Gout + heart damage

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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Patients with gout often have heart problems including high blood pressure, coronary artery disease, and congestive heart failure.

Hyperuricemia (elevated serum uric acid [SUA]), in fact, has been associated with a higher risk of death from these conditions. One 2001 study reported that disease activity in gout may contribute to elevated lipid levels.

Cozaar (losartan), an anti-hypertensive medicine may also have uric-acid lowering effects and thus may be useful for patients with gout who also have high blood pressure.

Researchers at the Johns Hopkins Children's Center report that allopurinol, a drug commonly used to treat gout, improved the heart function in mice with a rare form of heart disease. In the study, allopurinol was shown to delay the onset of damage, including heart failure.

"These findings are significant because we already know that allopurinol is a well-established, safe, and relatively inexpensive drug," said the study's lead author, Jennifer G. Duncan, M.D., a pediatric critical care medicine fellow at the Children's Center. "If these findings hold true in the human population, this may become an effective and economical method of treating patients with heart damage and heart failure."

Investigators created a mouse genetically altered to constantly produce abnormal troponin I protein, which has been shown in animal models to occur with an unusual condition called "cardiac stunning." Researchers noticed the stunned mice had elevated levels of xanthine oxidase, an enzyme that promotes oxidative stress. Elevated levels of xanthine oxidase also contribute to human heart failure. After one month of treatment with allopurinol, a xanthine oxidase inhibitor, the mice had normal xanthine oxidase levels and improved cardiac function.

In a second study, researchers from Iowa demonstrated that a drug used to treat gout - allopurinol - rapidly reversed the abnormal blood vessel constriction caused by smoking.

William G. Haynes, M. D., senior author of the allopurinol study and associate professor of internal medicine, University of Iowa College of Medicine, Iowa City, studied 14 heavy smokers aged 18 to 85 and 14 age- and sex-matched non-smoking volunteers. The subjects underwent tests to assess blood vessel functioning at baseline and after treatment. The subjects were randomized to receive either a single 600 mg oral dose of allopurinol or no drug on the day of the study.

At baseline smokers had impaired blood vessel function as measured by blood vessel dilation in response to the stimulant acetylcholine. A greater change in vessel dilation after acetylcholine indicates better endothelial function. The change in dilation produced by acetylcholine was significantly less in smokers (254 percent) than in non- smokers (390 percent). After taking allopurinol, smokers' response to acetylcholine improved to 463 percent, while non-smokers' response remained about the same (401 percent).

Allopurinol inhibits an enzyme called xanthine oxidase, which increases oxidative stress in the blood vessels.

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