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By Lawrence M. Ryan, MD, Professor of Medicine, Medical College of Wisconsin

Gout is a disorder that results from deposits of uric acid crystals, which accumulate in the joints because of high blood levels of uric acid (hyperuricemia). The accumulations of crystals cause attacks of painful inflammation in and around joints.

  • Accumulations of uric acid crystals can intermittently cause severe joint or tissue pain and inflammation.

  • Doctors remove fluid from the joint and check it for uric acid crystals.

  • Drugs are given to relieve inflammation and pain, prevent further attacks, and sometimes decrease blood levels of uric acid to decrease deposits of urate crystals in the joints.

Gout is more common among men than women. Usually, gout develops during middle age in men and after menopause in women. Gout is rare in younger people but is often more severe in people who develop the disorder before age 30.

Gout, caused by high blood levels of uric acid (hyperuricemia), often runs in families.

Blood levels of uric acid tend to be high in people with metabolic syndrome. This syndrome is characterized by a large waist (due to excess abdominal fat), high blood pressure, resistance to the effects of insulin (called insulinresistance) or high blood sugar levels, and abnormal levels of cholesterol and other fats in the blood.

Cardiovascular disease is common among people with gout.

Causes of Gout

Normally, uric acid, which is a by-product of the breakdown of the nucleic acids (ribonucleic acid [RNA] and deoxyribonucleic acid [DNA]) in the cells, is present in small amounts in the blood because the body continually breaks down cells and forms new cells. Also, the body readily transforms substances in foods called purines into uric acid. Purines are building blocks of RNA and DNA.

Abnormally high uric acid levels in the blood result from

  • Decreased elimination of uric acid by the kidneys (most common cause)

  • Consumption of too much purine-rich food and/or alcohol

  • Production of too much uric acid

Most often, the uric acid level in the blood becomes abnormally high when the kidneys cannot eliminate enough uric acid in the urine. This cause is usually determined by the person's genes. Too much uric acid in the blood can result in uric acid crystals being formed and deposited in and around joints. Conditions that can impair the kidneys’ ability to eliminate uric acid include

  • Some types of kidney disease

  • Certain drugs

  • Lead poisoning

Consuming too much purine-rich food (such as liver, kidney, anchovies, asparagus, consommé, herring, meat gravies and broths, mushrooms, mussels, sardines, and sweetbreads) can increase the uric acid level in blood. However, a strict low-purine diet lowers the uric acid level by only a small amount. In past times, when meat and fish were scarce, gout was considered a rich person’s disease.

Combining a high-purine diet with alcohol can worsen matters because alcohol both increases the production of uric acid and interferes with its elimination by the kidneys.

For unknown reasons, not all people who have hyperuricemia develop gout.

Did You Know...

  • In past times, when meat and fish (purine-rich foods) were scarce, gout was considered a rich person’s disease.

Less commonly, another disorder causes the body to produce too much uric acid. (Gout caused by another disorder is called secondary gout.) These disorders include

  • An inherited enzyme abnormality

  • Disorders that cause cells to multiply and/or be destroyed rapidly, such as leukemia, lymphoma, and hemolytic anemia

  • Drugs that cause cells to multiply and/or be destroyed rapidly, such as certain cancer drugs and radiation therapy

High levels of uric acid in the blood often lead to high levels of uric acid in the joints. This process may then result in the formation of uric acid crystals in the joint tissue and the fluid within the joints (synovial fluid).

Gout most often affects the joints in the feet, particularly at the base of the big toe (swelling, pain, and redness of the big toe is called podagra). However, it also commonly affects other areas: the ankle, instep, knee, wrist, and elbow. Gout tends to affect these cooler areas because uric acid crystals form more readily in cool than in warm areas. Rarely, gout affects the joints of the warmer, central part of the body, such as the spine, hips, or shoulders.

Sudden severe attacks of gout (called acute gouty arthritis) can occur without warning. They may be triggered by

  • An injury

  • Illness (such as pneumonia or another infection)

  • Surgery

  • Use of thiazide diuretics

  • Start of treatment with certain drugs (such as allopurinol and nitroglycerin, particularly nitroglycerin given by vein, which contains alcohol) that may suddenly change the uric acid level in the blood

  • Consumption of large quantities of alcohol or purine-rich food

Symptoms of Gout

Typically, severe pain occurs suddenly in one or more joints, often at night. The night-time pain occurs probably because fluid that has built up in the joint during the daytime leaves the joint faster than uric acid does when a person lies down, making the uric acid more concentrated and thus more ready to form crystals. The pain becomes progressively worse and is often excruciating, particularly when the joint is moved or touched.

The joint becomes inflamed—it swells and feels warm, and the skin over the joint may appear red or purplish, tight, and shiny.

Other symptoms of an attack sometimes include

  • Fever (which may reach 102° F [38.9° C])

  • A fast heart rate (tachycardia)

  • A general sick feeling

  • Chills (rarely)

The first few attacks usually affect only one joint and last for a few days.

The symptoms gradually disappear, joint function returns, and no symptoms appear until the next attack. However, if the disorder progresses, untreated attacks last longer, occur more frequently, and affect several joints. If left untreated, later attacks can last up to 3 weeks.

After repeated attacks, gout can become severe and chronic and may lead to joint deformity.

Over time, joint motion becomes progressively restricted by damage caused by deposits of uric acid crystals in the joints and tendons.


Hard lumps of uric acid crystals (tophi) are first deposited in the joint (synovial) lining or cartilage or in bone near the joints and then under the skin around joints. Tophi can also develop in the kidney and other organs and under the skin on the ears. They commonly develop in the fingers, hands, feet, the tough band extending from the calf muscles to the heel (Achilles tendon), or around the elbows.

Tophi are normally painless but can become inflamed and painful.

If untreated, tophi can burst and discharge chalky masses of uric acid crystals through the skin and may eventually cause deformities.

Complications of gout

About 20% of people who have gout develop kidney stones (urolithiasis) that are composed of uric acid. The stones may block the urinary tract, resulting in excruciating pain and, if untreated, infection and kidney damage.

In people with gout who also have another disorder that damages the kidneys (such as diabetes or high blood pressure), increasingly poor kidney function reduces the excretion of uric acid and makes the gout and its joint damage progressively worse.

Diagnosis of Gout

  • Microscopic examination of joint fluid

  • Sometimes x-rays and/or ultrasonography

Doctors suspect gout on the basis of its distinctive symptoms and an examination of the affected joints. The following suggest the diagnosis:

  • Podagra (sudden swelling, pain, and redness of the big toe)

  • Recurrent instep inflammation

  • A history of previous attacks that began suddenly and resolved spontaneously

Many people with gout have a high level of uric acid in the blood. However, the uric acid level is often normal, especially during an acute attack. Many people have high levels of uric acid in the blood but do not have attacks of gout.

The diagnosis of gout is usually confirmed when needle-shaped uric acid crystals are identified in a sample of a tophus or in joint fluid removed with a needle (joint aspiration) and viewed under a special microscope with polarized light.

X-rays may show joint damage and the presence of tophi (uric acid crystal tophi that displace bone and produce cysts). Doctors may also do ultrasonography to check for uric acid deposits.

Gout is often similar to and sometimes misdiagnosed as another type of arthritis.


With early diagnosis, treatment enables most people to live a normal life. For many people with advanced disease, significant lowering of the levels of uric acid in the blood can resolve tophi and improve joint function.

Gout is generally more severe in people whose initial symptoms appear before age 30. The metabolic syndrome and cardiovascular disease probably contribute to premature death in people with gout.

Some people do not improve sufficiently with treatment. The reasons can include failure to take drugs as prescribed, drugs are prescribed at too low a dosage, and alcoholism.

Treatment of Gout

  • Drugs to relieve pain and swelling resulting from inflammation

  • Rest, immobilization of a painful joint with a splint, and ice

  • Dietary changes and weight loss to lower the uric acid levels and help prevent further attacks

  • Drugs to prevent attacks by preventing inflammation caused by crystals

  • Drugs to lower uric acid levels and dissolve the crystals

Gout treatment has three goals:

  • Relieving the acute attack of inflammation

  • Preventing further attacks

  • Preventing further deposition of uric acid in the tissues by lowering blood levels of uric acid

Relieving acute attacks of gout

Nonsteroidal anti-inflammatory drugs (NSAIDs) are often effective in relieving pain and swelling in the joint. Sometimes additional pain relievers (analgesics), such as the opioid analgesic oxycodone, are needed to control pain.

Treatment with NSAIDs should be continued for several days after the pain and inflammation have resolved to prevent them from appearing again (a condition called relapse).

Colchicine is the traditional, but no longer the most common, first-step treatment. Usually, joint pain begins to subside after 12 to 24 hours of treatment with colchicine and is sometimes gone within 3 to 7 days. Colchicine is taken in tablet form, often as 2 pills given an hour apart. The first pill is taken as closely as possible to the beginning of an attack. A third pill may be taken depending on what the doctor prescribes.

Corticosteroids, such as prednisone, are sometimes useful to reduce joint inflammation (including the swelling) in people who cannot tolerate the other drugs.

If only one or two joints are affected, a corticosteroid suspension, such as prednisolone tebutate, can be injected using the same needle that is used to remove fluid from the joint.

As with NSAID therapy, corticosteroids that are taken by mouth should be continued until after the attack fully resolves to prevent relapse.

In addition to NSAIDs or corticosteroids, other pain relievers, rest, immobilization with a splint, and ice can be used to reduce pain. If people cannot tolerate corticosteroids, colchicine, or NSAIDs, drugs that suppress the immune system and inflammatory system (such as anakinra) can be used, but they are expensive. If there are underlying problems, such as chronic kidney disease or peptic ulcer disease , or if the person is taking certain drugs (such as anticoagulant drugs), the usual treatments for gout may not be used or may be modified.

Preventing further attacks of gout

The following can help:

  • Avoiding alcoholic beverages (such as beer and liquor) and nonalcoholic beer

  • Losing weight

  • Stopping drugs that cause elevated blood levels of uric acid

  • Eating smaller amounts of purine-rich foods

  • Substituting low-fat dairy products for other foods

But these measures are rarely all that is needed.

Most people who have primary gout are overweight. As they gradually lose weight, their blood levels of uric acid often return to normal or near normal, and gout attacks subsequently cease.

Preventive daily drug treatment may be needed for people who experience repeated, severe attacks. Colchicine may be taken daily to prevent attacks or to greatly reduce their frequency. NSAIDs taken daily can also prevent attacks. These drugs help prevent crystals from causing the inflammation that results in attacks. However, colchicine and NSAIDs may cause some side effects.

People with gout who take a diuretic (such as hydrochlorothiazide) to treat high blood pressure may have fewer attacks if they take losartan or a similar drug rather than a diuretic to control their blood pressure. Blood pressure should be controlled as well as possible regardless of how it is treated. Preventing attacks does not prevent or heal existing joint damage caused by uric acid crystals because the crystals are still in the joints, and the drugs do pose some risks for people who have kidney or liver disease.

Lowering blood levels of uric acid

A high level of uric acid in the blood causes problems for people with gout and may increase the risk of kidney disease in people without gout.

People with gout who especially need their blood level of uric acid lowered include those who have the following:

  • Frequent, severe attacks despite taking colchicine, an NSAID, or both

  • Tophi

  • Uric acid kidney stones

  • Conditions that make NSAIDs or corticosteroids risky to take (such as peptic ulcer disease and chronic kidney disease)

People taking drugs to lower the blood level of uric acid should know their level, just as people with high blood pressure should know their blood pressure. The goal of drug therapy is to decrease the level to less than 6 milligrams per deciliter. If the blood level is maintained below 6, uric acid will stop being deposited around the joints and in soft tissues, and the existing deposits will eventually dissolve.

Drugs can lower blood levels of uric acid by decreasing the body’s production of uric acid or increasing the excretion of uric acid in the urine.

Allopurinol is most often used to lower the blood level of uric acid. This drug blocks the production of uric acid in the body. However, allopurinol can upset the stomach and can rarely cause a rash, decrease the number of white blood cells, or cause liver damage or inflammation of vessels (vasculitis). Allopurinol also can trigger an acute attack when it is first taken (mobilization attack). Because low-dose colchicine or an NSAID can decrease this risk, one of these drugs is usually given at the time allopurinol is started and continued for a few months.

Febuxostat is another drug that lowers blood levels of uric acid. It is especially useful in patients who cannot take or have not been helped by allopurinol. As with allopurinol, attacks can occur as the uric acid level in the blood first decreases.

Uricase is used less often. It is given every two weeks by vein (intravenously) and can decrease uric acid by a large amount but can often cause acute flare-ups of gouty arthritis (when first started) or allergic reactions.

Uricosuric drugs (drugs that cause excretion of uric acid in the urine) also can be used to lower the levels of uric acid in the blood in people who have normal kidney function by increasing the kidney’s excretion of uric acid. These drugs include

  • Probenecid

  • Sulfinpyrazone

Aspirin can block the effects of probenecid and sulfinpyrazone, and high doses of aspirin should not be used at the same time as either of these drugs. Low doses that protect the heart (81 milligrams daily) should be continued because heart disease is a considerable risk in people with gout.

Mobilization attacks

Any treatment that decreases levels of uric acid in the blood can trigger an acute attack (sometimes called a mobilization attack). Mobilization attacks are particularly likely soon after a drug is started. A mobilization attack may be a sign that a drug is working well to decrease uric acid levels.

During a mobilization attack, people should not stop taking the drugs that decrease the uric acid level.

Low-dose colchicine or an NSAID can be given for a few months after treatment, when such a drug begins to help prevent or treat mobilization attacks.

Other treatments

Although uricosuric drugs lower the concentration of uric acid in the blood, they can increase the concentration of uric acid in the urine. Drinking plenty of fluids—at least 3 liters a day—may help reduce the risk of uric acid stones developing in the urinary tract. Making the urine basic (alkaline) or less acidic by taking acetazolamide or potassium citrate (which increases the solubility of uric acid in the urine) can further help reduce the risk of uric acid stones forming in the urinary tract. However, if the urine becomes too alkaline, crystals or stones of another and more dangerous kind—calcium oxalate and, less often, calcium phosphate—may form.

Most tophi on the ears, hands, or feet shrink slowly when the uric acid level becomes sufficiently low (less than 6 milligrams per deciliter). However, large tophi may rarely have to be removed surgically.

Uric acid stones in the urinary tract can be broken up, and thereby washed out in the urine, by using ultrasound directed at the stones from outside the body (extracorporeal shock wave lithotripsy—see Removing a Stone With Sound Waves).

Drugs Used to Treat Gout


Some Side Effects


Nonsteroidal anti-inflammatory drugs (NSAIDs)


Upset stomach


Kidney damage

High potassium levels

Retention of sodium and potassium

Swelling or high blood pressure (sometimes)

Used to treat an acute (sudden) attack or to prevent an attack

Antigout drugs


Suppression of blood cell production in the bone marrow (occurs very rarely if the drug is used properly)

Muscle pain and weakness (uncommon)

Interaction with many other drugs, sometimes causing severe side effects

Used to prevent and treat attacks


Flare-ups of gouty arthritis

Allergic reactions

Can decrease uric acid levels by a large amount

Should be avoided if people have glucose-6-phosphate dehydrogenase (G6PD) deficiency


Prednisone (taken by mouth)

Retention of sodium, with swelling or high blood pressure

Multiple side effects if used long-term

Used only if other treatments cannot be used, but the benefit is rapid

Prednisolone tebutate or triamcinolone hexacetonide (taken by injection)



Joint damage with overuse

Inflammation (occasionally)

Infection (rarely)

Injected into the joint if only one or two joints are affected

Uricosuric drugs (drugs that increase uric acid secretion in the urine)





Kidney stones

Can be used long-term to lower blood levels of uric acid to prevent attacks


Drugs that block uric acid production


Upset stomach

Rash (which can be serious)

Decrease in the number of white blood cells

Liver damage (rare)

Can be used long-term to lower blood levels of uric acid to prevent attacks and to remove crystals in the body or stones in the kidneys



Joint pains


Especially useful in patients who cannot take or have not been helped by high doses of allopurinol

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