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

Hello. My name is Atul Devdar. I'm a rheumatologist at Oregon Health and Science University. Perhaps the most important presentation at this year's meeting in the field of Excess Spondyloarthritis has been the classic study which was presented in the plenary session this morning. Classic study classic stands for classification of axial spondyloarthritis inception cohort.

And this study reported the the work that was done by Spartan and ASAS, ASAS, over nine years. The study basically started in 2016 with the understanding that we need to do something about the classification criteria that existed from 2009 regarding axial spondyloarthritis. The FDA thought that the original classification criteria were did not have enough specificity, and probably the non radiographic axial spondyloarthritis diagnosis could be misused, and fibromyalgia patients and mechanical back pain patients could be diagnosed or classified with non radiographic axial spondyloarthritis using the 2009, ASAS criteria. The classification criteria should not be used for doing diagnosis. Unfortunately, people were doing that.

And because of this concern, FDA suggested that in clinical trials, if this criteria are to be used, the 2,009 criteria, there has to be either positive CRP or positive MRI, high CRP or positive MRI. They also imposed a fifty two week placebo controlled study requirement for non radiographic excess spondyloarthritis. With all these limitations, it it was decided that we should revisit the 2,009 classification criteria by ASAS, repeat the study, and see what is the sensitivity and specificity of that criteria to validate the original criteria. We decided a priori that if the sensitivity is not 75% and the specificity is not 90%, then the criteria will be revamped. Over the last six years, when I participated in this study myself, we took care of we diagnosed or we saw one thousand and fifteen patients worldwide, five hundred and four in North America, which is US, Canada, and Mexico, and the remaining, patients from rest of the world.

This was done during COVID, and we these were patients referred to the rheumatologist with the suspicion of axial spondyloarthritis. And the rheumatologists were asked to make a diagnosis based on their just the history, then the physical findings, then with their blood test and HLAB twenty seven, then the CRP, and the MRI, and then the MRIs were centrally read. And the final diagnosis, when the when the, rheumatologist made the final diagnosis, they had all the information regarding these patients. What came out was that thirty six percent of the patients in this study had excess spondyloarthritis. Based on that, the old 2,009 criteria were looked at again, and we found out that they actually had 72% to 78% sensitivity, and the specificity was not nowhere close to ninety percent.

It was about eighty two percent. Because of that, the criteria were needed to be changed. We sat together lasso analysis, which is something similar. It's a statistical way of finding out which which different criteria which different parts of the spondyloarthritis, disease are important, and LASSO gives them a coefficient. So for example, HLAB 27 and the CRP, inflammatory back pain, etcetera.

And based on that, we came up with coefficients, for the important spondyloarthritis features. Finally, this criteria were developed two different models were developed. The Spartan and the SS members voted, and one of those two models, has come out as the winner of this classic, study. These criteria will soon be published. They are now in the table format.

There is a stem for this criteria, which is patients with chronic back pain starting before the age of 45. But then there are numbers, there are, there are points that you give. So MRI has eight points, X-ray has got seven points. Ultimately, if the patient has 11 points or higher, then they can be classified as excess spondyloarthritis. In my mind, this is a major advance in the field of axial spondyloarthritis because these criteria have more than 90% specificity, more than 75% sensitivity, and they will be used going forward in clinical trials, and we can be mostly reassured that patients who should not be included in the trial will not be included, because they will not fulfill this classification criteria.

Hello. My name is Atul Devdar. I'm a professor of medicine at Oregon Health and Science University in Portland, Oregon. My research interest is in axial spondyloarthritis and psoriatic arthritis. And today, I'm joined here by Doctor.

Mohammad Biktar, who is also an assistant professor at Oregon Health and Science University. Doctor. Biktar's research is very novel, and this is a big trend that actually I'm noticing in this particular conference as well and that's why I thought I will bring him here to discuss his research but just in short what we are finding is that nowadays in inflammatory arthritis, spondyloarthritis included, the morbidity is not because of the inflammation. We are pretty good at controlling the inflammation of our patients with our biologics. Leftover pain, leftover pain, leftover fatigue is the reason why people are becoming disabled.

And so doctor Bittar has some very novel research ideas. He had a poster here. He also was chairing a session on this particular entity of leftover pain. So Doctor. Bittar, take it from here.

Tell us a little bit more about this leftover pain and how can we measure it and what can we do about it.

Thank you so much for having me and this is an extremely important topic that has been neglected in rheumatology. As you mentioned, we always focus on treating inflammation, inflammation, but we forget about the leftover pain which is driving the patient's disability and the symptom and the burden of the disease and that's why it's time for us to focus on studying pain and rheumatic diseases. So I'm very happy to share that in this conference at the ACR we've seen a lot of new work on pain in rheumatic diseases, whether in rheumatoid arthritis, in psoriatic arthritis, of course in axial spondyloarthritis, our research interest. I can talk to you a little bit about the project that we've done, where is we are trying to look into the brain imaging and the CNS, central nervous system dysregulation in patients who have axial spondyloarthritis because this can explain why patients continue to have chronic pain without having inflammation. So in particular we're interesting at looking at resting state connectivity on how different parts in the brain connect to each other and also how the brain responds to a painful stimulus.

So for example the project that we've done on ACTFL patients that showed that axSpA patients respond differently to a painful stimuli compared to healthy controls. For example, mainly we got two signals from the default mode network and the salience network. Default mode network, it's usually is active when we are in a relaxed state. Whenever we get an input or an insult, this should be inactivated. Our study showed that in patients who have axSpA, actually default mode network got activated, which is abnormal that means patients are focusing on the brain is focusing on pain and that's why they go into a chronic pain state.

Also the salience network it got exaggerated responses Salience in network. Okay. In AXPA compared to healthy controls. So we got signals that different parts of the brain are working differently in axSpA patients who have chronic pain.

Yeah. So there were some abstracts yesterday, and you were chairing that one session, where some similar work has been done also in rheumatoid arthritis and psoriatic arthritis. Do you want to tell us about that?

Definitely. And there was a very interesting oral abstract that was presenting yesterday on rheumatoid arthritis where patients had, I believe it was twenty seven patients who had functional imaging of the brain and a task was an input or a painful stimulus was done on rheumatoid patients and the rest and it showed activity in the insula and the brain which is part of the salience network. Similarly, there is another session on psoriatic arthritis, but this was mainly on fatigue and that showed that insula played a role in it. So, are seeing a different mechanism that are non inflammatory playing a role in rheumatoid and PSA and axSpA, so we need to start looking at these pathways.

Yeah, this is going forward, we are going to be looking at more and more research as well as abstracts at annual meetings. And and we will hopefully one day find the differences of how the brain works with nociceptive and nocplastic and neuropathic. Those are the three different different types of pain. Which parts of the brain get activated and how we can intervene to prevent this? I think this is something that I would suggest, the viewers should keep, should be aware of and keep an eye on.

This is a very exciting new area in the field of rheumatology.

Hello, my name is Doctor. Guillermo Valenzuela. I'm a rheumatologist practicing in Florida and I'm happy to bring you today information about the recent poster that we presented about new immune modulation in the treatment of rheumatoid arthritis. And I will be presenting you a succinct version of study which reflects the results of the RESETRA study as it was named. So this study essentially has shown and demonstrated the benefits of an implantable device on the vagus nerve which produces a constant daily stimulation of approximately one minute.

And that device has shown to, produce results that we now have captured in the RESET trial. The results of the trial show that the primary endpoint were those of ACR20 at three months and the outcomes from that result showed that there was a statistical significant difference between the treatment group, which was the group of patients who received electrical stimulation of the vagus nerve on a daily basis versus the patients who had the implanted device. However, that was not turned on. And the difference was forty four percent in the treatment group versus eighteen percent in the placebo group. What is more interesting is that after the three months, all patients roll into the active treatment group.

And we see that by month six, the patients who were originally in the, control group were able to, accomplish the same ACR20 results that we saw originally in the first cohort of ACR20 treatment active patients. Those results continue to, remain, stable and within positive upward upward trends, towards the end of the year, which was twelve, twelve months of the complete, observation period. Important is to also mention the, adverse events noted in this study, the ones that were specifically related to the implanting of the device which was only one point five percent in one individual who received the treatment. After three months, the patients, if needed by choice of the physician or by requirements of the disease activity, patients had the option to add additional therapy to their regimen such as DMARS or targeted synthetic DMARS. However, only eighteen percent of those patients were added this therapy, whereas eighty two percent of the patients continued after three months of additional therapy besides the baseline therapy and continued in this way through month twelve.

These studies results certainly and strongly support the clinical use and demonstrate what the use of neuromodulation causes in patients with rheumatoid arthritis. And we invite everyone to become more familiar with this path pathophysiology of this process because it's the beginning of a new era.

Hi. This is Bella Mehta reporting for RheumNow from ACR twenty twenty five. This is a very interesting abstract that we came across. So what do you do after you fail the first TNF in an axSpA patient? This is late baking abstract zero nine.

And what they did is was a prospective randomized multicenter open label superiority phase four trial, of patients who, have a pretty active axSpA with an ASAS, AS DUS greater than 3.5 or BASDIG greater than four, and randomized them to either get a second TNF or IL 17 agent. So they call the study rock ROC SPA, ROC SPA, And this was a multicenter study study, 31 sites across France and Morocco. And the primary outcome that they were looking at was forty percent oh, sorry. ASAS 40 at week twenty four, and then the secondary outcomes were the same at week twelve and fifty two just to see how these patients do. And they had pretty good sizable numbers, one fifty two patients in the TNF arm and around one forty two patients in the sorry.

One forty two patients in the TNF arm and one fifty six patients in the IL 17 arm. And what they found was that the primary outcome was no different or at least they did not prove superiority of IL seventeen as the second agent when the first TNF fails. Now if a patient discontinued TNF because of an adverse effect, then going to the second TNFs may TNF made sense, which is what we do in clinical practice. But, you know, there was some very, very small exploratory data that they talk about where, you know, going to IL-seventeen might be better in patients who who are HLA B27 negative or those who have CRPs less than five. I don't know if, you know, if you talk about subtyping, they are a different subtype of patients that they are hinting to, but, I think it's, good to know that going to a second TNF versus going to an IL-seventeen agent is not wrong.

Like, you can choose whatever works better. And I think I think this is an important paper and that we look forward to and an abstract that would be interesting to see. Thank you.

Hello. My name is Doctor. Philip Meese. I'm the Director of Rheumatology Research, at Provident Swedish Medical Center in Seattle, and I conduct rheumatology practice in Seattle as well. Over the past two years I've been the PI for a variety of CAR T cell therapy trials in combination with our hematology oncology division at my institution and it's been quite a ride.

So I've been taking on many of the cell therapy trials that have been conducted in autoimmune disease ever since the initial report from Erlang in Germany from Bjork Schatz group showed how effective CAR T cell therapy can be in lupus. One of the sessions here at the ACR meeting was a overall review of CAR T cell therapy and a wonderful update from Joan Merrill. And she highlighted a meta analysis that was authored by Nord van Goemas in seminars in arthritis rheumatism and what he did was review 16 studies, 13 targeting CD19 and three targeting CD19 and BCMA. There were 12 autologous CAR T trials and four allogeneic ones, and for a total of one hundred and forty five subjects with lupus that were treated. Some summary from that included the fact that at baseline these patients had very active disease with an average CDI score of 13, and with treatment this decreased to 2.3 after six months and 1.4 after twelve months.

It does show that it takes a little bit of time, you don't get immediate results, but ultimately very, very significant improvement in overall disease activity scores, with doris remission seen in seventy percent of patients, LDAS in eighty nine percent of patients, and drug free remission in eighty four percent of patients. Highly effective, and this mirrors our own experience working in clinical trials with lupus patients, where the longest out that we have is a one year patient who is drug free and having essentially no signs of lupus. Occasional rash, mouth sore, but really doing very well. Now side effect wise, there are some very specific things that have been seen including something called cytokine release syndrome or CRS, and in this meta analysis that was seen in slightly over half of the patients, usually grade one or two, and this would be, for example, fever or slight change in blood pressure, but overall very well tolerated in our center, treated either with Tylenol or Tocilizumab. In these reports there were four cases of ICANS.

ICANS is what is called immune effector cell associated neurotoxicity syndrome, can be confusion, for example, or word finding problems, and usually quite responsive to either steroids and or other treatments. We're rarely seen either grade one, two or three most often. And then seven percent of patients developed serious infections and there was one case report of fatal pneumococcal meningitis. So there are potential side effects. In addition to the CRS and ICANS that I mentioned a moment ago, there can be cytopenias, hypogammaglobulinemia, and downwind reported in the cancer treatment literature.

Very, very rare risk of CAR related cancers. A new toxicity that has been reported is an interesting one, known as LICATS, or Local Immune Effector Cell Associated Toxicity Syndrome. What is happening with this condition is that the patient may report a flare of some of their basic lupus symptoms, such as skin rash or arthritis or proteinuria that occurs somewhere around three to four weeks after cell infusion, and this tends to be transient, pretty easily treated with steroids and or tocilizumab. It seems to be associated with an area where B cells have been ablated and this may be a reaction to the B cells that are dead there in that particular tissue. Again, this is transient and tends to be relatively benign.

We don't think that this represents a flare in their basic lupus activity. So what I liked about this overall presentation was how much it mirrored our own experience, both in terms of the degree of effectiveness that can be seen, many, many patients with Doris remission, but also some of the side effect profile. There

are

a number of us who are conducting these trials that are now gaining the experience that the hematology oncology physicians have gained in their years of using this type of therapy. So I think that clearly we're going to be moving into an era where this type of therapy can become available for other refractory lupus patients. It is expensive, pretty arduous, and there are going to be some possibly more practical off the shelf allogeneic therapies coming along and T cell engagers. We'll save that for another video to have a more in-depth discussion about those newer approaches. Thank you very much.

Hello. I'm Andrea Fava from Johns Hopkins University coming to you from ACR in Chicago. I wanna discuss today about the importance of addressing lupus nephritis early. There was a beautiful plenary session by Michel Petrie coming from the Accelerating Medicines Partnership group that showed that if we biopsy lupus patients when they have a proteinuria above 0.5, which is the agreed threshold, it may be too late. Biopsing at point five at point two five was already able to identify seventy one percent of lupus nephritis patients and fifty six percent of all these patients had actionable lupus nephritis.

If we identify nephritis early, we can intervene early, and there is a much lesser fire to put out. So think about biopsy patient at put point two five grams, you're gonna find lupus nephritis early is gonna make your life easier. The other is, point that will go in this direction is that there was data presented by Brad Roving that showed if you wait for proteinuria to be too high, two, three grams and more, is gonna take much longer to obtain a response. And we do know that having a high proteinuria baseline and a delayed response is associated with a higher risk of loss of kidney function, is what exactly we want to prevent in lupus nephritis. The other point about catching and addressing lupus nephritis early is that if we can get patients into remission early and if we can show that even the biomarkers that identify inflammation in the kidney can go down early, as early as three months, that early response is associated with a much lower risk of permanent loss of kidney function in the next five year.

So the, operative word is early, and so catch lupus nephritis early, address it early, address it aggressively, and we're gonna improve outcome for lupus nephritis. If you wanna learn more, go in the room now. Hi. I'm Andrea Fava coming to you from ACR in Chicago. Lupus nephritis is bad.

Among the lupus manifestation, among the severe manifestations is the most common one. And one of the most dreadful complication is end stage kidney disease, and and twenty percent of patients in the twenty years after diagnosis may develop that and end up on dialysis. So how do we prevent that? Recent data have shown that the more aggressive you are early in the disease, the better the outcomes. And in fact, the guidelines for the treatment of lupus nephritis, both from the ACR and EULAR, reflected that concept, that early intervention with aggressive treatment that is called combination or triple therapy, which is more than one immunosuppressant, is now the standard of care, and the data strongly support that.

So we need to invert the pyramid in lupus nephritis and in lupus as well. So treating very aggressively early is going to pay off. Now, how long to be aggressive for and how soon we can peel off medication, that's still to be determined, but I think that the theme needs to be, let's be very aggressive at the beginning. Let's use many medications so we could reduce steroids and we can reduce complication and bad outcomes. Now will this apply also to SLE?

Probably, yes, but we don't have the good data that we have in lupus nephritis. In lupus nephritis, the three major clinical trial that led to the FDA approval of the three medication we have for lupus nephritis shown that combination treatment works. In, SLE, we have some data coming from post hoc analysis of many of the other biologic trials showing that early intervention with biologics may reduce damage, but we need to do those clinical trial to show that the very aggressive treatment at the beginning is going to pay off and perhaps keeps patient from developing damage, which is exactly what we expect. If you want to learn more, please go on RheumNow.

Hi. This is Bella Mehta reporting for RheumNow from ACR twenty twenty five. We have Jeff Sparks with us who's from Brigham and Women's and he's the Director of Immuno Oncology. And

Autoimmunity.

Yes,

And

Autoimmunity at Brigham. There's a lot of talk at ACR about CAR T cells, we thought we'd hear from the expert here. Tell me, what do you think about CAR T cells and what are the best abstracts or sessions you could recommend people to go to?

Well, as in previous meeting, there's a lot going on with CAR T and I think the field is exploding and, you know, cells and cellular biomarkers, cells as intervention, it's just really been incredible to see it grow. As we know, maybe a few years ago, we were really only talking about auto CAR T, talking about chemotherapy, long hospitalizations. And now this year, it's moving even more into off the shelf, is Allo. Also doing in vivo CAR T, and then I think a lot more interest in T cell engagers both bispecific even trispecific antibodies. And the way I would term it is that at the moment there's some early adopters that are really trying to test out the field.

I think the rest of rheumatology is really trying to see where things fall into place. And are they going to have to get an oncologist on board, a pheresis unit, get familiar with chemotherapy, or is it gonna be something where you could do all this in vivo? But certainly it's been transforming the field.

Great. Great. So, just for people to understand, when you say in vivo, how does it work?

Well, we don't have

all the time here, but basically, lipid nanoparticle units are injected and basically give instructions for the engineering to actually occur within the body as opposed to having to extract cells carefully, engineer them, ex vivo, you know, freezing them. So you can imagine that there's a lot of appeal to do this in vivo because, you don't have to go through all those inefficiencies. However, of course, there's so many details, there's so many things to iron out that this is still very, very early days.

Okay. So does it change the cost and do you think that will open up this technology to more patients?

Yeah, cost and efficiency, access are gonna be the big issues and all of those we need a lot of work on as you probably know. Right now it's very expensive, it's a bit of a cherry pick patient that's able to be sick enough to qualify but adherent enough and have all those resources involved in order to undergo these really complicated protocols. And certainly it's very expensive now, and there's so much enthusiasm here. Am cautiously optimistic that many of these can be lessened.

Great. Great. Thank you. So is there any particular sessions that you would recommend people to go to? Any particular drug is here which is the big one,

do I think I'll highlight a few things. I think most rheumatologists understand that CD nineteen based therapies can really effectively deplete B cells and probably to a greater extent than our other therapies such as rituximab and other related items. But this is really a platform where you can choose many different targets and you can also choose other types of cells, not just T effector cells that have all these side effects. There's some really innovative cars looking at NK cells, but also T regulatory cells. And those in particular, I'm really excited about.

These recently run the Nobel Prize about T reg and you wouldn't expect much toxicity in here. You're basically injecting a peacemaker that hones in to where the, inflammation's going on and in theory at least there should not be a lot of the, you know, acute side effects that would be expected in other types of cells. So I'm not sure one really is standing out from the crowd, but to see the, depth and breadth. And also we're moving on from case reports. Like all the studies now are prospective, they're interventional, they're pre specified, we're and now getting into dozens of patients.

But certainly, we need to get into even more patients. We also need to think about at what point do we do a comparator group. So still early days, but it's incredible how much the field has advanced in, you know, just a few years.

Thank you so much. This is really, really helpful, and thank you to Jeff Sparks, and you'll see more coverage on CAR T at RheumNow. Thank you. Bye.

Hello, my name is Atul Devdar. I'm a professor of medicine at Oregon Health and Science University. I'm going to speak about biomarker discovery in axial spondyloarthritis. One of the issues we have in the field, one of the big unmet need that we have in the field of axial spondyloarthritis is lack of biomarkers. Beyond C reactive protein and HLA B27 and MRI of the sacroiliac joint or spine.

We don't have any other biomarkers. I found there were three studies presented here, two posters, one oral presentation, and they are on fourteen thirty three ETA, which is a protein, and the autoantibodies to that protein in external spondyloarthritis. Rheumatologists know about fourteen thirty three ETA as a blood test in patients with rheumatoid arthritis, and this is known for over a decade now. And the levels, high levels of fourteen thirty three ETA correlate with the disease severity in rheumatoid arthritis. It's also helpful in diagnosis of rheumatoid arthritis, etc.

During the investigation of this protein further, it was found out that the antibodies two fourteen-thirty three eta might be a biomarker for axial spondyloarthritis. It's a very exciting, or interesting, story how that was found out. But in any case, fourteen thirty three Eta is a intracellular protein. It's a chaperone protein, and it lives inside the cell, but if it is externalized, then the body can make autoantibodies against this protein. It was found that patients with axial spondyloarthritis have high levels of this particular autoantibody.

There was one poster at this meeting which compared the autoantibody levels of fourteen thirty three eta in patients with radiographic axial spondyloarthritis, or what we used to call ankylosing spondylitis, with normal controls, and it was found out that the levels were high. They also found out that if you combine this biomarker of autoantibodies to 14,038 with C reactive protein and age and sex and HLA B27, then the ROC area under the curve becomes 0.93, so it becomes a pretty strong diagnostic test. Second poster compared the autoantibody levels of this fourteen thirty three eta in axial spondyloarthritis, radiographic axial spondyloarthritis with patients with mechanical back pain because that is the closest differential diagnosis we have. And they found that the levels are high in radiographic axial SPA, but not so in mechanical back pain. So it works as a differential test.

And the third, which was an oral presentation, they actually looked at these levels in radiographic and non radiographic excess spondyloarthritis compared with controls, mechanical back pain patients, and found out that even in non radiographic excess spondyloarthritis, the levels are high. So this is an interesting development in the field of excess spondyloarthritis. Also, in the SPARTAN meeting, which was along with the ACR, it was declared that SPARTAN might be embarking on a study called Basis biomarker investigation in axial spondyloarthritis. So I'm happy to report that the field is moving and probably within a few years we might actually have more biomarkers for axial spondyloarthritis.

Hi, welcome to day one at the ACR. So excited to be here. I've been assigned the area of psoriatic arthritis and I decided to think about the themes of some specialized biomarkers. I wanted to go over one of the first abstracts. My name is Elaine Husney and really glad to be here at RheumNow talking about specialized biomarkers and PSA.

I have abstract five twenty nine, which I thought was really interesting today, and that is called the anti peptidyl arginine deaminase two or anti PAD two autoantibodies in psoriatic arthritis. So for this particular abstract, why I thought it was interesting, it was looking at a very specialized autoantigen in psoriatic arthritis. And what they did was take a look at a cohort of psoriatic arthritis patients that fulfilled a criteria, a Casper criteria. And interestingly, they found in this specialized cohort, they had about forty four out of one hundred and twenty four patients with some interesting biomarker assays. They discovered that PAD2 autoantibodies that are found in psoriatic arthritis, that twenty nine percent were positive for this anti PAD2.

And what was more interesting is that these were associated more with patients with active joint disease as opposed to active skin disease. And the clinical significance of this is that the anti PAD2, may be a biomarker for us, that, can be, possibly distinguish, specific phenotypes within psoriatic arthritis.

I'm Anthony Chan reporting here for RheumNow at ACR twenty twenty five in Chicago. And today, there was presentation, abstract number o eight five four, which is the revision of the axial spondyloarthritis classification criteria, and this came from the classic study. There was there was a joint project between ASAS and Spartan and presented today here at ACR twenty twenty five. The aim of this study was to refine the classification criteria for EXAS par, which was first developed by ASAS in 2009. The 2009 ASUS XBA criteria offered a sensitivity of eighty three percent and specificity of eighty four percent for rheumatologists confirmed diagnosis.

It's important to know that these are classification criteria, not diagnostic criteria. While there was a strong starting point, the high prevalence of back pain in a commune in the general population meant that we were looking for a greater specificity in this round in the classic study where that was the focus. The focus was to try to get to above 75% sensitivity, but higher specificity at 90 greater than 90%. And that was the goal of the classic study. The classic study recruited over 1,000 patients from 61 centers across 27 countries, and these patients had back pain for more than three months, and the age of onset was below the age of 45.

The diagnosis was assessed very stringent in the five stages, and stage five had a reference standard. This includes centralized imaging review by two primary readers and also an adjudicator. The cohort was split into testing and training sets and validation sets, and they used regression techniques, including LASSO and multivariable logistic regression. And the team identified the key SPA features that's strongly associated with a stage five diagnosis. And then following that, expert consensus was refined to, to refine the criteria further, and the final proposal was put to vote from both the ASUS and SPARTAN members.

The results of the classic study was, 370 patients, about thirty six five percent of patients finally met the stage five diagnosis of XBA. And from this, we achieved a sensitivity of 79.5 and also specificity of 90.4, which met the original target for the specificity and sensitivity. What is different from the 2,009 criteria is there is a greater weighting on MRI imaging of the sacroiliac joints, both in terms of active and also structural lesions, radiographic sacroiliitis, and then the clinical features, HLAB 27, presence of inflammatory back pain, inflammatory bowel disease, uveitis, heel antisitis, and elevated CRP. Notably, they have added in psoriasis, and also dactylitis was replaced by CRP based on expert consensus. The conclusion I've taken away from the classic study is that this revised, ASA spartan criteria hopefully, will try to improve the the specificity in the classification criteria and also to emphasize that the central role of imaging and to streamline the clinical variables to improve diagnostic precision.

So I think this is one further step for us to try to improve the accurate identification of XBAW, particularly for clinical trials and research studies where these classification criterias will help us to identify these patients more accurately. I'm Anthony Chen reporting here for RheumNow at ACR twenty twenty five in Chicago.