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This is an ACR twenty twenty five podcast coming to you from Chicago. Hope you enjoy it.

My name is Marina Magre. I'm a professor of medicine at Case Western Reserve University at University Hospitals, and I'm here today at ACR Convergence Meeting twenty twenty five and reporting for our room now. You know, this abstract was was very I found this abstract very interesting. NSAIDs remain the cornerstone of treatment for joint pains and even for axial spondyloarthritis. However, we are concerned that they may cause flares of inflammatory bowel disease and avoid with underlying inflammatory bowel disease.

This study was a retrospective study that looked at an Optum database over a period of two decades, patients with inflammatory bowel disease and there were about 8,000 patients that were reviewed and about, you know, thirty five-thirty six percent of these patients actually were on NSAIDs. The main, outcome was, hospitalization by flaring of the underlying inflammatory bowel disease in patients that consumed NSAIDs. What the study found was that the overall risk of hospitalization was low. For the group, the hazard ratio was about one. In fact, in ulcerative colitis patients, there was no increased risk, but there was a moderately increased risk in patients with Crohn's disease.

The conclusion from this study was that these patients with underlying inflammatory bowel disease, the risk remains low except in patients with Crohn's disease, so we may be able to judiciously use NSAIDs in some of these patients, and I think this data will help to formulate new guidelines about the use of NSAIDs in inflammatory bowel disease.

Hi, it's David Lu here reporting from ACI twenty five. Lots on the poster floor today on day two. Want to tell you just a little bit about RAILD screening. There's been a lot of attention about this. I think we've started to realize that a lot of us are doing it sub optimally, not screening enough people, especially high risk rheumatoid arthritis patients to screen them for the possibility of interstitial lung disease.

I think we know that HRCT is the gold standard, but some of us might be a little bit nervous about the ionizing radiation associated with it. So the temptation of course, is that maybe we should be using respiratory function tests and chest x rays instead of going full throttle with the HRCT. Is that a good idea? Certainly, the guidelines don't think so. And today I saw some data from Spain, Madrid, really outlines what the performance of those tests are like.

So they cohort that they've done HRCT as well as respiratory function tests respiratory function tests and chest x rays at baseline. And to give you some idea of the numbers as to how good respiratory function tests and chest x rays are, we're talking about in all comers, seventy percent sensitivity, fifty percent specificity. If you look just at asymptomatic patients, we're talking about fifty seven percent sensitivity, 56% specificity. And if you go to the symptomatic patient thinking, well, maybe those are the ones with advanced enough disease that we might see them on chest X-ray, you're still only hitting a 78% sensitivity and 30% specificity. Now, in a situation where we wanted to detect early so that we can potentially introduce anti fibroidics early and introduce a whole gamut of IOD care early enough, I think that just simply isn't good enough.

Lung ultrasound certainly looks promising, may or may not have access to that, but right now, HRCT is the gold standard. And if we're going to be screening for RA, ILD, we shouldn't be mucking about with other tests, HRCT is what we should be looking at. For plenty more on RA, ILD, and all the rest, you know where to go, roomnow.com.

Hello, everyone. I'm Richard Conway from Dublin, Ireland reporting for RheumNow from ACR twenty twenty five in Chicago. Today, I want to talk to you about abstract 2346. This is a poster presentation by Zavada and colleagues from Prague. And this poster looked at the effect of biologic DMARDs on sexual dysfunction in ankylosing spondylitis.

So they had fifty two men with radiographic axial spondyloarthritis. In these men, the baseline prevalence of erectile dysfunction was twenty three percent. And what they found was that six months after starting biologic agents, there was very significant improvements, both in erectile dysfunction and in other measures of sexual function. And there was a nice little companion piece to the study. There's another poster presentation by the same group, which is poster thirteen fifty, and this is looking at female populations, as women with rheumatoid arthritis starting biologic DMARDs.

And it found very similar findings with some baseline issues with sexual function and significant improvements after starting the biologic agents. So this might seem like a small thing to many of us, but I think it is something that's very, very important to patients. I think it's something that we may not be told about. These individuals may be kind of simultaneously attending their primary care and asking questions and looking for assistance with erectile dysfunction. But I think if we have the opportunity to raise this, then we can reassure both men and women that issues with sexual function may well improve after they start their biologic agent, and particularly after this agent gets the disease under better control.

So I'm Richard Conway. Follow me on Twitter at Richard P A Conway, and do tune into RheumNow for all the updates from ACR twenty five in Chicago.

Hi, everyone. This is Orelinage from Glasgow, Scotland reporting live from ACR twenty twenty five. Today has been such an amazing day. So many pastas, so many abstracts, so

many

presentation. I picked an interesting presentation for you guys presented at the psoriatic arthritis session, and it's number 877. So what I've been looking into is at risk PSA. This conference has loads of presentation on at risk array, and I and I wrote an article about this, so go check it out if you haven't yet on the RheumNow website, but for PSA, there's not that many data in at risk patients for many reasons. I think one of them is that because these patients have most of them psoriasis, so they're already kind of in the medical system, they're already seeing a dermatologist and if they have joint disease or joint arthralgia or pain, are usually sent to us from dermatology.

But in this specific work, and that's the reason why I selected it, they looked into patients with arthralgia at risk of progression into PSA that were identified through a different way. They were identified through a cohort of patients. So it's an Argentinian study and so they have this cohort of people called RheumCheck and these are patients that have arthralgia and they can self refer to the program and they're gonna get labs, ultrasound, clinical examination. And then if there is any signs of inflammation, they're actually gonna get a treatment. So, what they identified as at risk for PSA was having at least either psoriasis yourself or a person in your family.

So family history, arthralgia, and they had also identified risk factors in a previous cohort that was psoriasis for over fifteen years, family history or obviously ultrasound, synovitis or ensisitis. But in that case, we're already kind of looking at a very advanced sub pre clinical, subclinical PSA stage. In any case, out of fourteen hundred patients, part of their cohort, they identified eight point four percent that were corresponding to this definition that it came up with. And they looked into these patients specifically over the course of a year to see who progressed. And so over the course of a year, thirty percent of these patients developed PSA, which is quite a lot in a year.

That's what that kinda makes me think that they were probably already fairly advanced into the PSA path. But also, forty percent of them received the drug. And the main factor to predict whether or not they were gonna receive a drug was whether or not they had psoriasis. And I think it's just because as a clinician, you're more comfortable giving someone with strict say, because they've got arthralgia and psoriasis than if they just got arthralgia. But in any case, out of these people that progressed into clinical PSAs to the thirty percent, sixty two percent were already treated with anti inflammatory or methotrexate, but just suggestive that maybe prevention or at least interception doesn't work really well in this population.

So either the population was already, as I said earlier, very advanced into the kind of PSA path or maybe the intervention is already too late. We need to have intervention studies in PSA, but they do represent challenges on their own because there is no clear definition on what at risk for PSA means. And so I think the next steps is to identify clear criteria for that population and then potentially think about intervention studies. Certainly something to keep an eye on. Tune on RheumNow for more content and follow me on Twitter at AureliRomo.

Hi. This is Bella Mehta reporting for RheumNow from ACR twenty twenty five. This is an interesting abstract talking about how we should be measuring multidimensional pain in axial SpA patients. The abstract number is zero three eight six, and this is what they call as the West Haven Yale multidimensional pain inventory or MPI, and it is it has five domains that it covers, pain related to life interference, pain severity, effective distress, social support, and life control. They use this MPI versus the ace ASAS OMRAC core domain set, which has things like the usual ASDAS, BSDY, CRP, patient global, total back pain, morning stiffness, and they enrolled around 135 patients or so.

Out of them, only one hundred and nine patients completed all the surveys, but what they found that was the construct validity supported that the pain related life interference and the pain severity did correlate with some of the core domains. But what it also shows is that things like social support, life control, or effective distress is not really captured as well in the core domains. So maybe we need to expand what we are asking of these patients. And, again, I know in clinical practice sometimes it's difficult to get all these sort of domains, but as we go in the future, these patient reported outcome measures are gonna be more and more important, not only from the patient's perspective, but also insurances and drugs and whatever that we need to do for our patients. So it's good to start getting some of these core domains in to your clinical practice, see if it's feasible.

Sometimes patients who are in the hallways waiting for you for the next to get in to see you, this is probably a good questionnaires to have which is disease specific and still will help overall improving the quality of life with patients. With that, thank you so much for listening. Follow us more for more RheumNow content, and follow me on Twitter at Bella underscore Mehta. Thank you.

David Lu here for RheumNow. ACR twenty five day two, and there was a really fantastic RA abstracts oral oral abstract session. A lot of fantastic work, some of which we'd heard a bit about before, Kevin Dean's work on hydroxychloroquine and stop RA, which unfortunately was negative. We heard Mandy Cope talking about the Alto study, the continuation of epipipra and the benefit that upfront abatacept can deliver in people with clinically suspect arthralgias and high appetizers. But in fact, one of the things that I think was particularly interesting that we hadn't heard much about in terms of the most recent results was actually data from Leeds presented by Tusk Toyota.

What he showed was looking at a cohort of people who had upfront TNF inhibitor for a year at the time of rheumatoid arthritis diagnosis. What effect could that have? I think a lot of this go through a process which has been reflected in the data up until now, where we start conventional synthetic DMARDs for the first period of time after a rheumatoid arthritis diagnosis and escalate up. But especially in places like The UK, we are getting the temptation to think about whether maybe upfront biologics might have an advantage, especially because with biosimilars, they are getting a lot cheaper. And if you come up with that upfront hit, whether you might have a legacy effect going on, especially thinking about whether we hit that difficult to treat rheumatoid arthritis, which we become more and more conscious about.

So that's exactly what this has looked at over greater than ten years follow-up after an initial one year of TNF inhibitor. It's not a randomized trial, they've looked at a cohort that they treated and compared it to controls from their clinics, but you can get an idea as to where the potential benefit is. So at five years, I saw that in fact, that upfront TNF inhibitor treated group had less difficult to treat rheumatoid arthritis. We saw more remission at ten years in that group as well. We saw that in fact, more people had come off, had actually come off DMIs altogether at five years.

So drug free remission in that TNF inhibitor upfront group. We did see as well that actually the patients in that upfront TNF inhibitor group were slower to actually need a biologic later on. The median delay there was actually eleven months. And so it raises a question whether actually this might actually make sense from a cost point of view, as well as in terms of the clinical point of view. And in The UK, they are certainly focused on that.

It did seem from these data that it would support a pharmacoeconomic benefit from giving upfront TNF inhibitor. And with the cost of TNF inhibitors dropping down and down and down, the question will be, as biosimilars take hold, should we be giving a little upfront burst to try and get these patients to a better track than it would have otherwise been? It isn't quite enough to act on yet, but certainly raises some important questions that I'll bring back to the clinic and think of that with my patients. For plenty more about rheumatoid arthritis, everything else at this magnificent conference, you know where to go, roomnow.com.

Hi, it's Doctor. Janet Pope or JanetBurdope tweeting for AtRoomNow. This is ACR twenty twenty five in beautiful Chicago. So I wanted to talk about does your neighbor matter. And, of course, I'm not talking about where we live.

I'm talking about something from a basic perspective. So, doctor Sarah McCoy did a beautiful study that she presented in abstract number one six eight four. So as many of you know, she's a translational and clinical scientist in Sjogren's syndrome and a rheumatologist. So here was the question. If you have Sjogren's and you are rho positive versus rho negative, what does that look like in the milieu of the cells around the gland where you've had basically a biopsy of a salivary gland?

So she had some biopsies of patients with lymphocytic infiltrate who had Sjogren's disease who were rho positive and some who were rho negative. And she found that looking at the cells in the milieu and the potential signaling that rho positive patients were very different than rho negative. And then she went on to look at, well, what if you're row fifty two positive versus row 60? And even in row 52 and row 60, some of the cell signaling was different. Now what is the take home implication?

So right now, this is interesting. She had beautifully, illustrated pictures of how these cells are different and what the cell types around the rho positive versus rho negative are. But what might be really truly important is what would be the response to therapy in a rho positive patient versus rho negative or a rho, in the, 52 versus a rho sixty. So more will come, but I thought this was one of the ACR best that I've seen today because of the elegant science and a potential eventual clinical take home message. Thank you.

Please follow me at RheumNow.

Hey, everyone. This is Jeff Sparks from Brigham Women's Hospital in Boston, Massachusetts, and we are here at Chicago for day two of the twenty twenty five ACR Convergence Annual Meeting. Today, I'm gonna be talking about new paradigms for the treatment of rheumatoid arthritis. Obviously, we have a lot of great treatments for RA, but a lot of our patients are still suffering. And there haven't been a lot of advances over the past decade.

Certainly, a lot of other diseases have benefited from this, but I think RA has languished a bit. But luckily, there's three trials I wanted to talk about here that are really paradigm shifting, at least potential to be paradigm shifting for rheumatoid arthritis. The first I'll talk about is RESETRA, which is an implantable left vagus nerve stimulation. So, obviously, this is very different from any other treatment that's ever been approved for rheumatoid arthritis before. This involves a surgical procedure, overall relatively minor, but certainly different to refer your patient to a neurosurgeon to have this implantable device.

And this periodically stimulates the left vagus nerve, which has been shown to decrease inflammatory markers. So there were two abstracts that were interesting from this RESET RA study. The first abstract, 1675, reported the primary results. And the primary outcome was an ACR twenty at month three, and this was randomized to basically turn the device on or to have a sham where basically the the procedure was implanted but not turned on. So in 1675, that the ACR twenty was hit at around 40 of patients compared to less than twenty percent of those with the sham intervention, and this was statistically significant.

And this showed that this neuroimmunomodulation could be helpful and efficacious to treat RA, and many of these had failed several biologics. I think a particularly interesting part of this is that there continued to be improvement in month three where all patients crossed over into the active arm, and it seemed like this was overall pretty well tolerated. There were some patients who had, some hoarseness and dysphonia, but overall not thought to be too, severe. A corollary subgroup analysis of this was twenty six fourteen, and this was looking at, basically, radiologic progression, looking at MRI scores. And this is not something I necessarily expected that a neuroimmunomodulator would actually decrease the progression of structural damage in rheumatoid arthritis.

And overall, there was a trend towards statistical significant and the intention to treat analysis. However, in the subgroup analysis where they restricted it to people who are high risk of developing or worsening ROSENS, particularly if radiographic features at baseline, it was statistically significant. So this is a real proof of concept that this could be a very different therapy to offer our patients. The next, study I'll briefly highlight is the Rinnoir study at l b 19, a late breaker. This is a phase two b study looking at rosinilimab.

This is a study that depletes pathogenic, T cells. In one of my previous videos, we talked about T peripheral helper cells, T follicular helper cells, which seem to be present in higher numbers, particularly in people at risk for rheumatoid arthritis and those that are seropositive. So this study randomized people to rosnilimab versus placebo, and this also hit its primary outcome of hitting an ACR twenty and also had differences in ACR 70 as well as many other secondary outcomes and was also very safe and well tolerated. And I think that should lead this towards maybe perhaps a phase three study that would really needed to be established efficacy and safety. The last study is l b 23 that I'll highlight, and this is a CAR T study.

However, it's a different kind of CAR T study because the T cell that they use is a Treg. And because this cell is relatively a a peacemaker, if you will, this one doesn't actually need chemotherapy. It isn't expected to have much side effects. And it's also targeted against citrullinated antigens that are specifically implicated in RA pathogenesis as opposed to c d 19 that many of the other CARs. So this is a a different kind of CAR T trial.

And this is very early study, just phase one, and there did seem to be some transient benefit. I'll say that compared to the c d nineteen, this was not, as efficacious. However, this is a dose finding study, and perhaps a higher dose might be needed for more, lasting effects. But, again, I think this illustrates how, CAR T could be used in many different ways besides just a c d nineteen CAR T effector cell. So these are just, three examples of some potential paradigm shifting studies within rheumatoid arthritis.

To highlight, we're talking about neuroimmunomodulation with an implantable device. We're talking about depleting pathogenic T cells, and we're also talking about actually using CAR T regs as a anti inflammatory in a CAR T environment. So again, thank you for your attention, and hopefully you're learning a lot at ACR twenty five, and I'll look forward for more reports. Thank you.

Hi. This is Bella Mehta reporting for RheumNow from the ACR twenty twenty five. It's been an interesting conference so far, and I just attended a session talking about biomarkers in Still's disease and MAS. So again, Still's disease is an auto inflammatory disease, SGI in pediatrics, and adult onset Still's disease in adults. And there's many biomarkers that have been talked about.

Back in the 2000, there was a lot of talk about glycosylated ferritin, which seemed to be a good biomarker for detecting flares and disease activity, but it never really took a big stand in clinical practice. Ferritin, obviously, we all know has been something that is widely used, widely accessible, but the new biomarkers or sort of biomarkers that have been talked about in the past few years has been IL 18 levels. So this talk was about how IL 18 levels can be useful in the clinical diagnosis as well as management of Still's disease. Specifically, five to 10,000 IL-eighteen levels seem to be an important marker. And when it's combined with the ILA criteria or any of the other criteria, the sensitivity of this increases.

The next thing they talked about was biomarkers in MAS. CXCL nine seemed to be an easy one or something that should be sent out for patients with suspected MAS. The other one is the soluble I l two receptor alpha. Both of these are usually sent out, but in my clinical practice, I feel like it takes a while for these markers to come back. So you still have to go with the patient's overall clinical picture when you are trying to assess these patients, but these are definitely great tools.

And with their availability being more easier, it'll be good to use them widely. And the last thing they did talk about is the interferon gamma drugs that are out there, like the Gamifen, and how they, you know, some of these drugs can or or the drug can help decrease the biomarker levels, and this the decrease in the biomarker level almost corresponds to how good the patients get clinically. So with that, things to remember, ferritin is something that we've always sent for Still's disease. IL eighteen is probably a very good biomarker. We should try sending it out.

And for MAS, try and send out CXCL nine as well as soluble IL two receptor antibody. Thanks. With that, this is Bella Mehta signing off, and please follow us more for RheumNow contents. Thanks.

Hello, everyone. My name is Youssef. I'm a consultant rheumatologist from Leeds, and I'm reporting live in Chicago for the ACR two thousand twenty five conference. In this conference, there have been so many abstract pertaining to cell based therapy using CAR and also bispecific T cell engagers. So I usually don't cover early studies, you know, for the audience understanding, but I do find that this abstract really interesting.

It's super sexy and super new, therapy. That's why I just want to bring, this abstract into into the audience. So the abstract that, I'm talking about is abstract number one five three five. So this abstract is a T cell engagers, but it is using the pan gamma delta T cell engagers. So I'm here.

I'm so delighted, you know, to be joined by the co authors of the abstract. So we got doctor Kate Rocklin here. Hi. Hi, Kate.

Hi, thanks for having me.

Yeah, thanks for joining us as well. So what I just wanted to know, can you please explain about your compound? What make it different and exciting compared to other current T cell engagers?

That's a great question because there are a lot of T cell engager approaches out there right now. And what we really love about what we do is that we're leveraging the power specifically of the gamma delta T cells. So this is a subset of T cells that are incredibly cytotoxic, very powerful killing cells, but they don't secrete the cytokines that induce the toxicities that you see with a lot of the current T cell engager approaches on the market. So what we've actually done is we've built an engager that targets c d 19, and it targets the gamma delta t cells using the gamma delta TCR. So we don't target through c d three.

That means we don't run the risk of the toxicities that you typically see or the cell based exhaustion that you can see with other engager approaches. And then importantly, we've tried to overcome the challenge that gamma delta t cells are a very low percentage cell in the immune system. Very powerful, small but mighty. So what we've done is we've developed a gamma delta t cell expansion domain that actually allows those cells to expand in vivo. So we're activating and expanding those cells to be able to drive deep and complete B cell depletion using our engager.

Oh, that that's really exciting and certainly stand out from other T cell engagers. So in terms of this abstract itself, so you do you you've done some in vitro studies. Can you just briefly summarize what were the key points from the from the study?

So in our poster, we were able to demonstrate that our engager is in fact a pan gamma delta T cell engager, meaning that we target a region on the gamma delta T cells that hits multiple gamma delta T cell subtypes. So both the V delta ones and the V delta twos, so we're able to drive cells that both hone to the tissue as well as the cells that circulate in the lymphatic and blood systems. We've also been able to show that compared to commercial B cell depleters, such as, blinatumomab or Mazu, that we can drive complete B cell depletion in vitro comparable to those two depleters. And that's very exciting for us because it tells us that we don't need to activate through CD three and drive all of the T cells. We can specifically activate and expand the gamma delta T cells, they are powerful enough to drive complete depletion.

So that was very exciting data for us. And importantly, we do it without any elevation of the CRS inducing cytokines like IL-six that are so concerning, particularly as you move into that autoimmune space and you really don't have room for those toxicities at all.

Wow. That that this is sounds really exciting. And and in terms of where do you go from here, would you like to explain a bit more?

Exactly. So I think we've been able to show now that we really get nice T cell expansion. Importantly, we've shown that by activating both of these immune compartments, V delta one and V delta two, we can actually cover depletion across a spectrum of autoimmune conditions. So in some patients with more advanced disease, you have one compartment that's more responsive than the other. So now we're moving this into animal models.

We're looking forward to bringing that data out in the next twelve months or so, and then looking to bring it into the autoimmune space. And so we're just very excited to be here sharing our data and hopefully bringing the power of gamma delta t cells from oncology, which is where we started, into the autoimmune space where we really think there's room for a powerful cell type with a lower, toxicity profile.

Yeah. Thank you so much for the the wonderful, in the summary. And talking about space, I think we definitely will watch this space for this molecule. And so I hope you found the interview interesting. And follow me at use six yousef on x and also all other my colleagues at RheumNow for further content coverage.

Thank you, everyone. Bye bye.

Thank you. Hello.

Janet Pope here reporting at RheumNow. This is lovely Chicago at ACR twenty twenty five. I wanted to talk about a nice talk that I heard on, the heartbreak. There's a little heartbreak in quotes here of sarcoidosis. So, there was a big Stanford cohort of sarcoidosis, and they wanted to look at what's happening in cardiac sarcoid, how is the treatment algorithm, and how do you work these people up and follow them.

So in this cohort, as many as fifteen percent of patients with sarcoidosis had cardiac involvement. That's probably higher than many cohorts because they enrich for this, area of expertise. They had a really good algorithm, usually PET scan, not usually a cardiac biopsy. They've also had improved, mortality, with cardiac sarcoid. So the first thing to note is that you will start if you have active PET scan cardiac involvement with sarcoidosis.

Often, you'll have involvement systemically as well, but not always, hilar lymphadenopathy, etcetera, mediastinal nodes too. What you'll find is that one third of patients will respond well who have cardiac sarcoid, to methotrexate and glucocorticoids. Then when you taper the glucocorticoids, you wanna find out are they gonna rebound or not, so they usually do a repeat PET scan to see if it's active. If there's a failure or you can't get the person off, glucocorticoids are still smoldering, they'll use monoclonal antibody TNF. They'll usually use infliximab, but they might use adalimumab.

Usually, again, there's a very high response rate. If this doesn't work, anecdotally, data are emerging using a JAK inhibitor, so they might use a JAK inhibitor. Why am I telling you about this? I think, number one, we have to identify cardiac sarcoid in a patient with sarcoidosis. Number two, there are some risk factors of people who don't respond as well.

Often, right heart involvement is less responsive, and also people with a lot of systemic involvement are less responsive. Number three, there was an excellent algorithm, and I will take this home. I run a bit of a cardiac sarcoid clinic in order to get access for the drugs for my colleagues. And the final thing is mortality has improved by treating earlier identification, these advanced therapies, and I think also by implantable ICDs because many of these patients die of arrhythmias. Please follow me at RheumNow.

It's at Janet Burdope. Thank you. Bye.