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Gout is a painful inflammatory arthritis condition caused by deposits of uric acid crystals in the joints and soft tissues. The painful attacks often begin at night and may last for a week.

8.3 million people in the U.S. have gout. This number is growing because of an aging population, the rise in obesity, increasing numbers of people who also have other conditions such as heart disease, kidney disease, and/or diabetes. The use of diuretics by persons with cardiovascular disease is another cause of the increase in gout.

Treatment and Management

  • Medications are aimed at treating acute attacks by reducing pain and inflammation in the joints and other tissues. Medications also prevent future attacks by lowering uric acid in the body.
  • Lifestyle changes are important in preventing attacks and managing the condition. Measures include losing weight, limiting foods and beverages that have the chemical purine, and limiting alcohol.


Gout is a painful and common type of arthritis. It is caused when there is too much uric acid in the blood. This is called hyperuricemia. Uric acid is a waste product in the body and is normally excreted through urine. Buildup of uric acid results in needlelike crystals forming in the joints, soft tissues, and organs.

Cases of gout have increased in recent years. This increase is likely due to an aging population, dietary and lifestyle changes, greater use of medicines, such as diuretics (water pills), all of which can lead to a high uric acid level in the body.

Click the icon to see an animation about gout.

How Hyperuricemia and Gout Develop

Metabolism of Purines. The process leading to hyperuricemia and gout begins with the metabolism, or breakdown, of purines. Purines are compounds that are important for energy. Purines can be divided into two types:

Endogenous purines are manufactured within human cells.

Exogenous purines are obtained from food.

The process of breaking down purines results in the formation of uric acid in the body. Most mammals, except humans, have an enzyme called uricase. Uricase breaks down uric acid so it can be easily removed from the body. Because humans lack uricase, uric acid is not easily removed and can build up in body tissues.

Uric Acid and Hyperuricemia. Purines in the liver produce uric acid. The uric acid enters the bloodstream. Most of the uric acid goes through the kidneys and is excreted in urine. The remaining uric acid travels through the intestines where bacteria help break it down.

Normally these processes keep the level of uric acid in the blood below 6.8 mg/dL. But sometimes the body produces too much uric acid or removes too little. In either case, the level of uric acid increases in the blood. This condition is known as hyperuricemia.

If uric acid reaches 7 mg/dL or higher, needlelike crystals of a salt called monosodium urate (MSU) may form. The higher the level of uric acid, the higher the risk of crystal formation. As crystals build up in the joints, they trigger inflammation and pain. These are the symptoms of gout.


Symptoms of gout depend on the stage of the disease. Gout can be divided into four stages:

  • Asymptomatic hyperuricemia
  • Acute gouty arthritis
  • Intercritical gout
  • Chronic tophaceous gout

Asymptomatic Hyperuricemia

Asymptomatic means there are no symptoms. Increase in blood uric acid is the first stage of gout. This stage may last 30 years or more.

Note: Hyperuricemia does not always lead to gout. Less than 20% of cases devleop into arthritic gout disease.

Symptoms of Acute Gouty Arthritis

Acute gouty arthritis occurs when the first symptoms of gout appear. Sometimes the first signs of gout are brief twinges of pain (petit attacks) in an affected joint. These attacks can last several years before the full-blown condition occurs.

Symptoms of acute gouty arthritis often start in one joint and include any of the following:

Severe pain at and around the joint: may feel like "crushing" or a dislocated bone; physical activity and even the weight of bed sheets may be unbearable; usually takes 8 to 12 hours to develop; occurs late at night or early in the morning and may wake you up

Warmth over the joint

Red, shiny, tense skin over the affected area, which may peel after a few days

Chills and mild fever, loss of appetite, not feeling well in general

Monoarticular Gout. Gout that occurs in one joint is called monoarticular gout. About 60% of all first-time monoarticular gout attacks in middle-aged adults occur in the big toe. This is known as podagra. Symptoms can also occur in other locations such as the ankle or knee.

Polyarticular Gout. If more than one joint is affected, the condition is known as polyarticular gout. Multiple

joints are affected in only 10% to 20% of first attacks. Older people are more likely to have polyarticular gout. The most frequently affected joints are the foot, ankle, knee, wrist, elbow, and hand. The pain usually occurs in joints on one side of the body and it is usually, though not always, in the lower legs and the feet. People with polyarticular gout are more likely to have a slower onset of pain and a longer delay between attacks. People with polyarticular gout are also more likely to experience low-grade fever, loss of appetite, and a general feeling of poor health.

An untreated attack peaks 24 to 48 hours after symptoms first appear and goes away after 5 to 7 days. Some attacks last only hours, while others go on for as long as several weeks. Though symptoms can subside, the crystals are still present and future attacks are likely to occur.

Intercritical Gout

Intercritical gout is the term used to describe the periods between attacks. The first attack is usually followed by a complete disappearance (remission) of symptoms. But, untreated, gout nearly always returns. Over two-thirds of patients have at least one more attack within 2 years of the first attack. By 10 years, over 90% of patients are likely to have more attacks.

Symptoms of Chronic Tophaceous Gout

Chronic Tophaceous Gout and Tophi. After several years, persistent gout can develop into a condition called chronic tophaceous gout. This long-term condition often produces tophi. These are solid deposits of MSU crystals that form in the joints, cartilage, bones, and elsewhere in the body. In some cases, tophi break through the skin and appear as white or yellowish-white, chalky nodules that have been described as looking like crab eyes.

Click the icon to see an image of tophi gout. %img src="" /%

Without treatment, tophi develop about 10 years after the onset of gout, although the occurrence can range from 3 to 42 years. Tophi are more likely to appear early in the course of the disease in older people. In the elderly, women are at higher risk of developing tophi than men. Persons who have had an organ transplant and are on the medicine cyclosporine also have a high risk of developing tophi.

Chronic Pain. When gout remains untreated, the intercritical periods become shorter and shorter and the attacks, although sometimes less intense, can last longer. In about 10 to 20 years gout becomes a chronic disorder with constant low-grade pain and mild or acute inflammation. Gout may later affect several joints, including those that may have been free of symptoms at the start of the disorder. In rare cases, the shoulders, hips, or spine are affected.

Location of Tophi. Tophi may form in the following locations:

Curved ridge along the edge of the outer ear


Around the heart and spine (rare)

Tophi are usually painless. But they can cause pain and stiffness in the affected joint. In time, they can also wear aways cartilage and bone and destroy the joint. Large tophi under the skin of the hands and feet can cause severe deformities.


Uric Acid Nephrolithiasis (Kidney Stones). Persons who have kidney stones that formed from uric acid are more likely to have a higher level of uric acid in their blood than in their urine. This suggests that hyperurecemia is responsible for this type of kidney stone.

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Not all kidney stones in patients with gout are made of uric acid. Some are made of calcium oxalate, calcium phosphate, or substances combined with uric acid. Uric acid stones can also form in a person who does not have gout or hyperuricemia.

Chronic Uric Acid Interstitial Nephropathy. Chronic uric acid interstitial nephropathy occurs when crystals slowly form in the structures and tubes that carry fluid from the kidney. This condition is reversible and not likely to injure the kidneys.

Kidney Failure. Sudden overproduction of uric acid can sometimes block the kidneys and cause them to fail. This occurrence is very rare but can develop after any of the following:

  • Chemotherapy for leukemia or lymphoma, particularly acute forms of the disease
  • Other cancers, such as breast cancer and lung cancer
  • Epileptic seizures
  • Pregnancy related preeclampsia or eclampsia
  • Use of medications to prevent kidney transplant rejection, such as cyclosporine

Causes and Risk Factors

Gout is considered either primary or secondary, depending on the causes of the high uric acid level in the blood (hyperuricemia).

Nearly all cases of primary gout cases are idiopathic. This means that the cause of the hyperuricemia cannot be determined. Primary gout is most likely the result of a combination of genetic, hormonal, and dietary factors. Secondary gout is caused by medicines or by medical conditions other than a metabolic disorder.

The following factors increase the risk of gout:

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