APLAR 2026: GRAPPA Session Covers Obesity, Axial PsA, and Emerging Treatments

So, hi everyone. Peter Nash reporting from APLAR in Seoul, Korea 2026. It's still freezing outside. Today we're going to talk about the GRAPPA session that was held. It had three speakers. Katie Le Young talked about obesity, a hot topic in PsA. And just like Jack had his whole obesity session, they had a summary of how obesity affects PsA. The second talk was a presentation trying to define axial PsA. They didn't quite get into whether you should have an argument whether it's axSpA with a rash or axial PsA is a separate entity. There's another talk today by Murat Torgulov who's going to talk about that topic. And lastly, Philip Mease talked about future therapies and the latest therapies in PsA.

So Katie Le Young showed some nice data. Again, data that we've now seen quite a lot, talking about the obesogenic environment, combination of processed foods, inadequate exercise, sleep deprivation, gut dysbiosis, and various medications such as antidepressants, which puts weight on people. She talked a little bit about how being obese drives PsA, blocks its therapy, and makes assessment even difficult. Then she started talking about the GLP-1s and then she started talking about the TOGETHER study where they combined tirzepatide with ixekizumab and compared it with ixekizumab alone, and the combined endpoint of ACR50 and 10% weight loss of course was in favor of the combination. But if you just look at the ACR50 and if you even looked at the components of the ACR — joint counts, patient global, physician global, etc., swollen and tender joints — it was all in favor of the combination. Because she also showed quite nicely that the GLP-1s actually have an anti-inflammatory effect, and that when fat is turned on, adipose tissue releases lots of cytokines — IL-6, TNF, etc. — so that it's an active organ that drives chronic inflammation, and that you can make a big difference if you treat that obesity, as we are now learning in PsA.

I was impressed by a study from a couple of ACRs ago from Canada where they looked at a bunch of diabetics, half of whom got reimbursed GLP-1 and the other half who didn't. And these people had autoimmune diseases — the ones we know and love — PsA, RA, lupus, etc. And there were over 11,000 patients. And if you happened to be on a GLP-1 and diabetic and have an autoimmune disease, having a GLP-1 agonist meant less death, less stroke, less heart attack. That's hard to argue with. And I encourage all my patients with a BMI over 30 to either fund their own or to get some reimbursed GLP-1 for six months or so, lose 15 kilos — which they're never going to be able to do any other way except bariatric surgery — and then fight to keep it off and stop or microdose and keep it going. But the other thing we've learned is you lose muscle as well as fat, and you need to do some gym work to keep the muscle bulk and not become sarcopenic.

So the second talk was by Mitsugu Nishimoto and he talked about axial involvement in PsA, and he was leading up to the AXIS study. The point of all that was that they were able to define, in the AXIS study, the incidence of axial involvement in PsA, and it was about 27% of patients. All the different features were clearly labeled — peripheral and psoriatic features. But they used imaging criteria to prove the diagnosis and allow people in to have the label of axial PsA. And the minute you do that, you start selecting for the typical axial phenotype — so more males, higher CRP, baseline axial involvement. And they came up with an ASAS graphic consensus definition of axial involvement in PsA, which is going to be validated. The prerequisite is that the patient has a diagnosis of psoriatic arthritis — and they use the CASPAR criteria, even though that's a classification criteria not a diagnostic criteria. They've got to start off with someone who you think clinically and on imaging and bloods etc. has PsA. And then there are four clinical features: chronic back pain, inflammatory back pain, good response to NSAIDs, and a positive B27 — and you have one of those plus one of the imaging features, which is SI joints showing radiographic sacroiliitis using the New York criteria, or an MRI indicative of axial involvement in the SI joints. And they made the point that often the SI joints are not involved but lumbar and cervical spine are, and so you need to look at the rest of the spine and the presence of structural damage on any X-ray or an MRI indicative of axial involvement in the spine. And if you use that as a definition — one clinical, one imaging — if you use that as your definition of axial PsA, you have a sensitivity of 89% and a specificity of 92%.

But guess what? That's exactly the phenotype that people sitting in a back pain clinic see — the B27-positive male with the CRP who has sacroiliitis, bilateral often — and that's very different to the form that we see sitting in a peripheral arthritis clinic, where it's very asymmetrical, where the B27 is only seen in half the patients, where they have a lot of cervical involvement, they have chunky syndesmophytes, they don't have symmetrical SI joint involvement. So it's a circular argument — these are two phenotypes of the same disease. Otherwise, we're going to have to have PsA dactylitis, PsA enthesitis, PsA uveitis, and claim it's different to axSpA dactylitis, axSpA enthesitis, axSpA uveitis. So it depends entirely on what genes you inherit and what cytokines you make, which of the two phenotypes you show. In the peripheral arthritis clinic, you see the peripheral arthritis phenotype. If you sit in an AS back pain clinic, you see the axSpA symmetrical high-B27-positive phenotype. But that's an argument that we can continue to have and people will either agree or disagree.

Then Philip Mease finished off by talking about some of the novel therapies. He discussed the BBOLD study, a head-to-head risankizumab versus bimekizumab, with the IL-17 inhibitor having a quicker onset of response, significant at the 16-week level for ACR50. The MDAs track pretty similarly — the depths of remission also — the IL-17 had a quicker onset of efficacy and they came together by 24 weeks, and the skin was clearly in favor of the IL-17, but they came together again at 24 weeks. The full 24-week data we'll see at ACR coming up very very shortly.

He talked about the nanobody sonelokimab, another IL-17A/F inhibitor. He talked a little bit about deucravacitinib, the POETYK studies PsA2, with nice data and clean safety. He talked about the other TYK2 on the horizon called zasocitinib — Z-A-S-O-C-I-T-I-N-I-B — one million times more specific for TYK2 than deucravacitinib. But we'll never see a head-to-head, and it's hard to know if being a million times more TYK2-specific gives you any better efficacy than deucravacitinib has.

He talked about icotrokinra, the oral IL-23 inhibitor in psoriasis published in the New England Journal of Medicine, and showed the plaque psoriasis data. The PsA study has finished and they've reported as a press release, but we'll see the data soon — probably at ACR — from the PsA studies. So that looks very interesting, and it will be interesting to see the PK/PD of that oral agent and how effective it is.

He talked about the TL1A medications, in particular telitacicept — which has not only an anti-inflammatory property but also has antifibrotic properties — and a lot of evidence now showing that resistance in different rheumatic diseases is driven by the fibroblast, which takes on initially an inflammatory phenotype and then turns into a fibrotic phenotype, leading to resistance to therapy. And if you can nip that in the bud and treat it at the inflammatory level, you might prevent some of the resistance we see that gives us a ceiling effect from most of our medications in PsA as well as rheumatoid.

And then finally, he mentioned the very intriguing TRBv9 autoreactive T-cells seen in axSpA, and the bispecific T-cell engagers that can now block that. The TRBv9 comes from the Russian studies in ankylosing spondylitis. These are a 4% T-cell clone that can drive disease. And it looks like you can eliminate that T-cell clone but leave all the other T-cell clones alone, and you're not causing great immune suppression. So it looks interesting. They're only in B27-positive people. I'm going to try and do a study in psoriatic arthritis and see — maybe half the patients are B27-positive or less — and we'll see if they carry TRBv9 and whether it has efficacy in that group of patients. So we're looking forward to that.

And he finished with talking about the vagus nerve stimulator in rheumatoid, and suggested it might be applicable in PsA. We initially got involved in some of the early studies where they implant this thing in the neck, and there were patients who had recurrent left field nerve palsies and local infection — and whenever you have a side effect in your own patient it's worth 100 in the literature — and I'm not particularly keen on taking that approach.

So that was the GRAPPA symposium in a nutshell. Obesity — the GLP-1 agonists should be in the water supply. The argument over axial PsA and how you define it — is it different to axSpA with a rash? And lastly, lots of interesting therapies on the horizon. How many IL-17 inhibitors do we need? And oral IL-23 looks very interesting, and the TYK2 inhibitors as well look very interesting. And then you can ask yourself where does that fit in the treatment algorithm between methotrexate and the parenteral biologics. So watch this space for more evidence on imaging, without methotrexate, etc. etc. So, Peter Nash signing off for RheumNow, Seoul, Korea, APLAR 2026. Thanks very much for your attention.