All About Gout - Symptoms, Diagnosis, Treatment

Gout is a form of inflammatory arthritis that can cause extreme pain in the joints, most often in the big toe. Learn about the symptoms, risks, and causes of gout, as well as how to prevent and treat the condition.


Gout Overview

When gout causes severe joint pain, it is called a gout attack, a gout flare-up, or acute gout. Pain is typically accompanied by extreme joint tenderness, swelling, warmth, and skin redness. The symptoms may come on suddenly and without warning.

Experts estimate gout will affect 4% of Americans during their lifetimes, and often occurs in men and people over age 60.1 Typically, only one joint is affected at a time, but it is possible to have several joints affected during a gout attack.

Joints Affected by Gout

Gout can affect any joint, but some joints are more likely to be affected than others. Joints commonly affected include the big toe, the foot’s instep, heel, ankle, and knee.2 Less often, gout affects the elbow, wrist, fingertips, or spine.2,7

Gout is acute, painful swelling in the joints from uric acid buildup. Common areas include the foot and big toe.

Differences between men and women

Sex differences play a role in which joints are affected:

  • In men, about 85% of gout flare-ups affect joints in the lower extremities.8 About 50% of first-time gout attacks involve a big toe joint.9
  • In women, a gout attack is most likely to occur in a knee.9 In addition, women may be more likely to get gout in the upper extremities.9

While women are less likely to get gout, they are more likely to have multiple joints affected by gout.12

How a Gout Flare-Up Develops

Gout results from a build-up of uric acid crystals (monosodium urate crystals) in a joint. These needle-like, microscopic crystals collect in the soft tissue of a joint, causing pain that can be excruciating, as well as swelling, redness, and warmth.

Infographic displaying details about gout, hyperuricemia and purines
Gout, Hyperuricemia and Purines
(larger view)

How uric acid crystals form

The build-up of uric acid crystals begins with purines, a chemical compound found in many foods.

  • When the body metabolizes purines, it produces a substance called uric acid.
  • The uric acid enters the bloodstream.
  • The kidneys filter the blood and normally filter out excess uric acid. This uric acid is then excreted via urine (70%) or stool (30%).10
  • If the kidneys cannot adequately filter out excess uric acid, or if the body produces too much uric acid, there will be too much uric acid in the bloodstream.
  • Too much uric acid in the bloodstream is called hyperuricemia.
  • In some people, hyperuricemia leads to the formation of uric acid crystals that collect in joint tissue, leading to painful symptoms.

An inability to adequately process and excrete uric acid accounts for an estimated 90% of gout cases.8 Other cases occur because a body produces too much uric acid.

Read more about Hyperuricemia - High Uric Acid Levels and Gout

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Why Flare-Ups Happen at Night

It is not uncommon for gout to flare-up in the middle of the night, waking a person from a sound sleep. One research study of more than 700 gout patients found that flare-ups were 2.4 times more likely between midnight and 8 am than between 8 am and 4 pm.11

Researchers theorize gout attacks often occur at night because:

  • Uric acid is more likely to form crystals at lower temperatures. The body’s temperature drops slightly during sleep, encouraging the formation of crystals.12,13
  • Breathing rates slow down during sleep, and the lungs expel less carbon dioxide. Excess carbon dioxide can cause the blood to become slightly more acidic. This condition, called respiratory acidosis, may encourage the formation of uric acid crystals.14
  • People with sleep apnea take in less oxygen, which can lead to an increase in the body’s production of purines and cause hyperuricemia.15,16
  • The body’s cortisone levels tend to dip while sleeping. Cortisone suppresses inflammation, and a dip in cortisone may contribute to gouty inflammation.16
  • Overnight dehydration may facilitate hyperuricemia and/or increase the concentration of crystals in the joint fluid.16,23

More research is needed in this area.

Gout Attack vs. Chronic Gout

It is possible to have a gout flare-up and never experience another. Repeated instances of acute gout are called chronic gout.17

The treatment goals for a gout attack are different than those for chronic gout. When treating a gout attack, the goals are to relieve pain and inflammation. When treating chronic gout, the goals are to prevent future gout attacks and long-term joint damage.

While some people with chronic gout may get frequent gout attacks, others may have years in between attacks. If chronic gout is not treated, attacks may become more frequent and/or last longer.

Left untreated, a gout attack will usually resolve itself within a few days or weeks. Chronic gout can permanently damage a joint’s tissues and decrease its range of motion. For this reason, it is important to recognize symptoms, understand risk factors, get an accurate diagnosis, and treat and prevent gout.

Gout Symptoms

Many forms of arthritis occur gradually, and in the early stages a person may experience only occasional mild pain. In contrast, gout often strikes quickly, severely, and without warning.

Typical gout symptoms include all or some combination of:

Pain

The most notable symptom of gout is extreme pain at the affected joint. Gout pain has been compared to being constantly stabbed with tiny, hot knives.

Extreme tenderness

Touching the skin over the affected joint can be painful. Even covering the skin over the affected joint with clothing or a light blanket can elicit severe pain.

Swelling

The affected joint swells as the uric acid crystals create irritation and inflammation.

Reduced joint function

Pain, tenderness, and swelling can significantly limit the joint’s range of motion and ability to function. It may be uncomfortable—or even impossible—to put weight on an affected foot or knee.

Changes to the skin

The skin at and around the joint will be red and warm to the touch. The skin may also become visibly stretched.

Rapid onset

A gout attack can develop suddenly and without warning, taking only a few hours to become severely painful. The worst pain usually occurs within the first 24 hours.2 (While not typical, gout symptoms can appear more gradually.)

Symptoms that interrupt sleep

It is not uncommon for gout to flare-up in the middle of the night, waking a person from a sound sleep. The affected joint, often a big toe, causes so much pain that the person cannot tolerate even a bed sheet resting on it.

A single joint that is affected

In many gout attacks, only one joint is affected.18 The big toe, ankle, foot instep, heel, or knee is most likely to be affected.

Flu-like symptoms

A gout attack may also cause fever, fatigue, and a general feeling of being unwell. These flu-like symptoms are more common when more than one joint is inflamed.2

Short duration

If left untreated, gout pain typically tapers off and goes away within 10 to 14 days.2,9 A person’s first episode of gout may last just a few days while successive episodes may last longer.

Tophi

Uric acid crystals can collect together and create small white chunks, called tophi, that can be seen and felt through the skin. Tophi (sing. tophus) usually only occur in people who have had chronic gout for several years or longer. This condition is referred to as chronic tophaceous gout and is the most disabling form of gout.

Although gout symptoms normally resolve within several days or weeks, gout should not be left untreated. Over time, gout can become chronic, tophi may develop, and permanent joint damage can occur.

Read more: 5 Unusual Gout Symptoms

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Gout Causes and Risk Factors

Although experts do not fully understand why some people get gout and others do not, many causes and risk factors of gout are well established.

Sex

Experts estimate men are 4 to 10 times more likely to have gout than women.9 Women’s risk of developing gout goes up during menopause (estrogen seems to have protective effects).2,19

Age

Many people have their first episode of gout between the ages of 30 and 50, and the risk of gout continues to increase with age. It is estimated that less than 3% of men under the age of 50 and nearly 12% of men aged 70 to 79 have had at least one episode of gout.20,21

Race

African American men are nearly twice as likely to report having had gout as Caucasian men.22,23

Family history

Research suggests that certain genes that influence kidney function (SLC2A9 and ABCG2) and gut function (ABCG2) increase the risk of developing gout.9 These genes may make the body more prone to accumulating uric acid and developing the uric acid crystals that lead to gout.

Excess weight

People who are overweight have a greater risk of developing gout.24 They are also more likely to develop gout at a younger age.25

Diet

The risk of a gout flare-up is increased by the consumption of alcohol, sugary foods and drinks, meat, and seafood, which are high in purines.26 (Beans, fruits, and vegetables do not seem to increase risk, even if they are high in purines.2)

What Are Purines?

Purines are chemical compounds in food known to cause gout. Read More

Alcohol use

Drinking beer, wine, or liquor increases the likelihood of a gout attack. A study of 724 people diagnosed with gout found that consuming between 1 and 2 alcoholic drinks increased the likelihood of a flare-up by 36%.27

Certain medications

Taking certain medications can increase the risk of hyperuricemia and gout attacks. Common examples of these medications include9:

  • Diuretics, which are sometimes called water pills
  • Low-dose aspirin
  • Cyclosporine, an immunosuppressant sometimes prescribed to people who have rheumatoid arthritis or psoriasis, or who have had an organ transplant
  • Niacin (nicotinic acid), which is used to prevent and treat niacin deficiency (pellagra)
  • Teriparatide, a synthetic hormone used to treat osteoporosis

This is not necessarily a complete list. People who take medications or supplements are advised to talk to their doctor or pharmacist about how their medications may influence gout risk.

Chronic renal failure

A person with chronic renal failure no longer has fully functioning kidneys. When the kidneys’ ability to flush out uric acid is compromised, gout may develop.

A trigger event, such as injury, surgery, or medical therapy

Specific events can trigger a change in body chemistry and bring on a gout flare-up. Such events include, but are not limited to2,28:

  • Infection
  • Repetitive microtrauma from joint overuse
  • Traumatic injury
  • Surgery
  • Illness
  • Sudden and dramatic weight loss

Interestingly, many people who experience an episode of gout may not ever have symptoms again, or at least not for several years. People who do experience gout symptoms repeatedly may notice that episodes get longer and more severe. Gout and its precursor, hyperuricemia, should be addressed to prevent future joint damage.

Gout Diagnosis

A doctor will want to rule out other possible conditions that can cause symptoms similar to gout, such as septic arthritis and pseudogout. To confirm or disprove a gout diagnosis, a doctor may use some or all of the following:

All About Pseudogout

Learn about what causes pseudogout, symptoms of pseudogout, and how to treat it. Read More

Physical exam

A doctor will examine the patient’s affected joint, noting skin color, swelling, pain points, and range of motion.

The doctor will also look for the presence of bumps under the skin. These are collections of uric acid crystals (monosodium urate crystals) called tophi. Tophi are a strong indicator that a person has chronic gout.

Patient interview

A doctor will ask a patient about family history and to describe the onset and pattern of their symptoms.

Joint fluid analysis

The most dependable way to diagnose gout is by examining the joint fluid under a microscope and looking for uric acid crystals.

To obtain a joint fluid sample, a doctor will use a needle and syringe to draw fluid from the affected joint. This procedure is called arthrocentesis or joint aspiration. The procedure may be performed using medical imaging (such as ultrasound) to ensure accurate placement of the needle. If uric acid crystals are found in the fluid sample, then a gout diagnosis is confirmed.

A small percentage of gout cases are diagnosed even though uric acid crystals are not found during joint fluid analysis.29 Before such a diagnosis, additional tests must be done to rule out other possibilities, such as septic arthritis (infectious arthritis).

See Diagnosis through Synovial Fluid Analysis

Blood and urine test

A doctor may test a blood or urine sample for uric acid levels. Abnormally high uric acid levels, called hyperuricemia, indicate gout may be present.

It is possible for the levels of uric acid in the blood to return to normal once a gout attack strikes, so the absence of hyperuricemia does not completely rule out a diagnosis of gout.

Synovial biopsy

During a synovial biopsy, a doctor removes a small amount of tissue from the affected joint so it can be tested and examined for uric acid crystals and signs of gout. The tissue is taken from the joint’s synovial membrane, a normally thin layer of cells that surrounds the joint. A synovial biopsy is typically a minor, outpatient surgical procedure that can be done arthroscopically, so only small incisions are needed.

Ultrasound

A physician may use ultrasound to identify areas where uric acid crystals have deposited, such as in a bursa or on joint cartilage.

Dual-energy computed tomography

This type of medical imaging can distinguish urate crystal deposits from chemically different substances, such as calcium deposits. It may be used to identify uric acid crystals even when a joint fluid analysis does not detect them or in between gout attacks.2

Dual-energy computed tomography may be referred to as dual-energy CT or DECT.

X-rays

An x-ray of the joint may show the deposition of uric acid crystals. However, x-rays can be normal even when gout is present. Experts estimate that chronic gout must be present for 5 to 10 years before joint changes can be seen on an x-ray.30

Most gout cases are diagnosed with a joint fluid analysis. An accurate diagnosis is important to long-term treatment and health.

During an acute gout episode, the priority is to alleviate the immediate pain and other symptoms. Once steps are taken to relieve symptoms, a treatment plan to prevent future gout attacks can begin.

Without treatment and prevention, gout can become chronic, leading to repeated episodes of intense gout pain and possibly permanent damage to the affected joint(s).

Treating a Gout Flare-up

Infographic displaying 6 ways to deal with Gout: Take it Easy, Apply Ice, Elevate, Stay Hydrated, Take OTC Medications, Take Prescription Medications
6 Ways to Deal with Painful Gout
(larger view)

The immediate goals for treating a gout flare-up are to reduce intense pain, swelling, warmth, and redness. With proper treatment, gout pain and other symptoms can be under control within 24 hours and completely gone within a matter of days.

Avoid pressure

During the peak of gout pain, contact with any surface—even a bedsheet, may cause a sharp increase in pain. It is advisable to avoid putting even minor pressure on the joint until this phase has passed.

Rest

It is usually painful to use the affected joint, and resting it will help alleviate pain, swelling, and other symptoms.

Ice

If some pressure can be tolerated, a soft, cool compress applied to the affected joint may help relieve discomfort caused by inflammation.

See 3 Types of Cold Packs for Arthritis

Elevation

Elevate the affected limb to help reduce swelling. If the foot is affected, sit down with the foot resting on a footstool or lie down with the foot propped up on a pillow.

Over-the-counter anti-inflammatory medications

Ibuprofen, naproxen, and other nonsteroidal anti-inflammatory medications (NSAIDs) can relieve pain from a gout attack. These medications may be particularly effective if they are taken as soon as the person feels the gout attack coming on.31

While NSAIDs are an effective and recommended treatment for many people, they can have a negative effect on the kidneys, reducing their ability to filter out uric acid and increasing the risk of future gout attacks. NSAIDs can also cause gastrointestinal side effects. A doctor can advise whether or not to take NSAIDs and at what dosage.

See Pain Medications for Arthritis Pain Relief

Colchicine

A prescription drug called colchicine was developed to treat gout. Evidence shows that colchicine reduces gout pain, swelling, and inflammation decrease when it is taken within the first 36 hours of an attack.32 A second, smaller dose should be taken an hour or two later.9,33

Colchicine should be taken only as directed. Many people taking colchicine experience gastrointestinal side effects, such as vomiting or diarrhea.

Corticosteroids

A doctor may recommend corticosteroid treatment to alleviate inflammation. Corticosteroids may be taken orally or delivered by injection.

Steroid treatment is particularly useful for people with sensitivities to NSAIDs and colchicine.9 Repeated corticosteroid injections and/or long-term oral cortisone treatment can have side effects. Oral steroids should not be taken with NSAIDs.9

See Cortisone Injections (Steroid Injections)

Biologics

While the FDA has not approved biologics drugs to treat gout,9 they may be recommended. They may be particularly appropriate for people who have other medical conditions, such as kidney disease, heart failure, diabetes, and high blood pressure, that prevent them from taking traditional gout medications.34

Biologics can target and prevent inflammation from occurring, thereby reducing and possibly eliminating joint pain, swelling, redness. Examples of biologic drugs prescribed for gout include anakinra and canakinumab.2,9,35,36 Biologics tend to cost more than traditional medications.

See Biologics for RA and Other Autoimmune Conditions

Surgery

Gout cannot be cured with surgery. However, if untreated gout leads to the development and buildup of tophi, surgery to remove the tophi may be recommended.

Gout is usually so painful that a person cannot ignore it and will take steps to treat it. Once the symptoms of a gout attack are under control, a person can take steps to lower the uric acid levels in the blood and prevent another attack.

Gout Prevention

People at risk for chronic gout will want to take steps to prevent a painful attack. There are several lifestyle and dietary changes that can reduce the risk of a gout attack and joint degeneration associated with gout. When these changes are not enough to stop gout episodes from happening, a doctor may recommend allopurinol or another daily prescription medication.

This page describes gout prevention strategies.

Avoid or limit alcohol

Consuming alcohol inhibits the body’s ability to excrete uric acid, increasing the risk of hyperuricemia and a gout attack. Just one or two glasses of beer, wine, or hard liquor can increase the likelihood of a gout attack, and the risk increases with the number of drinks consumed.44

Drink plenty of water

Increasing water intake will help keep the kidneys healthy and help them flush out uric acid from the body. The recommended daily intake of fluids varies depending on an individual’s age, weight, sex, and other factors.37

Lose excess weight or maintain a healthy weight

Obtaining and maintaining a healthy weight through diet and exercise helps reduce the risk of gout.38

Research evidence47 suggests that sudden, dramatic weight loss, such as after bariatric surgery, may increase the likelihood of a gout attack in the short term. In the long term, excess weight loss—sudden or gradual—is an effective way to reduce risk.

Treat sleep apnea

While more research is needed, some evidence suggests that treating sleep apnea may significantly affect the frequency of gout episodes.16,21,39 Treatment typically includes using a C-Pap machine or another treatment device designed to increase oxygen intake while sleeping. Increased oxygen intake may lower uric acid production and reduce the risk of a gout attack.

The primary goals of sleep apnea treatment include improving sleep quality and heart health.40,41,42

Avoid foods that can trigger a gout flare-up

People who are prone to gout can prevent uric acid buildup in the bloodstream by avoiding certain foods, including seafood, red meats, organ meats, and sugary drinks and foods.

Avoid medications that trigger gout

Certain medications, such as diuretics, are associated with hyperuricemia.42 People who take these medications and have gout may ask their health care providers other medications or treatments approach might be appropriate.

Take prescription gout medication

A doctor may prescribe medication to reduce the amount of uric acid produced by the body. Urate lowering medication is typically recommended to people who9:

  • Experience more than two gout attacks per year
  • Have a gout attack and also have a history of tophi or renal stones (from previous attacks)
  • Have a gout attack and also have chronic kidney disease

Commonly prescribed medications include allopurinol and febuxostat.9 Additional or alternative medications may be prescribed depending on the patient’s circumstances.

Gout Diet

Consuming certain foods and drinks can raise uric acid levels in the blood and trigger a gout flare-up. Other food may help decrease the likelihood of a gout flare-up. Experts estimate that an appropriate gout prevention diet can reduce uric acid levels up to 15%.43

Infographic displaying which foods to avoid, moderate, or enjoy to balance purines.
Balancing Your Purines
(larger view)

Foods that may trigger a gout attack

Physicians recommend avoiding or limiting consumption of44:

  • Alcoholic beverages, especially beer
  • Sugary foods and beverages, particularly those made with high fructose corn syrup, such as sodas45
  • Meat, particularly organ meat or “sweetmeats,” such as liver, and game meats6
  • Seafood, particularly scallops, anchovies, and herring46

Alcohol increases the amount of uric acid in the blood and it limits the body’s ability to process and eliminate uric acid.47

Foods that may help prevent a gout attack

A gout prevention diet includes plenty of vegetables, fruits, and complex carbohydrates, including whole grains and beans. Such a diet may also include low-fat dairy products and cherries:

  • Low-fat dairy products, such as skim milk and yogurt, may decrease the levels of uric acid in the blood and thereby decrease their risk of gout attacks.48 High-fat dairy products do not have the same protective effect.
  • Cherries have long been thought to prevent gout flare-ups, and there is some scientific evidence to support this.49-53 Fresh or frozen tart cherries, 100% unsweetened tart cherry juice, or cherry extract may be beneficial. Avoid sweetened cherries, such as cherry pie filling.

Eating a healthy, plant-based diet and taking other preventative steps, such as drinking plenty of water, avoiding alcohol, and maintaining a healthy weight, can go a long way towards preventing gout, other types of arthritis, and heart disease.

See What Are Purines?

References

  • 1.Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum 2011;63(10):3136–41. As cited in Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45(2):213-236. doi:10.1016/j.pop.2018.02.004
  • 2.Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45(2):213-236. doi:10.1016/j.pop.2018.02.004
  • 3.Riddell CM, Elliott M, Cairns, AP. An Unusual “Gouty” Case of Back Pain and Fever. J Rheumatol October 2008 35(10):2076-2077 PMID: 18843766
  • 4.Bang SY, Jeong JH, Joo KB, Jun JB, Sung YK. A Case of the Lumbar Spine Involvement and Sacroiliitis in a Patient with Gout. J Korean Rheum Assoc. 2009 Dec;16(4):318-322. https://doi.org/10.4078/jkra.2009.16.4.318
  • 5.Mantle B, Gross P, Lopez-Ben R, Alarcón GS. Hip pain as the presenting manifestation of acute gouty sacroiliitis. J Clin Rheumatol. 2001 Apr;7(2):112-4. PubMed PMID: 17039107.
  • 6.Konatalapalli RM, Demarco PJ, Jelinek JS, Murphey M, Gibson M, Jennings B, Weinstein A. Gout in the axial skeleton. J Rheumatol. 2009 Mar;36(3):609-13. doi: 10.3899/jrheum.080374. Epub 2009 Feb 4. PubMed PMID: 19208604.
  • 7.Klauser AS, Halpern EJ, Strobl S, et al. Gout of hand and wrist: the value of US as compared with DECT. Eur Radiol. 2018;28(10):4174-4181. DOI: 10.1007/s00330-018-5363-9
  • 8.Slobodonick A, Toprover M, Pillinger M. Crystal Arthritis. In: Efthimiou P, ed. Absolute Rheumatology Review. Springer Nature Switzerland AG; 2020; chap 15. Accessed September 15, 2020. https://doi.org/10.1007/978-3-030-23022-7_15
  • 9.Dirken-Heukensfeldt KJ, Teunissen TA, van de Lisdonk H, Lagro-Janssen AL. "Clinical features of women with gout arthritis." A systematic review. Clin Rheumatol. 2010;29(6):575-582. doi: 10.1007/s10067-009-1362-1
  • 10.Scott JT, Pollard AC. Uric acid excretion in the relatives of patients with gout. Ann Rheum Dis. 1970 Jul;29(4):397-400. Review. PubMed PMID: 4916770; PubMed Central PMCID: PMC1031324. DOI: 10.1136/ard.29.4.397
  • 11.Choi HK, Niu J, Neogi T, et al. Nocturnal risk of gout attacks. Arthritis Rheumatol. 2015;67(2):555-562. doi: 10.1002/art.38917
  • 12.Neogi T, Chen C, Niu J, et al. Relation of temperature and humidity to the risk of recurrent gout attacks. Am J Epidemiol. 2014;180(4):372-377. DOI: 10.1093/aje/kwu147
  • 13.Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot?. J Foot Ankle Res. 2011;4(1):13. Published 2011 May 13. doi: 10.1186/1757-1146-4-13
  • 14.Martillo MA, Nazzal L, Crittenden DB. The crystallization of monosodium urate. Curr Rheumatol Rep. 2014;16(2):400. DOI: 10.1007/s11926-013-0400-9
  • 15.Zhang Y, Peloquin CE, Dubreuil M, et al. Sleep Apnea and the Risk of Incident Gout: A Population-Based, Body Mass Index-Matched Cohort Study. Arthritis Rheumatol. 2015;67(12):3298-3302. doi: 10.1002/art.39330
  • 16.Abhishek A, Valdes AM, Jenkins W, Zhang W, Doherty M. Triggers of acute attacks of gout, does age of gout onset matter? A primary care based cross-sectional study. PLoS One. 2017;12(10):e0186096. Published 2017 Oct 12. doi: 10.1371/journal.pone.0186096
  • 17.Gout. Medline Plus. Last Reviewed April 8, 2019. Accessed July 16, 2020. https://medlineplus.gov/ency/article/000422.htm#:~:text=It%20occurs%20when%20uric%20acid,one%20joint%20may%20be%20affected.
  • 18.Harris MD, Siegel LB, Alloway JA. Gout and hyperuricemia. Am Fam Physician. 1999 Feb 15;59(4):925-34. PMID: 10068714.
  • 19.Hak AE, Choi HK. Menopause, postmenopausal hormone use and serum uric acid levels in US women--the Third National Health and Nutrition Examination Survey. Arthritis Res Ther. 2008;10(5):R116. DOI: 10.1186/ar2519
  • 20.Kramer HM, Curhan G. The association between gout and nephrolithiasis: the National Health and Nutrition Examination Survey III, 1988-1994. Am J Kidney Dis. 2002 Jul;40(1):37-42. DOI: 10.1053/ajkd.2002.33911
  • 21.Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum. 2008;58(1):26-35. doi: 10.1002/art.23176
  • 22.Fang J, Alderman MH. Serum uric acid and cardiovascular mortality the NHANES I epidemiologic follow-up study, 1971-1992. National Health and Nutrition Examination Survey. JAMA 2000;283(18):2404–10. As cited in Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45(2):213-236. doi:10.1016/j.pop.2018.02.004
  • 23.Hochberg MC, Thomas J, Thomas DJ, Mead L, Levine DM, Klag MJ. Racial difference in the incidence of gout. The role of hypertension. Arthritis Rheum 1995;38(5): 628–632. DOI: 10.1002/art.1780380508
  • 24.Ansari S, Haboubi H, Haboubi N. Adult obesity complications: challenges and clinical impact. Ther Adv Endocrinol Metab. 2020;11:2042018820934955. Published 2020 Jun 22. doi: 10.1177/2042018820934955
  • 25.DeMarco MA, Maynard JW, Huizinga MM, et al. Obesity and younger age at gout onset in a community-based cohort. Arthritis Care Res (Hoboken). 2011;63(8):1108-1114. doi:10.1002/acr.20479
  • 26.Gout. Centers for Disease Control and Prevention. Page last reviewed January 28, 2019. Accessed July 14, 2020. https://www.cdc.gov/arthritis/basics/gout.html
  • 27.Neogi T, Chen C, Niu J, Chaisson C, Hunter DJ, Zhang Y. Alcohol quantity and type on risk of recurrent gout attacks: an internet-based case-crossover study. Am J Med. 2014;127(4):311-318. doi: 10.1016/j.amjmed.2013.12.019
  • 28.Nielsen SM, Bartels EM, Henriksen M, et al. Weight loss for overweight and obese individuals with gout: a systematic review of longitudinal studies. Annals of the Rheumatic Diseases 2017;76:1870-1882.
  • 29.Neogi T, Jansen TL, Dalbeth N, Fransen J, Schumacher HR, Berendsen D, Brown M, Choi H, Edwards NL, Janssens HJ, Lioté F, Naden RP, Nuki G, Ogdie A, Perez-Ruiz F, Saag K, Singh JA, Sundy JS, Tausche AK, Vaquez-Mellado J, Yarows SA, Taylor WJ. 2015 Gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis. 2015 Oct;74(10):1789-98. doi: 10.1136/annrheumdis-2015-208237. Erratum in: Ann Rheum Dis. 2016 Feb;75(2):473. PMCID: PMC4602275 DOI: 10.1136/annrheumdis-2015-208237
  • 30.Bloch C, Hermann G, Yu TF. A radiologic reevaluation of gout: a study of 2,000 patients. AJR Am J Roentgenol 1980;134(4):781–7. As cited in Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45(2):213-236. doi:10.1016/j.pop.2018.02.004
  • 31.Schlesinger N. Management of acute and chronic gouty arthritis: present state-of-the-art. Drugs. 2004;64(21):2399-416. Review. PubMed PMID: 15481999. DOI: 10.2165/00003495-200464210-00003
  • 32.Khanna D, Khanna PP, Fitzgerald JD, et al. 2012 American College of Rheuma- tology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res (Hoboken) 2012;64(10): 1447–61. As cited in Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45(2):213-236. doi:10.1016/j.pop.2018.02.004
  • 33.Terkeltaub RA, Furst DE, Bennett K, et al. High versus low dosing of oral colchicine for early acute gout flare: twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum 2010;62(4):1060–8. As cited in Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45(2):213-236. doi:10.1016/j.pop.2018.02.004
  • 34.Liew JW, Gardner GC. Use of Anakinra in Hospitalized Patients with Crystal-associated Arthritis. J Rheumatol. 2019 Oct;46(10):1345-1349. DOI: 10.3899/jrheum.181018
  • 35.Dinarello CA. An expanding role for interleukin-1 blockade from gout to cancer. Mol Med. 2014;20 Suppl 1(Suppl 1):S43-S58. Published 2014 Dec 16. doi: 10.2119/molmed.2014.00232
  • 36.Janssen CA, Oude Voshaar MAH, Vonkeman HE, et al. Anakinra for the treatment of acute gout flares: a randomized, double-blind, placebo-controlled, active-comparator, non-inferiority trial, Rheumatology, Volume 58, Issue 8, August 2019, Pages 1344–1352, https://doi.org/10.1093/rheumatology/key402
  • 37.Getting the Facts: Drinking Water and Intake. Centers for Disease Control and Prevention. Last Reviewed August 9, 2016. Accessed July 10, 2020. https://www.cdc.gov/nutrition/data-statistics/plain-water-the-healthier-choice.html
  • 38.Dessein PH, Shipton EA, Stanwix AE, et al. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis 2000;59(7):539–43. As cited in Sidari A, Hill E. Diagnosis and Treatment of Gout and Pseudogout for Everyday Practice. Prim Care. 2018;45(2):213-236. doi: 10.1016/j.pop.2018.02.004
  • 39.Abrams B. Sleep apnea and gout. Can Fam Physician. 2009;55(3):243-244. PMID: 19282526
  • 40.Giles TL, Lasserson TJ, Smith BJ, White J, Wright J, Cates CJ. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD001106. Update in: Cochrane Database Syst Rev. 2006;(3):CD001106. PMID: 16437429. DOI: 10.1002/14651858.CD001106.pub2
  • 41.Bouloukaki I, et al. (2014). Intensive versus standard follow-up to improve continuous positive airway pressure compliance. European Respiratory Journal, 44(5): 1262–1274. DOI: 10.1183/09031936.00021314
  • 42.Milleron O, et al. (2004). Benefits of obstructive sleep apnoea treatment in coronary artery disease: A long-term follow-up study. European Heart Journal, 25(9): 728–734. DOI: 10.1016/j.ehj.2004.02.008
  • 43.Paul BJ, Anoopkumar K, Krishnan V. Asymptomatic hyperuricemia: is it time to intervene?. Clin Rheumatol. 2017;36(12):2637-2644. doi: 10.1007/s10067-017-3851-y
  • 44.Ramirez-Sandoval JC, Madero M. Treatment of Hyperuricemia in Chronic Kidney Disease. Contrib Nephrol. 2018;192:135-146. doi: 10.1159/000484288
  • 45.Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of gout in women. JAMA. 2010;304(20):2270-8. doi: 10.1001/jama.2010.1638
  • 46.George C, Minter DA. Hyperuricemia. [Updated 2020 May 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459218/
  • 47.Kakutani-Hatayama M, Kadoya M, Okazaki H, et al. Nonpharmacological Management of Gout and Hyperuricemia: Hints for Better Lifestyle. Am J Lifestyle Med. 2015;11(4):321-329. Published 2015 Sep 2. doi: 10.1177/1559827615601973
  • 48.Choi HK, Liu S, Curhan G. Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2005;52(1):283-9. DOI: 10.1002/art.20761
  • 49.Schlesinger N. Dietary factors and hyperuricaemia. Curr Pharm Des. 2005;11(32):4133-8. Review. PubMed PMID: 16375734.
  • 50.Jacob RA, Spinozzi GM, Simon VA, Kelley DS, Prior RL, Hess-Pierce B, Kader AA. Consumption of cherries lowers plasma urate in healthy women. J Nutr. 2003 Jun;133(6):1826-9. PubMed PMID: 12771324.
  • 51.Chen PE, Liu CY, Chien WH, Chien CW, Tung TH. Effectiveness of Cherries in Reducing Uric Acid and Gout: A Systematic Review. Evid Based Complement Alternat Med. 2019;2019:9896757. Published 2019 Dec 4. DOI: 10.1155/2019/9896757
  • 52.Zhang Y, Neogi T, Chen C, Chaisson C, Hunter DJ, Choi HK. Cherry consumption and decreased risk of recurrent gout attacks. Arthritis Rheum. 2012;64(12):4004–4011. DOI: 10.1002/art.34677
  • 53.Collins MW, Saag KG, Singh JA. Is there a role for cherries in the management of gout?. Ther Adv Musculoskelet Dis. 2019;11:1759720X19847018. Published 2019 May 17. doi: 10.1177/1759720X19847018
Further Reading: 5 Unusual Gout Symptoms