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Preventing and treating acute gout attacks across the clinical spectrum: A roundtable discussion

June 1, 2010|Cleveland Clinic Journal of Medicine
Brian F. Mandell, MD, PhD;N. Lawrence Edwards, MD;John S. Sundy, MD, PhD;Peter A. Simkin, MD;James C. Pile, MD, FACP, SFHM
Author and Disclosure Information

Brian F. Mandell, MD, PhD
Department of Rheumatic and Immunologic Disease, Cleveland Clinic, Cleveland, OH

N. Lawrence Edwards, MD
Division of Rheumatology and Clinical Rheumatology, University of Florida, Gainesville, FL

John S. Sundy, MD, PhD
Divisions of Rheumatology and Immunology and of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC

Peter A. Simkin, MD
Division of Rheumatology, University of Washington School of Medicine, Seattle, WA

James C. Pile, MD
Divisions of Hospital Medicine and Infectious Diseases, MetroHealth Medical Center, Cleveland, OH

Correspondence: Brian F. Mandell, MD, PhD, Center for Vasculitis Care and Research, Cleveland Clinic, 9500 Euclid Ave., NA10, Cleveland, OH 44195; mandelb@ccf.org

The authors reported the following relevant relationships with commerical interests: Dr. Mandell—consulting (one-time consultation) for URL Pharma and consulting and teaching/speaking (in a funded CME program) for Takeda Pharmaceuticals; Dr. Edwards—consulting for Takeda Pharmaceuticals and Savient Pharmaceuticals; Dr. Sundy—consulting for Alnara Pharmaceuticals, Anadys Pharmaceuticals, Ardea Biosciences, Regeneron Pharmaceuticals, and Savient Pharmaceuticals; contracted research (through Duke University Medical Center) for Ardea Biosciences, Genentech, Neopharm, Regeneron, and Savient; membership on advisory committee/review panel for Ardea Biosciences; and teaching and speaking for Takeda Pharmaceuticals; Dr. Simkin—membership on advisory committees for Novartis and URL Pharma; Dr. Pile—membership on advisory committee/review panel for Pfizer.

This article was developed from an audio transcript of a roundtable discussion convened at Cleveland Clinic on February 6, 2010. The transcript was edited by the Cleveland Clinic Journal of Medicine staff for clarity and conciseness, and was then reviewed, revised, and approved by each of the authors/panelists.

Each author/panelist received an honorarium for participating in the roundtable that formed the basis of this article (Dr. Mandell’s honorarium was donated to the Cleveland Clinic Internal Medicine Residency Research and Education Fund). The honoraria were paid by the Cleveland Clinic Journal of Medicine from the educational grant from URL Pharma, Inc. (Mutual Pharmaceutical Company) underwriting the supplement in which this article appears. URL Pharma had no input on the content of the roundtable or this article.

SHOULD WE INTRODUCE URATE-LOWERING THERAPY AT THE TIME OF AN ACUTE ATTACK?

Dr. Mandell: Let’s consider the patient who presents with a first or second or third attack of gout but is not yet being treated for the underlying hyperuricemia. Should we introduce urate-lowering therapy at the time of the attack? After all, it’s a moment of opportunity, as the patient is “captive” and needs to be treated for his or her pain, so should we use that as a chance to also start the urate-lowering therapy that will be needed? There seem to be two schools of thought on this question. One is that if we start urate-lowering therapy immediately and drop the urate, the attack is likely to last longer. The other is that as we drop the urate by starting uratelowering therapy, we’re already treating them very aggressively for inflammation, so it may be an acceptable time to introduce urate-lowering therapy. What are your individual approaches?

Dr. Edwards: I’ve heard that argument of “we have them here now, let’s get it started.” I’d counter that when you start on this course of urate lowering, you need a very close connection to the patient during the long period of dose adjustment. Both the patient and physician need to understand that clearly. I’ve seen too many cases of a bad flare turning into a terrible flare when urate-lowering therapy is started during an acute attack. Patients are unhappy and get turned off of the idea of reintroducing allopurinol or any other urate-lowering therapy. So I don’t use that approach. Instead, I try to optimize the conditions for initiating urate-lowering therapy to minimize the chance that patients will have a bad experience. There’s no reason to rush, since most patients presenting with their first few flares have been hyperuricemic for 30 years, with urate slowly accumulating and depositing around their bodies. I’d promote an approach of letting the acute attack resolve and then getting the uratelowering therapy started about a month later.

Dr. Simkin: My approach is along the same lines as Larry’s. We all encounter gouty patients who say, “I can’t take allopurinol.” When you ask why, the most common response is, “It makes my arthritis worse.” Patients must understand that this is a hump they have to get over; we need to do everything we can to lessen that hump, and that involves good prophylaxis. But it’s also essential to educate them to expect the hump and to forewarn and forearm them in terms of how they’ll cope with it.

Dr. Sundy: A common rationale for starting urate-lowering therapy during the acute attack is that the patient may not follow up and you’ve got them on hand for intervention right now. But if follow-up is that unlikely, urate-lowering therapy is not going to be successful in any case, since frequent monitoring and dose adjustments are needed over many months. The notion that a patient can just be put on 300 mg of allopurinol and check back in 6 months is unrealistic.

Dr. Mandell: It sounds like we’re unanimous on this. One other consideration I would add is that I will avoid adding more than one drug in a patient at the same time whenever I can, to avoid confusion about which drug is causing any side effects that may develop.

REFINING THE PARADIGM: ACUTE ATTACKS AS THE ENTRY POINT TO A PROGRESSIVE DISEASE

Dr. Mandell: So our recommendation to the hospitalist who’s confronting acute gout is to treat the acute attack, start the education process, and make sure the patient understands this is a chronic disease that you’re going to make better in the hospital but which requires lifelong attention to prevent flaring up again. At that point the recommendation is to refer the patient back to the primary care physician or a rheumatologist with the understanding that the underlying hyperuricemia needs to be addressed and that the patient should make sure that happens.

Dr. Sundy: This raises some interesting handoff issues. How do we best ensure that the physician who’s going to pick up responsibility for chronic management is aware of these issues and on board with the necessary patient education efforts? There’s clearly an opportunity for doctor-to-doctor education here as well.

Dr. Pile: Yes, this is a microcosm of what we deal with all the time in the hospitalist world—safe transitions of care and trying to avoid information “voltage drop” as patients return to the care of their usual physicians.

Dr. Simkin: I think our education of both our colleagues and our patients needs to emphasize that this is not only a chronic disease but a progressive disease.

Dr. Edwards: That’s a great point, and it raises the question of the stage in the disease process where we should start urate-lowering therapy—a question without a clear-cut answer. Three decades ago, the thinking was that you should do it before the patient transitioned from acute intermittent gout to a more chronic and advanced tophaceous gout because of how terrible those joints looked and how destructive advanced gout is. Yet the destruction begins much earlier than that, and changes probably occur within the joint even before a patient has his or her first gout attack. There are soft-tissue changes around the joint as monosodium urate crystals accumulate, and the effects on bone and cartilage are occurring throughout the period of acute intermittent gout if the serum urate level hasn’t been lowered. As we’ve come to recognize this, we’ve pushed the initiation of uratelowering therapy earlier and earlier. The standard recommendation now is to start it as soon as a patient has two gout attacks within a year. Since 60% of patients have their second attack within a year of their first, that means initiating urate-lowering therapy after the second attack for about 60% of patients. An even larger majority of patients will be at that stage to qualify for urate-lowering therapy within the first few years after their initial attack.

Dr. Mandell: This is a good place to conclude, with a reminder that the acute gout attack is just one part of a chronic and potentially progressive disease. Although the acute attack is what gets the patient’s attention—and often the physician’s attention as well—it is really just the entrance into therapy for gout, a chronic disease.

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