Definition and Risk Factors of Gout

Gout is one of the most painful rheumatic diseases. It results from deposits of needle-like crystals of uric acid in the connective tissue, joint spaces, or both. These deposits lead to inflammatory arthritis, which causes swelling, redness, heat, pain, and stiffness in the joints. Arthritis is a term that is often used to refer to the more than 100 different rheumatic diseases that affect the joints, muscles, and bones, and may also affect other connective tissues. Gout accounts for about 5 percent of all cases of arthritis. Pseudogout, also a crystal-induced arthritis, is a condition with similar symptoms that results from deposits of calcium pyrophosphate dihydrate crystals in the joints. It is sometimes called calcium pyrophosphate deposition disease, crystal deposition disease, or chondrocalcinosis.

Uric acid is a substance that results from the breakdown of purines or waste products in the body. Normally, uric acid is dissolved in the blood and passes through the kidneys into the urine, where it is eliminated. If the body increases its production of uric acid or if the kidneys do not eliminate enough uric acid from the body, levels build up (a condition called hyperuricemia). Hyperuricemia may also result when a person eats too many high-purine foods, such as liver, dried beans and peas, anchovies, and gravies. Hyperuricemia is not a disease and by itself is not dangerous. However, if excess uric acid crystals form as a result of hyperuricemia, gout can develop. The excess crystals build up in the joint spaces, causing inflammation . Deposits of uric acid, called tophi, can appear as lumps under the skin around the joints and at the rim of the ear. In addition, uric acid crystals can also collect in the kidneys and cause kidney stones.

For many people, gout initially affects the joints in the big toe, a condition called podagra. Sometime during the course of the disease, gout will affect the big toe in about 75 percent of patients. Gout can also affect the instep, ankles, heels, knees, wrists, fingers, and elbows. The disease can progress through four stages:

  • Asymptomatic (without symptoms) hyperuricemia - In this stage, a person has elevated levels of uric acid in the blood but no other symptoms. The tendency to develop gout, however, is present. A person in this stage does not usually require treatment.
  • Acute gout, or acute gouty arthritis - In this stage, hyperuricemia has caused the deposit of uric acid crystals in joint spaces. This leads to a sudden onset of intense pain and swelling in the joints, which may also be warm and very tender. An acute attack commonly occurs at night and can be triggered by stressful events, alcohol or drugs, or another acute illness. Early attacks usually subside within 3 to 10 days, even without treatment, and the next attack may not occur for months or even years. Over time, however, attacks can last longer and occur more frequently.
  • Interval or intercritical gout - This is the period between acute attacks. In this stage, a person does not have any symptoms and has normal joint function.
  • Chronic tophaceous gout - This is the most disabling stage of gout and usually develops over a long period, such as 10 years. In this stage, the disease has caused permanent damage to the affected joints and sometimes to the kidneys. With proper treatment, most people with gout do not progress to this advanced stage.

A number of risk factors are related to the development of hyperuricemia and gout:

  • Genetics may play a role in determining a person's risk, since 6 to 18 percent of people with gout have a family history of the disease.
  • Being overweight increases the risk of developing hyperuricemia and gout because excessive food intake increases the body's production of uric acid.
  • Excessive use of alcohol can lead to hyperuricemia because it interferes with the removal of uric acid from the body.
  • Eating too many foods that are rich in purines can cause or aggravate gout.
  • An enzyme defect that interferes with the way the body breaks down purines causes gout in a small number of people.
  • Exposure to lead in the environment can cause gout.

Some people are at risk for high levels of uric acid in body fluids because of certain medicines they take or other conditions they may have. For example, the following types of medicines can lead to hyperuricemia because they reduce the body's ability to remove uric acid:

  • Diuretics, which decrease the amount of uric acid passed in the urine. Many people take diuretics for hypertension, edema, or cardiovascular disease.
  • Salicylates, or medicines made from salicylic acid, such as aspirin.
  • The vitamin niacin, also called nicotinic acid.
  • Cyclosporine, a medicine used to control the body's rejection of transplanted organs.
  • Levodopa, a medicine used to treat Parkinson's disease.

Gout occurs in approximately 275 out of every 100,000 people. Men are more likely to develop gout than women, and men aged 40 to 50 are most commonly affected. Women rarely develop gout before menopause. The disease affects men and women differently:

Men tend to develop gout at an earlier age than women, and alcohol is more often associated with the development of the disease in men. Gout is rare in children and young adults.

Signs and Symptoms of Gout

  • Hyperuricemia
  • Presence of uric acid crystals in joint fluid
  • More than one attack of acute arthritis
  • Arthritis that develops in 1 day
  • Attack of arthritis in only one joint, usually the toe, ankle, or knee
  • A painful joint that is swollen, red, and warm

Gout may be difficult for doctors to diagnose because the symptoms may be vague and often mimic other conditions. Although most people with gout have hyperuricemia at some time during the course of their disease, it may not be present during an acute attack. In addition, hyperuricemia alone does not mean that a person has gout. In fact, most people with hyperuricemia do not develop the disease.



To confirm a diagnosis of gout, doctors typically test the fluid in the joint, called synovial fluid, by using a needle to draw a sample of fluid from a person�s inflamed joint. The doctor places some of the fluid on a slide and looks for monosodium urate crystals under a microscope. If the person has gout, the doctor will almost always see crystals. Their absence, however, does not completely rule out the diagnosis. Doctors may also find it helpful to examine joint or tophi deposits to diagnose gout. A doctor who suspects a joint infection may check for the presence of bacteria.

With proper treatment, most people with gout are able to control their symptoms and live normal lives. Gout can be treated with one or a combination of therapies. Treatment goals are to ease the pain associated with acute attacks, prevent future attacks, and avoid the formation of new tophi and kidney stones.

The most common treatments for an acute attack of gout are high doses of nonsteroidal anti-inflammatory drugs (NSAID's) and injections of corticosteroid drugs into the affected joint. NSAID's reduce the inflammation caused by deposits of uric acid crystals. The NSAID's most commonly prescribed for gout are indomethacin (Indocin) and naproxen (Anaprox, Naprosyn), which are taken by mouth (orally) every day. Patients usually begin to improve within a few hours of treatment, and the attack goes away completely within a few days.

Scientists are studying whether other NSAID's are effective in treating gout and are analyzing new compounds to develop safe, effective medicines to treat gout and other rheumatic diseases. For example, researchers are testing to determine whether fish oil supplements reduce the risk of gout. They are also studying the structure of the enzymes that break down purines in the body, in hopes of achieving a better understanding of the enzyme efects that can cause gout.

- Questions and Answers About Gout - National Arthritis and Musculoskeletal and Skin Diseases Information Clearinghouse (NAMSIC)

National Institutes of Health
The NIAMS gratefully acknowledges the assistance of John H. Klippel, M.D., NIAMS; N. Lawrence Edwards, M.D., of the University of Florida in Gainesville; and Lawrence Ryan, M.D., of the Medical College of Wisconsin, in the preparation and review of this fact sheet.