Improving management of gout flares may require defying 'conventional wisdom'
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Reviewing old data and challenging conventional wisdom may yield benefits in managing gout flares, according to a presenter at the 2021 Congress of Clinical Rheumatology-West.
“Our gout patients are not getting adequately managed regardless of their chronic kidney disease,” Kenneth G. Saag, MD, of the University of Alabama at Birmingham, told attendees.
It is for this reason that Saag suggested that using all available options may yield benefit in treating flares. For example, “conventional wisdom” held that prednisone did not have efficacy in this setting, but Saag noted that the field has evolved. “What we have realized over the years is that it does work, but you have to use a bigger dose,” he said.
He noted that using prednisone at 30 mg to 35 mg daily can have similar efficacy in controlling gout flares as NSAIDs. But there is another reason to consider steroids. “I find in my practice, there are patients with contraindications to NSAIDs,” he said, highlighting chronic kidney disease, heart failure and hypertension as reasons to avoid indomethacin or naproxen.
Saag added, however, that complications can arise with long-term steroid use, and that a plan for tapering post-flare is essential to the efficacy of this approach.
There is a slightly different story for colchicine. There was some sense that a lower dose — 1.8 mg over the course of an hour — was not as effective as a dose of 4.8 mg delivered over 6 hours. In addition, diarrhea was seen as an inevitable complication with colchicine.
However, findings from the AGREE trial showed that while diarrhea is, in fact, a concern, the lower dose could be as effective as the higher dose in controlling gout flares.
If there is a caveat, it is that colchicine could be associated with myopathy in some patients, particularly those with chronic kidney disease, according to Saag.
Looking at data for the interleukin-1 inhibitor canakinumab (Ilaris, Novartis), Saag suggested that a 150 mg dose showed superior efficacy to triamcinolone 40 mg at controlling flares. “However, there were some safety concerns that the FDA had that did not lead to it getting approval for that indication,” he said.
Also in the IL-1 class, recent data showed similar outcomes for anakinra (Kineret, Sobi) when compared with triamcinolone. “It is nice to know we have a choice here with anakinra,” Saag said.
If there was one issue with this study, while the curves look the same, Saag noted that the trial was designed for superiority as opposed to non-inferiority. “That was the regulatory hurdle that needed to be crossed in order to get this drug over the finish line,” he said. “The drug has not moved forward for regulatory approval. While we use it off-label, it is not a drug that is likely ever going to be approved for gout.”
Despite this obstacle, the American College of Rheumatology included IL-1 inhibition as a possible strategy for managing gout flares in patients who are resistant or contraindicated to other approaches. “That is certainly our practice,” Saag said. “The train wrecks that we see in the hospital with bad gout flares and the big fluid shifts that occur in inpatient situations, that is a circumstance where we might consider IL-1 inhibition.”