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Patient education: Gout (Beyond the Basics)

Author: Fernando Perez-Ruiz, MD, PhD
Section Editor: Nicola Dalbeth, MBChB, MD, FRACP
Deputy Editor: Paul L Romain, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2021. | This topic last updated: Dec 13, 2021.

GOUT OVERVIEW

Gout is a form of arthritis. Like other types of arthritis, it causes pain and swelling in the joints. Gout develops in some people who chronically
have a condition called "hyperuricemia," meaning high levels of a substance called urate (also known as uric acid) in the blood. Urate can form
crystals that build up in different parts of the body, causing symptoms. Not everyone with hyperuricemia develops gout; up to two-thirds of people
with hyperuricemia never have any symptoms, although it is unclear why this is. In some people, uric acid crystals may form that can lead to
kidney stones and other problems with kidney function.

Gout is different from another disease called calcium pyrophosphate crystal deposition (CPPD) disease (formerly called "pseudogout"), which is
discussed separately. Nevertheless, symptoms may be quite similar for the joints that are involved in both diseases (such as the knee or the
ankle). This other condition develops in some people in response to the presence of a different type of crystal known as a calcium
pyrophosphate (CPP) crystal. (See "Patient education: Calcium pyrophosphate crystal deposition (CPPD) disease (Beyond the Basics)".)

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GOUT RISK FACTORS

Gout usually develops in adulthood and is rare in children. It commonly develops earlier in adult men (often between the ages of 30 and 45) than
in women (usually after age 55); it is particularly common in people older than 65 regardless of gender. It is estimated that gout affects nearly 4
percent of adults in the United States.

There are several medical conditions and lifestyle factors that increase a person's risk of developing gout, including:

● Obesity
● High blood pressure
● Chronic kidney disease
● Overeating or prolonged fasting
● Consuming excessive amounts of alcohol (particularly beer, whiskey, gin, vodka, and rum and other spirits) on a regular basis
● Consuming large amounts of meat or seafood
● Consuming beverages containing high fructose corn syrup (such as non-diet sodas)
● Taking medications that affect blood levels of urate (especially diuretics)

In people already diagnosed with gout (referred to as "established gout"), there are also certain characteristics that increase the risk of repeated
gout flares. These include:

● Injury or recent surgery

● Fasting
● Consuming excessive amounts of alcohol
● Overeating
● Taking medications that induce sudden changes in blood urate levels
● Dehydration

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GOUT SYMPTOMS

Gout flares (also called gout attacks) are sudden episodes of severe joint pain, usually involving redness, swelling, and tenderness of the joint.
Although a gout flare typically affects a single joint, some people develop several inflamed joints at the same time. Gout flares start more often
during the night and in the early morning hours than during the day, but they can occur at any time. The pain and inflammation usually reach
peak intensity within 12 to 24 hours and generally improve completely within a few days to several weeks, even if untreated. It is not clear how
the body "turns off" a gout flare.

The characteristic pain and inflammation of gout develop when white blood cells and cells in the joint linings attempt to surround and digest urate
crystals that have shed from deposits to the fluid that lubricates the joints (called synovial fluid). These cells recognize the crystals as foreign
material and release chemical signals that contribute to the pain, swelling, and redness associated with a gout flare.

PHASES OF GOUT

There are three main phases of gout: gout flare, intercritical gout, and tophaceous gout.

Gout flare — Initial gout flares usually involve a single joint, most often the big toe or knee. Over time, flares can begin to involve multiple joints
at once and may be accompanied by fever. People with osteoarthritis in their fingers may experience their first gout flares in the fingers rather
than the toes or knees.

Intercritical gout — The time between gout flares is known as an "intercritical" period. A second gout flare typically occurs within two years, and
additional gout flares may occur thereafter. If your gout is untreated over a period of several years, the time between gout flares may shorten,
and your gout flares may become increasingly severe and prolonged and involve multiple joints.

Tophaceous gout — People who have repeated gout flares or persistent hyperuricemia for many years can develop tophaceous gout. This term
describes the accumulation of large numbers of urate crystals in masses called "tophi." People with this form of gout develop tophi in joints,
bursae (the fluid-filled sacs that cushion and protect tissues), bones and cartilage, or under the skin. Tophi may cause erosion of the bone and
eventually joint damage and deformity (called gouty arthropathy).
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Developing tophi near the small joints of the feet or fingers can cause physical changes that can not only be distressing (due to the cosmetic
appearance) but also contribute to restricted movement and disability because they may act as a "chalk splint" on the joint and eventually cause
bone and joint lesions (recently named as erosive gout). Tophi are usually not painful or tender. However, they can become inflamed (
picture 1) and can cause symptoms like those of a gout flare.

Tophaceous gout was more common in the past, before effective treatment for hyperuricemia became available. Certain groups are still at risk for
tophaceous gout, including:

● People who have very high levels of urate in the blood (as may happen with chronic kidney disease, high-dose diuretics, and some
transplant medications)

● Those who cannot tolerate or do not receive adequate doses of medications to properly control hyperuricemia (for example, due to kidney
failure or drug allergy)

● Women who have already been through menopause, especially if they are taking a diuretic medication or develop chronic kidney disease,
as well as those with osteoarthritis

The known risk factors for gout can also increase a person's risk of developing tophaceous gout. (See 'Gout risk factors' above.)

KIDNEY-RELATED COMPLICATIONS

Normally, the kidneys filter urate in the blood and excrete it from the body through urine. In people with gout, urate crystals can build up in the
kidney or other parts of the urinary tract, leading to kidney stones. If a stone gets large enough, it can block one of the ureters (the tubes that
carry urine from the kidney to the bladder and out of the body) ( figure 1). Medications that increase the amount of urate excreted by the
kidneys, which are commonly used in people with frequent or severe gout flares, may increase the risk of developing kidney stones. The most
common symptom of kidney stones is pain in the side of the back ("flank pain").

Kidney stones caused by uric acid crystals occur in approximately 15 percent of people with gout. This compares with an 8 percent risk of kidney
stones in people without gout. Sometimes these kidney stones also contain calcium crystals.

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GOUT DIAGNOSIS

There are many illnesses that can cause joint pain and inflammation. Gout is strongly suspected if a person has one or more acute attacks of
intermittent and sudden joint pain, followed by a period in which there are no symptoms but there is persistent hyperuricemia. It is important to
confirm the diagnosis of gout to ensure that medications that should be taken for quite a long time are properly/accurately indicated.

The best way to diagnose gout is for a doctor to examine the fluid lining the affected joint (synovial fluid) under a microscope to look for urate
crystals. To do this, he or she uses a needle and syringe to withdraw a small amount of fluid from inside the joint. Tophi located just beneath the
skin can also be sampled with a needle to diagnose tophaceous gout.

If it is not possible to do a synovial fluid analysis, your doctor will consider your symptoms, physical exam, and blood test results. Also, some
imaging procedures may be useful to ascertain diagnosis. Among the criteria for suspecting gout are:

● Rapidly developing pain and inflammation initially involving one joint at a time, especially the joint at the base of the large toe

● Complete resolution of symptoms between flares

● High levels of urate in the blood (this is most accurate for diagnosis after a gout flare resolves because urate levels may be within normal
limits during the flare)

TREATMENT OF GOUT FLARES

The goal of treatment of gout flares is to quickly and safely reduce inflammation, and therefore your pain, and the accompanying disability. This
treatment is usually short-term and limited to the duration of the flare. Deciding which medication to use is based upon several factors, including
your risk of bleeding, kidney health, and whether you have a past history of an ulcer in the stomach or small intestine.

Antiinflammatory medications are therefore the best treatment for gout flares. They are most effective when started early in the course of a flare.

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If you have a history of gout, your clinician can give you medication to keep on hand in the event of a flare. This is important because early
treatment is key in minimizing the amount of time it takes to decrease the pain, severity, and duration of a flare.

Nonsteroidal antiinflammatory drugs — Nonsteroidal antiinflammatory drugs (NSAIDs) work to reduce swelling in a joint. They include
ibuprofen (sample brand names: Advil, Motrin), naproxen (sample brand names: Aleve, Anaprox), indomethacin (brand name: Indocin), and
celecoxib (brand name: Celebrex). NSAIDs are generally recommended for people under age 65 who have no history of kidney or liver disease,
have no bleeding problems, do not use anticoagulant medications such as warfarin (brand name: Jantoven), and have no history of stomach or
duodenal ulcer or of difficult-to-control high blood pressure. Some NSAIDs are available over-the-counter, while others require a prescription.
(See "Patient education: Nonsteroidal antiinflammatory drugs (NSAIDs) (Beyond the Basics)".)

NSAIDs are most effective in the treatment of a gout flare when they are started as early as possible in the flare and when taken in higher doses
than when used for minor pain relief alone. (At higher doses, these medications have antiinflammatory, not just pain-relieving, properties.) Your
doctor will work with you to figure out the most appropriate NSAID dose. People who have had previous flares may start taking an NSAID at the
first signs of a recurrence. NSAID treatment is stopped within a day or two after the gout flare resolves.

Although aspirin is an NSAID, it is not usually recommended for the treatment of gout because it can, depending upon the dose, either raise or
lower urate levels in the blood.

Colchicine — A prescription oral medication called colchicine may be prescribed for a gout flare instead of an NSAID. Colchicine does not
increase the risk of ulcers, has no known interaction with anticoagulants ("blood thinners"), and, in proper doses, does not affect kidney function.
However, colchicine can have bothersome side effects when given in excess, including diarrhea, nausea, vomiting, and crampy abdominal pain.
Lower doses of colchicine than formerly used have been shown to be as effective for gout flares as the higher doses recommended in the past,
and the gastrointestinal side effects have been much less of a problem.

Colchicine therapy seems to be most effective when started within 24 hours of the first symptoms of a gout flare. Your doctor will tell you what
dose you should take if you have a flare; people with kidney or liver problems may need a lower dose.

Glucocorticoids — Steroid medications, also known as glucocorticoids, are effective and frequently used for treating gout flares. They may be
given orally (as pills), by direct injection into an involved joint (called an intraarticular injection), or, in certain circumstances, by intravenous (IV)

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or intramuscular injection. Commonly used oral glucocorticoids include prednisone, prednisolone, and methylprednisolone.

Oral glucocorticoids can be given to people with impaired kidney function or at increased risk for bleeding, as well those with multiple affected
joints or who cannot take NSAIDs or colchicine. Certain people are generally not candidates for glucocorticoid treatment, including those who
have poorly controlled diabetes, in whom infection is a concern, or who cannot tolerate steroids for some other reason. If you have increasingly
frequent gout flares, reducing the dose of glucocorticoids too quickly can increase your risk of a recurrent (or "rebound") flare. In these cases,
your dose of glucocorticoid should be reduced slowly over a period of at least 14 to 21 days. Your doctor will work with you to figure out how to
reduce (taper) your dose.

PREVENTIVE TREATMENT

Preventive (also called prophylactic) antiinflammatory therapy aims to prevent or reduce the occurrence of gout flares. Colchicine is usually
recommended as preventive therapy; it is taken daily at low doses to avoid gastrointestinal side effects. Colchicine reduces the frequency of gout
flares, particularly while starting drugs that lower urate levels.

Preventive colchicine is not usually used alone as a long-term treatment (ie, for years), but can serve as a helpful "bridge" if you are transitioning
from treating a gout flare to longer-term urate-lowering therapy. Although not nearly as commonly prescribed as colchicine, daily nonsteroidal
antiinflammatory drugs (NSAIDs) are sometimes used for preventive therapy and may have an advantage for people who also have
osteoarthritis (due to their pain-relieving properties).

LONG-TERM URATE-LOWERING THERAPY

Over time, medications and lifestyle changes can lower urate levels and, as a result, prevent or reverse urate crystal deposits that can cause
joint damage, disability, kidney stone formation, and possibly kidney damage. People who have one or more of these complications are
especially encouraged to take a urate-lowering treatment.

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The goal of urate-lowering therapy is to achieve and maintain blood urate levels below a specific level. In practice, the recommended goal for
most people with gout is less than 6 mg/100 mL (360 micromol/L), except in people with tophaceous or severe gout, in which case the suggested
goal often lower (eg, less than 5 mg/dL [300 micromol/L]). Your clinician can talk to you about what your goal level should be.

Not everyone with gout will require urate-lowering therapy. If you only have rare or mild flares, you may be able to manage your gout by treating
the flares as they happen. However, if you have frequent, prolonged, painful, or disabling gout flares, joint damage, or tophi, your health care
provider will likely suggest urate-lowering therapy.

Medications — Medications lower urate levels in one of three ways: they increase urate excretion by the kidneys; they decrease the body's
production of urate; or they break down urate. Urate-lowering therapy is usually started after a gout flare has resolved. People who take their
medication regularly and maintain urate levels below the target range over months to years eventually experience fewer flares; sometimes, flares
stop altogether. Doctors recommend that preventive therapy be continued if needed to maintain blood urate levels in the goal range indefinitely;
stopping treatment is commonly associated with a return to hyperuricemia and recurrence of gout.

Medications that lower urate levels include the following:

● Allopurinol (brand names: Alloprim, Zyloprim) and febuxostat (brand names: Uloric, Adenuric) work by preventing the formation of urate.
Allopurinol is the most commonly used drug for lowering urate levels in people with gout. Allopurinol can cause side effects, including skin
reactions (rash), lowered white blood cell and platelet counts, diarrhea, and fever, although these problems occur in only a small
percentage of people. The starting dose of allopurinol needs to be reduced in people with impaired kidney function, but doses can usually
be gradually increased to achieve the target urate level. No such dose-lowering concern is present with febuxostat when used at the
approved doses. Regular blood tests to check liver function are recommended during treatment with allopurinol or febuxostat. Febuxostat
should be used with caution in people at high risk of cardiovascular disease or who have had a heart attack or stroke.

● Probenecid increases the efficiency of urate excretion by the kidney and is called a "uricosuric" drug. Benzbromarone is a more potent
uricosuric drug but is not available in the United States (although it may be in the European Union and Asia). Probenecid can cause side
effects, including rash, upset stomach, and kidney stone formation. Effective probenecid use requires two doses daily. Probenecid is not
effective in people with advanced kidney disease. Benzbromarone may infrequently cause liver problems. Both medications can increase
the risk of kidney stones.

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● Pegloticase (brand name: Krystexxa) works by breaking down urate. Pegloticase is a biologic compound that is given by repeated
intravenous (IV) infusions and can lower urate levels rapidly and profoundly. This medication is expensive; may cause allergic-like
reactions, some of which can be severe; needs careful monitoring; and is effective in the long term in only about 50 percent of cases. For
these reasons, it is recommended that pegloticase use be limited to people with advanced gout that cannot be controlled with oral urate-
lowering therapies.

Some other medications induce a reduction in blood urate levels. Losartan (brand name: Cozaar) is used to treat high blood pressure but also
has a useful, though weak, urate-lowering effect, as do the lipid-lowering drugs fenofibrate (sample brand names: Antara, Fenoglide) and
atorvastatin (brand name: Lipitor). These agents can be useful additions to urate-lowering treatment with allopurinol or febuxostat or with lifestyle
modifications in people with high blood pressure or high blood lipid levels, respectively.

It takes weeks or months to lower urate levels to where they should be. During this period, your doctor will gradually adjust your medication
doses to meet the goal. Very rapid urate lowering can cause more frequent gout flares. Adequate hydration with oral fluids is recommended for
people taking uricosuric medications.

If you also take antiinflammatory preventive therapy (with colchicine or nonsteroidal antiinflammatory drugs [NSAIDs]) (see 'Preventive treatment'
above), this can usually be safely stopped when blood levels of urate are normal and have been in the goal range for about six months. Some
people may need a longer period of preventive therapy, particularly if they have tophi. Blood levels of urate should be monitored periodically to
ensure that the goal urate level is maintained.

Dietary changes — Improving your diet may reduce the frequency of gout flares. Because obesity is a risk factor for gout, as well as for many
other health conditions, losing weight (if you are overweight) is an important goal. However, extreme or "fad" diets are not recommended. (See
"Patient education: Losing weight (Beyond the Basics)".)

Changes in diet are often recommended along with urate-lowering medications. Changing your diet alone is unlikely to lower blood urate levels
by more than about 15 percent, even if you make major changes to your diet. On the other hand, if you lose weight in addition to changing your
diet, it is possible to see more significant improvements in urate control, along with benefits to your general health.

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Dietary guidelines for people with established gout have changed over time, and it is not completely clear which combination of foods is best.
Until validated diet guidelines for gout are available, a reasonable approach is to try to establish and maintain a healthy body weight with a
balanced diet, drink adequate water to avoid dehydration, and limit your intake of alcohol and sugar-sweetened drinks.

WHERE TO GET MORE INFORMATION

Your healthcare provider is the best source of information for questions and concerns related to your medical problem.

This article will be updated as needed on our web site (www.uptodate.com/patients). Related topics for patients, as well as selected articles
written for healthcare professionals, are also available. Some of the most relevant are listed below.

Patient level information — UpToDate offers two types of patient education materials.

The Basics — The Basics patient education pieces answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read materials.

Patient education: Gout (The Basics)

Patient education: Calcium pyrophosphate deposition disease (The Basics)

Patient education: Ganglion cyst (The Basics)

Beyond the Basics — Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are best
for patients who want in-depth information and are comfortable with some medical jargon.

Patient education: Calcium pyrophosphate crystal deposition (CPPD) disease (Beyond the Basics)

Patient education: Kidney stones in adults (Beyond the Basics)

Patient education: Nonsteroidal antiinflammatory drugs (NSAIDs) (Beyond the Basics)

Patient education: Losing weight (Beyond the Basics)

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Professional level information — Professional level articles are designed to keep doctors and other health professionals up-to-date on the
latest medical findings. These articles are thorough, long, and complex, and they contain multiple references to the research on which they are
based. Professional level articles are best for people who are comfortable with a lot of medical terminology and who want to read the same
materials their doctors are reading.

Asymptomatic hyperuricemia

Clinical manifestations and diagnosis of gout

Diuretic-induced hyperuricemia and gout

Kidney transplantation in adults: Hyperuricemia and gout in kidney transplant recipients

Pathophysiology of gout

Pharmacologic urate-lowering therapy and treatment of tophi in patients with gout

Treatment of gout flares

Lifestyle modification and other strategies to reduce the risk of gout flares and progression of gout

The following organizations also provide reliable health information.

● National Library of Medicine

(www.medlineplus.gov/healthtopics.html)

● National Institute of Arthritis and Musculoskeletal and Skin Diseases

(301) 496-8188
(www.niams.nih.gov/)

● American College of Rheumatology

(404) 633-3777
(www.rheumatology.org)

● The Arthritis Foundation

(800) 283-7800

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(www.arthritis.org)

ACKNOWLEDGMENT

The editorial staff at UpToDate would like to acknowledge Michael A Becker, MD, who contributed to an earlier version of this topic review.

Topic 514 Version 24.0

Contributor Disclosures
Fernando Perez-Ruiz, MD, PhD Grant/Research/Clinical Trial Support: Cruces Rheumatology Association [Gout]; Spanish Foundation for Rheumatology
[Gout]. Consultant/Advisory Boards: Arthriti [Gout]. Speaker's Bureau: Astellas [Gout]; Menarini [Gout]; Spanish Foundation for Rheumatology [Gout];
Parexel/Selecta [Gout]. All of the relevant financial relationships listed have been mitigated. Nicola Dalbeth, MBChB, MD, FRACP Grant/Research/Clinical Trial
Support: AstraZeneca [Gout]; Amgen [Gout]. Consultant/Advisory Boards: AstraZeneca [Gout]; Arthrosi [Gout]; Selecta [Gout]; Horizon [Gout]; Dyve Bio [Gout].
Speaker's Bureau: AbbVie [Rheumatoid arthritis]; Janssen [Psoriatic arthritis]; Horizon [Gout]. All of the relevant financial relationships listed have been
mitigated. Paul L Romain, MD No relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review
process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

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