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By Nathan Wei
Gout is one of the most common forms of arthritis. It is due to an inborn error of metabolism that causes people to overproduce uric acid. Uric acid then accumulates and leads to deposits of monosodium urate inside joints, kidneys, and other organ systems.
Because gout is so inflammatory, it causes painful attacks that over a period of years have the potential to create a tremendous amount of damage and destruction.
The treatment of gout revolves around two major goals. Stopping the acute attack and also preventing monosodium urate accumulation.
Acute attacks of gout can be treated with a number of different medications including low doses of colchicines, non-steroidal anti-inflammatory drugs (NSAIDS), and glucocorticoids (steroids) given either by mouth, by vein, or into the joint. It is generally not difficult to break an acute attack.
The big problem is when it comes to chronic attacks and chronic arthritis. Because it is important not only to help with the painful symptoms of arthritis but also to find away to lower the amount of uric acid in the system.
To date, only two primary drugs are available for reducing uric acid.
Probenecid works by making a person urinate out more uric acid. This drug has three drawbacks. The first is that if a patient is already putting out a lot of uric acid in the urine (and a doctor should check this with a 24 hour urine collection before starting a patient on probenecid), then the patient is at increased risk for developing kidney stones. The second issue with probenecid is that it works only in patients with relatively normal kidney function. The final problem is that if a patient has a lot of uric acid in their system and they have large collections (called tophi) in and around their joints, probenecid is not usually strong enough to have a beneficial effect. One other drawback is that probencid has some drug interaction with medicines such as penicillin.
The second drug that is used is allopurinol. This is a purine xanthine oxidase inhibitor which means it works by reducing the production of uric acid. While it works well for many patients, particularly those with tophaceous gout, there are many drawbacks. These include drug interactions with multiple medications as well as other potentially serious toxicities. Allopurinol causes severe skin rashes, liver and kidney damage, as well as bone marrow problems. Allergic reactions can cause death.
Therefore, there is an unmet clinical need for new gout treatments. Even when patients are given desensitization treatments to try and help them take allopurinol, these treatments often fail.
Unfortunately, other treatment options are relatively limited. To lower uric acid, removing contributing factors such as medications, where possible, can be useful. For example, thiazide diuretics are a common cause of elevated uric acid.
Alteration in diet can be beneficial, but compliance is often difficult for many patients.
Other medications with uric acid-lowering properties, such as losartan (Cozaar) and fenofibrate (Tricor), can be tried if there are no contraindications.
A drug currently in late-phase development, febuxostat, is a non-purine xanthine oxidase inhibitor that has shown promise in clinical trials but has not yet been approved for gout. It can be used in patients who are allergic to allopurinol.
PEG-uricase is another drug in development. It converts uric acid into allantoin, a substance that does not induce inflammation.
There is anecdotal evidence suggesting that IL-1 inhibitors, drugs that are currently being used for other inflammatory types of arthritis such as rheumatoid arthritis, may be effective in gouty arthritis, and this approach is currently under study.
Nonsteroidal anti-inflammatory drugs (NSAIDs), in addition to being used for acute attacks, are commonly used for the treatment of chronic arthritis.
Comorbid conditions commonly found among patients with gout, including hypertension and kidney disease, which in some cases contribute to the disease, can limit the use of NSAIDs in patients with gout, however.
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:
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