Also Known As
Gouty Arthritis
This article was last reviewed on
This article waslast modified on November 13, 2020.
What is gout?

Gouty arthritis, also known as gout, is a condition caused by the deposition of needle-like crystals of uric acid (monosodium urate). These crystals accumulate in joint fluid and tissues, causing inflammation, swelling, and severe pain. The most frequently affected joint is the big toe, but gout can also occur in the hands, elbows, wrists, knees, ankles, and feet.

Attacks of gout may occur sporadically and last for several days. During these attacks, uric acid deposits may build up in cartilage, tendons, and soft tissues. They may also form lumps called tophi under the skin. Crystals that accumulate in the kidneys can lead to kidney stones and kidney damage. Most gout episodes are acute and last a few days, but the severity and frequency of attacks can increase, with some people developing a chronic form of gout.

Uric acid is an end product of the breakdown of purines, compounds found in all body tissues and in many foods, such as liver, dried beans, asparagus, mushrooms, and anchovies. Uric acid is normally carried through the blood and eliminated in the urine. If production of uric acid increases, a person eats a large quantity of foods high in purines, or if the kidneys are unable to adequately eliminate uric acid, then concentrations in the blood can rise (called hyperuricemia). When the crystals accumulate in the joints, they can cause the pain associated with gout.

Gout develops more frequently in men than women. It is more common in adults, usually occurring in men over the age of 30 and in women after menopause. People with a family history of gout or who are obese or who have hypertension, type 2 diabetes, hyperlipidemia, cardiovascular disease, or kidney disease are at increased risk of developing gout. Gout has also been associated with metabolic syndrome, a term often used to describe a cluster of these symptoms. Drugs such as cyclosporine, thiazide diuretics (used to treat hypertension), and salicylates (aspirin) can interfere with uric acid excretion as can excessive consumption of alcohol.

Gout must be distinguished from conditions that can cause similar symptoms, such as calcium pyrophosphate deposition (CPPD, formerly called pseudogout), a condition caused by the deposit of calcium pyrophosphate crystals, septic arthritis (caused by an infection in a joint), and rheumatoid arthritis (an autoimmune arthritis). The treatment of these conditions is different than those used in the management of gout.

Accordion Title
About Gout
  • Testing

    The goals with testing are to identify gout, to distinguish it from other conditions, such as other types of arthritis that may have similar symptoms, and to investigate the cause of increased uric acid concentrations in the blood.

    Laboratory tests

    • Synovial fluid analysis – used to detect the needle-like crystals derived from uric acid or other crystals that may be present; to look for signs of joint infection.
    • Uric acid – to detect elevated levels in the blood; if a diagnosis of gout is made, uric acid testing may be performed regularly to monitor levels.
    • Basic metabolic panel (BMP) – this group of tests may be used to evaluate and monitor kidney function.
    • Complete blood count (CBC) – to determine if there is an abnormal increase in the number of white blood cells (leukocytosis) and to help differentiate between septic arthritis and gout.
    • Sometimes other tests, such as an RF (rheumatoid factor) or an ANA (anti-nuclear antibody), may be ordered to rule out other causes of arthritis symptoms. A blood culture and/or synovial fluid culture may be ordered if septic arthritis is suspected.

    Non-laboratory tests

    • X-rays of the affected joints may show uric acid deposits and damage indicative of gouty arthritis.
  • Treatment

    The goals of treatment are to reduce inflammation and the pain by controlling uric acid levels. This will minimize future attacks and the potential for joint and kidney damage.

    During acute attacks, someone may be treated with nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or naproxen to relieve pain and inflammation and, if necessary, with corticosteroids like prednisone. If those do not help to control symptoms, colchicine may be useful within the first 12 hours of an attack. NSAIDs or oral colchicine may be prescribed in small daily doses to prevent future attacks as well. In some patients, anti-interleukin-1 therapy (anti-IL-1) has shown to be very effective in treating acute gout flare-ups.

    People can make lifestyle changes to minimize gout attacks. Examples of changes include:

    • Decreasing alcohol consumption, especially beer
    • Eating a diet rich in low-fat dairy products and vegetables but avoiding foods high in purines (such as liver and kidney) and high fructose corn syrup. Eating less beef, lamb, pork, shellfish, sardines, anchovies, and sugar and salt (see Gout Diet from the Gout & Uric Acid Education Society)
    • Exercising regularly and lowering their body mass index (BMI)
    • Increasing fluid intake to help the kidneys flush out uric acid

    If dietary changes are inadequate to improve signs and symptoms and lower uric acid levels, drug therapy may be needed. According to the American College of Rheumatology, the drugs allopurinol or febuxostat can be used to help lower uric acid levels by blocking the production of uric acid. Other drugs may be prescribed that can help the kidneys remove excess uric acid or break down uric acid. (See the links in Related Content section for more on treatment.)

    Always take any medications that your healthcare provider prescribes as directed and tell your healthcare practitioner about any other medicines or vitamins you are taking.

View Sources

Sources Used in Current Review

American College of Rheumatology. 2016. Gout. Available online at Accessed 6.20/2017.

John Hopkins Arthritis Center. 2017. Treatment of Gout. Available online at Accessed 6/20/2017.

Medscape. 2017. Gout and Pseudogout Workup. Available online at Accessed 6/20/2017.

National Institute of Arthritis and Musculoskeletal and Skin Disease. 2016. Questions and Answers about Gout. Available online at Accessed 6/20/2017.

Sources Used in Previous Reviews

Arthritis Foundation. Gout. Available online at Accessed June 2013.

American College of Rheumatology. Gout. Available online at Accessed June 2013.

UpToDate. Patient information: Gout. Available online at Accessed June 2013.

Gout & Uric Acid Education Society. Gout Treatment and Uric Acid Therapy. Available online at Accessed June 2013.

Stamp LK, Chapman PT. Gout and its comorbidities. Rheumatol 52(1):34-44, 2013.

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Chen, A. (2005 June 7, Updated). Synovial fluid analysis. MedlinePlus Medical Encyclopedia [On-line information]. Available online at

(Revised 2007 March). National Institute of Arthritis and Musculoskeletal and Skin Diseases. Fast Facts About Gout. Available online at Accessed June 2010.

(2006 December Updated). National Institute of Arthritis and Musculoskeletal and Skin Diseases Questions and Answers about Gout. Available online at Accessed June 2010.

(2009 August, Updated). Schumacher, H. Gout. American College of Rheumatology. Available online at Accessed June 2010.

ARUP Consult. Hyperuricemia - Gout. Available online at Accessed June 2010.

American College of Rheumatology. 2012 American College of Rheumatology Guidelines for Management of Gout. Available online at Accessed November 2012.

Walsh, N. ACR Puts Out Gout Guidelines. MedPage Today. Available online at Accessed November 2012.