Uric acid medical condition gout
by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
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Information, in part, from the American College of Rheumatology
Gout is classified as either primary or secondary, occurring as a result of another underlying medical condition.
In both types of gout, between 70% and 95% of hyperuricemia cases are the result of underexcretion of uric acid, rather than uric acid over-production.
Many people develop hyperuricemia, however, not all people with hyperuricemia develop gout.
More than 99% of primary gout cases are referred to as idiopathic, meaning that the cause of the hyperuricemia cannot be determined. The cause is most likely due to a combination of hormonal and genetic factors that cause metabolic abnormalities resulting in overproduction of uric acid or reduced excretion of uric acid. Consumption of certain purine-rich foods and certain alcoholic beverages may also contribute to primary gout. The remaining 1% of primary gout cases are due to rare inherited enzyme defects that affect purine synthesis in the cells.
In secondary gout, hyperuricemia is caused by drug therapy or by medical conditions other than a metabolic disorder that increase uric acid concentration.
Alcohol use, especially beer consumption, is a major contributor to gout and increases uric acid levels in three ways:
• By providing an additional dietary source of purines (the compounds from which uric acid is formed).
• By intensifying the body’s production of uric acid.
• By interfering with the kidneys’ ability to excrete uric acid.
Hyperuricemia occurs in between 30% and 85% of people who have kidney insufficiency. Kidney insufficiency is a major cause of gout in older people. This results in an impaired ability of the kidneys to eliminate waste products, including uric acid, which then build up in the blood. This condition, in turn, can be the result of the following:
• Thiazide diuretics (the “fluid pills” used to control hypertension). These agents are very highly associated with gout. In fact, 75% of elderly-onset gout patients report the use of diuretics.
• Organ transplantation. Kidney transplantation poses a high risk for renal insufficiency and gout. In addition, other transplantation procedures, such as heart and liver, increase the risk. The procedure itself poses a risk. In addition, cyclosporine an immunosuppressive agents used after these procedures to help prevent rejection of the implant, poses a particular risk for gout. It also interacts with indomethacin, a commonly used gout anti-inflammatory drug. (Alternative agents for rejection, such as tacrolimus, may be effective and pose less of a risk of gout.)
The list of drugs that cause hyperuricemia is long. In addition to diuretics and immunosuppressants, other agents that increase the risk for gout include the following:
• Pyrazinamide (used to treat tuberculosis).
• Aspirin. Low doses (not high doses) of aspirin reduce uric acid excretion and increase the chance for hyperuricemia. This may be a problem for older people who take baby aspirin (81 mg) to protect against heart disease. (High doses have the opposite effect.)
Chronic occupational exposure to lead is associated with build-up of uric acid and a high incidence of gout. The old "moonshiners" had a high incidence of gout due to the lead in their stills. A 2002 study also suggested that persistent low-level exposure to lead may also increase the risk for gout.
A number of other conditions can cause gout. They include the following:
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