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Future Looks Promising for Gout Sufferers
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Posted on: 11/30/1999
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Gout has been around for thousands of years. We know this from evidence seen in Egyptian mummies and written reports from ancient kings before the time of Christ. Although it is caused by a disorder of purine metabolism, it is often brought on by dietary excesses. In ancient days, only the wealthy could "afford" to have gout, but today, many more people (with access to the same foods) are affected.
Gout is a disease that involves the build-up of uric acid in the body. About 95 percent of gout patients are men. Most men are over 50 when gout first appears. Women generally don't develop gout until after menopause. But some people develop gout at a young age.
In gout, excess uric acid causes needle-shaped crystals to form in the synovial fluid of the joints. Synovial fluid is the fluid that the body produces to lubricate the joints. Uric acid is a normal chemical in the blood that comes from the breakdown of other chemicals in the body tissues.
The first symptom of gout is often a pain at the base of the big toe (the metatarsal phalangeal joint). The joint becomes swollen, warm, and red within eight to 12 hours. The attacks occur most often at night. Patients say the pain is so bad the joint can't even stand the slightest touch. Even the weight of a sheet causes excruciating pain. Walking and standing are almost impossible if the legs or feet are affected. Many patients have flu-like symptoms, including fever and chills. The pain may go away on its own in a few hours, or it may take a few weeks.
Gouty arthritis attacks come and go. There may be months between attacks. Over time the attacks happen more often, last longer, and involve more joints. Eventually the pain doesn't ever completely go away. The joints stay swollen and tender even between flare-ups, and the flare-ups start to happen every few weeks. Eventually, some patients develop tophi (visible crystals) on joints or pressure points and kidney stones.
We mentioned food in association with gout --what does food have to do with it? The breakdown of purines in the body releases uric acid. Purines are ingested through certain types of food such as sweetmeats (e.g., liver, kidney, brain, lunch meat, bacon, salami) and seafood. The increased intake of fructose-sweetened soft drinks has also been linked with an increased risk of gout. Alcohol (especially beer) also raises uric acid levels in the body and impairs the kidneys' ability to excrete the buildup.
Everyone has some uric acid in his blood. Usually the excess uric acid is then passed out of the body through the urine. As your immune system tries to get rid of the crystals, inflammation develops. For the person with too much uric acid, this inflammation can cause painful arthritis.
More than 90 percent of people with gout have kidneys that don't effectively get rid of uric acid. Sometimes this is caused by certain kinds of drugs, such as diuretics, cyclosporine, and low-dose aspirin. Other medical conditions, such as obesity, hypertension, and diabetes, can also make some people more likely to develop gout.
What can be done for those who suffer this disease? The first step is to make sure the person with painful joint symptoms has been properly diagnosed. Other joint diseases such as septic (infectious) arthritis or pseudogout can look like gout. In fact, it's possible to have both gout and one of these other joint problems.
An accurate diagnosis depends on removing fluid from the joint and examining it under a microscope. The presence of urate crystals is the "gold standard" for making the diagnosis. Other imaging studies may be ordered such as X-rays, ultrasound, CT scans or MRIs. Each of these tests offers a little piece of information that helps define the location, severity, and extent of disease.
In many cases, a change in diet is enough to resolve the symptoms and the patient never has another attack. But untreated acute attacks can become chronic (long-lasting) with joint inflammation leading to joint destruction. Besides the metatarsal phalangeal joint (big toe), the ankles, knees, elbows, and small joints of the fingers can be affected.
What happens if symptoms don't go away? The main goal of treating gout is to reduce the amount of urate in the blood. Joint crystals will not dissolve or go away unless the serum urate concentration is below six mg/dL.
Nonsteroidal antiinflammatory medications (NSAIDs) are used to combat the inflammatory process. Steroid-based anti-inflammatories called corticosteroids (oral by mouth or injected into the joint) can also be used to decrease swelling and relieve pain.
Another common medication that has been found effective with gout is called colchicine. Colchicine has an anti-inflammatory effect. It also inhibits urate crystal from forming deposits. Studies show that low-doses of this drug within 12 hours of an acute attack are very successful.
One other group of medications available to lower urate levels in the body is allopurinol. This drug is one of the serum uric acid (SUA)-lowering therapies. It works by inhibiting a substance called xanthine oxidase, which then reduces the production of urate.
Zyloprim is the brand name for allopurinol. Zyloprim does not take away the acute attacks of gout. But it is useful in preventing recurrence. Other allopurinol drugs on the market include Allohexal, Allosig, Progout, and Zyloric. As with all drugs, there are some patients who can't tolerate allopurinol. They develop an itchy skin rash, severe diarrhea, and fever.
What's new on the market for the pharmaceutical (drug) treatment of gout? New understanding of the exact mechanisms behind gout has led to the development of new agents for patients with refractory gout. Refractory means the symptoms won't go away and the condition has become chronic and unmanageable.
These new treatments called uricase therapy aren't available for use in the general public. They are just in the experimental stages. Drug companies are looking to find ways to use enzymes that convert uric acid into an acid that will be readily absorbed and passed out of the body. One of these enzymes is uricase. Humans don't have this enzyme naturally but other animals do. The use of pig and baboon uricase called pegloticase therapy is under investigation and pending FDA approval.
Some researchers are using medications already on the market but used for other problems. This practice is referred to as off-label use. One drug in particular (rasburicase) normally used to break down cancerous tumors has been tested. It seems to work but it is very expensive ($8000) per dose so that won't work if a patient is supposed to take it for a long time.
Right now uricase (biologic) therapy is an induction therapy, which means it is administered intravenously. Infusion reactions are holding things back a bit. At least 10 per cent of the patients receiving induction therapy experience severe adverse reactions including flushing, hives, low blood pressure, chest pain, and muscle cramping. It may be possible eventually to start with an intravenous dose, get the symptoms under control, and then switch to a pill form of the same medication to maintain results.
The future looks promising for gout sufferers. It seems certain that better understanding of purine metabolism will come to light in the very near future. Experts feel sure that it's only a matter of time before scientists hit upon a pharmaceutical "cure" for cases of gout that can't be managed otherwise with diet and exercise.
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References:
Preethi C. Kurakula, MD, and Robert T. Keenan, MD, MPH. Diagnosis and Management of Gout: An Update. In The Journal of Musculoskeletal Medicine. October 2010 Supplement. Pp. S13-S19.
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*Disclaimer:*The information contained herein is compiled from a variety of sources. It may not be complete or timely. It does not cover all diseases, physical conditions, ailments or treatments. The information should NOT be used in place of visit with your healthcare provider, nor should you disregard the advice of your health care provider because of any information you read in this topic. |
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