One of the most common forms of arthritis is gout. Gout is not a benign disease. It can lead to kidney failure. It also works together with other associated conditions such as elevated blood lipids, hypertension, diabetes, and obesity to cause significant morbidity and mortality. This article discusses general treatment concepts used by expert rheumatologists who treat gout(http://www.aocm.org)
An acute attack of gouty arthritis is an extremely painful experience. It is important to start appropriate therapy quickly in order to terminate it. This goal can be achieved with non-steroidal anti-inflammatory agents (NSAIDS), colchicine, or corticosteroids. The last drug can be administered orally, intramuscularly, or sometimes by injection directly into the inflamed joint(s).
Once the attack subsides, the next step is to lower the serum urate level below the limit of solubility- meaning the level at which crystals of urate deposit out in tissue- (i.e., below about 6.
0mg/dL). This step reduces recurrences, prevents further damage to end organs such as the kidney and joints, and begins to return the total body urate level to normal. This important goal can be achieved by two different groups of medicines. The first are the uricosuric agents (drugs that make a patient get rid of uric acid in the urine). An example is probenicid (Benemid). It is often administered as a combination tablet with colchicines (Colbenemid). The other category of anti-gout drug are the xanthine oxidase inhibitors (drugs that reduce the production of uric acid). Allopurinol (Zyloprim), a xanthine oxidase inhibitor, is the agent most commonly used, but it is a potentially toxic drug and side effects often require discontinuation. The most common side effect is rash although other side effects such as liver and bone marrow toxicity may be severe and even life-threatening.
Uric-acid lowering therapies should not be started during an acute attack since they can actually make that attack worse. When uric-acid lowering therapies are started they need to start low, go slow, and be accompanied by low dose colchicine for the first six months of therapy.
Febuxostat, a xanthine oxidase inhibitor, and pegylated uricase are new agents under development and may be helpful in these situations. Another consideration are co-morbid conditions which prevent the use of conventional treatments. Examples of co-morbid conditions that occur in gout patients include hypertension, diabetes, elevated blood lipids, and obesity. Alcohol and diet are also related to hyperuricemia (elevated blood uric acid) and acute gout. Recently beer, wine, and liquor were studied and the risk of gout varied according to the type of alcohol ingested. Recent data has shown that important dietary modifications may help in the treatment of gout. The role of protein ingestion, while still questioned, is not nearly the consideration it once was. The goal is to tailor medical regimens that directly prevent or reduce recurrent attacks of gouty arthritis. There are treatments for common comorbid conditions that may help with lowering serum urate levels. An example is losartan (Cozaar) which is used to treat hypertension but which also lowers serum uric acid. These recent findings may be particularly important for treating stubborn cases. Patient education remains a cornerstone to ensure compliance.
Dr. Wei 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 and consultant to the National Institutes of Health. He is a Fellow of the American College of Rheumatology and the American College of Physicians. For more info: Types of Arthritis
