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TORONTO — Contrary to popular opinion — and some guidelines — nonsteroidal anti-inflammatory drugs (NSAIDs) may not always be contraindicated in patients with axial spondyloarthritis (axSpA) who have inflammatory bowel disease (IBD).

“The [gastrointestinal] guidelines tell us not to use NSAIDs, but I think there are some patients in whom we can,” Adam Mayer, MD, assistant professor of internal medicine and pediatrics, Hackensack Meridian School of Medicine, Nutley, New Jersey, told Medscape Medical News.

Mayer, whose research focuses on earlier detection and optimal treatment of axSpA in patients with IBD, discussed the management of such patients during the Spondyloarthritis Research and Treatment Network (SPARTAN) 2026 Annual Meeting.

About 10% of patients with axSpA have IBD. Clinicians generally prescribe agents in four drug classes — NSAIDs, TNF inhibitors (TNFi), interleukin-17 inhibitors, and JAK inhibitors (JAKi) — in patients with axSpA. But only two classes, TNFi and JAKi, are typically prescribed for those who also have IBD because of the perceived risk of worsening of IBD symptoms with the other drug classes, Mayer said.

He noted there are different classes of NSAIDs — selective COX-2 inhibitors and those that are nonselective in inhibiting COX-1 and COX-2 — and different phenotypes of IBD, the main ones being Crohn’s disease and ulcerative colitis (UC). He stressed these “are phenotypically very distinct disease subtypes.”

No Evidence of Risk in UC

Research shows there’s an increased risk for flares in patients with Crohn’s disease who are taking NSAIDs, “but there has never actually been evidence of risk in patients with ulcerative colitis,” Mayer said.

His study, published last month in Arthritis Care & Research, looked at almost 300,000 patients with IBD, including 80,000 who were prescribed an NSAID. In patients with Crohn’s disease who were taking NSAIDs, Mayer and colleagues found a significant increase in risk for severe IBD flares, measured as an IBD-related hospitalization, but this risk was not seen in patients with UC.

“The signal was similar for COX-2 selective NSAIDs and nonselective NSAIDs,” Mayer noted.

(Nonselective COX-2 inhibitors such as ibuprofen are available over the counter, whereas selective COX-2 inhibitors such as celecoxib are available only by prescription.)

But the impact on the gut may be better with selective agents, Mayer said. “In general, the GI side effect profile is much better for those compared to nonselective NSAIDs.”

The research supports use of a COX-2 selective inhibitor in patients with UC, “assuming it’s safe from a cardiovascular standpoint,” he added.

When using COX-2 selective inhibitors in patients with UC, Mayer suggested a “shorter duration and lowest dose possible” to accomplish the intended goal.

More Use of Combination Therapy

Clinicians “more and more” are using combination advanced disease-modifying antirheumatic drugs (DMARDs) that are immune-suppressive in complex cases, Mayer said.

In such cases, a first drug might work for some “domains,” for example, tendons, fingers, toes, etc., but not for others. “ You can then select a second drug to combine with that to hit those domains that are still active.”

This strategy, he added, involves considering efficacy across gut and joint manifestations, and avoiding agents that can worsen the other domain. He suggests clinicians “escalate or switch” medications based on response and phenotype and to always coordinate care with gastroenterologists.

Another of Mayer’s tips is to explore IL-23 inhibitors. He noted research suggests that for patients with Crohn’s disease who have failed a TNFi, IL-23 inhibitors (eg, guselkumab, risankizumab, and mirikizumab) appear to be superior to other biologic DMARDs.

IL-23 inhibitors address an upstream pathologic mechanism shared between psoriatic skin and joint diseases as well as IBD.

“The nice thing about IL-23 inhibitors is you don’t dose very frequently, so patients love them,” Mayer said. “The dosing could be every 4 weeks, sometimes every 8 or 12 weeks, depending on the indication.”

These drugs also have “very minimal side effects”, he added. “They have a pretty good infection risk profile, especially when you look at some of the other immunosuppressing DMARDs that we use.”

Future treatment strategies might involve “more aggressive upfront therapy, which could modify long-term disease outcomes,” instead of the current approach of switching agents one by one if they don’t work, he said.

Elsewhere in the same meeting session, Patricia Remalante-Rayco, MD, a PhD student at the University of Toronto and clinical research fellow at the University Health Network’s Schroeder Arthritis Institute, both in Toronto, elaborated on the common gut-joint overlap in axSpA.

She said, the relationship between axSpA and IBD is likely bidirectional. And she noted research showing axSpA plus IBD appears distinct, but no more severe, compared to axSpA alone.

Does IBD Change AxSpA Outcomes?

An ongoing question has been whether having IBD changes axSpA outcomes. Remalante-Rayco referred to a recent study she conducted with her colleagues that found IBD does not confer higher disease activity or greater radiographic progression in axSpA.

She agreed that Individual treatment decisions should be guided by active disease domains. And she suggested that future research should consider the impact of IBD severity and duration.

Mayer disclosed having financial relationships with Med Learning Group, the Centers for Medicare & Medicaid Services, AbbVie, and Kyowa Kirin.