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.
Click here: Second Opinion Arthritis Treatment Kit
The most common anti-inflammatory drug, aspirin, has two potential effects on gout.
Gout is a metabolic condition characterized by abnormally elevated levels of uric acid in the blood, recurring attacks of joint inflammation (arthritis), deposits of uric acid in joints, and decreased kidney function and kidney stones.
While gout is often associated with an elevated blood uric acid level, serum uric acid levels can be normal during an acute attack. Also, many patients with elevated blood levels of uric acid (hyperuricemia) never develop gout.
Frequently, acute attacks are brought about by a rapid change of uric acid, either up or down.
Small doses of aspirin can increase the level of uric acid in the blood because aspirin can impair the excretion of uric acid from the kidneys. However, this change is typically only noted when aspirin is taken in the usual over-the-counter doses (two 325mg tablets every four to six hours).
Low dose aspirin (75-81mg per day), which is given, for heart attack or stroke prevention, should not significantly alter the level of uric acid in the blood. Furthermore, even the higher doses mentioned should only cause an attack of gout in a person who is at risk for an attack, not in an individual with normal metabolic function.
Aspirin has a very different effect when it is taken at very high doses. In very high doses, aspirin actually blocks the normal reabsorption of uric acid by the kidneys, thereby causing uric acid to be excreted in the urine and resulting in a lowering of the blood level of uric acid.
This was an effect that was noted initially in patients with rheumatoid arthritis who were being treated with high dose aspirin.
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