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Medical Encyclopedia:

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. 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.

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—in other words, the redness, swelling, and pain that are the hallmarks of a gout attack.

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Dictionary: gout  (gout) pronunciation
n.
  1. A disturbance of uric-acid metabolism occurring chiefly in males, characterized by painful inflammation of the joints, especially of the feet and hands, and arthritic attacks resulting from elevated levels of uric acid in the blood and the deposition of urate crystals around the joints. The condition can become chronic and result in deformity.
  2. A large blob or clot: “and makes it bleed great gouts of blood” (Oscar Wilde).

[Middle English goute, from Old French, drop, gout, from Medieval Latin gutta, from Latin, drop (from the belief that gout was caused by drops of morbid humors).]

goutiness gout'i·ness n.
gouty gout'y adj.
 
Sci-Tech Encyclopedia: Gout

A hereditary disease due to abnormal purine metabolism. The disease is characterized by increased amounts of blood uric acid (hyperurilcemia), acute and chronic inflammatory arthritis, tophaceous deposits of uric acid crystals, and renal insufficiency. The increase of uric acid is thought to be caused by increased production or decreased excretion of uric acid from the kidney or both. See also Arthritis; Purine.

Primary gout occurs most frequently in middle-aged males and is passed as a familiar or hereditary trait which for some unknown reason does not appear as often in females. Secondary gout refers to the disease when associated with some underlying disorder causing an elevation in uric acid production (for example, myeloproliferative disorders).

The uric acid becomes deposited as urates in soft tissues, especially around the joints, in the cartilages of the ear, along the shafts of long bones, in the kidney, and occasionally on the heart valves. Such deposits, when superficial, can be seen grossly as reddish, inflamed masses called tophi. See also Protein metabolism; Uric acid.

 
World of the Body: 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
 
Food and Nutrition: 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.

 
Food and Fitness: gout

A defect in metabolism resulting in an excessive build up of uric acid crystals in the bloodstream and joints. Crystals may be deposited in the kidneys (where they may contribute to the formation of kidney stones), tendons, and joints. Usually, the first symptom of gout is an intense pain felt in the first joint of the big toe. There are a variety of causes, but the main one is poor excretion of uric acid. High intakes of alcohol or fructose can increase the risk of gout.

 
Dental Dictionary: gout

n

A disease associated with an inborn error of uric acid metabolism that increases production or interferes with the excretion of uric acid. Excess uric acid is converted to sodium urate crystals that precipitate from the blood and become deposited in joints and other tissues. The great toe is a common site for the accumulation of urate crystals. This condition can be exceedingly painful with swelling of a joint and may be accompanied by chills and fever.

 
Alternative Medicine Encyclopedia: 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. .

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. .

[Article by: Patience Paradox; Rebecca J. Frey, PhD]

 
Britannica Concise Encyclopedia: gout

Hereditary metabolic disorder in which excess uric-acid salts, normally excreted in urine, are deposited as needle-sharp crystals in joints, causing attacks of severe inflammation. The most common site is the base of the big toe. One of the oldest diseases in medical literature, gout is far more common in men. Attacks usually do not begin until middle age. They cause heat, redness, and extreme tenderness and pain and often subside in a week or two. Colchicine is used to treat acute attacks. Drugs such as allopurinol inhibit uric-acid synthesis.

For more information on gout, visit Britannica.com.

 
Columbia Encyclopedia: 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.

 
Health Dictionary: gout
(gowt)

A disorder of metabolism characterized by attacks of painful inflammation in the joints, particularly those of the feet and hands. The inflammation is caused by the deposition of crystals of uric acid in the joints. Gout occurs most often in middle-aged men. The tendency toward developing gout is inherited. Stress, fatigue, or excessive exercise are among the factors that can bring on an attack.

 
Veterinary Dictionary: gout

A disorder of uric acid metabolism in which there is hyperuricemia and deposition of urates in and around the joints. Occurs in humans and anthropoid apes. Most animals possess the enzyme uricase that converts uric acid to allantoin. Dalmatian dogs excrete large amounts of uric acid in their urine, but the breed is not affected by gout. A disease called gout occurs in commercial chickens due to feeding of excessive amounts of protein.

  • articular g. — caused by gross excesses of protein in the diet. A chronic disease manifested by swelling of the joints which contain a thick white fluid consisting largely of uric acid crystals.
  • visceral g. — birds become weak and listless and die. The viscera are covered with a frosting of urea crystals. There is a primary renal disease and a fatal uremia. The high-protein diet exacerbates that original disease.
 
Devil's Dictionary: gout
A cynical view of the world by Ambrose Bierce


n.

A physician's name for the rheumatism of a rich patient.

 
Wikipedia: gout
Gout
Classification & external resources
Uric_acid.png
Uric acid
ICD-10 M10.
ICD-9 274.0 274.1 274.8 274.9
OMIM 138900 300323
DiseasesDB 29031
eMedicine med/924  orthoped/124 emerg/221 med/1112 oph/506 radio/313
MeSH D006073

Gout (also called metabolic arthritis) is a disease due to a congenital disorder of uric acid metabolism. In this condition, monosodium urate or uric acid crystals are deposited on the articular cartilage of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the blood stream. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material.

Signs and symptoms

The Gout, Cartoon by James Gillray (1799). The artist memorably illustrates the excruciating pain and swelling that are symptoms of the disease
Enlarge
The Gout, Cartoon by James Gillray (1799). The artist memorably illustrates the excruciating pain and swelling that are symptoms of the disease

The classic picture is of excruciating, sudden, unexpected, burning pain, swelling, redness, warmness and stiffness in the joint. Low-grade fever may also be present. The patient usually suffers from two sources of pain. The crystals inside the joint cause intense pain whenever the affected area is moved. The inflammation of the tissues around the joint also causes the skin to be swollen, tender and sore if it is even slightly touched. For example, a blanket or even the lightest sheet draping over the affected area could cause extreme pain.

Gout usually attacks the big toe (approximately 75 percent of first attacks); however, it also can affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, and spine. In some cases, the condition may appear in the joints of small toes that have become immobile due to impact injury earlier in life, causing poor blood circulation that leads to gout.

Patients with longstanding hyperuricemia (see below) can have uric acid crystal deposits called tophi (singular: tophus) in other tissues such as the helix of the ear. Uric acid stones can form as one kind of kidney stone in some common occasions.

Diagnosis

Hyperuricemia is a common feature; however, urate levels are not always raised.[1] Hyperuricemia is defined as a plasma urate (uric acid) level greater than 420 μmol/L (7.0 mg/dL) in males (or 380 μmol/L in females); however, a high uric acid level does not necessarily mean a person will develop gout. Urate is within the normal range in up to two-thirds of cases.[2] If gout is suspected, the serum urate test should be repeated once the attack has subsided. Other blood tests commonly performed are full blood count, electrolytes, renal function and erythrocyte sedimentation rate (ESR). This helps to exclude other causes of arthritis, most notably septic arthritis.

A definitive diagnosis of gout is from light microscopy of fluid aspirated from the joint (this test may be difficult to perform) to demonstrate intracellular monosodium urate crystals in synovial fluid polymorphonuclear leukocytes. The urate crystal is identified by strong negative bi-refringence under polarised microscopy and its needle-like morphology. A trained observer does better in distinguishing them from other crystals.

Pathogenesis

Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Uric acid is more likely to form into crystals when there is a hyperuricaemia, although it is 10 times more common without clinical gout than with it[3]

Purines can be generated by the body via breakdown of cells in normal cellular turnover, or can be ingested in purine-rich foods such as seafood. the kidneys are responsible for approximately one-third of uric acid excretion, with the gut responsible for the rest. It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.

There are also different racial propensities to develop gout. Gout is high among the peoples of the Pacific Islands, and the Māori of New Zealand, but rare in the Australian aborigine despite the latter's higher mean concentration of serum uric acid.[4] In the United States, gout is twice as prevalent in African American males as it is in Caucasians.[5]

A seasonal link also may exist, with significantly higher incidence of acute gout attacks occurring in the spring.[6] [7]

Hyperuricemia is considered an aspect of metabolic syndrome, although its prominence has been reduced in recent classifications. This explains the increased prevalence of gout among obese individuals.

Gout is a form of arthritis that affects mostly men between the ages of 40 and 50. The high levels of uric acid in the blood are caused by protein rich foods. Alcohol intake often causes acute attacks of gout and hereditary factors may contribute to the elevation of uric acid. Typically, persons with gout are obese, predisposed to diabetes and hypertension, and at higher risk of heart disease. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol.[8] It is known that lead sugar was used to sweeten wine, and that chronic lead poisoning is a cause of gout,[9][10] which condition is then known as saturnine gout, because of its association with alcohol and excess.[11]

Gout also can develop as co-morbidity of other diseases, including polycythaemia, leukaemia, intake of cytotoxics, obesity, diabetes, hypertension, renal disorders, and hemolytic anemia. This form of gout is often called secondary gout. Diuretics (particularly thiazide diuretics) have traditionally been blamed for precipitating attacks of gout, but a Dutch case-control study from 2006 appears to cast doubt on this conclusion.[12]

Gout with tophi on elbow and knee.
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Gout with tophi on elbow and knee.

Treatment

Acute attacks

The first line of treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are indomethacin, other nonsteroidal anti-inflammatory drugs (NSAIDs), oral glucocorticoids, or intra-articular glucocorticoids administered via a joint injection.

Colchicine was previously the drug of choice in acute attacks of gout, as it impairs the motility of granulocytes and can prevent the inflammatory phenomena that initiate an attack. Colchicine should be taken within the first 12 hours of the attack and usually relieves the pain within 48 hours, although side effects (gastrointestinal upset such as diarrhea and nausea) can complicate its use. NSAIDs are the preferred form of analgesia for patients with gout.

A randomized controlled trial found similar benefit from nonsteroidal anti-inflammatory drugs and oral glucocorticoids; however, less adverse drug reactions occurred in the glucocorticoids group.[13] In the nonsteroidal anti-inflammatory drugs group, each patient initially received diclofenac (75 mg) intramuscularly, indomethacin 50 mg orally, and acetaminophen 1 g orally. The patient was received a 5-days of indomethacin (50 mg orally every 8 hours for 2 days, followed by indomethacin 25 mg every 8 hours for 3 days), and acetaminophen 1 g every 6 hours as needed. The glucocorticoids patients received prednisolone 30 mg orally, and acetaminophen 1 g orally. The patient was then given prednisolone 30 mg orally once per day for five days.

Before medical help is available, some over-the-counter medications can provide temporary relief from pain and swelling. NSAIDs such as ibuprofen can reduce the pain and inflammation slightly, although aspirin should not be used as it can worsen the condition. Preparation H hemorrhoidal ointment can be applied to the swollen skin to reduce the swelling temporarily. Professional medical care is needed for long-term management of gout.

Ice may be applied for 20–30 minutes several times a day, and a randomized controlled trial found that patients who used ice packs had better relief of pain without side effects.[14] Keeping the affected area elevated above the level of the heart also may help.

Due to swelling around affected joints for prolonged periods, shedding of skin may occur. This is particularly evident when small toes are affected and may promote fungal infection in the web region if dampness occurs, and treatment is similar to that for common athlete's foot.

Some sufferers of Gout report an aggravation of the condition in the knees and toes associated with long periods of immobility, such as when sitting at a computer desk for long hours. This can be particularly unfortunate if the sufferer is searching for work as the aggravation can interefere with mobility. Sufferers who notice early swelling or early pain may appear to be able to arrest the aggravation when medical treatment is applied before the condition gets worse. Where this is the case, a medically prescribed anti-inflammatory oral treatment taken with food and bed rest may provide relief within 6-8 hours.

Another possibility is use of acetazolamide, one of the first diuretics discovered. This drug inhibits the action of carbonic anhydrase on the proximal convoluted tubules within the kidneys, which effectively inhibits reabsorption of bicarbonate, thus alkalinizing the urine. After two to three days of usage, the diuretic effects of this drug decline because of increased downstream reabsorption of ions and water by the renal tubules; however, the alkalinization of urine persists, and this basic urine attracts weak acids such as uric acid and cystine into the urine, thus increasing their urinary excretion.35

Chronic joint changes

For extreme cases of gout, surgery may be necessary to remove large tophi and correct joint deformity.

Prevention

Medications

  • Febuxostat ((2-[3-cyano-4-isobutoxyphenyl]-4-methylthiazole-5-carboxylic acid) - a non-purine inhibitor of xanthine oxidase seems to be an alternative that is superior to allopurinol; it is currently in Phase III trials.[15]
  • Probenecid, a uricosuric drug that promotes the excretion of uric acid in urine, is also commonly prescribed - often in conjunction with colchicine. The drug fenofibrate (which is used in treating hyperlipidemia) also exerts a beneficial uricosuric effect.[16]
  • It is suspected that in many cases gout may be secondary to untreated sleep apnea, when oxygen-starved cells break down and release purines as a by-product. Treatment for apnea can be effective in lessening incidence of acute gout attacks.[17]
  • A study in 2004 suggests that animal flesh sources of purine, such as beef and seafood, greatly increase the risk of developing gout. However, high-purine vegetable sources did not. Dairy products such as milk and cheese significantly reduced the chances of gout. The study followed over 40000 men over a period of 12 years, in which 1300 cases of gout were reported.[18]
  • PEG-uricase, a polyethylene glycol ("PEG") conjugate of recombinant porcine uricase (urate oxidase), which breaks down the uric acid deposits is being studied in Phase III clinical trials for the treatment of severe, treatment-refractory gout in the United States in 2006.Pipeline
  • Sodium bicarbonate (baking soda) is an old remedy,[19] thought to work by raising blood pH (lowering blood acidity). However, the added sodium may be inappropriate for some people.
  • Research from the University of British Columbia suggests long-term coffee consumption is associated with a lower risk of gout. [20][21]

Diet

See Saag and Choi, 2006, an open-access review article, for detailed references and further information.[22]

The serum level of uric acid is the primary risk factor for gout. The serum level is the result of both intake (diet) and output (excretion).

Reduce intake of purines

The solubility threshold for uric acid is approximately 6.7 mg/dl; above this threshold crystals may form. Healthy subjects in the Normative Aging Study who had serum levels of uric acid over 9.0 mg/dl suffered a 22% incidence of gout over six years, compared to less than one percent for those with 7.0-8.9 mg/dl. The average uric acid level in men is 5.0 mg/dl, and substitution of a purine-free formula diet reduces this to 3.0 mg/dl. A purine-restricted diet lowers the level nearly as much (1-2 mg/dl).

A diet low in purines reduces the serum level of uric acid. Notable sources of dietary purines include:

Protein is a crude proxy for purines; a more precise proxy is muscle. Apart from the notable dietary purines above, the main source of dietary purines is DNA and RNA, via their bases adenine and guanine. All sources of dietary protein supply some purines, but some sources provide far more purines than others. Meat (particularly dark meat) and seafood are high in purine because muscle cells are packed with mitochondria, which have their own DNA and RNA. In a large prospective study, high consumption of meat and seafood were found associated with an elevated risk of gout onset (41% and 50%, respectively). High consumption of dairy products, high in protein but very low in DNA and RNA, was associated with a 44% decrease in the incidence of gout. Consumption of the more purine-rich vegetables or a high protein diet per se had no significant correlation.

Consumption of beer is associated with a 49% increase in relative risk per daily 12-oz serving. By contrast, consumption of spirits was associated with only a 15% increase in relative risk, and no association at all was found with consumption of wine.[citation needed]

Some medical drugs are purine-based. Notable among these are the purine-analog antimetabolite drugs, sometimes used as chemotherapy agents.

Increase output of uric acid

Ingestion of 500 mg of Vitamin C per day has been shown[citation needed] to bring about a 0.5 mg/dl decrease in serum uric acid through increased excretion. Some Gout sufferers have recently found that taking up to 1,000 mg of Vitamin C, combined with a small dosage (approx. 10-15 mg./day) of Lithium have had very beneficial effects on their uric acid levels.

Vitamin C, taken in high doses, can help decrease blood uric acid levels, but should not be taken without a doctor's supervision. Note that there is a small subset of people with gout who will actually get worse with high levels of vitamin C. Also, a single high dose can free up too much uric acid and cause kidney stones. (University of Maryland Medical Center for Integrative Medicine).

Other approaches

Additional dietary recommendations can be made which reduce gout indirectly, by reducing gout risk factors such as obesity, hypertension, cardiovascular disease, diabetes, and metabolic syndrome.

The following suggestions do not meet with universal approval among medical practitioners.

Low purine diet:

  • To lower uric acid:
    • cherries were reported to reduce uric acid in a small study.[23][24]
    • celery extracts (celery or celery seed either in capsule form or as a tea) is believed by many to reduce uric acid levels (although these are also diuretics).[citation needed] Celery extracts have been reported to act synergistically with anti-inflammatory drugs.[25]
    • Cheese has been recommended as a low-purine food,[26] and dairy products have been found to reduce the risk of gout.
  • Food to avoid:
    • foods high in purines
      • limit food high in protein such as meat, fish, poultry, or tofu to 8 ounces (226 grams) a day. Avoid entirely during a flare up.[citation needed] Tofu has been proposed as a safe source of protein for gout patients due to its small and transient effect on plasma urate levels.[27]
      • sweetbreads, kidneys, liver, brains, or other offal meats.[28][29]
      • sardines and anchovies [30]
      • seafood [31]
      • alcohol.[32] Some claim that this applies especially to beer, on the basis that brewer's yeasts are very rich in purine. Since most modern commercial beer contains only trace amounts of yeast, this claim requires further substantiation.[citation needed] Formerly, port wine was sweetened with litharge, causing lead poisoning, of which gout is a complication. Ironically, red wines, particularly those produced by traditional methods,[33] contain procyanidins released from grape seeds during wine making, which have been reported to lower serum uric acid levels by an indirect mechanism.[34] However, withdrawal of urate-lowering therapy is associated with recurrence of acute gouty arthritis.[35]
      • meat extracts, consommés, and gravies[36]
  • To avoid dehydration:
    • Drink plenty of liquids, especially water, to dilute and assist excretion of urates;
    • Avoid diuretic foods or medicines like aspirin(aspirin should be avoided from those suffering from gout, unless specified by a trained physician), vitamin C, tea and alcohol. The role of diuretics in triggering gout has been disputed.[37]
  • Moderate intake of purine-rich vegetables is not associated with increased gout.[18]

History

Writing ca. 30 AD, Aulus Cornelius Celsus appeared to recognize many of the features of gout, including its link with a urinary solute, late onset in women, linkage with alcohol, and perhaps even prevention by dairy products. [2] "Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera." and "Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed. Upon the commencement of pain blood should be let; for when this is carried out at once in the first stages it ensures health, often for a year, sometimes for always. Some also, when they have washed themselves out by drinking asses' milk, evade this disease in perpetuity; some have obtained lifelong security by refraining from wine, mead and venery for a whole year; indeed this course should be adopted especially after the primary attack, even although it has subsided."

The Roman gladiatorial surgeon Galen described gout as a discharge of the four humors of the body in unbalanced amounts into the joints. The Latin term for a drop, as a drop of discharge, is gutta -- the term gout descends from this word.

See also

References

  1. ^ Sturrock R (2000). "Gout. Easy to misdiagnose". BMJ 320 (7228): 132–3. PMID 10634714. 
  2. ^ Siva C, Velazquez C, Mody A, Brasington R (2003). "Diagnosing acute monoarthritis in adults: a practical approach for the family physician". Am Fam Pghysician 68 (1): 83–90. PMID 12887114. 
  3. ^ Virsaladze D, Tetradze L, Djavashvili L, Esakia N, Tananashvili D. (2007). "Levels of uric Acid in serum in patients with metabolic syndrome.". Georgian Med News 146: 34–7. PMID 17595458. 
  4. ^ Roberts-Thomson R, Roberts-Thomson P (1999). "Rheumatic disease and the Australian aborigine". Ann Rheum Dis 58 (5): 266&ndasgh;70. PMID 10225809. 
  5. ^ Rheumatology Therapeutics Medical Center. What Are the Risk Factors for Gout?. Retrieved on 2007-01-26.
  6. ^ Schlesinger N, Gowin KM, Baker DG, Beutler AM, Hoffman BI, Schumacher HR Jr.. Acute gouty arthritis is seasonal.. Retrieved on 2007-09-27.
  7. ^ Gallerani M, Govoni M, Mucinelli M, Bigoni M, Trotta F, Manfredini R.. Seasonal variation in the onset of acute microcrystalline arthritis.. Retrieved on 2007-09-27.
  8. ^ Robert S. Ivker, D.O. , et al (1999). The Complete Self-Care guide to Holistic Medicine, 186–8. ISBN0-87477-986-J. 
  9. ^ Lin JL, Huang PT. (1994). "Body lead stores and urate excretion in men with chronic renal disease". J Rheumatol 21 (4): 705–9. PMID 8035397. 
  10. ^ Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. (2000). "Effect of low level lead exposure on hyperuricemia and gout among middle aged and elderly men: the Normative Aging Study". J Rheumatol 27 (7): 1708–12. PMID 10914856. 
  11. ^ Ball GV. (1971). "Two epidemics of gout". Bull Hist Med 45 (5): 401–8. PMID 4947583. 
  12. ^ Janssens H, van de Lisdonk E, Janssen M, van den Hoogen H, Verbeek A (2006). "Gout, not induced by diuretics? A case-control study from primary care". Ann Rheum Dis 65 (8): 1080–3. DOI:10.1136/ard.2005.040360. PMID 16291814. 
  13. ^ Man CY, Cheung IT, Cameron PA, Rainer TH (2007). "Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial". Annals of emergency medicine 49 (5): 670–7. DOI:10.1016/j.annemergmed.2006.11.014. PMID 17276548. 
  14. ^ Schlesinger N, Detry MA, Holland BK, et al (2002). "Local ice therapy during bouts of acute gouty arthritis". J. Rheumatol. 29 (2): 331–4. PMID 11838852. 
  15. ^ Becker M, Schumacher H, Wortmann R, MacDonald P, Eustace D, Palo W, Streit J, Joseph-Ridge N (2005). "Febuxostat compared with allopurinol in patients with hyperuricemia and gout". N Engl J Med 353 (23): 2450–61. PMID 16339094. 
  16. ^ Bardin T (2003). "Fenofibrate and losartan". Ann Rheum Dis 62 (6): 497–8. PMID 12759281. 
  17. ^ Abrams B (2005). "Gout is an indicator of sleep apnea". Sleep 28 (2): 275. PMID 16171252. 
  18. ^ a b Choi H, Atkinson K, Karlson E, Willett W, Curhan G (2004). "Purine-rich foods, dairy and protein intake, and the risk of gout in men" (PDF). N Engl J Med 350 (11): 1093–103. PMID 15014182. 
  19. ^ The British Pharmaceutical Codex. Published by direction of the Council of the Pharmaceutical Society of Great Britain, 1911. Sodium
  20. ^ Hyon K. Choi, Walter Willett, Gary Curhan (2007). "Coffee consumption and risk of incident gout in men: A prospective study". Arthritis & Rheumatism 56 (6): 2049–2055. PMID 17530645. 
  21. ^ Choi HK, Curhan G. (2007). "Coffee, tea, and caffeine consumption and serum uric acid le