The therapeutic landscape for polymyalgia rheumatica (PMR) has grown and will grow further, allowing prolonged use of glucocorticoids (GCs) to be minimized, Anisha B. Dua, MD, MPH, of Feinberg School of Medicine, Northwestern University, Chicago, said at the 2026 Rheumatology Winter Clinical Symposium (RWCS) in Maui, Hawaii.

“Do all PMR patients need to be treated with glucocorticoid monotherapy? No, we have options that have shown [and are showing in ongoing research] to have efficacy in both new-onset and relapsing PMR,” she said.

PMR, the most common inflammatory rheumatic condition in people older than 50 years, “still humiliates us. It’s still [largely] steroid dependent [with prednisone] used both diagnostically and therapeutically…and it’s still very much a diagnosis of vibes,” said Dua, director of the Vasculitis Center and professor of medicine (rheumatology) at Northwestern.

However, “we’re learning more,” she said. Two years ago, the FDA approved the interleukin (IL)-6 receptor inhibitor sarilumab for patients with PMR who have an inadequate response to GCs or intolerance of tapering, and research on other therapeutic mechanisms of action — such as IL-17 inhibition and JAK inhibition — is advancing.

“I’m excited about the mechanisms of action under investigation. And I’m excited there seems to be increasing awareness of this disease state generally…and a focus on recognizing gaps and unmet needs,” Dua said in an interview after the meeting, referring to needs such as identification of biomarkers, longer-term data on biologics, larger blinded randomized controlled trials, and patient access to specialist care and biologics.

Questions about “subclinical giant cell arteritis (GCA)” in PMR — chiefly whether to screen with imaging and how to respond to findings — are getting attention but thus far are largely unanswered, Dua noted at the meeting.

“Should we screen for large vessel involvement in all patients with PMR? Probably not,” she said. “We need validation of [current research findings] and blinded studies to determine the true prognosis of [subclinical GCA] and if treatment modifications change short- and/or long-term outcomes.”

‘A Lot of Improvisation,’ Dua’s Approach

Joint guidance issued in 2015 by the European League Against Rheumatism and the American College of Rheumatology recommends starting GCs at an oral prednisone equivalent of 12.5-25 mg/d and then tapering after improvement to 10 mg/d within 4-8 weeks. Once remission is achieved (following adjustments for relapses), tapering by 1 mg/d every 4 weeks is recommended.

“It’s a pretty wide range [of initial GC therapy]. We could use a lower dose if they have comorbidities [as recommended] or a higher dose if they have a more aggressive phenotype,” Dua said. “But what’s an aggressive phenotype? Female, high inflammatory markers, peripheral arthritis…. That’s most people with PMR.”

Her approach with most patients, she said, is “to essentially go down the middle and start with 15 mg/d” of oral prednisone equivalent. In her experience, most patients, she said, have improvement within a few days.

Relapses are “more the rule than the exception,” however, and “we do a lot of improvisation in treating these patients,” Dua said. Relapses occur without increases in erythrocyte sedimentation rate or C-reactive protein (CRP) in 20%-50% of cases and are especially common during GC tapers — particularly at doses < 5 mg/d.

Dua usually tapers the dose to 10 mg/d within 2 months and then to 2.5 mg — an amount that matches the size of each prednisone tablet — every 1-2 months until the patient reaches 5 mg/d. From there, she tapers the dose by 1 mg/d every month.

When patients relapse, she increases prednisone to the last effective dose for 1 month and tries again to taper. “And if that doesn’t work, I increase prednisone to the last effective dose and add sarilumab,” she shared. “So far I have not stopped sarilumab, but I have tapered off prednisone and dose-reduced the sarilumab.”

For patients who develop severe GC-related side effects or have sensitive comorbidities, “I try to taper glucocorticoids within 6 months and start sarilumab at the first clinical sign of relapse,” she said.

In real life, prolonged GC use has been prevalent, Dua said. A 2022 systematic review and meta-analysis of PMR management concluded that the pooled proportions of patients still taking GCs at 1, 2, and 5 years were 77%, 51%, and 25%, respectively.

“And patients are really upset with steroids. They comment on side effects, tolerability, inefficacy as they’re weaning their prednisone, and the comorbidity burden,” said Dua, referring to a recently published analysis of social media posts from patients in the US and Germany. In discussions of treatment, most patients were not happy and viewed steroids more negatively than biologics, she said.

Regarding the impact of steroids on patients’ quality of life, “posts covered the gamut —physical, emotional, social, functional, and financial,” Dua said. “And when you home in on the physical piece, they’re unable to walk, have pain and fatigue, and difficulty sleeping.”

IL-6 Inhibition and Other Mechanisms of Action, New European Guidance

IL-6 levels are elevated in patients with PMR than in healthy control individuals, and levels correlate with PMR disease activity. Persistently elevated levels are associated with the risk for future relapses, Dua said. Of the three phase 3 studies that tested IL-6 inhibition to treat PMR, two trials (SEMAPHORE and SAPHYR) studied patients with relapsing or refractory disease, and one (the SPARE trial) studied patients with new-onset disease.

Investigators of the 118-patient SAPHYR trial, which led to the approval of sarilumab, reported sustained remission at 52 weeks in 28% of patients randomly assigned to receive twice-monthly subcutaneous injections of sarilumab 200 mg along with a 14-week taper of GCs compared with 10% of patients receiving placebo every 2 weeks with a 52-week GC taper. The sarilumab group had significantly lower cumulative GC exposure and better GC Toxicity Index, Dua said. (Participants in the SAPHYR trial had flared on ≥ 7.5 mg/d of prednisone or equivalent during tapering.)

In the 100-patient SEMAPHORE trial, GC-refractory patients with PMR were randomly assigned to intravenous tocilizumab or placebo every 4 weeks for 24 weeks, combined with GC tapering. The primary endpoint — a CRP PMR-Activity Score < 10 along with a prednisone dose ≤ 5 mg/d or a decrease from baseline of ≥ 10 mg/d — was achieved in 67% of the tocilizumab group and 31.4% of the placebo group.

The smaller phase 2/3 SPARE trial randomly assigned patients with new-onset PMR to receive either subcutaneous tocilizumab (162 mg/wk) or placebo for 16 weeks, along with prednisone tapered from 20 mg/d to 0 over 11 weeks. The primary endpoint of GC-free remission at week 16 was achieved in significantly more patients on the biologic. These patients had a decreased cumulative GC dose and increased time to flare, Dua noted.

Interestingly, Dua said at the meeting, the upfront use of IL-6 receptor inhibitors with GCs in patients with major comorbidities or at high risk for GC-related adverse events is recommended in 2024 new guidelines issued by the French Society of Rheumatology and in 2024 updated guidelines from the German Society for Rheumatology and Clinical Immunology (along with Austrian and Swiss societies).

For patients not at high risk, both guidelines “suggest going ahead with the glucocorticoids and trying the regular taper and adding the IL-6 receptor inhibitor if that doesn’t work,” she said at the meeting. “One of the differences is that the French guidelines recommend methotrexate if the IL-6 inhibitors don’t work, and the German guidelines give the option of rituximab.”

“It makes sense that MTX [methotrexate] would fall after the use of IL-6 inhibition,” Dua said in the interview. But rituximab “is a strong immunosuppressive treatment, and I’d want to know more about the safety, risks, ideal dosing, and which patients it should be considered in.”

Dua said she awaits findings from the phase 3 REDUCE-PMR-1 and REDUCE-PMR-2 trials underway in Netherlands. The trials are looking, respectively, at the efficacy of rituximab vs placebo on GC-free remission at 52 weeks in newly diagnosed patients and in patients who relapse during a GC taper.

B cells have been implicated in the pathogenesis of PMR, and a proof-of-concept trial (BRIDGE-PMR) that randomly assigned patients to a single infusion of rituximab 1000 mg or placebo with a 17-week GC taper found 48% vs 21% (P =.049) in GC-free remission at 21 weeks. At 1 year after infusion, more patients in the rituximab group remained in GC-free remission, but the difference was no longer statistically significant.

“And a post hoc analysis suggested more efficacy in new-onset patients,” Dua said at the meeting.

Research on IL-17 inhibition has advanced, meanwhile, with the completion of the phase 3 international REPLENISH trial of secukinumab 300 mg (and 150 mg) or placebo every 4 weeks in combination with a 24-week GC taper. The results were recently reported at the International Vasculitis Workshop 2026 in Melbourne, Australia. At 52 weeks after starting therapy, 41.2% of patients in the 300-mg regimen group and 40.6% of patients in the 150-mg group had achieved sustained remission — defined as no recurrence of disease signs or symptoms from week 12 to week 52 — compared with 20.4% of patients in the placebo group.

JAK inhibition for PMR is also under investigation, Dua said. There are early data to support the use of tofacitinib from the EAST PMR trial and baricitinib from the BACHELOR trial. “But these are smaller trials,” she said. Findings “need to be replicated in larger trials with longer follow-up.”

Subclinical GCA in PMR

The relationship between PMR and GCA is well known: About half of the patients with GCA have features of PMR, and about 15% of patients with PMR will go on to develop GCA. Some experts have spoken “about the idea of a PMR-GCA spectrum,” and the concept of subclinical GCA is gaining attention, Dua said at the meeting.

Recent imaging studies have attempted to characterize subclinical GCA in PMR and define its prevalence. In one study using ultrasound in patients with newly diagnosed PMR, 23% had findings consistent with GCA without symptoms or signs suggestive of the vasculitis.

And in studies using PET, the pooled prevalence of subclinical GCA (evidence of large vessel inflammation with only PMR symptoms) was 29% in a systematic review and meta-analysis of individual patient data.

“Big questions” involve the clinical significance of such findings and whether screening is warranted. “And what do we do with the information?” Dua said. “Will more aggressive therapy prevent ischemic manifestations?”

Not enough is known at this point, she said. Asked at the RWCS session whether rheumatologists should think about subclinical GCA in patients who aren’t improving significantly on treatment, Dua said, “we do have to think about GCA and other disease processes, but we have yet to identify the group that would benefit from us noticing the subclinical GCA.”

“And I don’t think we know what to do with that information yet,” she said. “It would probably just [prompt us] to do what we’d do anyway, which is bump up the steroids.”

Dua disclosed consulting for AbbVie, Amgen, AstraZeneca, GSK, Novartis, Sanofi, and Zenas. She reported receiving research support from Amgen, Novartis, and the Rheumatology Research Foundation. She reported being a board member for the Rheumatology Research Foundation, Vasculitis Foundation, and Chicago Rheumatism Society.