Gout Causes, Diagnosis, Symptoms, Treatment and Information on MedicineNet.com

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Gout (cont.)

How is gout treated?

There are two key concepts essential to treating gout. First, it is critical to stop the acute inflammation of joints affected by gouty arthritis. Second, it is important to address the long-term management of the disease in order to prevent future gouty arthritis attacks and shrink gouty tophi crystal deposits.

The treatment of an acute attack of gouty arthritis involves measures and medications that reduce inflammation. Preventing future acute gout attacks is equally as important as treating the acute arthritis. Prevention of acute gout involves maintaining adequate fluid intake, weight reduction, dietary changes, reduction in alcohol consumption, and medications to lower the uric acid level in the blood (reduce hyperuricemia).

Maintaining adequate fluid intake helps prevent acute gout attacks. Adequate fluid intake also decreases the risk of kidney stone formation in patients with gout. Alcohol is known to have diuretic effects that can contribute to dehydration and precipitate acute gout attacks. Alcohol can also affect uric acid metabolism to cause hyperuricemia. Therefore, alcohol has two major effects that worsen gout by impeding (slowing down) the excretion of uric acid from the kidneys as well as by causing dehydration, both of which contribute to the precipitation of uric acid crystals in the joints.

Dietary changes can help reduce uric acid levels in the blood. Since purine chemicals are converted by the body into uric acid, purine-rich foods are avoided. Examples of foods rich in purines include shellfish and organ meats such as liver, brains, kidneys, and sweetbreads. Researchers have reported, in general, that meat or seafood consumption increases the risk of gout attacks, while dairy food consumption seemed to reduce the risk. Protein intake or purine-rich vegetable consumption was not associated with an increased risk of gout. Total alcohol intake was strongly associated with an increased risk of gout (beer and liquor were particularly strong factors). Fructose in soft drinks also increases the risk of gout.

Weight reduction can be helpful in lowering the risk of recurrent attacks of gout. This is best accomplished by reducing dietary fat and calorie intake, combined with a regular aerobic exercise program.

There are three aspects to the treatment of gout with medications. First, pain relievers such as acetaminophen (Tylenol) or other more potent analgesics are used to manage pain. Secondly, antiinflammatory agents such as nonsteroidal antiinflammatory drugs (NSAIDS), colchicine, and corticosteroids are used to decrease joint inflammation. Finally, medications are considered for managing the chronic underlying metabolic derangement that causes hyperuricemia and gout. This means treating the elevated levels of uric acid in the blood with medications that reduce these levels.

NSAIDS such as indomethacin (Indocin) and naproxen (Naprosyn) are effective antiinflammatory medications for acute gout. These medications are tapered after the arthritis resolves. Common side effects of NSAIDS include irritation of the gastrointestinal system, ulceration of the stomach and intestines, and even intestinal bleeding. Patients who have a history of allergy to aspirin or nasal polyps should avoid NSAIDS because of the risk of an intense allergic (anaphylactic) reaction. Colchicine for acute gout is administered by mouth to reduce inflammation as well as to prevent gouty arthritis attacks while correcting hyperuricemia with medications such as allopurinol (Zyloprim) or febuxostat (Uloric). For acute attacks, it is given hourly or every two hours until there is significant improvement in pain or the patient develops gastrointestinal side effects such as severe diarrhea. For prevention, it is given once or twice daily. Other common side effects of colchicine include nausea and vomiting.

Corticosteroids such as prednisone, given in short courses, are powerful antiinflammatory agents for treating acute gout. They can be administered orally or injected directly into the inflamed joint. Corticosteroids can be prescribed to patients who have accompanying kidney, liver, or gastrointestinal problems. Long-term chronic use of corticosteroids is discouraged because of serious long-term side effects.

In addition to medications for acute gout attacks, other drugs can be taken over prolonged periods to lower blood uric acid levels. Lowering blood uric acid levels reduces the risk of recurrent attacks of arthritis, kidney stones, and kidney disease, and also slowly dissolves hard tophi deposits. Medicines used to lower blood uric acid level work either by increasing the kidney's excretion of uric acid or by decreasing the body's production of uric acid from the purines in foods. These medicines are generally not started until after the inflammation from acute gouty arthritis has subsided because they can worsen the attack. If they are already being taken prior to the attack, they are continued and only adjusted after the attack has resolved.

Probenecid (Benemid) and sulfinpyrazone (Anturane) are medications that are commonly used to decrease uric acid blood levels by increasing the excretion of uric acid into the urine. Since these drugs can, in rare instances, cause kidney stones, they should be avoided by those patients with a history of kidney stones. These medications should be taken with plenty of fluid so as to promote the rapid passage of uric acid out of the urinary system in order to prevent kidney stone formation.

Allopurinol lowers the blood uric acid level by preventing uric acid production. It actually blocks the metabolic conversion from purines in foods to uric acid. This medication is used with caution in patients with poor kidney function, as they are at a particular risk of developing side effects, including severe rash and liver damage.

Febuxostat was approved by the U.S. Food and Drug Administration (FDA) for the chronic management of hyperuricemia from gout in 2009. Febuxostat has been shown to be more effective than allopurinol in preventing acute attacks of gouty arthritis and is effective in shrinking tophi deposits of uric acid in the tissues such as the fingers, elbows, and ears. Because febuxostat is not significantly metabolized by the kidneys, it may have advantages over allopurinol in patients with underlying kidney disease. While taking febuxostat, patients have uric acid and liver function blood tests monitored regularly.

Again, uric acid-lowering medications such as allopurinol and febuxostat are generally not started in patients who are having acute attacks of gout. These medications, when started during an acute attack, actually can worsen the acute inflammation. Therefore, uric acid-lowering drugs are usually instituted only after complete resolution of the acute arthritis attacks, but if patients are already taking these medications, they are maintained at the same doses during the acute attacks. In some patients, increasing the dose of uric acid-lowering medications can precipitate gout attacks. In these patients, low doses of colchicine can be given to prevent the precipitation of acute gout.

Home remedies which can alleviate the symptoms of acute gout include resting and elevating the inflamed joint. Ice-pack applications can be helpful to reduce pain and decrease inflammation. Patients should avoid aspirin-containing medications, when possible, because aspirin prevents kidney excretion of uric acid.