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How Do Experts Treat Gout? Part 2

Oct 9, 2007
In an earlier article I discussed the aims of treatment and some of the pitfalls in treating gout. In this article I will discuss types of treatment.

Before jumping into the exact drugs used to treat gout, let's look at the metabolic pathway that explains why gout develops.

Foods that are high in purines (shell fish, red meat, beer, wine, etc.) are converted to hypoxanthine and then to xanthine. Xanthine is then transformed into uric acid. Patients who have a metabolic abnormality that causes them to produce an excessive amount of uric acid will have a big problem if the ingest a diet high in purines.

There are three major drug treatment strategies for gout:

* Uricosurics (these are drugs that cause patients to eliminate uric acid in the urine). Examples include probenecid, losartan, and fenofibrate). These drugs should be used in people who are under the age of 80 with normal kidney function, who are not already putting out more than 800 mgs of uric acid per day in their urine, and who are not kidney stone formers. Patients should be adequately hydrated and avoid aspirin doses higher than a baby aspirin per day because of potential drug interaction.

* Drugs that reduce urate formation. Medicines in this class block the conversion of hypoxanthine to xanthine and xanthine to uric acid. Examples include oxypurinol, febuxostat, and allopurinol. Of these only allopurinol is available for general use. This drug should be used for patients who cannot tolerate uricosuric drugs, who already put out more than 800 mgs of uric acid per 24 hours, who are stone formers, and who have chronic kidney disease. The dose of allopurinol can range from 100 mgs per day up to 800 mgs per day.

The most common dose used is 300 mgs per day. The problem is that this dose fails to get the blood uric acid to below 6 mg/dL, which is the ideal target, in more than 50 per cent of patients!

Other problems having to do with allopurinol:

o propensity for patients who are started on the drug to get acute attacks of gout,

o gastrointestinal side effects (elevated liver function tests being among the most common), drug interactions with other medicines such as azathioprine, ampicillin, and 6 MP),

o need for reduction in dosage in patients with abnormal kidney function,

o bone marrow toxic effects,

o life-threatening skin rashes,

o a peculiar hypersensitivity syndrome consisting of fever, rash, kidney and liver dysfunction, and elevated white blood cell count.

* Drugs that convert uric acid to allantoin. This is an extra step in the metabolic pathway of uric acid. By converting excess uric acid to allantoin, there is less uric acid available to cause gout. Examples include investigational drugs such as PEG uricase, rasburicase.

Unfortunately, many patients still either don't respond to current therapies or develop a side-effect. For patients intolerant to drug therapy, strategies that can be used include lifestyle modification (diet and alcohol reduction), allopurinol desensitization, and combining uricosuric drugs.

The role of diet should not be minimized. Foods high in purines should be removed from the diet. Alcohol (particularly beer and red wine) needs to be minimized. Anecdotal evidence supporting the role of fresh cherries and fresh cherry products are interesting and should be supported by further research. (Articles written by this author on both diet and gout and cherries and gout can be found elsewhere).

Another issue relates to non-compliance of the patient with their medical regimen. Factors that appear to be responsible include: lack of proper instruction, taking of multiple medications for other diseases, development of attacks during the early part of treatment leading to discouragement, and so on.

There is an obvious need for more effective medicines to treat gout. As mentioned earlier, PEG-uricase, febuxostat, and rasburicase are currently in clinical trial testing and they show promise.

Until then, rheumatologists who see gout patients on a frequent basis should be the ones consulted as soon as possible.
About the Author
Nathan Wei, MD FACP FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland. He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine. For more info: Arthritis Treatment
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