Clinical practice guideline for acute gout recommends corticosteroids, NSAIDs, low-dose colchicine
For diagnosis, a separate guideline recommended that physicians use synovial fluid analysis when clinical judgment indicates that diagnostic testing is necessary in patients with possible gout.
Physicians should use corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), or colchicine to treat patients with acute gout, according to a new clinical practice guideline.
If colchicine is used, it should be at a low dose, as evidence suggests that lower doses are as effective as higher ones but are associated with fewer gastrointestinal adverse effects, the guideline concluded.
The guideline also recommended against starting long-term uric acid-lowering therapy in most patients after a first gout attack or in patients with infrequent attacks. While evidence supports the benefits of using uric acid-lowering therapy for shorter duration to reduce gout flares, the benefits of using it for 12 or more months in patients with a single or infrequent gout attacks have not been studied, the guideline authors noted. In cases of recurrent gout, physicians and patients should discuss the benefits, harms, costs, and individual preferences before beginning uric acid-lowering therapy.
The guideline on management of acute gout was published online Nov. 1 by Annals of Internal Medicine. A guideline for diagnosing gout was published in the same issue.
For diagnosis, the guideline recommended that physicians use synovial fluid analysis when clinical judgment indicates that diagnostic testing is necessary in patients with possible gout. Misdiagnosis or delayed diagnosis of gout can result in unnecessary surgery, hospitalization, delays in adequate treatment such as antibiotics for septic joints, and unnecessary prescription of long-term treatment to patients, the guideline authors said.
The authors of an accompanying editorial questioned the lack of evidence to support the “treat-to-avoid-symptoms” strategy recommended by the management guideline and pointed out that the physiology of gout is well known. They suggested that physicians should additionally consider treating excess uric acid in the blood with urate-lowering therapy to prevent gout recurrence and more severe disease.
“With this strategy, providers might consider suppressive anti-inflammatory therapy or treatment of each flare as a sufficient strategy without addressing underlying hyperuricemia,” they wrote. “When patients never receive ULT [urate-lowering therapy] or receive inappropriately low doses, ongoing urate deposition occurs, leading to progression of tophaceous deposits, further joint damage, and functional limitations. At this stage, such patients need much more aggressive (and expensive) treatment than they would have if their serum urate level had been appropriately targeted early on.”
A second editorialist from ACP's Clinical Guidelines committee stressed the importance of evidence and outlined the criteria ACP follows to develop its recommendations. Evidence reviews supporting the management and diagnosis recommendations were also published.