As is true for many painful conditions, the first-line treatment for a gout attack is taking one of the nonsteroidal anti-inflammatory drugs (NSAIDs), such as diclofenac, ibuprofen, or indomethacin. For people who can't take NSAIDs, a drug called colchicine is an alternative. It's been used for centuries — maybe even longer — specifically for gout. The trouble with colchicine is its side effects, especially the copious diarrhea. If neither an NSAID nor colchicine is an option, then gout attacks can be treated with an oral corticosteroid, such as prednisone, or with corticosteroid injections into the joints.
For years, gout patients were told they had to follow a purine-restricted diet to stave off attacks, but those diets weren't very effective and people had a difficult time sticking to them. Now the easier-said-than-done advice is to lose weight, and also to cut back on alcohol, especially beer. Big meat and seafood eaters may be told to curb their appetites and instead eat more low-fat dairy foods. Diuretics tend to increase uric acid levels. If someone with gout is taking one, a doctor might explore lowering the dose or switching to a different medication.
But the most important fork in the road for gout sufferers is whether to start taking a drug that will lower their uric acid levels. Once people start taking these drugs, they usually must take them for the rest of their lives. Going on and off a uric acid–lowering medication can provoke gout attacks. Experts have differing opinions, but many agree that the criteria for starting therapy include frequent (say, three times a year) attacks, severe attacks that are difficult to control, gout with a history of kidney stones, or attacks that affect several joints. Another quirky aspect of gout is that uric acid–lowering medications can't be started during an attack because they can make the attack worse.
Allopurinol has emerged as the first-line uric acid–lowering drug because it needs to be taken only once a day and reduces uric acid levels regardless of whether the root problem is overproduction of uric acid or inadequate clearance by the kidneys. Sometimes people develop a mild rash when they start allopurinol, although rarely there's a dangerous allergic reaction. Guidelines warn against prescribing allopurinol for people with kidney disease, but if it's a mild case, the drug is usually well tolerated. Underdosing has long been a problem. The standard daily dose of allopurinol is 300 milligrams (mg), but that might not be enough to reach the commonly accepted target level for uric acid of 6 milligrams per deciliter (mg/dL). Most people can take doses of 400 mg (or even more) without any problems, although higher doses do mean taking extra pills.
A new drug, febuxostat (Uloric), is similar to allopurinol in the way it works. In head-to-head trials, febuxostat looked to be more effective than allopurinol at controlling uric acid levels, although that may have been because the allopurinol dose in the study was too low. As a new, brand-name drug, febuxostat is far more expensive than allopurinol.
Probenecid is a third choice. Like allopurinol, it's been on the market for decades, so it has a long track record. Probenecid works by increasing uric acid excretion by the kidneys so it can trigger the development of kidney stones and is not a good option for people with kidney problems. Another drawback to probenecid is that it has to be taken twice a day.
Perhaps the biggest problem with the uric acid–lowering therapy is sticking with it. A study done several years ago showed that over a two-year period, less than 20% of patients on allopurinol were taking it as prescribed. Poor adherence is understandable. Once people are taking gout prevention medicine, there are usually no immediate symptoms to remind them to take the pills daily. And the memory of the last attack is bound to fade, no matter how excruciating it might have been.
The Health Letter thanks Dr. Robert Shmerling for his help with this article. Dr. Shmerling is the clinical chief of the Division of Rheumatology at Beth Israel Deaconess Medical Center in Boston.