EULAR 2026 Daily Podcast Day 1a Save

You're listening to a RheumNow podcast coming to you from London in EULAR 2026. Enjoy. Hi, everyone. Welcome to EULAR 2026. I'm in London.

We're gonna do a little preview of the meeting that starts tomorrow, Wednesday, and, we've been over the program, there's a lot of really exciting stuff. I'll just give you some highlights of things I'm gonna be looking forward to, things that I think are maybe game changing in rheumatology. Two late breakers, actually there's a bunch of late breakers that come to mind. The Be Bold data is going to be presented by Joan Marola on Saturday. There are other late breakers that also look really, really good.

I like the, Jack Spare study, that's, LB005. This is a, phase three trial of baricitinib, given to people with early PMR. They have less than three weeks. It's a 46 patient study, it's not a big study, but they, either get Barrie four milligrams or placebo for sixteen weeks, and then part two, they either continue or they crossover. The primary endpoint is glucocorticoid free remission, and Barry is a clear cut winner.

And it's not surprising that a JAK inhibitor would work, there's a lot of other data out there about other JAK inhibitors working, in polymyalgia rheumatic, and I think it will be, something we'll see more of in the future. Another really important abstract that's coming up, as part of the late breakers is a long awaited study as a follow-up to oral surveillance, where we found out that JAK inhibitors don't do as well as TNF inhibitors when it comes to cardiovascular outcomes and cancer and infection in high risk individuals. The follow-up to that, another big study, not with tofacitinib but with baricitinib, was a regulatory commitment by Lilly to study baricitinib and its venous thromboembolic risk. So, they set up many years ago these studies called RA Bridge and RA Branch, it's baricitinib versus TNF inhibitors in over, three thousand five hundred patients who have risk factors for, VTE events, DVT, PE, and so we're talking there age, BMI, are the main risk factors on having had a prior event. And the bottom line on that study is that it confirmed what we already knew.

Baricitinib was the first of the JAK inhibitors to be, labeled, and right out of the gate, labeled with a VTE risk and warning, and this study confirms it, but interestingly, again, another high risk population, they were average age around 60, but it did not show, the study did not show that baricitinib compared to, a TNF inhibitor was associated with either a risk of, cardiovascular MACE events, cancer events, or, it did show infection, serious infectious events, but did not show an increased risk of, opportunistic infection. So, in some ways it argues against the data for the oral surveillance study, but those are two very important studies that I think will be coming up this week as late breakers. There's a lot of data that I'm going to be covering with my colleagues on, ILD. The bottom line there is it looks like all the risk factors everyone's saying, suggest, yeah, risk factors for ILD in RA is being male, being older, being seropositive, throw in their smoking, throw in their disease activity, and now you've got the profile. The question is, who needs to be screened?

There are a number of studies here this week that look at that issue and they all say the same thing. ACR guidelines says you need to have one risk factor, the, ERS, UR guidelines from last year say you need to have two risk factors, but the bottom line is that almost all RA patients have one or two of these risk factors. Does that mean you do high risk CT in everyone? Well, that remains to be seen. I like this report, it's going to be, an oral presentation maybe tomorrow, on, it's called the Sun Star Study, and it is a head to head study of, tocilizumab or abatacid after someone fails a biologic or targeted synthetic, and turns out in this study ninety five, ninety six percent of people were TNF inhibitor failures, and it looked like there was no real difference except for when you do the analysis a new way, a different way, there was an edge for tocilizumab, but we need to cover that to see where that's gonna go.

Other things, there are a lot of studies that have been recently published that are going to get big airtime at this meeting. The Together PSA study, that's the combination of, of tirazepatide and the IL-seventeen inhibitor, ixekizumab, that data is going to be presented in full here, the AFFINITY study of, with golimumab, the, what else? There's another one that's out there that's going to be presented, again, but I like this, data on, there's going be follow-up data. There's a lot of CAR T cell therapies and B cell depletion therapies, and everybody's excited about it except for me, because one, we're a long ways off from seeing CAR T cell in the clinic Two, I'm not seeing studies that are of good controls and are blinded. I'm seeing, you know, twelve people with Munchausen syndrome getting CAR T and being cured.

I'm making that up, that's a joke. But it looks very good, as you would imagine in lupus, and, somewhat good in, scleroderma, maybe not so good in the synthetase myositis patients, and a big question about what it's going to do in RA. The early report on the what's going to be presented here is a small study showing that not everybody gets better but a few people do, and the question is who are they and why are they getting better? The Neptunus study, in Sjogren's syndrome, there'll be a number of Sjogren's presentations. Neptunus was presented at ACR, that's, enalumab showing its success, now they have some long term data that they're gonna, look at, they have teletacept in Sjogren's, it's also gonna be presented here, and what else?

An anifrolumab study with, Sjogren's. And then the, Phonics study was just recently presented, and that's going to be shown here as well, that seems to look good as far as the data goes. So anyway, this is how you can best follow EULAR when you're not in London with the few of us who are here. I think the best way depends on how you like to learn. The Twitter feed's gonna be active, the RheumNow faculty is gonna be out there, they're gonna do, you know, six, seven, 800 tweets, you can follow that.

There'll be daily recaps starting Thursday night. We're gonna do a day one, day two recap that will, play Thursday evening, probably 7PM, and then there'll be a day three recap on Friday and a day four, final day recap, on Saturday. The recap is where a few of the faculty and myself get together and say, what was great today and what do you want everyone to know about? There'll be great articles that you can follow on your phone and, on the website, and they'll come to you as emails. And the other way to follow is, to look at take the quiz at the end of the week.

Do the weekly quiz on this Saturday and next Saturday, and you'll learn just by doing 20 or 30 quiz questions about, what the take home message from the meeting was. Anyway, it's gonna be a fun time in London. Hopefully, you'll have fun listening to our coverage. Take care.

Hello. Welcome to At Room Now, our great coverage of EULAR twenty twenty six in London. And just to let everyone know, London had a heat wave. It's gone now. It's gonna rain every day.

There's a tube strike and the sun's not out. It's cold, but it's still a fun meeting. So I want to talk about strong treatment predictions in inflammatory myositis. So I think everyone's aware for many years we treated inflammatory myositis really going down an algorithm glucocorticoids, steroid sparing drugs like methotrexate, MMF or tacrolimus, and then more severe cases IVIG or rituximab and rarely cyclophosphamide. And let's be honest, all this stuff was off label.

Then there were some data of JAK inhibitors such as JAK1 tofacitinib, no RCT, but an observational study that could help both inflammatory myositis, but also helping calcinosis a bit. But we got a new kid on the block. So what am I gonna tell you about? It's a TYK2 JAK1 inhibitor. And if I don't say it right, please forgive me.

It's called Brepocidenib. And this drug has actually now had a publication of a positive phase three study. It's called the VALOR, VA LOR trial. And there are going to be two abstracts presented or are being presented at EULAR here. And the abstracts are poster two sixty four and oral presentation OP one six six.

So what did they learn? I think it's really important to understand that in this positive trial, it was inflammatory myositis that was dermatomyositis. So they looked at muscle and skin and they looked at steroid sparing potential. And in all cases, the active treatment was superior with about a double response on average in two forty one patients with dermatomyositis. So steroid tapering, better improvement on skin and on the muscle features that they looked at.

And they use various scores that you really don't need to go into. I think the bottom line is that it was positive. And then where I want to put this for you to understand is in a context. So there are a lot of studies going on in inflammatory myositis, the FcRn blockers. There's three of them in studies.

Then there's also other studies like interferon beta signaling with a drug called dazucibart. There's anifrelimumab, so interferon. And then there's the toll like receptor and patteron, which also is in positive phase two lupus study, it's in phase three. And then there's a whole bunch of other drugs. So I think the most important thing is we now have strong data to guide our treatment.

And I think that when we get these other results from other phase two and three studies, we're going to have a lot to offer our patients hopefully in the future on label. Keep following us. It's JanetBurdo, and you'll be hearing lots at ULAr twenty twenty six from the AtRoomNow crowd. Thank you.

Hello. My name is Rinalini Day. I'm a fellow rheumatology and internal medicine working in King's College London in The UK. And I'm delighted to be reporting from EULA twenty twenty six for RheumNow from here in London. And today, I would like to highlight one of the imaging abstract imaging abstracts being presented at EULA twenty twenty six, and this comes from the Mayo Clinic.

It's o p zero three four eight. So this work used advanced CT based body composition analysis to better understand how rheumatoid arthritis alters fat and muscle biology. So, we know from many prior studies, that body composition does change in rheumatoid arthritis, and most of these studies have relied on the use of BMI or DEXA scans, for example. But importantly, these approaches can miss important differences in where fat is distributed and how healthy muscle tissue, actually is. So here, the investigators analyzed, abdominal CT scans from almost 900 individuals using a validated deep learning segmentation approach, to quantify subcutaneous fat, visceral fat, intermuscular fat, muscle area, and muscle radio density.

The key finding from their study was that patients with rheumatoid arthritis had a very distinct body composition profile compared with matched non RA controls. So they had significantly more subcutaneous fat, more intermuscular adipose tissue, and essentially fat infiltration between muscle groups and lower muscle radio density, which is a marker of reduced muscle quality or myosteatosis. Now what is particularly interesting here is that overall skeletal muscle area and visceral fat were not significantly different. So, rheumatoid arthritis seems to be associated with a qualitative remodeling of muscle and fat tissue that conventional metrics like BMI, which we are so used to measuring, may completely actually fail to capture. And that matters because, clinically, intramuscular fat accumulation and myosteatosis are increasingly associated with frailty, disability, insulin resistance, and cardiovascular risk.

So this does have important implications for our rheumatoid arthritis patients, for the development of comorbidities, which, of course, we know that they are already presusceptible to. It may help explain why some patients with rheumatoid arthritis appear metabolically unhealthy despite having relatively normal body weight. Another important aspect is the imaging methodology itself. So the use of deep learning CT segmentation allowed detailed phenotyping, in this case, from routine clinical imaging, suggesting that opportunistic CT analysis could eventually become a scalable way to identify high risk metabolic and musculoskeletal phenotypes in people with rheumatoid arthritis. So overall, this study shifts that conversation away from simply looking at just obesity or sarcopenia, but towards understanding how chronic inflammation may fundamentally alter tissue composition and muscle quality in ways that are, very clinically meaningful.

So if you want to know more about this particular work, it is, it's OP0348, in the imaging abstract session. And if you'd like to know more about everything going on here at ULA twenty twenty six, do be sure to follow us along on room now. Hello, my name is Runaalini Day, I'm a fellow in rheumatology and internal medicine working in London in The UK, which is the home of EULA twenty twenty six, I'm very excited to say, and I am reporting for RheumNow. And this year at ULA, I'd like to highlight one of the abstracts which I'll be presenting, which is OP0220. So I'm delighted to be presenting data from a large and diverse study examining physical function and psychosocial health in systemic lupus erythematosus.

And this is going to be presented on Thursday morning in the abstract session, Doris and the Wolf, outcome measures in SLE. So what's so great about this study? So this study combined two major US lupus cohorts. So the APEAL cohort from Georgia and the CLUES cohort from California, and this gave us a total sample size of just over a thousand patients, so around four fifty from APEAL and five 80 from CLUES. Now, the key thing to note is that these cohorts do differ socio demographically.

So APEAL was predominantly composed of black individuals, while the CLUES cohort included larger proportions of Asian, Hispanic and white patients. And despite these differences, the findings which we were able to demonstrate were actually remarkably consistent between the two groups. So we wanted to understand what factors are associated with poorer physical functioning in lupus, not just disease activity or organ damage, which we will all be used to measuring in clinic, but also psychosocial and patient reported factors. So we measured physical function using the PROMISE physical function score, and we also measured fatigue, depression, stress, coping, resilience, self efficacy, and learned helplessness, all using validated patient reported outcome tools. And what we found was that fatigue and psychosocial health were very strongly linked to physical function.

So across both cohorts, higher fatigue, greater depression, and higher perceived stress were all associated with worse physical functioning. And conversely, patients with greater resilience, stronger coping and higher self efficacy reported significantly better physical functioning. Now interestingly, these relationships actually persisted even after adjusting for demographics, lupus damage, and disease activity. So the strongest associations within each cohort was that in appeal, severe fatigue appeared to be very strongly associated with impaired physical function, while includes depression and self efficacy were particularly strong in their relationships with physical functioning. Another key observation to note from this study is that adjusting for disease activity attenuated these associations more than adjusting for organ damage.

And this suggests that a patient's current symptom burden and psychosocial stress state and stress may influence day to day functioning more than the irreversible damage alone. So why is this all relevant? So this all reinforces that physical functioning in lupus is not explained just by inflammation and organ damage. Patient reported outcomes, particularly fatigue, mood, stress, and coping, they are clearly quite central to how a patient is able to function in day to day life. And importantly, many of these factors are potentially modifiable.

So if we want to improve outcomes that matter most to our patients, I believe that care in lupus has to therefore extend beyond controlling disease activity alone. And actually, perhaps there is an argument for integrating more psychosocial assessment and patient reported outcomes into routine care, which may be just as important as ensuring that our medications and immunosuppression strategies are equally good in improving quality of life and physical functioning. If you'd like to know more about this study, as I said, it's going to be presented on Thursday morning at the Congress in the Lupus Abstracts session, and it is also now published in a CNR journal. If you'd like to know more about everything that's going on here at ULA twenty twenty six, do be sure to follow us on RheumNow. Thank you for listening.