As with most illnesses, effective treatment of gout depends on a correct diagnosis. Gout can be unequivocally diagnosed by telltale uric acid crystals in joint fluid. But appropriate treatment is often started after a "clinical" diagnosis based on painfully obvious signs and symptoms and other relevant factors, such as the patient’s:
- uric acid levels
- alcohol use
If this picture adds up to a strong suspicion of gout, treatment can be started with the immediate goal of arresting the acute attack
Acute gout is treated with drugs that block the inflammatory reaction. One of the oldest agents known to be effective against acute gout is colchicine, which comes from a common European plant, the autumn crocus, and is marketed in this country primarily as a generic drug. An English clergyman, Sidney Smith, said a century and a half ago that he had only to go into his garden and hold out his gouty toe to the plant to obtain a prompt cure. This may have been an exaggeration, but a rapid response to colchicine suggests that the patient does indeed have gout.
This old, powerful remedy is now used less often than it once was because it can be quite toxic, causing nausea, vomiting, diarrhea, and stomach cramps when taken by mouth and severe (even fatal) blood disorders when taken intravenously.
NSAIDs (nonsteroidal anti-inflammatory drugs)
Modern agents, specifically NSAIDs (nonsteroidal anti-inflammatory drugs) are highly effective against acute gout and less toxic than colchicine.
Steroid drugs, such as Deltasone (and other brands of prednisone) and Acthar (and other brands of adrenocorticotropic hormone), may be used if NSAIDs fail to control an acute attack. Steroids may be taken by mouth or by injection into the bloodstream or muscle.
Drug Treatment Approaches
Drug treatment usually relieves the symptoms of acute gout within 48 hours. Subsequent treatment, which may well be lifelong, is aimed at preventing further attacks by controlling uric acid in the blood—keeping it below concentrations at which crystals can form.
Two main drug treatment approaches are used, in some cases simultaneously.
One approach is to slow the rate at which the body produces uric acid.
Zyloprim (allopurinol) has been approved for the treatment of gout and is frequently prescribed for gout patients who have uric acid kidney stones or other kidney problems. Side effects include skin rash and upset stomach, both of which usually subside as the body becomes used to the drug. Zyloprim makes some patients drowsy, so they need to be cautious about driving or using machinery.
The other approach to controlling gout following an initial acute attack is to increase the amount of uric acid excreted in urine.
Two so-called uricosuric drugs commonly used for this are Benemid (probenecid) and Anturane (sulfinpyrazone), both approved by FDA for gout treatment. In addition to lowering blood uric acid levels, these drugs help dissolve deposits of uric acid crystals around joints and in other tissue. (Sulfinpyrazone is not currently available in the U.S.) Zyloprim is also used to dissolve tophaceous gout in uric acid over-producers. Uricosurics can cause nausea, stomach upset, headache, and a potentially serious skin rash.
Drugs to control uric acid levels may, paradoxically, prolong an acute attack. For this reason, Benemid, Anturane and Zyloprim are not used during the acute stage of gout. They may, in fact, induce gout flare-ups during the early part of long-term use. Accordingly, colchicine in a dose low enough to avoid toxic side effects is sometimes prescribed to prevent acute attacks during this phase of treatment.