Gout

Gout


The "disease of kings"

Gout is a painful arthritis caused by raised blood levels of a chemical called uric acid. It produces an acute joint inflammation. In a more chronic state, gout can also produce deposits of uric acid crystals around soft tissue, called tophi, and uric acid kidney stones.

A first attack of gout usually begins in one joint -- most commonly the big toe. Other targets include the ankles, heels, knees, and wrists. The first attack is intense: the pain can be so severe that it can be excruciating to put a even a bedsheet over the area.

Middle-aged men who drink heavily, are overweight, and eat excessive protein are most likely to get gouty arthritis. People with gout can feel in good company, for this is the "disease of kings."King Philip II of Spain had it. Were he alive today, King Philip would be relieved to find many treatments available to control blood levels of uric acid and ease the pain of gout.

Pronunciation

GOWT

Synonyms

    • Gouty arthritis
    • Podagra
    • Hyperuricemia

Detailed Description

Gout is characterized by sudden, intense attacks of joint inflammation. Deposits of monosodium uric acid crystals, accumulated in the joints due to an abnormally high level of uric acid in the blood, are the culprit here.

How does uric acid get too high? Your body continually breaks down cells and forms new ones. Some uric acid, a byproduct of cell breakdown, is normally found in the blood. But when the kidneys can't eliminate enough in the urine, the level of uric acid becomes abnormally high. Some people also produce large amounts of uric acid due to a hereditary enzyme abnormality or disease, like cancer of the blood, in which cells multiply and are destroyed rapidly. In addition, certain drugs and some types of kidney disease can impair the kidneys' ability to excrete uric acid.

Gout attacks without any warning, often at night. Severe pain stabs one or more joints. The first target is frequently the big toe, a condition called podagra. It is believed that uric acid crystals accumulate in the outer joints (toe, ankle, knee, wrist, and elbow) because they are cooler than the middle part of the body, and uric acid tends to crystallize at cooler temperatures. Gout seldom affects the shoulders, spine, or hips.

When a gout episode occurs, the affected joint swells and the skin becomes taut, shiny, and reddish-purple, and feels warm. Touching it is an agonizing experience. Usually, the first few attacks only affect one joint and last a few days. Life goes back to normal until the next attack. But if the disorder progresses, untreated episodes last longer, happen more often, and affect additional joints. Permanent damage can be done.

Severe, chronic gout can cause a deformity that increasingly limits joint movement. Hard lumps of uric acid crystals called tophi are deposited under the skin around joints. They can also form in the kidney and other organs, under the skin, on the ears, or around the elbows. Tophi usually appear about 10 to 15 years after the initial attack, in the tendons, cartilage, bursae, and other soft tissues. While the tophi themselves are painless, they can restrict movement and erode joints. In 10% to 20% of those with gout, uric-acid kidney stones form. Most stones pass spontaneously, some painlessly and some with flank pain. In more extreme cases, there may be bloody urine or obstruction.

Gout can be easily diagnosed. Treatment starts with easing the pain by controlling the inflammation. The second step is establishing a regimen to prevent recurrences.

How Common Is Gout?

Gout strikes less than 1% of the population in North America. It usually affects those between ages 30 and 60. Gout affects men much more often than women; but after menopause, the number of women with gout increases.

What You Can Expect

Subsequent attacks are common. A majority of gout sufferers have another episode within a year. Joint inflammation can become chronic and deforming after repeated attacks. However, gout is easy to diagnose and symptoms can be eliminated with treatment. Chronic gout is rare these days due to dietary therapy and drugs that lower and control uric acid levels.


Established Causes

Gout refers to joint inflammation due to uric acid crystal deposits. Almost all gout sufferers are hyperuricemics (have a high blood uric-acid level). However, not all hyperuricemics develop gout. Therefore, the exact relationship between gout and hyperuricemia is still unknown.

Theoretical Causes

The theoretical causes of gout -- whether it is hereditary or acquired -- all have to do with fluctuating or increasing blood uric acid or purine levels.

    • A dysfunction in purine metabolism is thought to contribute to approximately 10% of cases. This leads to abnormal production and excretion of uric acid.
    • Gout may also be a secondary condition caused by other disorders. Drugs used to treat other disorders might raise blood uric acid level.
    • A diet high in purine is also thought to contribute to gout. When excess purine is present, your body naturally breaks down the excess for excretion, and uric acid is one of the end products.
    • Radiotherapy rapidly destroys cells, and may raise the blood's uric acid level.

Risk Factors

Risk factors for gout include the following:

    • High alcohol intake
    • Family history
    • Pacific islander heritage (for example, Filipinos and Samoans)
    • Certain medications (diuretics, salicylates, and others)
    • Obesity
    • Disorders like hypertension, vascular disease, diabetes, and renal failure
    • Disorders caused by dysfunction in purine (a precursor to uric acid) metabolism
    • High cell-turnover states (leukemia, hemolysis, lymphoproliferative disorders)
    • Radiation therapy

Risk factors are traits or behaviors that may make you statistically more likely than others in the general population to have a certain condition. They are not necessarily "causes" of the condition.


Symptoms

The most common symptom is acute joint pain. Other indications include the following:

    • Affected joint displays redness, swelling, tenderness, and warmth
    • Fever, chills, fatigue, and loss of appetite
    • Recurrent attacks last longer and become more frequent
    • No symptoms between episodes of attack
    • Usually affect joints in the extremities (most common in the big toe)
    • Uric acid deposits in connective tissues
    • Kidney stones
    • Flank pain or bloody/red urine (with kidney stones)

Conditions That May Be Mistaken for Gout

The following conditions may confuse a diagnosis of acute gout:

    • Osteoarthritis
    • Rheumatoid arthritis
    • Traumatic arthritis
    • Psoriatic arthritis
    • Infectious arthritis
    • Acute rheumatic fever
    • Reiter's syndrome
    • Bursitis
    • Tendonitis
    • Pseudogout (acute joint inflammation by calcium pyrophosphate crystals)

For chronic gout:

    • Osteoarthritis
    • Rheumatoid arthritis
    • Traumatic arthritis

How Gout Is Diagnosed

A combination of medical history and laboratory studies is necessary to make a definitive diagnosis for gout. The following procedures are usually used:

    • Medical history and physical examination by your physician.
    • Appropriate laboratory tests to check the blood's uric acid level and the presence of uric acid crystal deposits in the affected joint. These are the diagnostic markers.
    • Systematic exclusion of differential diagnoses like pseudogout.
    • Possibly an X-ray study, to evaluate extent of joint damage.

Your Medical History

If you are a heavy, middle-aged man who consumes large amounts of alcohol and has a diet rich in purine, you are at increased risk of developing gout. Organ meats, legumes, and high-protein foods usually contain a lot of purine. Having a high blood uric acid level also makes you more susceptible to gout. In addition, there is a hereditary basis for gout; if someone in your family has it, you are more likely to get it.

Laboratory Work

Laboratory tests look for diagnostic markers. In the case of gout, lab tests check for various forms of uric acid in the body:

    • Blood sample to check for elevated blood uric acid level (over 7.5 milligrams per deciliter)
    • Urine analysis for checking under-excretion of uric acid by the kidney
    • Aspiration of joint fluid to check for the presence of uric acid crystals
    • Complete blood count (CBC: white blood cell count may be elevated)

Specific Tests

A detailed examination of joint fluid can help diagnose gout. Polariscopic examination fluid smears may also be used.

Imaging

Imaging is useful for evaluating the damage done by the disease:

    • X-rays of an affected joint don't show much in early stages of gout. However, joint erosion is visible in later stages of gout.
    • Bone scans of affected joints are used to check nuclide concentration.

Goals of Treatment

Gout cannot be cured, but it can be almost completely controlled by a combination of medical treatment, diet, and self-care. Drugs are available to correct purine metabolism problems. The immediate aim of treatment is to relieve any painful symptoms and to reduce inflammation and swelling. The long-range goal is to prevent recurrence of episodes by controlling blood uric acid levels.

Treatment Overview

Treatment for gout works toward:

    • Relieving inflammation and pain of an acute attack
    • Preventing future attacks with drugs and diet

Drug Therapy

Drugs most commonly prescribed

    • Prescription NSAIDs, including Indocin (indomethacin) for relief of symptoms during acute attacks
    • Colchicine for acute attacks and preventing recurrences
    • Glucocorticoids (such as Prednisone) for acute, severe attacks
    • Allopurinol for decreasing uric acid production to prevent acute attacks
    • Benemid (probenecid) for increasing urinary output of uric acid
    • Combination drugs, such as ColBenemid, for improved output of uric acid and prevention of future attacks

A word of caution: Older folks or those taking many other drugs should be sure to tell their doctor or pharmacist about all medications-- including herbs and supplements-- they are taking to avoid a drug interaction.

Also, in general, don't take aspirin while you're taking drugs to control uric acid levels because aspirin blocks their effect on the kidneys. That being said, a daily low-dose aspirin taken for cardiovascular health might be fine; ask your doctor.

A note about medications: Many drugs prescribed for gout have side effects. Be sure to discuss treatment benefits and risks with your doctor.

Considerations When Selecting Treatment

    • Nonsteroidal anti-inflammatory drugs (NSAIDs) are usually favored over colchicine. Colchicine taken orally is associated with gastrointestinal side effects, and it also clears less well when there is reduced kidney function.
    • Opioids (analgesics) are useful to relieve the sharp pain. Avoid aspirin, though, as it aggravates hyperuricemia.
    • Resting the affected region will help joint healing.

Appropriate Healthcare Settings

Care is given in an outpatient setting, unless you also have an associated joint infection.

Healthcare Professionals Who May Be Involved in Treatment

A variety of health professionals participate in managing different aspects of this disorder, including the following:

    • Primary physicians
    • Family medicine physicians
    • Internists
    • Rheumatologists
    • Orthopedic surgeons
    • Dieticians

Activity and Diet Recommendations

Rest of the affected area is recommended. Put that foot up. Rest that joint until it's comfortable to use again.

Special Diets

Drink plenty of water to help flush uric acid from your body. Reduce alcohol consumption. Keep protein intake adequate but moderate.

Make sure your diet is low in purine until hyperuricemia subsides. Avoid the following purine-rich foods:

    • Anchovies
    • Sardines
    • Organ meats like kidney and liver
    • Sweetbreads
    • Beer and wine

Foods (that are somewhat higher in purine content) to eat moderately include the following:

    • Lentils and dried beans
    • Meat and poultry
    • Shellfish
    • Oatmeal
    • Spinach
    • Wheat bran and wheat germ

Monitoring the Condition

Monitor your responsiveness to acute gout drug treatment. If your inflammation is not responding to drug therapy, ask your physician to prescribe an alternative drug. If drugs to lower uric acid are used, regular follow-ups with your physician are recommended. When gout is treated in its early stages, chronic impairment is much easier to avoid.

Possible Complications

Left untreated, gout may lead to the following complications:

    • Deformed joints and reduced motility
    • Kidney stones
    • Inflammation of the bones, tendons, and ligaments

Considerations for Children and Adolescents

Gout in young children is rare and usually indicates an inherited abnormality in purine metabolism. There are drugs specifically designed to treat this problem.

Considerations for Older People

Adverse reactions to and side effects of medications may be more frequent and severe in older people. Remind your doctor which medicines you are already taking when discussing a possible gout medication.


Supplements
 

    • Vitamin E: helps prevent the inflammation of gout attacks.
    • Essential fatty acids: gamma-linolenic acid (GLA) and eicosapentenoic acid (EPA). Like vitamin E, these nutrients have anti-inflammatory effects. One way to get them is to take fish oil -- four to six standard fish-oil capsules a day. Another is to take borage or black currant oil -- one standard capsule a day.
    • Vitamin C and niacin: avoid large doses -- they can increase uric acid levels. The amounts of these nutrients found in typical multivitamin supplements probably won't hurt, but make sure you don't take more than 2,000 mg/day of vitamin C and/or 50 mg/day of niacin.

 

Preventing Gout

No definite way exists to prevent gout. Minimizing your intake of high-purine foods, drinking plenty of water, and maintaining an optimal weight for your body-frame size may all reduce your risk. Avoiding drugs that raise uric acid levels may also be beneficial.

Self-Care Measures

    • Avoid purines, compounds that raise your uric acid level and increase your risk of gout attacks. Foods high in purines include the following: meats, organ meats (liver, brains, sweetbreads, etc.), dairy foods, shellfish, sardines, herring, mackerel, anchovies, and anything high in protein (like beans, fish, and poultry).
    • Limit or eliminate alcohol from your diet. Alcohol increases uric acid production, which is why gout attacks often follow an evening of drinking.
    • Drink plenty of nonalcoholic fluids, which help promote the excretion of uric acid from your body.
    • If you want to lose weight, don't go on a crash diet, which would tend to involve liberal use of diuretics. These eliminate fluid, which in turn increases the concentration of your urine, boosting your uric acid level and your risk of gout attacks.

Websites & Organizations

American Academy of Family Physicians Foundation
P.O. Box 8418
Kansas City, MO 64114
Phone: 800-274-2237, ext. 4400

American Academy of Orthopaedic Surgeons Research
6300 North River Road
Rosemont, IL 60018-4262
Phone: 847-823-7186 or 800-346-AAOS (800-346-2267)
Fax: 847-823-8125

American College of Rheumatology
1800 Century Place, Suite 250
Atlanta, GA 30345
Phone: 404-633-3777
Fax: 404-633-1870

Arthritis Foundation
National Office
1330 West Peachtree Street
Atlanta, GA 30309
Phone: 404-872-7100 or 800-283-7800

National Health Information Center
P.O. Box 1133
Washington, DC 20013-1133
Phone: 301-565-4167 or 800-336-4797
Fax: 301-984-4256
Email: nhicinfo@health.org

U.S. National Library of Medicine
8600 Rockville Pike
Bethesda, MD 20894
Phone: 800-272-4787 or 301-496-6308

Wheeless' Textbook of Orthopedics

Sources for This Article

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Hardman, Joel G. and Limbird, Lee E. Goodman and Gilman's The Pharmacological Basis of Therapeutics eds. New York: McGraw Hill, 1996.

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Articles

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Tikly, M, Bellingan, A, Lincoln, D, Russell, A. "Risk Factors for Gout: A Hospital-Based Study in Urban Black South Africans." Rev Rhum Engl Ed. 225-31. Apr 1998.

Wise, CM, Agudelo, CA. "Diagnosis and Management of Complicated Gout." Bull Rheum Dis. 2-5. 1998 Jun.

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