Philadelphia—An estimated 8.3 million adults in the United States have gout, and most don’t have the inflammatory arthritis well-controlled.

To help remedy that, the American College of Physicians (ACP) has developed a new evidence-based clinical practice guideline for the management of gout and published it recently in Annals of Internal Medicine.

The guidelines recommend that physicians should use corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), or colchicine to treat patients with acute gout. If colchicine is used, according to the ACP, it should be at a low dose, as evidence suggests that lower doses of colchicine are as effective as higher doses, but are associated with fewer gastrointestinal adverse effects.

Gout, one of the most common forms of inflammatory arthritis, is caused by excess uric-acid crystals accumulating in joint fluid, cartilage, bones, tendons, and other sites, which results in joint swelling and pain. However, the new guidance recommends against initiating long-term uric acid–lowering therapy in most patients after a first gout attack or in patients with infrequent attacks.

While the evidence supports the benefits of using uric acid–lowering therapy for shorter duration to reduce gout flares, the ACP advises, it says the benefits of long-term usage for 12 or more months in patients with either single or infrequent gout attacks have not been studied.

In cases of recurrent gout, meanwhile, guidelines suggest that physicians and patients discuss the benefits, harms, costs, and individual preferences before initiating uric acid–lowering therapy. Comparative effectiveness studies are recommended to evaluate the incremental benefits and harms of a treat-to-target strategy over a treat-to-avoid-symptoms strategy.

The ACP recommendations have generated some controversy, however.

The authors of an accompanying editorial question the lack of evidence to support a treat-to-target strategy, especially since the physiology of gout is well-known. They suggest instead that physicians should treat the underlying cause of gout—excess uric acid in the blood—with urate-lowering therapy.

“Further, not checking uric acid levels once starting treatment makes it impossible to know if patient symptoms are due to inadequate medication dosage, lack of adherence or some other reason,” commentator Tuhina Neogi, MD, PhD, professor of medicine at Boston University School of Medicine, stated in a press release. She recommended lowering uric acid to below the level at which it crystalizes in the blood (6.8 mg/dL), since it is this crystallization that leads to symptoms in gout.

The concern with the “treat-to-avoid-symptoms” approach, according to Neogi, is that it would encourage just treating flares of gout with anti-inflammatory therapies, which do not affect the underlying high uric acid levels that are causing gout in the first place. “That would be akin to treating patients with heart disease only when they experience angina, by using medication to alleviate those symptoms without treating the underlying disease process itself,” she explained.
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