WHAT CAUSES GOUT?

Gout is classified as either primary (the most common type) or secondary, depending on the cause of the associated hyperuricemia. In both types of gout, between 70% and 95% of hyperuricemia cases are the result of under-excretion of uric acid, rather than uric acid overproduction.
 
Primary Gout
More than 99% of primary gout cases are referred to as idiopathic, meaning that the cause of the hyperuricemia cannot be determined. They are most likely due to a combination of hormonal and genetic factors that cause metabolic abnormalities resulting in overproduction of uric acid or reduced excretion of uric acid. The remaining 1% of primary gout cases are traceable to either of two rare inherited enzyme defects that affect purine synthesis in the cells.
 
Secondary Gout
In secondary gout, hyperuricemia is caused by drug therapy or by medical conditions other than an inborn metabolic disorder that increase uric acid concentration.
Medications. The list of drugs that cause hyperuricemia is long. They include the following:

Alcohol Use. Alcohol use is a major contributor to gout and increases uric acid levels in three ways:

Kidney Insufficiency. Renal (meaning kidney) insufficiency is a major risk factor for gout in older people. This condition results in an impaired ability of the kidneys to eliminate waste products, including uric acid, which then build up in the blood. Hyperuricemia occurs in between 30% and 85% of people who have renal insufficiency from kidney transplants or certain medications (eg, immunosuppressive agents or diuretics).
Other Conditions. A number of other conditions can cause gout. They include the following:

Purine-Rich Diet. A purine-rich diet rarely causes hyperuricemia, although it may precipitate an attack in some people with existing gout. [For a list of purine-rich foods, see What Lifestyle Measures Can Help Prevent Gout?, below.]

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WHAT ARE THE SYMPTOMS OF GOUT?

Asymptomatic Hyperuricemia
Asymptomatic hyperuricemia, in which MSU slowly builds up, always precedes gout and is considered the first stage of the disorder. It lasts for an average of 30 years.

Note: Hyperuricemia does not inevitably lead to gout. In fact, less than 20% of the hyperuricemic population develops the full-blown arthritic disease.

Acute Gouty Arthritis
Acute gouty arthritis occurs when the first symptoms of gout appear. Sometimes gout is heralded by brief twinges of pain (petit attacks) in an affected joint, which can precede the actual full-blown condition by several years. MSU crystals form at normal body temperature when concentrations in the blood reach 7 mg/dL. At lower temperatures, crystals form at lower concentrations. Since blood temperature falls with distance from the heart, gout strikes the toes and fingers first.

The symptoms of acute gout arthritis are described as follows:

Intercritical Gout
Intercritical gout is the term used to describe the periods between attacks. The first attack is usually followed by a complete remission of symptoms, but left untreated, gout nearly always recurs at some point in the future. One study reported that 62% of subjects experienced at least one further attack within a year. At the end of two years, 78% of patients experienced a recurrence. After 10 years, 93% of the patients had had repeat attacks.
 
Symptoms of Chronic Tophaceous Gout
Development of Chronic Pain. When gout remains untreated, the intercritical periods typically become shorter and shorter, and the attacks, although sometimes less intense, can last longer. Over the long term (about 10 to 20 years) gout becomes a chronic disorder characterized by constant low-grade pain and mild or acute inflammation. Gout may eventually affect several joints, including those that may have been free of symptoms at the first appearance of the disorder. In rare cases, the shoulders, hips, or spine are affected.

Symptoms of Tophi. Tophi, the knobby MSU crystal deposits that form during chronic gout, generally form in the following location:

Tophi, generally, are painless. However, they can often cause pain and stiffness in the affected joint. Eventually, they can also erode cartilage and bone, ultimately destroying the joint. Large tophi under the skin of the hands and feet can give rise to extreme deformities.

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Triggers for Gout Symptoms

Gout symptoms may be precipitated by various conditions including the following:

Symptoms occur more frequently in the spring, with the peak in April, according to some studies.

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HOW SERIOUS IS GOUT?

Gout rarely poses a long-term health threat if properly treated. It does, however, remain a source of short-term pain and incapacity for thousands of Americans.

Pain and Disability
Left untreated, gout can develop into a painful and disabling chronic disorder. Persistent gout can destroy cartilage and bone, causing irreversible joint deformities and loss of motion. Tophi can grow to the size of handballs and can destroy bone and cartilage in the joints, similar to the process in rheumatoid arthritis. If they lodge in the spine, tophi can cause serious damage including compression, although this is very rare. In extreme cases, joint destruction results in complete disability.

Kidney Conditions
Kidney Stones. Kidney stones occur in between 10% and 40% of gout patients, and can occur at any time after the development of hyperuricemia. Although the stones are usually composed of uric acid, they may also be mixed with other materials.

Kidney Disease. About 25% of patients with chronic hyperuricemia develop progressive kidney disease, which sometimes ends in kidney failure. It should be noted, however, that many experts believe that chronic hyperuricemia is unlikely to be a common cause of kidney disease. In most cases, the kidney disease comes first and causes high concentrations of uric acid.

Conditions Associated with Gout

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WHAT ARE THE RISK FACTORS FOR GOUT?

Risk factors are attributes or activities associated with a greater-than-normal likelihood of developing a particular disorder. Sometimes a causal connection between the attribute or activity and the disorder can be established, but at other times there is simply a statistical correlation. The risk factors for gout, of which there are several, are identical to those for hyperuricemia.

Prevalence
Gout is one of the most common types of arthritis. Based on self-reports, gout is estimated to affect about 2.1 million Americans (1.56 million men and 550,000 women). Some experts believe, however, that this may be an overestimate. The prevalence of gout has been rising in recent decades, not only in America but in other developed countries, possibly because of dietary and lifestyle changes, greater use of medications that cause hyperuricemia, and aging populations.

Gout is very uncommon in less developed countries, however, and in 1952 it was said to be unknown in China, Japan, and the tropics.

Age
Gout usually first occurs in middle-aged adults, although it becomes increasingly prevalent as people age. Among children, the levels of uric acid in both girls and boys are low, on average 3 to 4 mg/dL. Except for rare inherited genetic disorders that cause hyperuricemia, gout in children is almost unheard of.

Gender
Men. Men are significantly at higher risk for gout. In males, uric acid levels rise substantially at puberty, with the result that the level exceeds 7 mg/dL (considered to indicate hyperuricemia) in about 5% to 8% of American men. Gout typically strikes only after 20 to 40 years of persistent hyperuricemia, however, so men who develop it usually experience their first attack between the ages of 30 and 50 years. In one study that followed male medical students for 28 years, the prevalence of gout was 5.8% in Caucasian men and 10.9% in African American men.

Women. Before menopause women have a significantly lower risk for gout than men, possibly because of the actions of estrogen. This female hormone appears to facilitate uric acid excretion by the kidneys. (Only about 15% of female gout cases occur before menopause.) After menopause the risk increases in women so that after age 60 the incidence is equal in men and women, and after 80, gout occurs actually more often in women.

Family History
A fairly substantial proportion of patients with gout (10% to 20%) has a family history of the arthritic condition.

Major Risk Factors
Obesity. Researchers report a clear link between body weight and uric acid levels; obesity may be an especially important risk factor for gout in men. In one Japanese study, overweight people had between 2 and 3.4 times the incidence of hyperuricemia as those of normal or low weights.

Hypertension and Diuretics. The use of diuretics, which are agents used to treat high blood pressure, are highly associated with gout. Hypertension (high blood pressure), itself, is found in 25% to 50% of patients with gout, but whether it causes hyperuricemia is uncertain.

Alcohol Use. Alcohol use is highly associated with gout in younger adults. Binge drinking particularly increases uric acid levels. It appears to play less of role among elderly patients, especially among women with gout.

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HOW IS GOUT DIAGNOSED?

Medical History and Physical Examination

Examination of Synovial Fluid
Examination of synovial fluid is the most accurate method for diagnosing gout. It may even be helpful in detecting gout during intercritical periods. The synovial fluid is the lubricating liquid that fills the synovium (the membrane that surrounds a joint and creates a protective sac). The fluid cushions joints and supplies nutrients and oxygen to cartilage, the slippery tissue that coats the ends of bones.

Procedure. The procedure for taking a sample of synovial fluid from an affected joint is called aspiration:

Aspiration can cause infection, though this occurs in less than 0.1% of patients. Aspiration sometimes eases a patient’s symptoms by reducing swelling and pressure on the tissue surrounding the joint.

Analyzing the Fluid. After the sample is taken, it is sent to a laboratory, where a specialist examines the sample through a microscope under polarized light. This special light will reveal the presence of monosodium urate (MSU) crystals, which will nearly always confirm a diagnosis of gout. The laboratory can also test the sample for infection.

Blood Test for Uric Acid Levels
A blood test is usually given for measuring uric acid and detecting hyperuricemia. A low level of uric acid in the blood makes a diagnosis of gout much less probable, and a very high level increases the likelihood of gout. Some experts argue, however, that such measurements are not very useful, given what is known about the variability of uric acid levels in people with gout:

24-Hour Urine Sample
It is sometimes helpful to gauge the amount of uric acid excreted by the patient over the course of 24 hours, particularly if the patient is young and has pronounced hyperuricemia that might be related to a metabolic disorder.

To provide a urine sample, the following steps are taken:

If uric acid exceeds a particular value in the urine, further tests for an enzyme defect or other identifiable cause of gout arising from uric acid overproduction are justified. Greater-than-normal amounts of uric acid in the urine also indicate that the patient faces a greater risk of developing uric acid kidney stones, and can guide the physician in his or her choice of drug therapy for chronic gout.

X-Rays
For the most part, x-rays do not reveal any abnormalities during the early stages of gout, and their usefulness where gout is concerned lies in assessing the progress of the disorder in its chronic phase and in identifying other health problems whose symptoms may resemble those of gout. Tophi can be seen on x-rays before they become apparent on physical examination.

Ruling Out Other Disorders
As part of the diagnosis, other disorders that produce gout-like symptoms or cause hyperuricemia should be ruled out. In general, it is easy to distinguish acute gout that occurs in one joint from other arthritic conditions. The two disorders that may confuse this diagnosis are pseudogout and septic arthritis. Chronic gout can often resemble rheumatoid arthritis. A number of other conditions may at some point in their course resemble gout. [See Conditions with Similar Symptoms to Gout.]

Pseudogout. Pseudogout is a condition most likely to be confused with gout but the crystals are made of calcium and not uric acid.  See section on Pseudogout.

Rheumatoid Arthritis. Rheumatoid arthritis can cause distortion in the joints of the fingers, inflammation, and pain that may mimic gout. It is particularly difficult to distinguish chronic gout in older people form rheumatoid arthritis. A proper diagnosis can be made with a detailed medical history, laboratory tests, and identification of MSU crystals.

Osteoarthritis. Gout can coincide and be confused with osteoarthritis in older people, particularly when it occurs in arthritic finger joints in women. In general, gout should be suspected if the joints in the fingers tips are unusually enlarged.

Septic Arthritis. Septic arthritis is a widespread and potentially life-threatening bacterial infection that can cause inflamed joints, chills, and spiking fever. The severity of the fever and a high white-blood cell count in the joint fluid helps differentiate septic arthritis from gout, but at times it is difficult to tell the conditions apart. A correct diagnosis is critical.

Bunions. A bunion is a deformity that usually occurs at the head of the first of five long bones (the metatarsal bones) that extend from the arch and connect to the toes and may be confused with gout. The first metatarsal bone is the one that attaches to the big toe. A bunion begins to form when the big toe is forced in toward the rest of the toes, causing the head of the first metatarsal bone to jut out and rub against the side of the shoe; the underlying tissue becomes inflamed, and a painful bump forms. As this bony growth develops, the bunion is formed as the big toe is forced to grow at an increasing angle towards the rest of the toes.

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Diseases with Similar Symptoms to Gout

The following diseases also cause joint and muscle pain:

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WHAT ARE THE GENERAL GUIDELINES FOR TREATING GOUT?

Acute attacks of gout and long-term treatment of gout and its associated hyperuricemia require different approaches. All phases are treated mainly with drugs. There are also specific treatment regimes for conditions associated with gout, including uric acid nephropathy and uric acid nephrolithiasis.

Lifestyle Changes
Many patients do not require medications. During the period between gout attacks, patients are advised to avoid foods high in purines and to maintain a healthy weight. Patients should also avoid alcohol and reduce any stress. [ See What Lifestyle Measures Can Help Prevent Gout?.]
 
Treatments for Asymptomatic Hyperuricemia
Because asymptomatic hyperuricemia usually does not lead to gout or other health problems, and would have to be treated with drugs that present certain risks and can be expensive, treatment to prevent a first attack of gout in hyperuricemic patients is considered inadvisable. In unusual circumstances, for example when very high uric acid levels threaten the kidney, treatment may be justified.
 
Treatment of an Acute Attack of Gout
Drug treatments for acute attacks of gout are aimed at relieving pain and reducing inflammation. They should be started as early as possible.

Rest, applying cold, and protecting the affected joint with a splint can also promote recovery. After the first attack, some physicians advise their patients to keep a supply of medications on hand so that self-medication can begin at the first sign of symptoms of a second acute attack.
 
Treatments to Prevent Attacks during Intercritical Gout
After an acute attack patients remain at risk for another for several weeks during the intercritical period. In such cases, low doses of either of the following agents may be used to during this period for prevention.

These agents should be taken in low doses for one to two months after an attack or longer in patients who have experienced frequent attacks. These are simply anti-inflammatory drugs, however, and have no effect on hyperuricemia. [For Description of individual drugs see What Are the Specific Drugs Used for Gout?, below.]
 
Drugs Used to Reduce Uric Acid Levels in Chronic Gout
In some cases, patients will use agents (antihyperuricemic drugs) to reduce uric acid levels. The goals of antihyperuricemic therapy are to reduce the frequency of attacks and to dissolve monosodium urate (MSU) crystals and tophi.

Candidates. Long-term treatment of hyperuricemia may be recommended for the following situations:

Normal kidney function is essential for taking these drugs. This therapy, then, may not be as beneficial in many elderly patients, who often have some kidney insufficiency.

Agents Used to Reduce Uric Acid. A number of effective antihyperuricemic agents are available. In general, their effects differ depending on whether a patient's high uric acid is due to overproduction or a failure to eliminate enough in the urine. [For Description of individual drugs see What Are the Specific Drugs Used for Gout?, below.] They including the following:

Certain steps must be made in undertaking hyperuricemic therapy:

The decision to use anti-hyperuricemic and if so, at what point, is not entirely clear, however. Some physicians do not prescribe them if hyperuricemia is mild or until a patient has had two attacks. Others prescribe them immediately after a single attack. Most of the time, antihyperuricemic therapy means taking a drug routinely throughout life, which many people find difficult to adhere to.

Surgery
Surgery is sometimes used to remove large tophi that are draining, infected, or interfering with the movement of joints. Several other surgical procedures are available for relieving pain in and improving the function of affected joints. It is sometimes necessary to replace joints.

Treatment of Kidney Disorders Related to Gout

Uric Acid Nephropathy. Uric acid nephropathy is common in chemotherapy patients. In such cases it is preventable if they are adequately hydrated and given allopurinol before chemotherapy begins. Treatment has reduced the death rate in cases of uric acid nephropathy from about 50% to close to zero.

Uric Acid Nephrolithiasis. Uric acid stones are dissolved by giving the patient allopurinol to reduce the concentration of uric acid in his or her urine. The patient also takes oral sodium bicarbonate or acetazolamide (Diamox) to alkalinize the urine. Drinking at least 10 to 12 eight-ounce glasses of water and other nonalcoholic beverages every day is important as well. [For more information see Kidney Stones, Comprehensive Version. ]

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WHAT ARE THE SPECIFIC DRUGS USED FOR GOUT?

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandins, the substances that dilate blood vessels and cause inflammation and pain. They are the drugs of choice for young, healthy adults without any other serious medical condition. NSAIDs are usually taken orally at their highest safe dosage as long as gout symptoms persist and for three or four days after. Low doses of NSAIDs may be used to prevent gout attacks, including in patients who are starting anti-hyperuricemic therapies.

NSAIDs Used. Indomethacin (Indocin) in doses up to 200 mg a day is the usual choice for gout. The first dose of indomethacin usually begins to act against the pain and inflammation within 24 hours and often much sooner. Ibuprofen, naproxen, sulindac, or others are good alternatives particularly for elderly patients who might experience confusion or bizarre sensations with indomethacin. Aspirin is an NSAID, but is associated with a higher risk for gout and should be avoided. There are dozens of NSAIDs available. [S ee Box Ulcers and Gastrointestinal Bleeding, for a list of NSAIDs].

Side Effects and Complications. Regular use of even over-the-counter NSAIDs may be hazardous for anyone and has been are associated with the following side effects:

COX-2 Inhibitors
Celecoxib (Celebrex), rofecoxib (Vioxx), and meloxicam (Mobic) are known as COX-2 (cyclooxygenase-2) inhibitors, the so-called super-aspirins. These agents may prove to be as effective and less harmful to the GI tract than NSAIDs. Theoretically, they may even have properties that produce less adverse effects on cartilage than NSAIDs may have. They may be effective for gout, although there is no data on the use of these agents for gout patients as yet.

Some studies have found that patients taking COX-2 inhibitors have the same gastrointestinal symptoms (eg, diarrhea, abdominal discomfort) as standard NSAIDs. (Other side effects found with short-term use include headache, and dizziness.) Importantly, however two 2000 studies reported a lower incidence of ulcers and other toxic side effects in patients taking the COX-2 inhibitors than in those taking NSAIDs. The drugs were all equally effective in relieving pain. (One study compared celecoxib with the NSAIDs ibuprofen or diclofenac and the other compared rofecoxib with the NSAID naproxen). One 1999 study even found the rate of GI problems with celecoxib was equal to that in people who do not take NSAIDs at all. COX-2 inhibitors are currently more expensive than traditional NSAIDs, however, and some insurers do not pay for them.
Possible Negative Effects. In spite of their promise, some researchers theorize that inhibiting COX-2 may have some negative side effects over the long term:

Other Investigative Alternatives to NSAIDs
NO-NSAIDS. Experimental agents are being developed that combine nitric oxide with NSAIDs (NO-NSAIDs). Nitric oxide increases blood flow in the mucous lining and secretions of mucus and bicarbonate. Combining nitric oxide with NSAIDs may provide benefits similar to the COX-2 inhibitors.
Arthrotec. Arthrotec is a combination of misoprostol and the NSAID diclofenac that may reduce the risk for gastrointestinal bleeding. One study found that patients taking Arthrotec had 65% to 80% fewer ulcers than those who took NSAIDs alone.
 
Colchicine
Colchicine, a derivative of the autumn crocus (also called the meadow saffron), has been used against gout attacks for centuries. It is highly effective though no longer the first drug of choice because of its frequent, unpleasant, and sometimes very serious side effects. The drug is generally not appropriate for elderly patients or those with kidney, liver, or bone marrow disorders. It can also effect fertility.

Oral Regimen. The oral regimen requires doses every hour until the symptoms either improve or side effects develop; improvement should be evident by the tenth dose. Oral colchicine usually eliminates the pain of an acute attack within 48 hours. It is unsuitable for many patients, however, because of nausea, vomiting, diarrhea, or abdominal cramps, which occur at the high doses necessary to relieve symptoms. Low doses are helpful for preventing further attacks, including in patients who are starting anti-hyperuricemic therapies. Low doses do not pose as high a risk for GI symptoms. (Taking low doses for a long duration, however, may suppress bone marrow function and cause some nerve and muscular injury in certain people.)
Note. The antibiotic erythromycin or H2 blockers, such as famotidine (Pepcid AC), cimetidine (Tagamet), ranitidine (Zantac), may intensify the gastrointestinal side effects of colchicine.

Intravenous. Intravenous administration of colchicine relieves episodes of gout without gastrointestinal effects and for a time, physicians hoped it could be used routinely. The intravenous route has some serious side effects, however, and poses an increased risk for injury to the kidney, liver, central nervous system, and bone marrow.
Warning Note: Overdose of Colchicine can be fatal, and there have even been reports of fatalities with low doses.
 
Corticosteroids
Corticosteroids, known commonly as steroids, are used when patients cannot tolerate other anti-inflammatory drugs or they prove ineffective for an attack of gout. They are becoming popular in elderly people. Corticotropin (ACTH), a drug that converts to a steroid, is another option. Corticosteroids can be administered in different forms:

Uricosuric Drugs
The uricosurics prevent the kidney from reabsorbing uric acid and so increase the amount excreted in the urine. They are usually the choice for preventing gout in the following patients:

Specific Uricosurics. Probenecid (Benemid, Parbenem, Probalan) and sulfinpyrazone (Anturane) are the standard uricosurics. An investigative uricosuric, benzbromarone, may prove to be beneficial, even in patients with some renal insufficiency.

Probenecid is taken twice to three times a day and sulfinpyrazone begins at twice a day and increases to three or four times daily. The initial doses should be low and then gradually built up. Probenecid combined with colchicine is more effective than probenecid alone, but patients respond differently to this regimen depending on the dosage balance, so it needs to be carefully individualized. A uricosuric combined with allopurinol [ see below ] is occasionally effective in cases where using just one drug is not.
Side Effects. The possible side effects of these two drugs include skin rashes, gastrointestinal problems, anemia, and kidney stone formation. To help reduce acidity and the risk for kidney stones, patients should drink plenty of fluids (ideally water, not caffeinated beverages). Sodium bicarbonate supplemented by acetazolamide can also reduce acidity and the risk for stones.

Interactions. Adding low-dose colchicine or an NSAID may help prevent gout attacks, but NSAIDs, particularly aspirin, as well as other salicylate drugs, interfere with uricosuric drugs and reduce effectiveness, so they should be avoided if possible. Patients who require minor pain relief should take acetaminophen (Tylenol and others) instead. Uricosurics interact with many other drugs, and a patient should be sure to inform the physician of any medications they are taking.
 
Allopurinol
Allopurinol (Lopurin, Zyloprim) blocks uric acid production and is the drug most often used in long-term treatment for older patients and over-producers of uric acid (levels of excreted uric acid are over 800 mg during a 14-hour period). It is also considered the drug of choice for patients with impaired kidney function, a history of kidney stones, and for tophaceous gout. Allopurinol is taken orally once a day in doses of 100 mg to 600 mg, depending on the patient’s response to treatment. When it is first used, allopurinol can trigger further attacks of gout, and thus during the first months (or longer) of therapy the patient is also given a NSAID or colchicine to forestall that possibility.

Side Effects . The drug’s side effects, experienced by 3% to 5% of patients, include leukopenia (a reduction in the number of white blood cells), thrombocytopenia (a reduction in the number of platelets), diarrhea, headache, and fever. The drug may also increase the risk for cataracts.
About 2% of patients experience an allergic reaction to allopurinol that causes a rash. In rare cases, the rash can become severe and widespread enough to be life-threatening. Allergic individuals who had experienced only a mild rash may be able to build up their tolerance for the drug by undergoing a desensitization process.

Interactions. Allopurinol interacts with certain other drugs, such as azathioprine.

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WHAT LIFESTYLE MEASURES CAN HELP PREVENT GOUT?

Avoiding Excessive Energy Demands

Any activities that increase energy demands also increase metabolism or purines that produce uric acid. Avoiding stress and staying healthy are important for preventing attacks.

Dietary Recommendations
Reduce Foods Containing Purines. Because uric acid levels are only minimally affected by diet, dietary therapy does not play a large role in the prevention of gout. Still, people who have suffered an attack of gout may benefit from reducing their intake of purine-rich foods if they habitually eat unusually large quantities of such foods. (Because purines are found in all protein foods, no one should eliminate all purines.)

Purine-containing foods include the following:

Maintain Healthy Weight
A supervised weight-loss program may be a very effective way to reduce uric acid levels if the patient is overweight. Crash dieting, on the other hand, is counterproductive because it can increase uric acid levels and can cause an acute attack.
 
Maintain Fluids
Drinking plenty of water and other nonalcoholic beverages helps remove MSU crystals from the body. Some researchers are studying the anti-inflammatory properties of green tea, which might have some benefit for gout. It should be noted, a Japanese study reported a higher association between gout and tea drinking (although the study did not describe the type of tea).
 
Avoid Alcohol
Alcohol should be avoided, since it promotes purine metabolism and uric acid production; it also may reduce excretion of uric acid. Heavy drinking, especially binge drinking of beer or distilled spirits, should especially be avoided.
 
Avoid Joint Injury
People with gout should also attempt to identify and avoid activities that cause repetitive joint trauma, such as wearing tight shoes.
 
Prevention During Travel
Travel is an example of an activity that increases the risk for gout. It not only increases stress, but eating and drinking patterns may change. Before traveling, patients should discuss preventive measures with their physicians. The doctor may prescribe a prednisone tablet to be taken immediately at the first sign of a gout attack; in most cases this stops the episode.

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