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Although an elevated blood level of uric acid (hyperuricemia) is associated with an increased risk of gout, the relationship between the two is not fully understood.

If members of your family have had gout, then you are more likely to develop the disease.

Prevention includes dietary changes, medications, and other strategies to reduce hyperuricemia.

Uric acid is produced by the body when it breaks down purines, substances that are found naturally in the body and in food. Purines are particularly rich in certain foods, such as liver, anchovies, herring, asparagus and mushrooms. Normally, uric acid dissolves in the blood and passes through the kidneys into the urine. However, when the body either produces too much uric acid or the kidneys excrete too little uric acid, it can build up, forming sharp, needle-like urate crystals in joints or surrounding tissues that cause sudden inflammation, pain, swelling and stiffness in the affected joint, a condition referred to as gout. However, people with elevated levels of uric acid in their blood do not always develop gout and conversely, not everyone that experiences repeated attacks of gout have elevated levels of uric acid.

Gout usually attacks the big toe (approximately 75% of first attacks), but it can also affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, and spine. Untreated and chronic gout can lead to deposits of hard lumps of uric acid (tophi lumps) in and around joints, kidney stones and decreased kidney function.

Approximately one million people in the United States suffer from attacks of gout. Gout is about nine times more common in men than in women. Among the male population in the United States, approximately 10% have hyperuricemia.

Two genetic variants have been found to be associated with gout. The first variant is in the GLUT9/SLC2A9 gene and the second is in the ABCG2 gene.

The deCODEme Complete Scan identifies these variants and provides an interpretation of the associated risk for the development of gout for individuals of European descent.

Risk Factors

Although an elevated blood level of uric acid (hyperuricemia) is associated with an increased risk of gout, the relationship between hyperuricemia and gout is not fully understood. Risk factors for hyperuricemia and/or gout include the following:

• Age and gender: Gout is nine times more common in men than in women, primarily because men tend to have higher levels of uric acid in their blood than women. The disease predominantly attacks males after puberty and is most common in males between 40 and 50 years of age. Women become increasingly susceptible to gout after menopause.
• Ethnicity: In the United States, gout is twice as prevalent in African American males as it is in males of European descent.
• Genetics: If members of your family have had gout, then you are more likely to develop the disease. Twenty percent of people with gout have a family history of the disease.
• Diet: High levels of uric acid in the blood are mostly caused by protein rich foods. Alcohol intake can cause acute attacks of gout. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol.
• Medication: The use of thiazide diuretics, which are commonly used to treat hypertension, and low-dose aspirin can increase uric acid levels. So can the use of anti-rejection drugs prescribed for people who have undergone an organ transplant.
• Other diseases: Typically, persons with gout are obese, predisposed to diabetes and hypertension, and at higher risk of heart disease.

Prevention and Treatment

Prevention of hyperuricemia and acute gout involves maintaining adequate fluid intake, weight reduction, dietary changes, reduction in alcohol consumption, and use of medication to reduce hyperuricemia:

• Dietary changes: Reducing the amount of animal protein in your diet is important, because high-protein foods increase the blood level of uric acid. Organ meats (liver, brains, kidney and sweetbreads), anchovies, herring and mackerel are particularly high in purines, a substance which the body breaks down into uric acid.
• Reduce alcohol consumption: Alcohol can inhibit the excretion of uric acid via the kidneys and hence cause an acute attack of gout. When suffering a gout attack, it is best to avoid alcohol completely.
• Fluids: Adequate fluid intake is particularly important as fluids help dilute uric acid in blood and urine.
• Weight reduction: If overweight, weight loss can be helpful in lowering the risk of recurrent attacks of gout.
• Medication: Medication can be prescribed to lower blood levels of uric acid. These medications either decrease uric acid blood levels by increasing the excretion of uric acid into the urine (such as probenecid and sulfinpyrazone), or lower the blood uric acid level by preventing uric acid production (such as allopurinol).

Treatment for acute gout usually involves medication, prescribed according to health status and previous medical history. These can include Nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine or steroid medications such as prednisone. Elevating the inflamed joint and applying ice packs can be helpful to reduce pain and decrease inflammation. Patients should avoid medication containing aspirin, when possible, because aspirin prevents kidney excretion of uric acid.

More Information

• Arthritis Foundation on Gout
• National Center for Chronic Disease Prevention and Health Promotion
• National Institute of Arthritis and Muskuloskeletal and
  Skin Diseases

Scientific References

1. Stark K, Reinhard W, Neureuther K, Wiedmann S, et al. Association of common polymorphisms in GLUT9 gene with gout but not with coronary artery disease in a large case-control study.PLoS ONE. 2008 Apr 9;3
2. Vitart V, Rudan I, Hayward C, et al. SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout. Nat Genet. 2008 Apr;40(4):437-42. Epub 2008 Mar 9.
3. Wallace C, Newhouse SJ, Braund P, et al. Genome-wide association study identifies genes for biomarkers of cardiovascular disease: serum urate and dyslipidemia. Am J Hum Genet. 2008 Jan;82(1):139-49.
4. Döring A, Gieger C, Mehta D, Gohlke H, et al. SLC2A9 influences uric acid concentrations with pronounced sex-specific effects. Nat Genet. 2008 Apr;40(4):430-6. Epub 2008 Mar 9.
5. Li S, Sanna S, Maschio A, Busonero F, et al. The GLUT9 gene is associated with serum uric acid levels in Sardinia and Chianti cohorts. PLoS Genet. 2007 Nov;3(11): e194.
6. Dehghan A, Köttgen A, Yang Q, et al. Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study. Lancet. 2008 Sep 30.

This content was last reviewed on February 08, 2010.

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