Daily Recap Day 1 + 2 EULAR 2026 Save

You're listening to a RheumNow podcast coming to you from London in EULAR twenty twenty six. Enjoy. Hello, everyone. Welcome to EULAR twenty twenty six. We're all here in London and have had a busy day one and day two.

This program is our daily recap of highlights from the meeting as seen through the eyes of the four of us, the faculty who've been scouring the meeting for the interesting oral presentations and abstracts. The meeting started yesterday in the afternoon, another busy day today. So today's recap is a day one or day two, and the faculty get to choose what they want to present. We're gonna do our first round and then a shorter second round. So we'll cover at least eight abstracts in this.

I'm gonna begin by asking our faculty to introduce themselves. Jack Cush from Dallas, Texas. Bella?

Hi, I'm Bella Mehta from New York here in London looking at abstracts for EULAR.

Very good. Orly.

Hi, guys. This is Orly Naj from Scotland, and I'm live from London as well.

Live from London. Hi, Janet Pope. I'm from the other London in Ontario, Canada, but it is on the Thames.

That's a But cool little

I'm hearing the real one.

That's a cool little twist. She just only lectures in London, only teaches in London. And she's got a few of them to choose from. Okay, so let's begin with orally. What's one of your favorites from the first two days?

Yeah, so on the first day I went to this RA session and there was a lot of therapy, how do we treat, how do we manage new drugs and so on, but there was one abstract that caught my attention, OP zero two zero four actually was today, not yesterday, anyways. It's the back study and it's, you know, when we talk about shared decision making in RA, it's always qualitative study or you know, surveys and it's never really randomised or high level of evidence. So, this is why and I noticed this one and I wanted to report on it. It's was a randomized controlled trial where they were looking at two groups of people living with rheumatoid. One group of 50 people that were just assigned the first biologic based on standard of care, the the physician chooses or they were watching a three minute video.

So, it's not a super long education therapeutic education session. It's a three minute video that they watch and they get leaflets on the drug and then they to choose. Do they want a jack? In which case it was filgotinib? Or do they want a subcut TNF inhibitor?

And what's what's really interesting as well is that the way people choose, first of all, everyone was able to make a decision within forty eight hours and second of all, the way they choose was basically half and half. There was like 28 wanting the the Jack and 23 wanting the TNF. So, it's not like everyone wanted the oral drug. And what came out of this was that obviously if people get to choose their drug they're actually more happy. Not only they're more satisfied but also they experience less adverse events.

They're more likely to stay on the drug over time, so the retention is much better and they're less likely to switch drug. Why is that interesting? I think it is interesting because obviously it doesn't mean it works better, but what it means is that people are less likely to want to discontinue it if it's working, which I think is important. Obviously, there's one caveat in this study, which is they started recruiting before the oral surveillance results. So, at the time when they started, obviously, it was anyone could choose anything but then as the warnings appeared, then they had to obviously be much more careful with who they were suggesting filgotinib to.

But in any case, I think it is interesting because I don't think I often tell people, okay, you have all these options. Which one would you like? You know, we cannot direct them obviously based on comorbidities and all but I'm I'm I'm curious how I could inform my practice with this, you know, just a bit.

You know, I used to get accused in the clinic of tricking my patients or trying to trick them because I would give them three choices. And then they would say, Well, Doctor. Cush, why are giving me three choices? Because you yell at me if I don't choose number one. And it's sort of like, that's not really what the intention was, but I love this idea because when you do clinical trials, people get randomized to A arm, B arm, why not a C arm where patients get to choose?

Because when they choose, the story in their head is so much better and the buy in and the retention and adverse, I thought that was so cool. I think that this really should inform how we do clinical trials, but really, like you said, what are you gonna do in practice? So how could you do this in practice? Do you have to make video packages that you say, I'm gonna send it to you and watch it at home after they talk to you? That's one way.

I mean, we all give handouts. Sorry. Yeah.

No. Go ahead. No.

We all give something like handouts to read up, but I don't know. I think videos are so maybe a better way of communication sometimes.

Yeah. It's

It's I was just gonna say I have a bit of a different take on it because I thought that people willing to be randomized would be more likely to stay on something because they had a willingness to say, we don't know what's going to be better or we don't know what to choose, so I'll just try it out. So I thought they'd be more open minded and would stay on drug and finding that they're more apt to come off drug. I mean, trying to do clinical trials, it informs me a little bit that a parallel group might be important to look at what happens in the real world of those eligible who don't really get randomized. So I was actually a little bit surprised that it was very different and it was. But I think we have to remember if we're going to give handouts or inform patients, you can't give too many choices.

Like Jack, as you were saying, two choices, maybe a third one that they won't choose anyway, but too many choices, people get overwhelmed as well. So I thought it was actually a neat little study.

You know, maybe the answer, you know, Doctor. Cavanagh from Galway used to, played with a tool that he liked for a while that was where you could send a patient a recording after the visit and it would summarize what we did today and it was a nice way of doing the follow-up, but we don't have to do that in this era. AI can do this if you have ambient dictation and whatnot, and it's covering this, it can send a package of either audio and maybe even a video that could let patients make decisions afterwards. But yeah, I mean, this is probably the best example of shared decision making, is it not? Cool paper.

Bella, what do you have?

So I wanted to talk about the plenary on obesity and RMDs and the potential of GLP one agonist. So this was a plenary today talking about a lot of things, but why GLP-1s are important to rheumatologists. I think, you know, there's data that they are present on leukocytes, which sort of change the pro inflammatory cascade to the anti inflammatory cascade in terms of the cytokine profile, they're also present in the synovial fibroblast. So these receptors are present, which makes sense that a lot of my patients who are on GLP ones for many different reasons sometimes respond you know, some of their disease activity measures get better. You know?

And there's a abstract sort of going on with this is or or a recent study published talking about ezekumab for psoriatic arthritis along with tirzeparatide. So, again, these are studies that are gonna be coming in more and more, and you'll see that patients, especially metabolic syndrome plus some of the rheumatic diseases, we'll see much more uptake of these medications. And there's, like, so many indications that they're trying, especially osteoarthritis, things that we're gonna be treating. I have you know, again, there's a lot of patients that are on this. Six percent of The US population apparently has been exposed to this.

I I think the one thing that everybody always talks about with GLP ones is muscle loss and make sure you, you know, do exercise and resistance training and all that. The second thing that people are not talking as much about, I feel, is osteoporosis. And there was a abstract, o p zero one seven seven, talking about osteoporosis. It was, like, a huge dataset, TriNetX, but more importantly, looking at adults who are on GLP one and bisphosphonates and did a propensity match control with GLP one. Patients sorry.

Patients who are on bisphosphonates and not GLP one. And they were looking at sort of adverse effects of bisphosphonates, you know, hypoglycemia, femoral fractures, atypical femoral fractures, etcetera. And seems like they were not different. Again, it's a five year study looking at this, but more importantly, the fact that we don't know the actual incidence of osteoporosis on this drug, it needs to be highlighted and looked at because, you know, losing a dramatic amount of weight may cause that, and we need to be mindful with our patients. Yeah.

I I think it's an interesting drugs I mean, a set of drugs like GLP plus GIP. As you know, that's the second generation. There's third generation. Fourth generations coming in. And, we as rheumatologists are not using these medications right now as much, but I think in the next few years, we'll be sort of starting to combine some of them with as treatment strategies for our patients.

So it's important to get to know them.

Donna, what do you think?

So I have probably two comments. So I never even thought about the OP. I mean, we have patients say hospitalized that lose a lot of weight by starvation, they lose a lot of bone mass when they're lying around in bed. So I guess if someone's on a GLP-one losing weight, but exercising and eating healthy, who knows? One thing.

And then I think you're right about the indications. They'll go on and on. And of course, published in New England Journal was the Lilly IL-seventeen drug with the combo GLP-one plus GIP or the Lilly drug alone, so the ixekizumab. And it showed that it was better on, it was active PSA patients, that it was better in the active PSA being on the weight loss drug. I think the big question though is if you are normal weight and a non diabetic or slightly overweight but not meeting obesity criteria, will you also get bang for your buck on these drugs as I'll call them more anti inflammatory than weight loss losing some of the visceral fat or whatever other fat around our organ side is probably pro inflammatory.

I don't think we know that yet.

Yeah, go

ahead.

No. There are studies on the way, and I know the fact that these receptors are present in synovium, you know, things that we care about. We and there's some early data on how these drugs may change some of the inflammatory cytokine profiles even before significant weight loss happens. Right? Again, you know, these studies need to happen and will happen, but even with data on retrospective stuff, patients are on it for various reasons, and you can look up their outcomes.

Jack?

Yeah. The cardiovascular benefits are there even in the cardiac patients and in sleep apnea patients where there are indications here, and when the weight loss isn't all that great. Other interesting thing is that in people that don't have diabetes, their blood sugars don't change substantially. Go down a little bit, but nobody, hypoglycemia is quite uncommon, with this. But the muscle mass is a gigantic issue, I think.

And then there's all these weird things about blindness and whatever. It's going to be these small, fringe, serious adverse events that everyone's got to be expert at because even if you're not using them in the treatment of your rheumatic disease patient, everybody else is using them. And it's going to be on board. And there doesn't seem be any musculoskeletal or rheumatic adverse event associated with this. Although I've read that increases the risk of RA in some people, think that's a little goofy, but we'll see if that ever pans out.

But yeah, we need to talk more about this stuff because it's gonna be in the literature, it's gonna be all over the place and there's a lot of it here at this meeting. So Janet, what did you like from today or yesterday?

So right. So this one's from today. So the same session Orly was in. This is a head to head trial. So I picked it.

I like it because we're always asking for head to heads, and then we seem to not act on the data. So this was an investigator initiated trial from one country and it was an active rheumatoid arthritis. They were TNF inadequate responders and they were randomized to IL-six inhibition, so tocilizumab or abetacept. And the primary outcome was a change in C. Dye, so the Clinical Disease Activity Index at week twenty six.

So the first question is, was it supposed to be a non non inferiority? Like did they be about equal or was it supposed to be a superiority? And in quite honest I'm not sure but I kind of got a sense that they wondered if one would be superior to the other but I'm not really sure what was said that way. So the first.

They they said a priori that their experience before suggested tislelizumab might be better.

Correct. That's right. But they didn't really explain the stats, but that's what I wondered too. So number one, change in C. At twenty six weeks was equal.

So the graphs were fairly close. There was a little bit more reduction in C. Diffeye on tocilizumab, but it was basically equal. It was non inferior. Number two, two other important points because then you can interpret the trial however you want.

So they said if the patient was on monotherapy, tocilizumab was better than Avatacep. And that was a portion of the patients, maybe about a third. And that's no surprise to any of us. And then he didn't say because it wasn't really part of the study. But another question was, what about the retention?

So he also said retention was better on tocilizumab. So it was an intent to treat. So if you went off the drug you were randomized to, once randomized, always analyzed, and that's what you're supposed to do. So if you believe they're equal, they're equal by the C. I.

Change at twenty six weeks. If you have a belief system that one is better than the other, then you could say tocilizumab had better retention and was better in monotherapy. So I think it's yet another head to head where I don't know the take home message and whatever I believe before I'll continue to believe. However, good for them for doing it and to have an investigator initiated study to ask you a question post TNF that they found was valuable.

You know, the thing about this is that UR guidelines, which I really think are great on RA, have said, you know, you're one and done. When you use a class, you should move on with a class, as opposed to, you know, primary non responder, secondary responder, you know, changing your TNF inhibitors and staying just, know that you should move on. And it's data like this that proves a point. So these people had to fail a TNF inhibitor, ninety five percent, they let someone at the end, but ninety five percent failed a TNF inhibitor, and this showed that it worked. So if you looked at the graphs, it looked like they were the same, but does that mean it worked?

Then they had a mean or median C. Dye score of 24 going in. Quite high disease activity. Yeah, they were on the upper end of moderate and had other indications of severe disease, but the magnitude of change was 10 C. Di points or more.

And the fact was that they're both good alternatives for people failing a TNF inhibitor. And maybe Jenna's point about the monotherapy is what guides you.

Right, and I think the bottom line too is we can put it in the context that the AbbVie Group had recently looked at TNF to TNF, RCT and our active RA, or TNF to upadacitinib, and the idea was is TNF cycling okay or not, because people say they don't do it, but lots of people still TNF cycle NRA for various reasons. And what they found in that case is going other MOA that you had mentioned, Jack, going to another MOA was was superior. So I think, you know, we start gathering up these head to head and what to do next, but I think habit is strong and we end up doing what we believe or what we get easier access to, etcetera.

Okay, so my, first one I'm going talk about was another plenary from yesterday. It's the COMPARE trial OP008. This was CAR T cell therapy in, refractory seropositive rheumatoid arthritis patients. It's an open label, uncontrolled, six patient study. Now the form of CD19 CAR T cell therapy is under investigation.

They have another cohort that's currently being studied. These people were refractory and they had very active disease, they had, DAS 28 scores ranging from, I think it was 4.7 to 7.1. Most of them were really quite high. They failed really about five, six, seven prior biologic or targeted synthetic drugs. And they were all on a DMARD, and the DMARD was stopped.

They underwent, lymphocyte depletion with cyclophosphamide and fludarabine, And then they were given, one injection of this, CAR T cell, just out of respect, I should say the name of it, it's, MIV shortened to MIV CAL, cal, and then observe. And they all dropped their B cells, all of them got neutropenic. They all dropped their CCP and RF antibodies significantly. When you look at the, on one hand, the presenter said that they all achieved DAS remission, but it really wasn't quite that simple. Meaning that they all didn't like just drop like we saw in Gaylord Shetz's lupus trials, all parameters went to zero and stayed down for a long time.

That was magical. You know, here at the end of, by week 12, the ACR20 responses were 50%, ACR50 was thirty three percent. If you wanted to look at the maximum response, you had to go out to twelve months, when you're already having B cells and others coming back. So I thought this was revolutionary because people keep talking about CAR T cell as being the great savior in rheumatology, and I'm cautioning saying, you only have uncontrolled data in the worst possible cases. It's not a real scenario for most of us and our patients.

But we have to go through this step of drug development, phase one, phase two, and train wreck patients, showing safety as the primary outcome. The good news is safety data on CAR T cell and rheumatic disease has been good, but it looks great in lupus, it looks really promising in systemic sclerosis. And the question is, where does it stand in RA? I've heard rumblings and rumor. This is the first good data and I'd say it's encouraging, but we need more studies.

Orly we did you see this?

Yeah, yeah, no, I saw that. I think I fully agree with you. I think it also made me think about this OSA abstract where I think it was OP204 where they used this the T cell engager as well. I'd have to dig back to the name of the molecule but you know, it's like, it it looks like there's a whole bunch of data we get from SLE and from sugar and from systemic sclerosis where we think, oh my god, this is amazing and then we translate that into RA but we need to keep in mind the safety as well as it's not the same disease. So I'm not sure if I would put it anywhere in the management strategy of RA at all right now.

Yeah. Go ahead.

I mean, it's it's about how what risk would you take. Right? Like, for an RA patient versus a lupus patient whose kidneys are going off, like, how much risk you wanna take and what target do you have? Right? Like, this whole CAR T, I mean, sometimes it feels like, you know, every other disease is gonna be targeted with this, but we don't even know which exact cell is causing it.

There's subtypes of all these. And for the right subtype, there might be a right CAR. But if you if the subtype is all muddy, doing a B cell CAR for a T cell predominant patient, I I I don't know what's the right strategy for those.

So when you use CAR T in RA or, bites and T cell engagers and you don't get the same kind of thing you see in lupus, what is that telling you about the biology of RA? That it may not be as heavily B cell dependent, it may be more this orchestrated derangement of T and B cells together leading to the cytokine story and target that we usually make. Janet, what do you think?

Yeah, I think it also leads to the fact that with synovial biopsies have helped to say, if your B cell predominant, because about, it's not quite what I'm about to say, but about a third of patients look like organized B cells with active RA who have a synovial biopsy who have been somewhat treated but ineffectively fully treated. And about twenty five percent are fibrotic and there's people in between that look B cell but it's not as organized as a B cell kind of lymph node look. So I think the fibrotic folks, maybe this wouldn't work anyway, but I'm hazarding a guess. So I think interesting data, not ready for prime time. We need more N and we need longer follow-up, and then we'll make a decision.

If you were poly refractory on pretty much everything, would you go for it with RA? Well, sure. If you're young enough that you've already got damage and you haven't turned off your disease in years and you're adherent to what's out there, I think you'd probably be consenting to it saying, well, I want to spare my joints for the next twenty five years if somebody's like 45 years old or something. But I don't know yet. No opinion yet.

Yeah, I wanna remind us that we discussed in the past, you know, Doctor. Pizzales' R4RA study that shows that, and others have shown that the big bad, you know, 800 pound gorilla the synovium is the fibroblasts and interstitial cells that are tremendously damaging and we're not attacking it. And maybe that's why we see incomplete responses when we target specifically CD19 B cells with this. All right, our final round, I want this to be faster, a minute each on your presentation and start with Bella.

Okay. So this is o p zero two four four. This is looking at pregnancy and autoinflammatory diseases. You know, there's a lot of talk of pregnancies and lupus, etcetera, but this is good data for autoinflammatory diseases. They included forty three percent FMF, seventy sorry.

Thirty seven percent Still's disease and other periodic fevers. Total of fifty one patients, and ninety three percent patients had live births. So that's important to educate our patients. Only ten percent preterm births, again, very, very important. And no preeclampsia help or all the vascular complications that are usually seen with lupus, etcetera.

So auto inflammatory patients, you know, again, these are small groups, you know, much more rare diseases, but important to counsel because a lot of our patients are young.

Right. And so I was gonna ask you that question, Bella, as you follow this literature, there often are reports about pregnancy causing stills, pregnancy causing auto inflammatory disease. What do you think about that?

I think it's the same, like, you know, some things, the immune system is triggered and here it's the innate immune system during pregnancy, but I don't think it causes these diseases. You're predisposed. I think I give that answer to most people.

Very good. All right, Orly, what do you have?

Yeah, I wanted to talk about the first abstract presented at the plenary yesterday, OP001. It's an RCT on gout, we don't have that many of them, so I thought it was interesting. And also, I mean, I think the result was expected but I think it's a great thing that someone did it and so what they did is they literally looked at people with gout, treated with urinary therapy, followed them up twenty four months and do we continue or do we deescalate? So do we taper down the uro lowering therapy? So the rule of thumb is we never stop and I think really it confirms that we shouldn't stop.

So yeah there was three hundred people in the study and all of those who had the escalation. Most of them weren't in remission at on the last six months of the two years follow-up period. Three times three times more more flares. More consumption of coal casino and so on. However one thing that I found quite interesting within all of that is that there still was a subgroup that seems to not be flaring at all.

So can we identify these people? I think we need further research because there might be a contingent of patients in whom we could reduce, but we don't know who they are yet.

Yeah, well, we definitely need more gout research. And I think that, you know, the good news is we have drugs coming down in development that will spurn not just the research, but also discussion and better education. Janet, what do you have?

So a really quick one. So it came in New England Journal at the same time a couple of days ago. So yesterday was OP-eighteen. So it's the largest RCT and IgG4 active disease. So one hundred and ninety four patients and they were randomized to I hope I'll say it right to Obaxilib.

I'm sure I'm probably not saying it right. I apologize. And or placebo. They were on glucocorticoids and then were forced to taper to see if they flare or not. So let's be honest, they weren't on background immune suppression.

So they might have been exposed in past of things like rituximab. They were all on glucocorticoids with active disease. So they looked at primary outcome time to flare and there was like almost a sixty percent reduction. So hazard ratio 0.44 if you're on active treatment. The rate of flares were approximately double on the people on as they tapered prednisone on placebo versus active.

They had one third less cumulative steroid dose, about three hundred milligrams in that first year versus about nine hundred milligrams and less serious adverse events. So how is this drug different from the other kid on the block, inebilizumab, which I'm also probably not saying right? It's because they're both affecting B cells, but the new one, the Oboxy, is basically a non depleter, whereas the other one is a depleter. So the big take home here is we have two drugs now, but none of them in fairness have been compared to regular immune suppressives that are used post steroids in many people, or and they haven't been compared to rituximab, which I think a lot of people that treat IgG4 get access to rituximab one way or another. So at least we'll have, I suspect quite soon now, a second drug that we'll be able to consider utilizing.

How will we choose between one and the other? I don't know, whatever we get access to, I guess. Yeah.

So here's the upside downside. Upside is more drugs for a hard to treat disease is a great thing. More education, more options, more whatever, but more drugs for a rare disease is maddening. Like how many drugs are we gonna need for IgG4 to manage? I mean, we're using rituximab before the current approval, and now this looks really good.

And there are other trials that are in play.

Right, JAKs are in trials and other B cell depleters or B cell modulators are also in trials. So you're right. We're going to have a rare disease with a plethora of drugs. However, I think what it does is it it does as you say, Jack, bring the research in and the education because there's probably people misdiagnosed over and under diagnosis, I suspect.

All right. So mine, I've changed my mind four times during this recording as to what my second one was going to be. I'm really going to go a little off the path here. Mine's a poster from today, POS0788 from UMESH and colleagues in India. This is a report on the efficacy of colchicine withdrawal in patients with palindromic rheumatism.

It seemed kinda oddly boring, but the fact is this is a real important decision. And so they have a retrospective experience with, their number was seven sixty five patients, and when they did all their exclusions and whatnot, they had one hundred and fourteen patients who were in remission on colchicine with or without hydroxychloroquine, that being a minority. Then they followed them up and the idea was that when they stopped the colchicine, that out of the one hundred and fourteen, sixty four remained in remission and that fifty relapsed. And so that does add up to one hundred and fourteen. Of the ones that relapsed, they reintroduced colchicine and 36 regained control, so that's about two thirds, whereas 11 continue to be, not well controlled.

So, I thought it was interesting. I thought it's got real practicality to what we need to do in folks. If you make the decision and someone has enough, I think it's a PR, first off, I think is another version of clinically suspect arthralgia, at risk RA, etcetera. But it's really kind of managed like gout, is it not? If they have more than one attack a year, you're talking about suppression.

If they're having three attacks or more, you're definitely all over them about putting them on something, and then what are you going to use? And colchicine certainly, needs to be considered because it's cheap. Well, it used to be cheap. In Canada, it's cheap. In The United States, they went crazy.

And the rest of the world, it's cheap. Which is why I get all my colchicine from Canada. But still, I think it's a very safe drug, and is effective. So, I'd like to know what, the panel thinks about this.

I mean, I think

Sorry. Yeah. Orly, go Go

ahead, Janet. No. No. Go ahead.

Or or Bella. Okay. I was just gonna say we just had professor McGonigal come and talk about I I never thought of it as a stills kite type picture of the innate pathway going on because honestly, until he just gave a talk to our group about a week ago, I was was not using colchicine and palindromic rheumatism. So after hydroxychloroquine, I would just go to methotrexate if they had too many attacks and I thought they were adherent and there is that Abitacept RCT of preventing more flares but I can't get access to Abitacept after hydroxychloroquine. So, I I kind of like the whole idea.

So that's where I'll stand is I don't have much experience in p in palindromic, but kinda makes sense to me.

I think people people add colchicine for different reasons even for, like, you know, PMR or maybe, like, you know, trying to figure out what inflammatory process there is. One abstract that I saw today was colchicine megadoses used by inflammatory arthritis patients for suicide risk. Right? Like, for suicide. So that's something to be careful about.

I I didn't even know that's a thing, but, apparently, this was like an app an app a poster. I don't have the number right by me, but so so if you are using it, I would just put a caution there, said you should not be given, like, mega doses. Like, you know, they shouldn't have, like, six months supply or something. So that's there was, like, twenty one patients with FMF, young people, mean age 28, and there was like it's a mode of suicide, I didn't know that. So that's something I learned.

That's crazy.

Bad off label, and God help you if you're doing that because there are a lot of deaths with colchicine when it's used improperly. And that's a good example of that, but that scares me to no end. Anyway, final word orally.

Yeah, no, I think it's one of these drugs where the toxicity dose is actually quite close to the terrapate dose and I think that's the issue. So yeah, always be careful, but I'm definitely open to using it in palindromic for sure.

All right, I want to thank the panel for a great review of the first two days. Encourage all of you to tune in tomorrow for our day three recap from EULAR. We'll have a whole new cast of characters. Take care everyone.