Charlotte, NC—How many rheumatologists can say they can cure gout? Not many can confidently say so, according to an informal poll taken during the 2014 North Carolina Rheumatology Association annual meeting.
“The key in treating gout flares is that when you start therapy is more important than which agent you use,” stated Robert T. Keenan, MD, MPH, Assistant Professor of Medicine, Division of Rheumatology, Duke University School of Medicine. Other key factors in treatment include selecting an agent based on patient comorbidities; starting treatment as soon as possible; avoiding attacks at the earliest hint of a flare; and educating patients on the role of diet, risk of flares upon initiation of urate-lowering therapy (ULT), and adherence.
Risk Factors and Stages
Citing data analyzed from the Framingham Heart Study—a study that examined the relationship between risk factors and the incidence of gout in 2476 women and 1951 men over a 52-year period—Dr Keenan explained that higher levels of serum uric acid increase the risk of gout in a graded manner among women, but the rate increase is lower in men (Bhole V, et al. Arthritis Rheum. 2010; 62:1069-1076). In addition, he discussed the different stages of gout, including asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout, and chronic tophaceous gout. “[Intercritical gout] is a very important, underappreciated, stage of gout,” Dr Keenan stated. “This is really where, as you will see, a lot of destruction and joint damage occurs.”
All gout is tophaceous gout, he added. “In my mind—and this is where I differ with the guidelines—if you have 1 gout attack, you have trophaceous gout,” according to Dr Keenan. “Whether or not you see tophi or the patient has another attack in 5 years, if they have 1 attack, especially if it’s crystal-proven, then the patient has tophaceous gout.”
Taking a closer look at the American College of Rheumatology (ACR) guidelines for the management of acute and chronic gout, Dr Kennan suggests using a serum uric acid target level of <5.0 mg/dL for all of his patients, instead of the recommended target level of <6.0 mg/dL for most patients and <5.0 mg/dL in some populations. That way, he explained, there is room for patients if their diet fluctuates, for example. He also discusses the importance of patient education when continuing ULT during flares and prophylaxis against flares.
He cited the example of patients coming into his office concerned they were experiencing an allergic reaction to allopurinol because they experienced a flare, when in fact that is an indication that the therapy is working. “It boils down to education and making sure that the patient understands what to expect from their medication,” Dr Keenan stated.
When to start prophylaxis of acute gout is controversial. The ACR guidelines recommend starting 1 to 2 weeks prior to the initiation of ULT. “I usually start, depending on the patient, a week or 2 ahead,” he explained. Among agents used for acute gout prophylaxis, Dr Keenan spent some time discussing colchicine toxicity. “I have seen more people going to the emergency room due to colchicine toxicity than anything else,” he emphasized. Colchicine toxicity is associated with gastrointestinal events, bone marrow suppression, neuromyopathy, cardiac toxicity, liver toxicity, and rarely death.
“Gout is curable,” Dr Keenan emphasized. The first step in lowering a patient’s serum urate levels is through prevention, including education, changing diet and lifestyle, as well as controlling comorbidities. More patients then are being treated probably need ULT, he added. These patients have chronic kidney disease stage 2 or higher with 1 or more attacks, patients with clinically evident tophi, 2 more attacks in a 12 month period, and/or a history of urolithiasis.
Dr Kennan suggested that under treatment can lead to significant chronic gouty arthropathy and disability. ACR guidelines are just that, he reminded the audience, and individualized therapy should be used for patients to reach their appropriate serum urate goals.