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About Gout

ACE is committed to using inclusive language that is free from words, phrases and tone that reflect discriminatory or stereotyped views of underrepresented people or groups. In our attempt to avoid bias or using language that appropriates other cultures as it relates to Indigenous Peoples health and wellness, ACE consults with Indigenous advisors to ensure its website and other written materials use terms and expressions that align with Indigenous identities and are culturally appropriate.
What is gout?

Gout is a form of arthritis which is caused by a build-up of a crystal called uric acid in the body. Normally, uric acid is processed by the kidneys and eliminated from the body through urine. In the case of gout, the kidneys do not eliminate uric acid well enough, or in some people with gout, too much uric acid is produced. Chronically high levels of uric acid in the blood form crystals, which are then deposited in joints, and sometimes tendons and skin as well.

The main symptoms of gout

These deposits can cause pain – often severe – and swelling in the affected area or areas. Gout symptoms come on very quickly and pain and swelling are often severe. The first signs of gout include 1,2:
  • Intense pain, usually in one joint at the start and most often in the big toe. Other joints sometimes affected by gout in the beginning include the feet, ankles, knees, hands, and wrists.
  • Swelling, heat and redness in the affected joint(s).
  • Fever, in severe cases.
Gout pain often first occurs at night. An individual may go to bed feeling healthy and be awakened in the night by an acute attack of gout. Pain may be so severe that even the weight of a blanket on the affected area feels unbearable. Most often, gout initially affects only one joint at a time, unlike in other forms of arthritis like rheumatoid arthritis, where multiple joints are often affected simultaneously.

Who can get gout?

Gout is estimated to occur in 1–4% of the general population; however, men are 2–6 times more likely to get gout than women. It can strike at any age but tends to affect men after the age of 40 and women after menopause, meaning that age is a risk factor3.

There also seems to be a disproportionate burden of disease on ethnic minorities due to an increase prevalence and subpar care10. Previous studies have found that Chinese in the U.S.11, Indigenous peoples of Alberta Canada12 and Māori of New Zealand have a higher prevalence of gout13.

The chance of getting gout goes up if a person is carrying extra weight or considered obese, or have one or several other health issues1,2:
  • family history of gout (genetic link6)
  • high blood pressure
  • narrowing of the arteries due to plaque build up (arteriosclerosis)
  • diabetes
  • kidney disease
  • take water pills
Alcohol, particularly beer, can increase risk of gout4. Sugary beverages such as soft drinks and fruit juices will increase risk of gout. Meat in excess, especially organ meats (e.g., liver, kidneys, brains) and shellfish can trigger an episode of 5. Limiting consumption to weekly should be the aim. All vegetables or plantbased foods are fine to consume for people with gout.

Some people who live with gout have frequent “attacks”, but others may go years in between them. When gout is not managed by ongoing treatment, the attacks can become more frequent and last longer. Repeated attacks can happen in the same joint(s) or can travel to other joints, greatly effecting a person’s quality of life. Repeated attacks of gout typically will start to damage the joints and can deposit in the skin and other organs.

Getting a diagnosis of gout

Doctors diagnose gout using several methods:
  • Taking a complete family history and carefully listening to and recording a person’s description of the symptoms, how often they occur and how long they last.
  • Performing a thorough physical exam, especially of the areas affected.
  • Ordering blood tests to measure the amount of uric acid crystals (A caveat is that the blood test for uric acid may become normal during a gout attack and for up to 2 weeks afterwards)
  • Ordering x-rays, ultrasound or specialized CT scan of the affected joint or joints. The gold standard of diagnosis is identification of characteristic uric acid crystals in the synovial fluid using polarized light microscopy7.
  • A holistic assessment of patient lifestyle factors may also provide insightful information to optimize treatment.
Treatment of gout

We acknowledge diverse values and beliefs around treatment. Your health care provider will be able to discuss and recommend personalized treatments that may differ from the information below. If you have questions about what is written here or if there is a section that needs updating, please do not hesitate to contact us at feedback@jointhealth.org.
Once a doctor has confirmed a diagnosis of gout, there are several simple, effective methods to help manage symptoms and prevent future gout attacks. These include diet, lifestyle changes and medications.

Diet1,2

Some simple changes in diet can help to reduce uric acid levels in the body. People with gout should avoid foods rich in purine, which is a chemical that is converted into uric acid in the body. These foods include red meats and some types of seafood, specifically organ meats, like liver, kidney, and brain, as well as shellfish. All plant-based foods are acceptable for people with gout. Cherries or cherry juice may help urinary excretion of uric acid.

Alcohol intake, especially beer and liquor, is associated with increased disease activity. If you have gout, you should discuss your alcohol consumption habits frankly and honestly with your doctor.

In addition, it is very important for people who have gout to avoid becoming dehydrated, which occurs more often in hot weather or when drinking alcohol. Individuals with gout should make sure they avoid dehydration as preliminary research has found that lower water intake is associate with hyperuricemia9.

Healthy body weight8

Healthy body weight maintenance is another vitally important component of a well-rounded treatment plan for gout. In people who are overweight, weight reduction may help to limit the risk of recurrent gout attacks.

Medications1,2

There are several main types of medications used in the treatment and long-term management of gout. These include medications to reduce inflammation, medications used between or to prevent attacks.
  1. Non-steroidal anti-inflammatory medications (NSAIDs) are to be used to temporarily manage painful symptoms of gout. These are potent medications which can reduce joint inflammation and pain, but do not work to prevent joint damage. It is important to know that NSAIDs can rarely cause serious cardiovascular, kidney or gastro-intestinal side effects, like stomach ulcers; for this reason, it is vital to speak with your doctor before adding an NSAID to any treatment plan for gout.

    Examples of NSAIDs available without a prescription include ibuprofen (Motrin® or Advil®) and naproxen (Aleve). Some more powerful NSAIDs require a prescription. These include higher dose naproxen (Naprosyn®) and diclofenac (Voltaren). It is thought that one of the most powerful NSAIDs for gout is indomethacin (Indocid).
  2. COX-2 inhibitors are a class of NSAID which work to reduce inflammation but do not carry the same risk of gastrointestinal side effects as non-COX-2 inhibitors. Celecoxib (Celebrex) is an example of a COX-2 inhibitor. It is important to know that while COX-2 inhibitors cause fewer gastrointestinal side effects, research has shown that they may have the same or higher risk of cardiovascular (heart) side effects compared to traditional NSAIDs. Celecoxib has been used “off-label” for gout.
  3. Corticosteroids (like prednisone) may be used to treat gout but only short-term because of the risk of side-effects. A corticosteroid injection or 'cortisone' injection into the joint is frequently a safer way to treat gout in a single joint.
  4. Colchicine is in a class of medications called anti-gout agents. It works by stopping the natural processes that cause swelling and other symptoms of gout; however, the most common side-effect is diarrhea. Colchicine, like NSAIDs, do not slow the progression of gout or reduce damage that gout can do.

    It is important to note that people with gout may be advised not take medications containing acetylsalicylic acid (ASA, Aspirin®), as these may decrease or prevent the kidneys' excretion of uric acid. Of course, if ASA is required for other medical reasons, it may still be used. Other medications that typically worsen gout include certain water pills or diuretics (thiazide diuretics).

  5. Prevention8

    After an initial gout attack has died down, there are several types of medications that work to reduce uric acid levels in the body going forward. These medications are highly recommended for those people who have had 3 attacks of gout despite lifestyle medication. These medications help to prevent gout attacks and ultimately, minimize long-term joint damage that is a direct result of untreated gout. These medications reduce uric acid production. Allopurinol is the most common medication used to prevent gout attacks. In certain ethnic groups such as east Asians and those of African origin, a genetic test called HLA-B5801 should be done prior to starting allopurinol. People with this gene have a higher risk of developing a severe rash and allergic reaction to allopurinol. For those who cannot take allopurinol, another medication called febuxostat can be used to reduce uric acid. This group of medications is almost always used only after an acute attack of gout has passed. For reasons not yet fully understood, these medications can worsen inflammation when taken during an acute attack of gout.

    Key take-aways

    • Gout is one of the only forms of arthritis that is curable. With advances in imaging technology and medication, management of the condition is achievable with prevention of gout attacks long term.
    • Education and discussions with a health care provider are keys in addressing patient-specific risk factors and ensuring adherence to an individualized management plan.
    • Self-management for gout include limiting consumption of alcohol, staying hydrated, avoiding food rich in purine and sugary beverages, and maintaining a healthy body weight.
    Thank you to Dr. Kam Shojania, Head, Division of Rheumatology, Vancouver General Hospital and Medical Director at Mary Pack Arthritis Program, for his medical review of the content on this page.

    References
    1CDC website
    2American College of Rheumatology website
    3Kuo et al. (2015). Global epidemiology of gout: prevalence, incidence and risk factors. https://doi.org/10.1038/nrrheum.2015.91
    4Nieradko-Iwanicka (2021). The role of alcohol consumption in pathogenesis of gout. https://doi.org/10.1080/10408398.2021.1911928
    5Li et al. (2018). Dietary factors and risk of gout and hyperuricemia: a meta-analysis and systematic review. https://doi.org/10.6133/apjcn.201811_27(6).0022
    6Major et al. (2018). An update on the genetics of hyperuricaemia and gout. https://doi.org/10.1038/s41584-018-0004-x
    7Rees et al. (2014). Optimizing current treatment of gout. https://doi.org/10.1038/nrrheum.2014.32
    8Ragab et al. (2017). Gout: An old disease in new perspective–A review. https://doi.org/10.1016/j.jare.2017.04.008
    9Kachur et al. (2017). Hydration and Gout: Looking at New Modes of Uric Acid Management. https://acrabstracts.org/abstract/hydration-and-gout-looking-at-new-modes-of-uric-acid-management/
    10Singh (2013). Racial and gender disparities among patients with gout. https://doi.org/10.1007/s11926-012-0307-x
    11Wahedduddin et al. (2010). Gout in the Hmong in the United States. Journal of clinical rheumatology: practical reports on rheumatic & musculoskeletal diseases. https://doi.org/10.1097/RHU.0b013e3181eeb487
    12Barnabe et al (2017). Inflammatory Arthritis Prevalence and Health Services Use in the First Nations and Non-First Nations Populations of Alberta, Canada. https://doi.org/10.1002/acr.22959
    13Rose (1975). Gout in Maoris. Seminars in arthritis and rheumatism, 5(2), 121–145. https://doi.org/10.1016/0049-0172(75)90002-5