EULAR 2026 Daily Podcast Day 3a Save

You're listening to a RheumNow podcast coming to you from London, and you are twenty twenty six. Enjoy.

Hey, everyone. This is Bella Mehta reporting for RheumNow from London for EULA. And one of the most practical and immediately relevant abstract at EULA was this one which looked at cost effectiveness of digital patient education in newly diagnosed rheumatoid arthritis patients. This is o p zero zero five, and this builds on a Web RA randomized control trial where patients with newly diagnosed RA were randomized either to digital patient education or standardized face to face education and followed over twelve months. In this economic evaluation, they analyzed data from one seventy five patients, eighty four in the digital group and ninety one in the control group, and both groups who are matched in terms of demographics, disease characteristics.

Again, the average age was mid to late fifties, and about sixty percent were females. And all of these patients had some amount of disease activity, very moderate, with DAS 28 scores about 4.4 to 4.6. They what they looked at was not just clinical outcomes, but also cost and quality of life or QALYs, quality adjusted life years, which was their primary outcome. And they took a broad societal perspective, which is important because it's it included not just health care utilization, but also things like productivity loss, transportation, and municipal services. And the results are quite interesting.

The digital education group had overall mean health care costs compared to the face to face group by around 500 or €600 and slightly improved quality or quality of life. And the quality quality adjusted life year gain difference, so quality gain difference was 0.013. It's a small number, but it's still in the in the right direction. When they calculated the incremental cost of effectiveness ratio, their digital intervention was actually dominant, meaning better outcomes at a lower cost. And then they ran, like, probabilistic analysis.

Again, this seems like a lot of math, but, you know, we they did simulations and which which fell into the best case quadrant, better outcomes at lower cost, and overall probability of cost effectiveness was around 70% even at a zero cost willingness to pay threshold, increasing slightly to about 71.5 at standard thresholds. So, again, most of the cost savings were driven by hospital utilization, which was reduced, which I think is a key thing that a lot of patients, physicians, insurances care about. And, you know, for the secondary outcome self efficacy, the results were mixed, and it's difficult to interpret in a small RCT, but it is in a small trial like that. But mainly what this suggest is that structured digital education tools can reduce cost without compromising outcomes and potentially improve access and efficiency in early RA care. In a setting where we are facing, you know, workload shortages, increasing patient demand, this might be highly useful.

But I think there's nuance here again that it's not about replacement. It's about augmentation. Digital education can standardize and scale information delivery, but it does not account or does not take care of individual concerns or health literacy differences or nuances of shared decision making. Again, this ties to the broader shift that we are seeing that patients are increasingly willing to engage with digital tools, whether structured education platforms or informal AI based systems. But even if these tools improve baseline understanding, they don't replace the need for a contextual interpretation, which we as clinicians can do.

So, you know, with these tools, this I don't think they'll replace us, but they will change how we spend our time and focusing more on complex decision making. But, again, all I when I see these abstracts, it makes me think that, slowly, the spectrum of how we are trying to treat these diseases and patients, is changing, and there's a lot of food for thought here. So with that, signing off. This is Bella Mehta at RheumNow, and please follow me on Twitter at Bella underscore Mehta. Thank you.

Hello. I'm Jonathan Kay reporting from EULAR twenty twenty six at the Excel Center in London, England. Today, on the third day of EULAR, there was a very interesting, debate, between Maya Book Maya Butch and Jacques Eric Gottenberg about combination targeted therapies for the treatment of rheumatic diseases. This is a very interesting area because, doctor Gottenberg, who's from France, suggested that there are a number of combinations that might be safe and more effective for the treatment of rheumatologic diseases. And in France, he has no difficulty getting approval or having dispensed, to his patients the multiple, targeted therapies.

There are recent data in psoriatic arthritis of the combination of ixekizumab and a GLP one agonist compared to ixekizumab alone, and this was more effective, achieving PASI 100s, greater, with the ixekizumab and the, GLP-one agonist than with ixekizumab alone. In rheumatoid arthritis, the potential for combination therapy is most interesting with the combination of a JAK inhibitor and a TNF inhibitor. JAK inhibition does not block signaling of the through the TNF receptor so that a patient who is inadequately responsive, to a JAK inhibitor might benefit from the addition of a TNF inhibitor. Now with biosimilars of adalimumab, available at a lower cost, this might become a feasible therapeutic option in rheumatoid arthritis. The addition of GLP-one agonists to biologic therapies is very promising, especially in patients with peripheral spondyloarthritis where an IL-seventeen inhibitor might be inadequately effective alone, but the addition of a low dose of a GLP-one agonist for its anti inflammatory effect may potentiate the effect of the IL-seventeen inhibitor.

Maya Butch said that she agrees with the idea of combination biologics,

but

the data are not yet there, and we need to learn more about mechanism, before embarking on this. This is a very interesting potential topic. More on this to come. For more about this and other topics at EULAR twenty twenty six, go to rheumnow.com. I'm Jonathan Kaye.

See you again soon from

Hello. I'm Anthony Chan reporting here from EULA twenty twenty six in London and today there are important presentations on dual therapy or combination therapy in Spar Spondyloarthritis. There have been more studies in psoriatic arthritis but today I want to focus on Spar Spondyloarthritis. First oral presentation OP351 which is a study from Spain. So the first thing in order for us to treat patients is we need to do what we call treatment to target or T2T.

That measurement allows us then to escalate the treatment into combination therapy. But what was very interesting from this presentation this morning from this oral abstract is that in SPAR only forty percent of patients had documented measurement of their S test or the outcome measure that allow you to escalate the therapy compared to seventy percent PSA and rheumatoid arthritis. This means that in most of the time these documents, this documentation did not take place. And what was quite interesting is that there's a treatment inertia that results as a result of not calculating your ASH test. In about a third of patients there was reassurance more than escalation of therapy compared to seventy percent in the PSA group.

So while we have guidelines and while we have the approach to treat to target, most of the time the problem is structural. The problem is documentation rather than clinical. And so they suggested prompts to get people to do the S test to be able to check the CRP prior to the patients coming. Many are ways for us to escalate the treatment. And then going into that, the next oral presentation was OP352.

And here is the study looking at the use of combination therapy in spa. And this includes people with peripheral spondyloarthritis as well. What they found is the biggest combination was the TNF and IL12 stroke twenty three followed by TNF combination of IL17 and then finally TNF with IL23 combination. The results were quite startling that if you did combination therapy and you escalated the treatment, more than fifty five percent of these patients would achieve S test remission or S test low disease score compared to the other patients who are on standard types of treatment. And when we think about combination therapy, obviously we think about the safety, whether this is safe.

In this cohort of patients that they studied, were no new safety signals. There were no unexpected results as a result of the combination therapy. So these are very refractory patients. The median number of biologics either targeted synthetic or DD marts were a median of four. So these are truly refractory patients who are not achieving their S test.

Putting these two together, I think the first thing is to be able to measure. If we don't measure these, then we are not going to be able to escalate. And when we do measure and the patients do not meet the standard for remission, then the ability now to escalate into one will be two biologics. And we need long term data to know how safe would this be in the long term or whether we de escalate patients down the line once they achieve the target. So very interesting presentations today.

I'm Anthony Chan from RheumNow, EULA twenty twenty six.

Hi. This is doctor Arti Kavanagh from UCSD coming to you for RheumNow. I'm at EULAR twenty twenty six in beautiful London, and, of course, a tremendous amount of material being presented here. I'll talk about one oral presentation, and that was by Mikhail Ostergard. The abstract is o p one eight six, and this was on an important study.

This is a combination therapy study called Affinity. Now this follows on the VEGAS study in ulcerative colitis, very successful, showing that the combination of the IL-twenty three inhibitor gazelkumab and the TNF inhibitor galimumab did what we had always hoped the combination therapy would do, and that is get greater efficacy and yet not have increased toxicity. Based on the results of that study, there's great interest in psoriatic arthritis looking at combination therapy, and this is one of the first studies to do that. Affinity looked at two of those groups, looked at gazelkumab and galimumab versus guselkumab alone in psoriatic arthritis. Now, the primary outcome was a very stringent one, and that was minimal disease activity or MDA, and while numerically superior, it did not reach significant statistical significance in this somewhat small study.

This abstract, was presented by Michael Ostegard, looked at MRI findings. So they looked at the SAMRIS, the, OMRIAC way to look at MRIs in, hands and feet of patients with psoriatic arthritis. They also looked at the hemorrhage which looked at enthesitis. They looked at inflammation and they also looked for structural damage. And what they found is that in the subset of patients treated with the combination therapy, there was a statistically significantly greater reduction in overall inflammation in the hands and feet than with just the therapy with gazelkumab, the IL-twenty three inhibitor alone.

So I think that raises some interesting questions. This is yet another way to look at the efficacy of therapy, and in this case, an important question about combination therapy. The study was short, and as you probably would have expected, no difference in structural changes in the MRI. I think this points out that MRI imaging may be a very useful adjunct in studies to get proof of concept, and that the combination therapy is certainly an idea worth exploring more in psoriatic arthritis. So coming to you, you are twenty twenty six in London for RheumNow.

This is Artie Cavanagh.

Hello, everyone. This is Nelly Ziadev from Beirut, Lebanon. I'm in London reporting on EULAR twenty twenty six for RheumNow. Today I will talk about combo therapy. R2 better than one.

This is a case for dual pathway blockade and refractory psoriatic arthritis. Psoriatic arthritis is by nature a disease of multiple inflammatory pathways, joints, antisis, skin, dactylitis. There's a role for TNF, interleukin-seventeen, 23, TYK2, and no single agent controls all of them optimally in every patient. Actually, forty to fifty percent of PSA patients on TNF inhibitors monotherapy fail to achieve minimal disease activity. So this treatment gap has long prompted a question among rheumatologists: What happens if we block two pathways at once?

And I will talk about two abstracts at EULAR that explore these questions from different angles. One is reporting MRI data from a complete phase 2a trial, and the other is just a starting study of a phase four entering recruitment. So the first abstract is AFFINITY OP 0.16086 by Weilen et al. They explored MRI findings from the phase 2A AFFINITY study. They randomized 91 TNF inadequate responders, PSA patients, two to one.

First arm is guselkumab associated, so an interleukin twenty three inhibitor plus golimumab HNF inhibitors, compared to the other arm of guselkumab monotherapy over twenty four weeks. So the rationale is mechanistically elegant. Interleukin 23 and TNF may play a complementary non redundant role. And so if you block both of them, you could have interesting results. And this is reporting the MRI data, which they scored using the OMRACT framework.

So in the hand pharyngeal joints, they found that the combination therapy produced a numerically greater reduction in the composite inflammatory score compared to monotherapy. So change minus five compared to minus 0.4. However, the P value did not reach statistical significance. However, the foot results were more striking and they reached nominal statistical significance. So, the composite foot inflammation score improved by minus 3.5 in the combination therapy versus a worsening of plus 2.7 with monotherapy.

Structural damage scores were stable in both groups, which is reassuring, knowing the basal crema established effect on radiographic progression. And here, antisitis scores showed no significant differences between the groups. So this is an exploratory study. It was not powered for more endpoints, so we need to be cautious. As the sample size was modest, we didn't find a significant difference for the hands, but it was important for the foot, and it is biologically coherent.

So we look forward to have more data on this combination. The second abstract by Merola et al, poster four ninety nine, is a different approach. So this is a combo trial pairing doclavacitinib, a TYK2 inhibitor, with ongoing TNF therapy. So target population is a patient with PSA and partial response to anti TNF, defined by persistent skin involvement or active joint, despite at least six months on TNF. So this is the, like the classical scenario where the patients are okay with TNF, but not really well enough to reach the treatment goal.

So the trial is ongoing. They were randomized 128 adults to clavacitinib once daily plus TNF or placebo plus TNF for twenty four weeks and followed by a twenty four week open label extension where everybody will receive the combination. The primary endpoint is a composite skin joint target, BSA less than 1% and swollen joint count less than one, less or equal to one at week twenty four, which is a bit stringent, but this is what our patients ask for. They have also interesting secondary endpoints, MDA, very low disease activity, antizitis, and the full PROs battery, also cardiometabolic biomarker profiling, adding in a new dimension. So recruitment is just beginning and also we look forward for the result.

So, I have two concerns to address when I see this combo treatment. First, the safety data of both agents. So, when used individually, the safety is well established. However, the incremental risk of combining both of them is still unknown. And the second one is the cost and the cost effectiveness of this combination, which also needs to be addressed.

So the question is whether this is ready to move from hypothesis to practice in psoriatic arthritis. Thank you.

I'm Anthony Chan reporting for RheumNow here in London in July 2026. One of the areas that had been discussed in this conference is the use of combination treatment or dual targeted therapy in the field of both psoriatic arthritis and also axospondyloarthritis. One of the presentations was the AFFINITY study, which is OP0186, which is the study of gusilcomab in addition to golimumab in patients who had failed one or two TNF inhibitors. This was a phase 2A study which tested the IL-twenty three inhibitor gusilkomab combined with golimumab, which is a TNF alpha inhibitor, versus gusilcumab monotherapy in patients who had failed one or two prior TNF inhibitors. Ninety one PSA patients were studied in this study, and this earliest, report is about the MRI findings, as an exploratory outcome.

The key findings is the combination therapy. Patients who had received both gusilcumab in addition to golimumab did better with regards to some of the MRI findings compared to patients who had just received the TNF inhibitor alone or with the gusilumab monotherapy. The combination therapy produced numerically greater reductions in the hand inflammation, compared to the monotherapy group. And also the foot MRI showed a statistically significant reduction in the total inflammation versus the monotherapy group. The structural damage was stable in both groups.

The combination did not accelerate any damage. There was no obvious difference in the heel and ascites data that were seen. So the question is what is the significance of this? This is very early data. It's looking at MRI changes.

So it's very much looking at the imaging outcomes and the MRI data certainly in the hands and feet would support the clinical signals, the dual pathway, the dual blockade of IL-twenty three and TNF, may actually raise the ceiling with regards to reducing joint inflammation in patients who had failed TNF or TNF inadequate responders, particularly seen in the foot. And it does not appear to increase our structural risk. So this is, I thought was interesting because it's using in the exploratory phase, the MRI result rather than the typical outcome measures that we would use in standard reporting. Obviously, we'll await further data as the study is carried out in the longer term. But we are increasingly seeing in patients who had failed one or two TNFs that we are going for more the combination treatment in these patients to try to get the treatment refractory patients and to get them into a more better clinical state and also hopefully reduce structural damage in the long term.

I'm Anthony Chan reporting here in London at EULA twenty twenty six.

Hi, everyone. Peter Nash reporting from reporting for RheumNow, London, EULA Twenty Twenty Six. There's many abstracts on variety of different treatments, new TYK2 inhibitors, combination therapies, etcetera. But probiotics are very popular, and this is post February, where because of the microbiome in the gut joint axis, people are very interested in whether adding a probiotic has any efficacy in psoriatic arthritis. So they took a number of people who had moderately active PSA.

They gave them a lactobacillus and a bifidobacterium, probiotic and compared it to placebo. And over twelve months, the primary endpoint was their PASTAF remission or low disease activity. And unfortunately, they were unable to show any difference in controlling or improving disease activity, whether you took a placebo or a probiotic. So probiotics look like they aren't the answer. We're working on a lactobacillus probiotic ourselves.

We've done it in rheumatoid with some modest efficacy, and we're about to do it in PSA, but that study really argues against it being of efficacy. More work needs to be done because nothing changed. The microbiome didn't change, the gut permeability didn't change, and the composition of the immune, subsets didn't change either with the probiotic. Now everyone is talking about late breaker one, which is going to be presented tomorrow by Joe Marola. This is the sixteen week data, and it's a head to head study between bimekizumab and risankizumab.

He'll present the twenty four week, and we look forward to hearing about that tomorrow. But we don't have many head to heads in psoriatic arthritis. We have two head to heads TNF versus, 17 inhibitors, one with and one without methotrexate, and that was very educational. It helped us, increase discontinuations in the, TNF group. The TNF group had much more serious adverse events than the 17 group, but this was a head to head for the first time, a active comparative study, including superiority, and they looked at a 17 versus a twenty three inhibitor.

Sixteen week data presented, twenty four weeks tomorrow, and these patients were all be DMARDs naive, or they had one TNF, and up to about twenty percent had one TNF. And they used the labeled dose. The risankizumab dose was one hundred fifty, at baseline four weeks, and then week sixteen, whereas the bimekizumab dose was the, one hundred sixty milligrams, that was dosed as per protocol, but up to sixteen percent who had moderate to severe psoriasis or body surface area greater than 10% or, an IGA greater than three, we're allowed to use the label dose, which was double the dose, and that was about sixteen percent of patients. The primary endpoint was ACR fifty at week sixteen, and a whole series of secondary endpoints including MDA. And there was significant difference at week sixteen, forty 9% versus 38% ACR50.

They looked at a whole series of other endpoints, including PASI 100. There was a difference of 53 versus 47. Because the second endpoint MDA didn't reach statistical significance, but just numerical significance, all the other endpoints were nominal, and they couldn't work out confidence intervals and significance there. But, dapsa, low disease activity and remission, numerically in favor of the 17 inhibitor, and all the way down the line, we didn't see any major differences in safety. There was a candida signal which is known with the 17.

So first, head to head 17 to 23 in favor of the 17. We look forward to the 24, results, and they'll hive off the percentage of patients with double dose and see if the significance is maintained, whether you can whether that was a reason for the difference or not. So we look forward to hearing about that tomorrow.

What does it mean to you?

To me, I think we're starting to get a treatment algorithm that has evidence based rather than, elderly bull fat men in a room sitting around a table deciding which drug should be used before which other drug. Hi, everyone. Peter Nash reporting for RheumNow from EULA London twenty twenty six. I've got a little theme, a couple of abstracts, and a couple of presentations talking about the transition of psoriasis to psoriatic arthritis, how we can prevent it perhaps, and how we can use some imaging to help. So the first is an Austrian group that have put together a nice prospective longitudinal program where they've taken a couple of 100 people who are at risk of developing psoriatic arthritis but don't have any synovitis, don't have any swelling, negative inflammatory markers, they only have PSO, and they have some morning stiffness, and they have an improvement with NSAID, but that's about all.

And they've done a nice lot of work with this group, and even at the baseline, they find four percent have rheumatologists diagnosed PSA, and they're gonna follow this group over a length of time. Now we did a similar thing in eight dermatology clinics, and we turned up about nine percent of pay PSO patients hiding amongst the p the hunt eight percent PSA patients hiding amongst the PSO population. Now the next transition is is anything can stop that transition from PSO to PSA. So the Greeks have done an, o PO72. They have done a retrospective observational cohort study where they took PSA, derm diagnosed, but no PSA, and they're all on a biologic for over six months.

And they looked to see, and they followed these patients up over seventeen years and they looked to see how many developed rheumatology diagnosed PSA. Again, three forty patients, three ninety four patients, sorry, and in the seventeen years twenty two percent developed frank PSA and of that twenty two percent, given that they were all given a biologic by their dermatologist for their rash, forty five percent of them happened to be on the TNF when they developed PSA, fourteen percent on an IL-seventeen inhibitor, ten percent twenty three, and eleven percent on a twelve twenty three. So these are three hundred people, twenty two percent actually have PSA that evolves and they diagnose it, and they had been on a variety of different biologics. And there was a hazard ratio difference adjusting for the disease time on a biologic and methotrexate background. And the 17s and the 23s and the eleven twenty 12 23s, there's no difference between them, but you're more likely to prevent and not get progression on those agents compared to a TNF in a group, all of them on a biologic.

So that was of some interest. People, including Lihi Ida, have presented ultrasound to help pick the PSA in the PSO population. But previous meetings have shown, and this is abstract two six one three, that if you use a technique called FAPI PET, you can show fibroblast activation. And the fibroblast is gonna become very interestingly more important as a measure of chronicity in rheumatoid, in PSA, in people who are not responding and not going into remission. And it's a watch this space as a number of companies are developing anti fibrotic drugs.

But this FAPI PET CT, if you have a high index compared to if you don't, you're six times more likely to develop psoriatic arthritis whilst you started off with psoriasis compared to those who do not have an elevated FAPI PET CT. It's an expensive research tool, but people are looking for ways to pick PSA in a PSA population and do something about it early.