Gout is a particularly painful form of arthritis triggered by an accumulation of uric acid crystals in your joints. Uric acid, a byproduct of the day-to-day recycling of cells in your tissues, is normally eliminated in your urine and bowel movements. Any condition that increases your blood level of uric acid, such as cancer chemotherapy or kidney disease, can increase your risk for an acute “flare” of gout. Nonsteroidal antiinflammatory drugs, corticosteroids and colchicine are most commonly used to treat acute gout.
When uric acid crystals accumulate in a joint, they generate an intense inflammatory response that is driven by immune cells emerging from the joint lining and the surrounding bloodstream. As these cells enter your joint, they release inflammatory compounds that dilate blood vessels, recruit additional immune cells and stimulate pain messages in nearby nerves. Among these inflammatory compounds are substances manufactured from arachidonic acid, which is a fatty acid normally found in your tissues. Nonsteroidal antiinflammatory drugs, such as indomethacin (Indocin), sulindac (Clinoril), naproxen (Naprosyn, Aleve) or ibuprofen (Advil, Motrin), prevent the conversion of arachidonic acid, quelling one arm of the inflammatory response.
Your own immune cells are the instigators of the inflammatory response that characterizes gout. Calming these cells’ activity is a principal goal of managing an acute episode of gout. Corticosteroids, such as prednisone, triamcinolone (Kenalog) or methylprednisolone (Depo-Medrol), act in a general fashion to reduce the activity of immune cells. Prednisone, which is administered orally, is typically started at moderately high doses for 2 to 3 days and is then tapered over the next 10 to 14 days. Methylprednisolone or triamcinolone can be injected into a muscle or directly into an inflamed joint.
Stabilizing Immune Cells
In an effort to isolate the uric acid crystals in a joint, your immune cells engulf them just as they would any other foreign invader. Once the crystals are consumed, your cells attempt to destroy them by enclosing them in lysosomes, which are packets of digestive enzymes that are typically used to destroy bacteria. But uric acid crystals damage the membranes of the lysosomes, leading to release of the digestive enzymes and the cells’ death. This process simply heightens the inflammatory response within your joint. Colchicine (Colcrys), a drug originally derived from the autumn crocus, suppresses a gout attack through a variety of mechanisms. According to a 2012 review in “Therapeutic Advances in Chronic Disease,” colchicine’s principal action is to prevent the union of ingested uric acid crystals with lysosomes, which prevents immune cell death and the “dumping” of digestive enzymes into the joint space.
Acute gout is extremely painful, and it may take 1 or 2 says for nonsteroidal antiinflammatory drugs, corticosteroids or colchicine to take effect. In the meantime, your doctor may prescribe narcotic painkillers to control your discomfort. Ice packs are helpful, but applying them to an acutely inflamed joint may be difficult. Newer agents, such as anakinra (Kineret), which target specific inflammatory chemicals produced by immune cells, may be useful for those who cannot take more commonly used drugs. These medications have not yet been licensed for use in people with gout, but doctors are allowed to prescribe them for the condition if they deem it appropriate.
Like all medications, the drugs used for treating acute gout may cause side effects. Nonsteroidal antiinflammatory drugs can cause stomach ulcers and fluid retention, and they may aggravate kidney, liver and heart disease. Corticosteroids -- even those injected directly into a joint -- can increase your risk for infections and elevate your blood glucose level. Colchicine commonly causes nausea, abdominal pain and diarrhea, and it can worsen kidney and liver disease, suppress bone marrow function and injure your muscles and nerves. Your doctor, who is familiar with your medical history, will determine the best treatment for you.
- Clinical Interventions in Aging: Management of Hyperuricemia in Gout: Focus on Febuxostat
- Arthritis Research & Therapy: Gout. Mechanisms of Inflammation in Gout
- American Family Physician: Gout: An Update
- Therapeutic Advances in Chronic Disease: Latest Evidence on Gout Management: What the Clinician Needs to Know
- International Journal of Nephrology and Renovascular Disease: New and Improved Strategies for the Treatment of Gout
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