-1698. (800) 366-8227. (301) 571-9200. [email protected]. 〈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

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,

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 are not 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 does not 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. 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 do not necessarily rule out gout and high levels do not 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.

(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. 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), 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, 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.

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 hyperurice-mia 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.

Caregiver concerns

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

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.

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. [email protected]. http://www.acfas.org/index.html.

American College of Rheumatology. 1800 Century Place, Suite 250, Atlanta, GA, 30345. (404) 633-3777. [email protected]. http://www.rheumatology.org.

American Podiatric Medical Association. 9312 Old Georgetown Road, Bethesda, MD 20814-1698. (800) 366 8227. (301) 571-9200. [email protected]. 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).

L. Fleming Fallon Jr., MD, DrPH