EULAR2025 Topic Podcast SpA Save

You're listening to a RheumNow podcast coming to you from Barcelona, Spain, and EULAR twenty twenty five. Hope you enjoy it.

Hi, everyone. This is Adela Castro from Memphis, Tennessee reporting from EULAR here in Barcelona. I wanted to go over a representation. The abstract number is OP0102, and it's called the efficacy and safety of a new IL-17A blocker called selegakimab in patients with ankylosing spondylitis. This is a Chinese study performed in four sixty five patients with ankylosing spondylitis and the primary efficacy was to achieve ASAS 20.

And then after week sixteen, it showed a significant proportion of patients achieved the primary outcome. And this was also noticed that this efficacy was sustained up until week forty eight in both doses of the medication. As far as safety, there was no major significant safety events. It did show a little bit of high proportion of mild elevation of LFTs, but in general, it seemed really safe. Something that is very interesting about this medication is that it's a fully humanized IgG4 antibody, which seems that one of the benefits is that it can last a little bit longer on the body and it can also minimize the drug antibody production.

For more, please follow RheumNow. Hi, everyone. This is Adela Castro from Memphis, Tennessee reporting from EULAR here in Barcelona, and I want to summarize a little bit of the How to Treat session today in the updates of asthma management, particularly in the lessons learned from uveitis. It is important to remember that up to forty percent of patients with uveitis present before the diagnosis of asthma, and uveitis itself has been associated with longer time to diagnosis in patients with asthma. Regarding treatment, it was reported that network meta analysis of 44 clinical trials that show that all standard of care, including TNF inhibitors, IL-seventeen inhibitors, and JAK inhibitors are effective for management of anterior uveitis and are actually protective against uveitis in patients with ACFA.

Something that was also noted here in this session was that there were very low rates of uveitis in patients with bimekizumab, which means that bimekizumab could also be protective against anterior uveitis. For more, follow-up over here at RheumNow.

Hello, I'm Anthony Chan. I'm reporting from Barcelona, EULA 2025 for RheumNow and there have been a lot of, important discussions about difficult to treat in the field of spondyloarthritis at this meeting and today I'm delighted to have, Marina Margreave from Cleveland USA who presented a very nice work looking at risk factors for the detection of difficult to treat in ankylosing spondylitis. So Marina welcome and I wonder whether you could tell us about your your poster.

Thank you for inviting me for you know to present this abstract. And you know this we have all faced in our clinical practice these conundrums of some patients that do not respond to treatment or some that have difficult to manage. So in order to look at some risk stratification, we explored a database called TriNetX. It's a large global database. It has information from 86 healthcare organizations with about 125,000,000 patients.

And we use the ICD-nine or 10 code for ankylosing spondylitis. And then we looked at those patients, using the ASAS definition for difficult to treat, which was published recently. So those patients that had actually failed two or more of biologic DMARDs and also had an elevated CRP. So we tried to take a very stringent patient population, those which had active inflammation and had failed at least two biologics from two different classes. So we found there were about ninety one thousand patients.

And out of that, the prevalence for difficult to treat was actually very small. It was about two thousand two hundred patients which were difficult to treat based on that definition. So the oral prevalence was low. It was lower than there were a lot of other abstracts that were presented at EULAR this year regarding difficult to treat from different countries and ours was the lowest prevalence. The reason for that was because we used the stringent criteria of elevated CRP and these patients median CRP was high.

So, when we looked at their baseline characteristics, these patients who were difficult to treat, they were more females and they were actually had high BMI's, they were obese, they had a lot of extra articular manifestations, psoriasis, inflammatory bowel disease, comorbidities were there, and then we used multi variable regression analysis to identify those factors at baseline, which increase the risk of these patients being difficult to treat. And these patients were HLA B27 positive females, mainly they were the high BMI's obese and had a comorbidity of depression. So, I felt, you know, it is important for us as a clinician to understand this because these may be the patient when we see them in our practices kind of, you know, start thinking about the response to treatment and educate them at the very beginning that there may be some lifestyle modifications they may need to do in order to respond better, maybe try lose weight. And if there are any comorbidities, we need to handle them too so that the response to treatment increases.

Very nice work. Lot of patients in your analysis as well. Were there any particular factors that were you know waiting strongly or more independent for the prediction of a d to t?

Yeah. So we tried doing, like, you know, some sensitivity analysis to avoid confounders between since the two groups are so different in n numbers. And the only three things that in the end that stood up was BMI, obesity and depression and HLA B27 positivity.

And how about, you know, sex male or female was there any

There was yeah females were obviously larger in number in the difficult to treat patients and that's kind of you know shown by all the abstracts that were presented there. Hewlett, every one of them had the risk was higher in females than males. And it's an interesting question in terms of, you know, response to treatment also differs and it's usually delayed in females compared to males and we still haven't been able to nail it, nailed it further, whether it's because of biological difference. Is it because, you know, central sensitization in females that the we are not able to get the pain under control? Is it a different disease phenotype?

Yeah, that's very interesting and wonder whether we should have a different outcome measures sometimes for different groups of population. What's the what's what's the next step from here? I mean you've done some great work. You've identified this cohort. What would you be sort of thinking of doing in in sense of following up from this study?

We are actually, that's a very important question you asked, and we are actually trying to see if we could do some transcriptome studies to see if there is a difference in, you know, some genetic differences between these two groups groups and looking for other like you know inflammatory pathways that may be driving this inflammation in these patients who are difficult to treat.

Yeah, think that will be very important for us especially when we are thinking of the treatments as well and how we are moving from one treatment to the other and trying to identify the patients who are at most at risk. Are there any plans to, you know, look at the other cohort which is what we call the difficult to manage where, maybe they have less objective or less inflammation and more non inflammatory pain?

You know, this database actually doesn't give us that kind of, you know, information like about what was the patient's perception of their disease, patient reported outcomes to look at that, whether other than that's why we use the stringent criteria, but in, you know, we do have a registry at our institution where now we may be able to look at that group separately and see if there is, because we have been collecting longitudinal data for some time now. So we do have some longitudinal data seeing how the patients are perceiving. We give them questionnaires, patient reported outcomes to do them at home after every visit. So that may help us to understand if there is some other factors that are impacting this.

Yeah, I think that's one of the challenges that we have seen here at EULA twenty five, the some of the other non inflammatory factors that sometimes can affect the outcome measures that we are using. So Marina, thank you very much for your time and thank you for sharing with us your great work. So everyone, this is a poster zero one one seven presented on the poster tour at Eula twenty twenty five. I'm Anthony Chan presenting for RheumNow. Thank you very much.

Thank you, RheumNow. You guys are doing a great job in disseminating all this information from EULA.

Good. Thank you. Bye.

Bye bye.

Hi, everyone. This is Adela Castro from Memphis, Tennessee, reporting here from Mueller in Barcelona. And I'm gonna discuss the abstract OP0310. And in this abstract, this is data from the state cohort, which analyzed the difference between structural lesions on MRI of the spine between patients with early asthma and patients with non asthma and chronic back pain for two years. The patients on this study underwent imaging at baseline and two years follow-up.

And it was found that at baseline, both groups were similar in conventional s rays. However, two years later, patients with asthma had significant difference compared to baseline, predominantly showing a little bit of undermines on the fat lesions. And this was not observed in patients that did not have asthma. So, this shown that the significant change on fat lesions can be a potential signal of structural lesions in patients with asthma. For more, follow-up in IrinNow.

Hello, everyone. I'm Nelly Zadeh, Associate Professor of Rheumatology from Beirut, Lebanon, reporting for RheumNow from the EULAR Congress in Barcelona. Now I will talk to you about emerging therapies in axial spondyloarthritis. I want to tackle three treatments that were discussed at the Congress. First one is Exeliezumab, an anti interleukin-seventeen A inhibitor.

The second one is Ivarmacitinib JAK1 inhibitor. And the third one is not an old one. It's not a new one. It's an old one, but with a new delivery mechanism, it's colchicine. So let's start with the new one, with the first one.

It's always difficult to pronounce the name. This is OP01O2. It's gzelegecumab in radiographic axial spondyloarthritis, efficacy and safety. This is a phase three trial. So this is a fully human monoclonal antibody that selectively neutralizes interleukin 17A.

This was a forty eight week phase three multicenter study conducted in China, comprising a sixteen week core treatment period, then a sixteen week maintenance period and a sixteen week follow-up period. The eligible patients were randomly assigned to receive GZELI-one hundred, GZELI-two hundred, or placebo. At week sixteen, the patients receiving placebo were then re randomised to receive either GZELI-one hundred or GZELI-two hundred. What was the primary endpoint? It was a proportion of patients achieving an ASAS-twenty response at week sixteen.

So they included four sixty five patients. At week sixteen, there was a significant higher proportion of patients in the treated group, two hundred and one hundred, achieving SS20 remission compared to placebo. So seventy four percent in the two hundred milligram, sixty five percent in the one hundred milligram, and thirty six percent in the placebo group. The efficacy was sustained through week forty eight in the Exeli treatment group. They also saw a significant reduction in disease activity as measured by Asthdas, ESR and CRP.

Also, improvement in physical function and spinal mobility, with 200 showing slightly better benefits. Concerning adverse events, there were no surprises. One point six percent of SAEs, no unexpected safety concerns. So we hope that this is, again, a new option for treating our patients with axial spondyloarthritis. The second poster is POS0757.

It's about ivarmicitinib in patients with active ankylosing spondylitis. This is a post hoc analysis that stratifies the initial results by baseline characteristics of a two phase two phase three trial. So what is Ivarmacitinib? It is a selective GYANOSKINAS1 inhibitor and has shown already efficacy in patients with active AS. And this time they are trying to see if it stays active significantly efficient in patients across different categories.

So, one hundred and eighty six received placebo, one hundred and eighty seven received ivamacitinib, and they showed a significant improvement in ASAS 20 in all subgroups. So, what did they study? Age, less than 40, more than 40, male or females, BMI below twenty four and more than 24, people with a disease duration less than five years or more than five years, with and without history of biologic or JAK inhibitor, with a VAS score of back pain less than 60 and more than 60. Across all categories, the treatment was effective, but mostly in patients who were young, so less than 40, with a lower BMI, with assess duration of less than five years, and without a history of biological or JAK inhibitor treatment. So no real surprises.

Again, another option for our patients. And the last treatment, as I said, it's not a new treatment, it's an old treatment. It's called SHISINE, our old friend. It's POS thirteen, and what they did is they did intra articular slow release treatment with microspheres containing colchicine in an inflammatory arthritis CRAT model. So this is a novel intra intra articular combination, sustained release colchicine and ropivacaine, an anaesthetic, in a RAC model of acute inflammatory arthritis.

They encapsulated colchicine with microspheres of biodegradable PLGA polymer to enable sustained release. They combined it with the anesthetic ropivacalline. They adapted a model of intra articular carrageenan induced arthritis in knees or ankles in the mice. They induced the arthritis and in the following one minute, injected either the colchicine or other also parallel group, including dexamethasone, for example. So after injection of the car, all animals developed an inflammation.

And they found, for example, that dexamethasone exerted a significant effect on pain, inflammation, and joint destruction, but also colchicine was effective for all these three parameters. So pain relief, inflammation, or destruction. And as a concentration in blood over seventy two hours after injection remained at very low levels and significantly below toxic thresholds. So what hope does this study give us? So we know that Cushisin is a very effective drug.

However, in several times, you are limited by the dose that we can deliver because of the toxicity. So this could be a very good option for treating acute inflammatory arthritis to limit all the toxicity of oral colchicine. And with that, I would like to thank you for listening and to follow RheumNow for more coverage from EULAAR twenty twenty five in Barcelona.

I'm Anthony Chan reporting here at EULAAR twenty twenty five for RheumNow. And today there was an interesting presentation on chronic pain in XBA, the whole concept of fibromyalgia and also central sensitization. This is from poster O213 which was presented here at EULA twenty twenty five. Chronic pain as you know is common in XBA even if effective, anti inflammatory treatment. Historically, chronic widespread pain is often labeled as fibromyalgia, but this sometimes doesn't capture the full picture.

And so this study explored the role of central sensitization as an important contributor to chronic pain in XBA. Why do I think this is important? We know that forty percent of patients of XBA can continue to experience chronic pain despite treatment. And chronic pain we know in XPAS complex, it is a combination of nociceptive pain which is inflammation driven and nocciplastic pain which is central sensitization. And ICD-eleven recognizes that chronic secondary musculoskeletal pain as being distinct from fibromyalgia.

So accurately characterizing these patients are essential for better targeted treatment. In this study which came from the Gila LES cohort, the Groningen Lewarden XBA cohort, they had one hundred and ninety nine patients of XBA fulfilling ASAS criteria and they were assessed for a few things. Firstly, they were assessed for fibromyalgia based on ACR criteria, then they were assessed for central sensitization inventory CSI and quantitative sensory testing QST and then they were also assessed for the Estes, Basti and CRP. They stratified the groups into three groups, firstly the fibromyalgia group that made up about twelve percent, the non fibromyalgia group these were people with either high CSI which is a score of above 40 and low CSI which is a score of below 40. The high CSI made up about thirty percent and the low CSI fifty eight percent.

What were the results of this study? This study essentially said that fibromyalgia underestimated central sensitization which I thought was quite interesting. So only twelve percent of these patients met fibromyalgia criteria. Over thirty percent of the remaining showed evidence of central sensitization so a CSI score greater than 40 and this suggests that central sensitization is much commoner than fibromyalgia and XBA And also patients if a CSI of more than 40 had significantly worse disease activity, pain and also QST abnormalities compared to those with less than, CSI 40. Regards to the traditional outcomes that we measure such as STAS and Basti, the patients were divided into those with fibromyalgia.

The mean disease activity STAS was three and those who had high CSI was 2.4. In contrast, those with low central sensitization the S test was lower at 1.8 and the same similar result was seen for Basti fibromyalgia and, people with CSI greater than 40 had higher best eye, whereas those with a lower CSI less than 40 had a lower best eye. These were quite interesting, the CRP did not differ between the group suggesting that non inflammatory pain mechanisms were probably driving this and also we found that, the people with a high CSI and also fibromyalgia group also had more confirmed pain facilitation scores as well. So I thought this was quite interesting, chronic pain in XBA is a spectrum, it is not just inflammation, and not just fibromyalgia. Many patients experience central sensitization, without fulfilling fibromyalgia criteria and these, composite measures that we have at the moment such as S test and best eye may be influenced by these non inflammatory pain mechanisms, possibly leading to over treatment if not recognized.

So pain management needs to be individualized, we have to think of it beyond our traditional methods of assessing patients and I think combining anti inflammatory therapies with strategies such as to manage central sensitization such as exercise, cognitive behavioral therapy or neuromodulators might be important. So chronic pain it's, remains a major unmet need in XBA. I thought this study today, was quite helpful in terms of trying to determine whether patients have more fibromyalgia phenotype or maybe more central sensitization type phenotype and we have tools such as CSI and QST to assess these patients and we should probably use these to evaluate the pain phenotypes so that we can optimize management for our patients. So I'm Anthony Chang, reporting here for RheumNow in Barcelona, at EULA twenty twenty five. I'm Anthony Chang reporting here for RheumNow in Barcelona at EULA twenty twenty five and there were interesting presentations on novel therapies in axial spondyloarthritis here at EULA twenty twenty five and I wanted to share with you some highlights of emerging treatments in the field of XBA.

And there were three key developments. One, a new IL-17A inhibitor, Vanakizumab, JAK inhibitor, Evamacitinib and then a highly individualized exercise intervention study. So let's, go through these and explore their clinical implications. The first one is post two fifty four which is a vunakizumab. It's a novel IL-17A monoclonal antibody which was studied for, its use in ankylosing spondylitis.

In the post hoc analysis four forty patients both TNF naive and TNF experience were treated. At sixteen weeks the ASUS20 response in the TNF experience was 67% versus 45% in the placebo and the TNF naive was 65% versus 41% in the placebo. So fairly similar in both TNF experience and TNF naive and the ASUS 40 responses were also significantly improved. Importantly, the response rates were similar as, in both the, TNF exposed and TNF naive groups suggesting quite broad utility of this treatment and, in terms of safety there were mild to moderate adverse events but no serious infections or malignancy seen. This study suggests that possibly Vunecizumab could offer additional IL-seventy in, A option for those, even those who were exposed to TNF, inhibitor therapy.

The second poster was, poster O262 which is, evamacitinib. We are obviously now moving towards a JAK inhibition. Evamacitinib is a selective JAK1 inhibitor. In phase twothree trials in three seventy three patients, They studied this and after twelve weeks the total back pain, visual analog scale, dropped by twenty five point six percent versus seventeen percent and this was significant. The night pain, visual analog scale also dropped by 25% versus 14.3% in the placebo and morning stiffness also dropped by 24.5% versus 15.8% in placebo all meeting, statistical significance.

The, patient global assessment and SQL also improved, significant. These are the quality of life measures. So even, patients who switch from placebo to the active drug after twelve weeks caught up and showed a rapid improvement. So again I think this supports, the what our current experience and JAK1 inhibition is a highly effective target for XBA offering rapid symptomatic relief, across multiple domains. So, another, one to add to our list of drugs that we could use to treat XBA.

Moving away from this drug therapy, there was an interesting presentation, post February and this is about individualized exercise program, beyond medications. I think structured, exercise is crucial. This was an eight week study so quite a short study. They looked at cardiopulmonary exercise, training and also they looked at, trunk strength and mobility exercises using a specialist devices. And the results were the strength were improved by about fourteen percent in mobility, improved by fifteen percent in people who underwent this, this, treatment and the improvements were in, things such as ventilatory efficiency, the anaerobic threshold and also chest expansion.

The best time also decreased from 3.5 to 2.9. So supervised individual exercise program, can significantly improve function, mobility and overall patient well-being, in XBA and this is again shown I think important that we don't just focus on the drug therapies but also the exercise as well. So what did I take away from these, three, presentations today? Firstly, the treatment landscape for XBA continues to evolve. We have another IL-seventeen inhibitor option, Vunakizumab, another JAK1 option, Evomacitinib, it was a rapid response and also comprehensive.

The L17, drug here responded both, in both TNF naive and TNF experience and finally, support an adjunctive therapy individualized exercise, remains important and I think these developments underscore and tell us the importance of multimodal personalized treatment approach to our patients. So thank you for joining me for this update on, the latest, developments in XBA I'm Anthony Chan reporting here at Barcelona at twenty twenty five.

Hi, David Lu reporting from day four of EULA twenty twenty five, the final day. I was wondering the poster floor today, and I came across poster twelve thirty two, the subject of which was everyone's favourite new class of medicines, the GLP-one receptor receptor agonists. And I think we started to see more and more data about how these drugs might affect our patients, knowing as well that we might not necessarily be the ones prescribing them right now, but actually our patients, because they live in the world and because they hear about these drugs, are getting them possibly for diabetes, possibly for weight loss, possibly just in general. So, what about for axSpA patients? Well, colleagues from Philadelphia in this study looked at TriNetX data, so big insurance data.

It looked specifically at ankylosing spondylitis because it's how it was coded. And it's over five thousand patients in this analysis, adjusted for relevant factors. And what washed out knowing as well that there's always a risk of residual confounding. But actually, they saw that for ankylosing spondylitis patients, the patients on GLP-one receptor agonists did better than the ones that did not, as far as major adverse cardiovascular events are concerned, specifically stroke, and then also with chronic kidney disease as well. Now, there's certainly reasons why that might make sense.

And we do know that our axial spondyloarthritis patients do have a base risk of cardiovascular disease. So it's not entirely surprising, but I think there's a lot that comes into the interaction here. It's hard to know whether a rheumatic disease does represent an extra factor that might be a reason why patients should consider GLP-one receptor agonists consider that kind of approach for diabetes or weight loss, or for other indications potentially. And it still seems like a bit of a moving face because it is being used off label so much as well. Nevertheless, we will see in our patient populations what this does.

I think the real question though is more than the comorbidities, as important as they are, and certainly as important as cardiovascular events are. We're really interested in seeing what happens with disease activity, and really look forward to seeing how that plays out across the spectrum of rheumatic diseases, especially the ones which are linked to the metabolic syndrome. Seeing how that plays out over the next few years, we will definitely get data to play with. So, for plenty more, for all things spa, and really all things rheumatology, you know where to go. Rheumnow.com.