ACR24 - SPONDYLOARTHRITIS Save

Hi, everyone. Jack Cush. I'm on the floor of the ACR Exhibit Hall. It's ACR convergence twenty twenty four. We're in Washington DC.

This is day one, morning one. We're excited to be here. Looks like a lively meeting. Lots of folks, lots of buzz. The exhibit floor and our booth is really happening.

If you're here at the meeting, come by, visit us. We'd love to meet you. Say hello. Give you one of the new RheumNow pens. Hope you like that.

I want to talk to you about what I think you should be doing and what's new at this meeting. You know, the meeting is is really the same meeting. Right? It's face to face and that's what people want. Some things are new.

And we have the same old sessions, the great debate. This morning they had the the year in review. We're gonna have knowledge bowl and other highlights including a wrap up at the end. But plenary sessions are have flipped. They're in the morning at 09:00, and the posters are beginning right about now at 10:30.

So that's something that's new. I think for you watching this video, how am I gonna learn the ACR? I'm gonna give you a few pointers that I think you should pay attention to. Number one, come to the meeting. See us at the booth.

Go to your favorite sessions. Number two, if you're at home, I'd recommend that you follow us on Twitter. On Twitter, you're gonna get this constant stream of information and what's happening really right to the minute. And it's almost like watching the ticker tape of what's going on at the meeting. I think that's kind of exciting, but maybe you're not a Twitter person.

And maybe you want to get a feel for what happened at the meeting. I'm gonna give you three ways that you can do that. Number one, that is at the end of every day at 6PM eastern time. We're gonna live stream the daily recap where it's gonna be me and three or four of the faculty. We're gonna review the happenings of that day and what was notable, exciting, and something you wanna take home.

Number two, starting next week when you get home, you can view the video that's gonna be called the lupus topic panel or the RA topic panel or the PSA. We have topic panels with me and four experts in lupus, RA, etcetera. And we're gonna do RA, PSA, SPA, lupus, JAK inhibitors, tick inhibitors, and IL seventeen drugs. And so that's like six different videos that you'll be able to look at. And the third way that makes the most amount of sense is to go to the RheumNow website and you might already subscribe and get a daily email or a weekly email.

But if you're an RA person or a lupus person, we have an email list and you could sign up, check the box. I want the topic email list that'll come out once a week. And if you check the box on whatever topic you like, you're gonna get an email after ACR and all the lupus stuff that we produce. So you'll have that in your inbox to review. By the way, everything I just said that's in video form will also be in podcast form.

You can listen to the daily recap podcast. You can listen to the topic panels in a in a podcast. And you can also listen to podcast accumulated podcast reports from all our faculty who are here covering the meeting for you. Hope you enjoy this meeting. I'm going to.

We'll talk more.

Hello. I'm Adela Castro at ACR twenty twenty four in Washington DC, and I want to tell you about the CLASSIC study, which is abstract eight twenty. So the CLASSIC study is a large, prospective multicenter trial that included over a thousand patients with chronic back pain and the investigators aim to evaluate the performance of the ASAS 2,009 classification criteria for axSpA in this patient population with an endpoint of obtaining more than 75 sensitivity and over 90% specificity. Diagnostic assessments were performed in five stages. The first stage was after the history and physical exam.

The second stage was after obtaining laboratory, which included evaluation of CRP and HLAB27 positivity. The third phase was by plain radiology of SI joints, which was read by a local radiologist. And then the fourth phase was actually MRI evaluation of the SI joint, which was read by the local radiologist. And the fifth phase was the overall compilation of the history, the exam, the laboratory, the x rays, and the previous MRI that were interpreted by central radiologists specialized in imaging of the SI joint, and there was an adjudicator in case there were some discrepancies between these two central radiologists. The patients that were classified with AHPPA had some common clinical variables.

Most were male, most of them had inflammatory back pain, There were high chances of them having peripheral arthritis, dactylitis, anterior uveitis, compared to the non asthma patients. Also, as we can imagine, the labs were elevated CRP and presence of HLA B27 positivity. And imaging patients that had axSpA were most likely to have a positive x-ray findings and MRI findings. Unfortunately, the 2,009 ASA specification criteria did not meet the set targets of 75% sensitivity and 90% specificity as the investigators were expecting, which is going to lead to the revision of these criteria, which I think is going to be very helpful to have very accurate criteria, particularly for the classification of patients appropriately for research trials. And then, it's going to be very important, of course, a of what they found in the results was something about the imaging.

So there was a lot of over diagnosing on imaging, particularly on MRI in the local radiology. It definitely involved education for our radiologists that are reading MRIs to kind of like look more into what are the specific findings required to classify these patients as ACFA. For more information, go to rheumnow.com.

I'm Anthony Chan reporting here for RheumNow here in ACR twenty twenty four in Washington. And there have been some very interesting abstracts today, looking at the assessment of exospondyloarthritis. Firstly, in the whole area of using the scores that we use to measure outcomes. So we traditionally have been using something called the PASCA score, which is the Bare F ankylosing spondylitis disease activity index. And for a long time, there have been an arbitrary cutoff of less than two or more than four in terms of assessing whether the patient is in remission or whether the disease is active.

But that actually hasn't been validated. So here in, ACR twenty twenty four, abstract number zero eight one eight looks at the assessment of, the VAST score in comparison to other outcomes such as the S test, the ankylosing spondylitis disease activity score, excess spondyloarthritis disease activity score, and it develops some new cutoffs. And the new cutoffs in remission is the VAST score of less than 1.4, Low disease activity is best time of less than 2.8, and very high disease activity is best time of 5.9. One of the things about coming to these meetings is to kind of think of what we would do when we get back to our clinics and how we could be using some of the new information. So this is one abstract that I think will will help us to kind of use the new data in terms of assessing our patients with this using these new cutoffs, which has some validation.

The second, abstract in the field of XBAW is in, abstract number zero eight one nine, and this is about the definition of difficult to manage access spondyloarthritis. All of us will have these patients in our clinic where sometimes they can be difficult to manage for a few reasons. And they have defined the the situation of these patients who who have difficult, treatment response. They have high disease activity scores. They have, raised inflammatory markers such as CRP or positive MRI.

And also that they can be clinically assessed as difficult to manage that despite, having good objective measures, the patient still has a poor quality of life. So here are some of the things that we can be using in terms of trying to define this population a bit better, And this is a work that has come from the ASAS group with eighty nine percent concordance among the people who voted for this new definition of difficult to manage access point neurofibrosis. So here we are in ASEA '24 with these two abstracts on today, o eight one eight and O eight one nine, which I think will help us inform how we manage our patients with excess spondyloarthritis going forward. I'm Anthony Chan reporting for RheumNow here in Washington, ACR twenty '24. I'm Anthony Chan reporting here for RheumNow here in ACR twenty '24 in Washington.

And there have been some very interesting abstracts today, looking at the assessment of axial spondyloarthritis. Firstly, in the whole area of using the scores that we use to measure outcomes. We traditionally have been using something called the BEST DIS score, which is the Bare F ankylosing spondylitis disease activity index. And for a long time, there had been an arbitrary cut off of less than two or more than four in terms of assessing whether a patient is in remission or whether the disease is active. But that actually hasn't been validated.

So here in, ACR twenty twenty four, abstract number eight eighteen looks at the assessment of the best eye score in comparison to other outcomes such as the S test, the ankylosing spondylitis disease activity score, axial spondyloarthritis disease activity score, and they've developed some new cutoffs. And the new cutoffs of remission is the best die of less than 1.4, low disease activity is best die of less than 2.8 and very high disease activity is best die of 5.9. Now one of the things about coming to these meetings is to kind of think what we would do when we back to our clinics and how we could be using some of the new information. So this is one abstract that I think will will help us to kind of use the new data in terms of assessing our patients if this using these new cutoffs, which has some validation. The second, abstract in the field of XBA is in, abstract number eight nineteen and this is about the definition of difficult to manage excess spondyloarthritis.

All of us will have these patients in our clinic where sometimes they can be difficult to manage for a few reasons. And they have defined the situation for patients who have difficult treatment response, they have high disease activity scores, they have raised inflammatory markers such as CRP or positive MRI, And also that they can be clinically assessed as difficult to manage that despite, having good objective measures, the patient still has a poor quality of life. So here are some of the things that we can be using in terms of trying to define this population a bit better. And this is, work that has come from the ASAS group with eighty nine percent concordance among the people who voted for this new definition, of difficult to manage access spondyloarthritis. So here we are in ACR 24 with these two, abstracts from today, eight eighteen and eight nineteen, which I think will help us inform how we manage our patients with access spondyloarthritis going forward.

I'm Anthony Chan reporting for RheumNow here in Washington in ACR 2024.

Hi, everyone. My name is doctor Trish Harkins reporting for RheumNow from ACR twenty twenty four. Today, I have the absolute pleasure of being joined by professor Barry O'Shea, a consultant rheumatologist and professor at Trinity College Dublin, Ireland. Today we're going to discuss his Abstract fourteen forty entitled Significant Factors Identified for Carotid Doppler UseUltrasound Use in axial spondyloarthritis patients without conventional cardiovascular risk factors. So firstly, thank you so much Professor Hsieh for joining us today.

To begin, I just want to know what was the inspiration for your group study?

So thank you very much for giving us the chance. So this work is largely done by my colleague Doctor. Brona Deneen. So it's a pleasure to present it on her behalf. So as you are probably well aware, EULAR have told us that we really need to screen for subclinical cardiovascular disease in various forms of inflammatory arthritis axial spondyloarthritis being no different.

So we were interested in trying to figure out exactly what is the role of carotid Dopplers in this. It's not really feasible to be doing carotid Dopplers on an entire cohort. So we felt if we could, examine this in a little bit more detail, we might shed some light on it. So we went to our clinic in St. James Hospital and we took out our axial SPA patients that had no history of cardiovascular disease are significant risks for it.

And then we put them through a carotid Doppler, specifically looking for their carotid intima media thickness to see as pointer towards carotid artery disease. It was a small sort of proof of concept idea. There was only thirty in the entire cohort that we did this, but these were asymptomatic patients with no risks. So they all went off and had their carotid Dopplers and a little over a third. So eleven of the cohort had abnormal, carotid intimal media thickness.

So 11 abnormal, 19 normal. So then we examine these in a little bit more detail, looking and seeing if we could get particular any predictors for, you know, what might guide us towards, identifying these patients earlier. So some were maybe obvious, but it was reassuring that those patients that had higher blood pressure, in the cohort that were abnormal versus normal, More abnormal cholesterol and lipid profile were the ones that pointed out. Also another useful clinical indication in our clinic is the waist hip ratio. So patients that we would think would be a pointer towards cardiovascular disease and they were the ones that turned out to have normal carotid ultrasound.

We had a couple, like anything research, there was a couple of maybe or more unusual findings that we need to examine a little bit further. We thought or we presumed, and maybe you shouldn't ever do that, we presumed that the cohort that would turn out to have abnormal carotid Dopplers would have maybe a strong family history, of cardiovascular disease. In fact, was the other way around. It was the normal cohort, that's, where that was identified. So we need to, examine that.

The other bit of a red herring was we presumed maybe would be the cohort with the longer disease duration. But again, that was the other way around. It was the patients with the normal carotid Doppler's that had the longer disease duration. So it was interesting. So like any good research, think it's thrown up, given us some good information, thrown up some, some more questions that we need to work on.

And did you look at any laboratory parameters like look at inflammation, CRP, sore, any kind of VASDI scores or anything like that?

Yeah, so we had CRP on the entire court and again maybe thinking there might be a difference between those with a high inflammatory burden, so high CRP, again there was no difference. We had the various indices that are frequently used to assess these patients, their Basai questionnaire and probably a better marker of disease activity, the ASDAS. But again, there was no difference. So it doesn't seem to be a feature of disease activity. The other features we looked at obviously frequently we assess a BASFI, so functional index and a metrology index of ASMI.

Again, maybe thinking that it might reflect longer disease duration, more impaired function. But there was actually interesting no difference between the BASMI and the BASFI scores in the patients that had normal and abnormal, crawdits on their ultrasound.

And I suppose moving on from that, do you guys have a plan to expand to a larger cohort or what's the future plans for the research?

Yeah, so this was done in our own unit on a sort of a pilot group so to give us a feeling of where we should go with this. We have a national registry in Ireland with a number of different centers that are still actually recruiting. So there certainly will be the opportunity to roll it out to bigger cohorts because it'd be nice to bulk up these numbers and see if it's reproducible. Other things we'd like to look at was obviously other indicators or markers for cardiovascular disease. Coronary CTs would be interesting, very interesting effect that can be difficult to get in some institutions.

We may have to come up with some kind of research question and see if we can get some funding for that because it'd really nice to take this in another modality, just crawdits, but seeing what their coronary arteries are like.

Absolutely. Well, thank you so much for talking to us today. So guys, that was abstract fourteen forty. And follow us all on RheumNow for further coverage of ACR twenty twenty four.

Hello, everyone. Leahy Heather here from, the University of Toronto reporting from RheumNow. This the abstract that I decided to present today, number six zero three, cycling versus switching after first failure of TNF inhibitors in patients with axSpA. So this is a very relevant to us because of the limited options that we have. This is a study from a big check registry that evaluated patients who failed their first TNF inhibitors, and they evaluated whether persistence on a TNF inhibitor versus IL-seventeen inhibitor is better in one or the other.

The bottom line is that there is really no difference. The retention was similar for TNF inhibitors and IL-seventeen inhibitors, but uniquely there was a difference in response. So the study did have information about ASDAS in response to treatment, and they showed some superiority of TNF inhibitors compared to IL-seventeen inhibitor. On the other hand, there was a little bit of more safety issues, including severe adverse effects in the TNF, inhibitor group compared to the IL-seventeen inhibitor group. So even though the retention was similar, there were some differences in terms of efficacy and safety.

So I think for us as clinicians, both options are available, either switching to a different mode of action or staying within class of TNF inhibitors, but we obviously need to take into consideration issues like safety, and some patients might benefit from maybe IL-seventeen inhibitors if safety issues are a major concern. Personalized treatment still remains intact until we have biomarkers that could help us predict response. Thank you. Hello everyone. Lihi Edder here from the University of Toronto reporting from the ACR here in DC.

I'll be, talking about a presentation, a new definition for difficult to manage that was presented. It's abstract number eight nineteen. This is the new definition, ASUS definition for difficult to manage axSpA. So this new definition refers to the patients that we all see in our practice. These are patients who failed multiple modes of action and are more difficult to manage and in order to understand better how we can better take care of these patients, we need a new definition.

So ASAS proposed that these patients include those that failed two separate modes of action but also have some additional definition which include high burden of symptoms as measured by ASAS or a high level of CRP or evidence of active inflammation by MRI as well as patients who showed progression in radiographic damage. Importantly they also emphasize the patient perspective here. So if the symptoms are perceived to be difficult or important by the patients that is also important and counts not just a rheumatologist perspective. They also include in this new definition a subgroup of refractory to treatment patients. And this means that these patients in addition to having symptoms, they also need to have objective evidence of inflammation either by blood tests, CRP, or by MRI, the evidence of inflammation in their spine.

And this is to separate them from those who have other confounders that might affect symptoms like depression, fibromyalgia, and so on. And this subgroup of maybe truly immunologically resistant patients might be a more focused target group for research or combination therapy or other approaches. So overall, I think this new ASUS definition is important. It's step forward that is similar to other projects of difficult to treat patients in PSA and RA, and hopefully we'll move this field forward and address this major issue that we all face in clinic as a source or as tool to help us do better research and better manage our patients. Thank you.

Hi. I'm doctor Sheila Reyes from The Philippines, and I'm here at Washington DC reporting live for RheumNow at the ACR Convergence twenty twenty four. I'm joined this afternoon by doctor Dennis Padavni from the University of Toronto where he will be talking about abstract number eight nineteen regarding the newest definition of difficult to manage axial spondyloarthritis. So Professor Padamy, thank you for joining us this afternoon and congratulations on your paper.

Thank you.

Yeah. So could you like walk us along how the criteria came about or the definition what criteria used or how you came about with the consensus definition?

Well so that was long process, took about three years in total to find a consensus among experts on what difficult to manage spondyloarthritis is about. So we started this initiative some time ago and there was clear there was an unmet need in the field. We see everyday patients coming to us not responding to the most advanced treatment and rheumatologists are very well aware of various problems which might lead into treatment non response or insufficient response to the therapy. It can be a biological non response so inflammation is not controlled well but more commonly these are other problems like chronic pain not related to inflammation so called, nociplastic or neuropathic pain. It might be a bit surprising but this fact is not really reflected in the management guidelines.

If you look into the management guidelines you will see that in a patient who is not responding to the treatment the recommendation is to check the diagnosis and to change treatment. But the problem is much deeper so you need to understand what is the structure of reasons behind this treatment non response. So that is why we decided to develop this consensus definition to define the group clearly to be able to study this. And in addition to that and that what was the development during the whole process, we came across a definition of a narrow, smaller group of truly treated refractory patients or patients where we have uncontrolled inflammation despite effective presumably anti inflammatory treatment.

Okay, thank you. So it's also interesting to note because it's giving more of a practical application that we can also use in our clinics, right, and not just in research as defining difficult to manage spondyloarthritis. I

think this is the first important step on that ways. We certainly will need to study these patients, difficult to manage patients to understand what is the best approach how to address all the problems outside of inflammation to find an appropriate way how to manage those patients. I think many rheumatologists they have ideas how to deal with those patients, to manage pain in these patients, but there is no unified approach. This is something that will come as a next step.

As a next step. Okay. So before we wrap up, could you give us the different elements, the important elements of the definition that you came up with?

Absolutely. There are three main pillars in that definition. First is a history of treatment with sufficient number of advanced treatment options. In the case of extra spondyloarthritis we define that as a history of at least two biological or targeted synthetic DMARDs given an appropriate amount of time to see a response. Second pillar is presence of signs and symptoms indicative of uncontrolled disease.

That can be defined by a composite outcome measure like ASDAS. It can be defined by presence of symptoms such as fatigue, extramuscular manifestations, it can be defined by rapid structural damage progression, or it can be defined even by other symptoms not mentioned here but still bothering the patient. And of course it can be uncontrolled inflammation is reflected by CRP or MRI. And then the third pillar is that this situation, so having signs and symptoms with history of previous treatment is perceived as problematic by a physician and or by a patient. So all three should be fulfilled cumulatively and then we can talk about difficult to manage situation.

Treatment refractory is a fraction of the big patient population, difficult to manage population, where we ask for treatment failure and presence of objective signs of inflammatory activities obligatory criteria.

Okay, all right. So thank you very much for giving us insights on the new classic, I mean on the definition of difficult to manage and the refractory type of spondyloarthritis. Hopefully we get to know more about or we get to use the definition and also that will help us in the management of our patients and also, you know, control disease activity and even improve quality of life. K. So there you have it.

Tune in to RheumNow for more updates and use of the a on the ACR convergence twenty twenty four. Follow me on Twitter at Rheuma Rampa, and have a good day. Hi. I'm doctor Sheila Reyes from The Philippines reporting live for RheumNow at the ACR convergence twenty twenty four here in Washington DC. I would like to talk about abstract fourteen forty seven from the group of doctor Gazelle and colleagues.

It struck me a little bit interesting because they compared the frequency of cervical dish in patients with SPA versus age and sex matched controls. So their findings showed that the frequency of DSH is the same for both populations and that SPA patients with DSH were significantly younger. Now interestingly, DSH was seen more in ex PA patients who were HLA b twenty seven positive while DISH was reported more among psoriatic arthritis patients who were HLA b twenty seven negative. Now how can these results help us in clinical practice? Probably not as much, but at least knowing that dish is not just a mimic of axSpA, but that it can co occur or it can occur simultaneously with axSpA helps us to understand disease the disease of our patients, especially when we're already giving our biologic DMARDs or a traditional DMARDs, and patients do not respond to treatment, probably because it's not the inflammatory type of back pain that's causing the symptoms, but it's more of the mechanical type.

So knowing these can also guide treatment decisions for clinicians. Follow me on X at RheumNow for more updates and news on the ACR convergence twenty twenty four.

Hello. I'm Adela Castro at ACR twenty twenty four in Washington DC, and I wanted to talk to you about the sex related differences in responses of biologic, which is abstract number five ninety nine. So this was a very interesting study that was a systematic review and meta analysis of over 11 studies that included over 11,000 patients. And the intention here was to evaluate if there was any difference between female or male in responses to efficacy of biologics predominantly TNF inhibitors and IL-seventeen inhibitors in terms of BUSD I50, ASDAS and ASAS 40 responses rate. Over here in the study, the majority of the patients with AHPSPA were predominantly male, sixty percent, and more of the male patients had also HLA27 positivity.

So in the results, in terms of efficacy, it seems that in terms for VAST I50 and low disease activity responses, male patients were actually higher in achieving these response rates compared to female patients. Whereas as far as the ASOS four is, there was no difference between male or female patients in achieving this response rate, which makes us wonder whether do females have higher disease activity versus should we be utilizing a more gender neutral efficacy measure for these patients? Thank you for more information follow-up on RheumNow.

Hello, I'm Marina Magre, the division chief of rheumatology at University Hospitals and professor of rheumatology at Case Western Reserve University. Today I'm reporting for RheumNow in Washington DC ACR convergence twenty twenty four. So it has already been an incredibly informative meeting and a lot of new data that were presented today, and I am going to walk you through some key highlights of today's meeting. So, you know, the ASAS consensus definition for difficult to manage axial spondyloarthritis was presented today, and the definition included treatment failures, which was defined as using two, biologics or more from two different classes. It also included persistent ongoing inflammation, either elevated CRP or on an MRI, or high disease activity and impure quality of life.

I think the definition took into account both objective measures as well as some subjective measures like patient or physician's perception of, bothersome symptoms, again telling us that how, you know, multidimensional, you know, challenges we face when treating these problems. But I'm very excited that this definition would allow clinicians to recognize these patients early on and also enable us to do more research. Another interesting abstract that was presented today was the much awaited data from the classic study. This study was a combined project of ASAS and SPARTAN order to refine the 2,009 classification criteria, even though they were a landmark step in research in axial spondyloarthritis, allowing us to expand those criteria, including patients with early disease. But, these criteria were often sometimes used for diagnostic purposes, so it was felt that we needed to refine and increase the specificity of those criteria.

This study tested these criteria using some predefined cutoffs with a sensitivity of 75% and specificity of 90%. And the data that were presented today showed that the study did not meet those criteria. And what the take home message is that the 2,009 ASAS classification criteria may need to be revised. Another interesting abstract which I found in this meeting today was there was an abstract presented from Meteor Spondyloarthritis database, which is data from seven different countries, and they used artificial intelligence and tried to develop some predictive models looking at patients who are at risk of flares with axial spondyloarthritis. So they this machine utilization, what they found was that those patients who have history of flares or have had, you know, been on treatment for a long duration of time, or those patients with low SDAS scores were actually at increased risk of flares.

And so these data, I think, are paving way for personalized medicine. So allowing clinicians to recognize these patients and maybe starting preemptive therapy to prevent flares. Hi. I'm Maureen Emeagre, professor of medicine at Case Western Reserve University, division chief of rheumatology at the University Hospitals Cleveland, once again reporting from for RheumNow from ACR twenty twenty four convergence meeting in Washington DC. I wanna touch upon some of the hot topics in axial spa that were presented today.

One of the hot topics that was presented was gender based differences in treatment response. Our group represented a poster which, did, you know, with a systematic review and meta analysis, and this abstract showed that the VASD I 50 responses and ASDAS low disease activity response was more robust in men compared to women. Not as many women were able to achieve this response in this meta analysis. Keeping up with the similar kind of research, another abstract is presented by the Toronto group. They also did a systematic review and meta analysis looking at gender based baseline characteristics and differences in response to treatment and safety, and their results were no different from our abstract.

They showed that the efficacy endpoints were reached in larger numbers in males compared to females and, you know, not much difference in safety signals. And now it needs to be determined what's driving these differences in treatment response. You know, these responses were seen across all biologics in this systematic analysis, both TNF alpha inhibitors and IL-17A inhibitors. Another interesting topic that was discussed today was, difficult to manage axial SpA, and as the consensus definition was presented, our group also presented another abstract which was a real world data looking at, patients, difficult to treat patients defined as those requiring three biologics, at least two, from two different families. And, that, abstract highlighted some clinical features in these patients.

These patients tend to have higher BMIs. They also had comorbidities like hypertension, chronic renal failure, depression, and extra articular manifestations of axial SpA. HLA B27 positivity was also associated with difficult to manage axSpA suggesting maybe there is a genetic role into it. Thank you so much.

Hi, my name is Doctor. Philip Nies. I'm a rheumatologist in Seattle, Washington and direct the Rheumatology Division of the Providence Swedish Medical Center there. I'm very glad to present data from an abstract on integrated safety across all of the trials of bimekizumab in axial spondyloarthritis and psoriatic arthritis. These were all the 2B and phase three studies as well.

So it gives us a very comprehensive picture of patient safety in over fifteen hundred patients observed for up to two years. What

we

saw were relatively low rates of infection, about one point three or one point four events per 100 patient years in both the AXPA and PSA studies. We saw relatively low rates of candida infection. This is something of interest because we know that IL-seventeen as a cytokine protects us from surface candida. So there were occasional cases of thrush, for example, usually just occurring once and easily treatable with topical treatments for the most part. Only occasionally were we to see patients with recurrent episodes more than one.

So this rate was also low, and there were no systemic fungal infections noted nor any cases of tuberculosis. Another area of interest is inflammatory bowel disease. This was seen in very low rates in the axial spondyloarthritis population, slightly more than the psoriatic arthritis population. Again, this is something that we have seen, with this mechanism of IL-seventeen inhibition. Usually these are cases in patients who have a past history of inflammatory bowel disease and there's a flare.

Occasionally, we have seen some new onset cases. So this happens, the frequency is low, we do need to talk to our patients about it. Another issue that is being monitored for in current trials of psoriasis and psoriatic arthritis is the issue of depression and suicidal ideation because these are issues that are more prevalent in a patient population with these diseases. Again, here the rates were low. There were slightly more patients in the bimekizumab arm that reported let me start that one again.

Again, these rates were low, and I think, if anything, what this reminds us to do is to talk to our patients about their mood, to talk about depression openly, and be ready to care for this issue if the patient is meaningfully depressed or has potential ideation. Another issue that is of interest, especially in a group of patients who have a proclivity to obesity, is the potential for liver transaminase changes because sometimes if a patient has underlying fatty liver or is on methotrexate, we may see perturbations in LFTs. This was seen on occasion, so we do occasionally see upticks in liver transaminases, but these were generally transient and would return to normal and generally did not lead to any concern about the ongoing use of bimekizumab. Another topic of interest is that of uveitis. Itis.

We know, for example, that when we use a monoclonal TNF antibody that we can see reduction, in UVitis flares, which can occur in patients with PSA or axial SpA. The rates of uveitis in this integrated safety analysis were quite low, and so it doesn't look like there's, in any case, a significant increase in number of cases of uveitis, and overall the rates were very low. We saw no signal, for malignancy, no signal, for, cardiovascular disease of concern. So in general, this report, underlines the relative safety and tolerability of bimekizumab and IL-17A and F inhibitor, a dual mechanism that has been recently approved for the treatment of psoriatic arthritis and the full spectrum of axial spondyloarthritis.

Hi. I'm doctor Sheila Reyes from The Philippines, and I'm here at Washington DC reporting live for RheumNow at the ACR Convergence twenty twenty four. This time, I'll be talking about abstract number five five nine by doctor Diego Beneffant and his group on the use of machine learning in predicting future flares for patients with XPa. The study aimed to develop and validate a predictive model for XPa flares in patients who are treated with biologic and synthetic DMARDs using machine learning. And their results showed that among the predictive models, they selected the reduced logistic regression because it had high performance, interpretability, and simplicity.

And this model identified the following factors that are predictive of a flare within six months. So this included low ASDAS, history of enthesitis among the patients, a number the number of previous flares, as well as a longer disease duration. More data might still be needed to establish its utility in in practice or maybe its future use in clinical trials. But knowing these risk factors and from a clinical standpoint can help can help us profile our patients and monitor them closely so that we would give the proper treatment and we can also educate them in knowing what to look for, when they do develop flares. Follow me on x at RheumNow for more updates and use of the ACR coverage of the ACR convergence rather twenty twenty four.

Hello. This is Marina Magre again reporting for RheumNow at ACR Convergence twenty twenty four in Washington DC. I'm going to report this very interesting abstract which is talking about precision immunotherapy in ankylosing spondylitis. This abstract, was presented this afternoon. As we all know, ankylosing spondylitis is a T cell mediated disease.

However, you know, trying to deplete T cells is not possible because that would put the patients at a very high risk of infections. A subset of T cells have been incrinated in pathogenesis of ankylosing spondylitis. The this subset carries this unique receptor, t receptor b v nine. And this is this these cells are thought to, know, bind with the antigen presented by HLA B 27 positive cells and have been implicated in pathogenesis. In this abstract, a bispecific antibody was developed against this subset of T cells carrying this receptor, TRBV nine receptor.

They neutralized these cells showing to be with using this antibody, the risk of infections was low. Cytokine release was low with this binding. So the concern for cytokine release syndrome was minimum. And the recommendation was that by binding and, you know, or depleting this subset of T cells, one could reset these autoreactive T cells and produce long term remission in axial spondyloarthritis in AES. So it was very exciting, and, you know, I we have to wait till actual human studies are done with this bispecific antibody.

There there has been a case, report from Russia last year, which was published showing that these antibodies are work. So something very exciting for the future of axial spondyloarthritis. There was another abstract keeping up with the same theme presented today, which was which took patients with the you know, which had uveitis, acute anterior uveitis, HLA b twenty seven positive. So they took their ocular cells and blood cells, and they found that blocking this TR this t receptor b v nine T cells may not be enough. They also found another receptor that may be implicated in patients with uveitis, TR b v five.

So they were and what can the gist from that abstract was that blocking one one receptor may not be enough and maybe need to block both receptors. Well, this is, you know, very early data. Ultimately, it needs to be vetted in real human studies and see what works for our patients. Thank you so much.

Hi. I'm doctor Sheila Reyes from The Philippines reporting live here DC for the ACR Convergence twenty twenty four. I'd like to talk about Abstract five seventy one. It's an interesting abstract because it talks about the gender specific differences among the disease activity measures in AXPA and how these disease activity measures would affect gender. This study was from the group by Doctor.

Sabrina Hamroun. The objective was to evaluate the influence of gender on disease activity assessment tools and the ability of these disease activity tools to discriminate the PASS or the patient acceptable symptom state based on gender. So what are the findings rather? Well, they showed that in the overall population of the axSpA patients, VASDI, ASDAS CRP, and the patient global assessment performed well in discriminating paths, meaning that they were able to get clinically significant or relevant results from the trial. More importantly, VASDAI scores were seen to have better discriminating performance in women, whereas ASDAS ERP did not really or it was homogenous among the genders.

Okay, so what did this translate for us? Well, I think it makes sense because we know that there are gender differences in AXPA and that women present more with fatigue, with peripheral arthritis, with extra intestinal manifestations, or I mean, extra articular manifestations rather. And so we should also use disease activity measures that would really define or measure those domains. And probably in future clinical trials then, and especially if women are involved, then the VASD diet can be used as a disease activity measure. Follow me on Twitter at RheumNow, and tune in to RheumNow for more coverage of the ACR twenty twenty four.

Hi. Marina Mayagre from Case Western Reserve University once again reporting for RheumNow at ACR Convergence twenty twenty four. Great meeting so far and a lot of exciting data. And today, I attended, it was a session for difficult to manage AxleSpA, which has been a very hot topic at this meeting. This session, you know, doctor Dennis McGonigal from UK did a very nice discussion about difficult to manage expa.

And the take home message from that, what I got was what he mentioned was these patients that are difficult to manage, first thing one needs to know is go back to the drawing board and make sure that these patients have a right diagnosis. Because sometimes it may not be the right diagnosis, and that's why these patients may not be responding to the therapeutics as we expect them to be. So so maybe they don't have XPA. Maybe they have degenerative arthritis or some other form of arthritis that needs to be taken into account. He also mentioned about some anecdotal reports of using a combination biologics in these patients.

So what he showed was that patients, you know, particularly those patients with psoriatic disease, there have been some reports using combination biologics like an IL twenty three inhibitor along with the TNF inhibitor. However, it seems, you know, to be determined, and we need actual clinical trials to show the efficacy of these combination biologics in these patients. Thirdly, the point he emphasized was that these patients may have other reasons for being in pain, and they may have central sensitization, other, you know, other causes for pain, sleep deprivation. So these need to be thoroughly also looked into these patients and make sure that those areas are also addressed when trying to manage these patients. So that was the take home message from that session.

Another abstract that I like today that was presented was it was an poster actually, was this group tried to look at it was a French group trying to look at the time to low disease activity in patients that have been previously treated with TNF inhibitors. And what that abstract showed us that those patients that were previously treated with TNF inhibitors, either one, two, or three, when they switched to another TNF inhibitor, it the duration to reach low disease activity was longer. So the bio naive patients took lesser time to reach low disease activity compared to those patients that were previously active treated with TNF inhibitors, whether they started a new TNF inhibitor or they started an IL seventeen inhibitor. They also looked at the durability of, you know, the low disease activity in these patients, and they found that those patients that switched from a TNF inhibitor to IL seventeen inhibitor, the durability of low disease activity was decreased. However, the durability of low disease activity was not decreased in those patients who are naive or switched from a TNF inhibitor to another TNF inhibitor.

So the take home message from this abstract was that those patients who now show inadequate response to previous TNF inhibitors and when we are switching treatment to them, I think it may be it may be advisable to let our patients know that it may take longer for them to reach the low disease activity. So they need to be more patient, you know, stay on the treatment rather than cycling treatments from one class to another. It may be better to wait and give them more time till they attend attain low disease activity. Thank you so much.

Hi. I'm doctor Sheila Reyes from The Philippines, and I'm reporting live for RheumNow here at Washington DC for the ACR Convergence twenty twenty four. I'm here with professor Walter Maximowicz from Alberta, Canada, and we will be talking about their, study, abstract number eight two one, on answering the question of what is a positive MRI in spondyloarthritis. So let's get to the meat of the discussion. Professor Walter, thank you for joining us this afternoon.

Pleasure. Yep. So congratulations again to the to your study and to your presentation. It was presented earlier. So now I would just like to ask, could you give us a brief overview of what this study is about and probably the reason why this was done or this was pursued?

Thank you. So MRI is really important in the assessment of spondylo arthritis. It's the most sensitive tool that we have and it's really the best way to make an early diagnosis. But it's not an easy tool. It's not an easy scan to interpret.

And both rheumatologists and radiologists often lack the experience to do the interpretation. And so it's really important that we try and establish some operational rules that might help radiologists and rheumatologists understand if they should be thinking about spondyloarthritis when they're looking at a scan. So there are different types of lesions, both inflammatory and structural lesions that can occur on a scan. And the question that we posed when we thought about the study was, well, can we find a way of operationalizing the extent, how much of the sacroiliac joints should demonstrate, for example, bone marrow edema or erosion. So how extensive does it have to be before you start thinking that maybe this is ankylosing spondylitis?

Okay.

Now minor degrees of inflammation can occur, for example, in very active people. Uh-huh. So some people have called this bone contusion. Okay. Minor degrees of bone marrow edema can occur in healthy people if they're very active, for instance.

So what we wanted to see is there a way where we could look at defining, well, what's the extent of a lesion before we really start thinking it's axial spondyloarthritis. So what we did was we had a whole bunch of scans from people with spondylitis and different variants spondylitis like spondylitis plus psoriasis.

Alright. So the other

Arthritis and other subtypes. Mhmm. And we had nonspecific back pain controls.

Okay.

And readers were evaluating the scans, but they were blinded to the diagnosis. And they were doing two things. First of all, they were just looking at the scan, all the sequences that were done, and they were doing two things. Number one, they were responding to a question in the case report form that asks, do you think this scan is indicative of axial spondyloarthritis?

Oh, and that's just based on the image that you're looking at?

That's just a global assessment of the image. Okay. And then what you can do is you can divide each sacroiliac joint quadrant into four into quadrants using a line through the joint cavity and then through the midpoint of that line. So there are four quadrants. And then you can evaluate consecutive slices.

So, typically, there's about 12 to 15 slices through the sacroiliac joint. And then you're going to ask the question, well, how many sacroiliac joint quadrants with bone marrow edema, erosion, fat lesion, best reflect the diagnosis. Right? And differentiate between spondyloarthritis and a nonspecific back pain control. Okay.

And what our findings were were actually something that's kind of easy to remember. And so it's the three four five

rule. Okay.

Three sacroiliac joint quadrants with erosion gives you specificity of ninety five percent Mhmm. In favor of ankylosing spondylitis versus nonspecific

back pain.

For bone marrow edema, it's four sacroiliac joint quadrants. And for fat lesion, it's five sacroiliac joint quadrants. That's why it's the three four five rule. So it's something easy to remember because those are amongst the commonest lesions. Erosion, bone marrow edema, fat.

Fat.

And so we call it the three four five rule that gives us really good discrimination between an MRI scan from a spondylitis patient and a non specific back pain control.

Okay. So wow, that's very good. The findings are really interesting. And now that you're saying the three, four, five rule, it's easier to understand. And I don't know if this was included in the study, but does the specificity further increase if you include a history of a patient with, inflammatory back pain, or is it independent of the findings on MRI?

This is just purely focused on the findings in MRI. This is a radiologist or rheumatologist who may be looking at the MRI scan and won't have a history or a physical exam. Okay. And that's usually the case, of course, right? The amount of clinical information provided to the radiologist is fairly minimal.

Maybe age, there may be gender. You know, occasionally, it may be b 27 finding or a CRP, but usually, it's only age and gender. That's all you've got. And so this is just like an MRI scan. Now this isn't, you know, this isn't something that's kind of should be interpreted as written in stone.

Mhmm. It's guidance. Okay. Right? And at the end of the day, the rheumatologist makes the final decision based on the history, the physical, the labs, and the reporting from the radiologist.

So this is meant to to help make that decision well, how much bone marrow edema, how much erosion, before I really get concerned that this is spondyloarthritis.

Yeah. Correct. And it's because sometimes the reader it depends on the reader as well. So I like what you said about getting everything in context. There should be your history that should be appropriate.

And then of course make the use of imaging because we know that imaging is really an integral part of the diagnosis and Okay. So I'd just like to sum up what you've said, because it's really, well, if you take a look at it from your point of view of how you said it, it's really easy. The three, four, five rule. So again, that's three sorry, three erosions, three lesions, erosions, and then four bone marrow edema and five fat lesions, correct?

That's correct, yes.

That could tell you or increase the specificity that this may be spondyloarthritis on MRI.

Yeah. It gives you more confidence.

Yes. It gives you

more So the the you know, once you start seeing those targets, if the bone marrow edema is only one or two slices Yeah. You're probably not dealing with spondyloarthritis.

Correct. Correct. Yeah.

If all you see is, you know, a couple of slices of bone marrow edema without erosion, without fat, you know, this this is probably not.

Not or probably just a mimic. Right?

Yeah. Yeah. And and if if you think you're seeing erosion in maybe one location, that's probably not bone marrow. Not bone Not spondylitis. Okay.

So it's really giving some guidance about how extensive these lesions should be before you really start getting concerned that this is spondyloarthritis.

Okay. So thank you very much Professor Walter for joining us this afternoon and sharing the findings of your very interesting research. So again, ladies and gentlemen, remember that in the diagnosis or in the assessment of patients, when we consider spondyloarthritis, we have to take into consideration also apart from an appropriate history, PE, then we also request for imaging, which in this case is MRI. And Professor Walter explained very beautifully how they came up with the diagnosis of MRI with the three, four, five rule. I'm Sheila Reyes, and follow me, with my X handle, at RheumMarampa, and tune in to RheumNow for more updates on the ACR convergence twenty twenty four.

Hey, everyone. It's Brian Jaros here. I'm reporting live from ACR convergence twenty four here Washington DC. Today I'll be telling you about abstract number seventeen fifty six. Now this is an abstract, that's being presented with the ankylosing spondylitis therapy group.

It's out of, a group from Europe and their question is really interesting. They're looking to see whether patients who were previously exposed to TNF therapy had longer times to remission when they used another TNF inhibitor or an IL-seventeen inhibitor compared to those that had never been on TNF treatment before. And in order to do this, they had a very clever, design where they used a bunch of registries from across Europe in order to really gather a strong pool of patients to help answer this question. And I think this is a really important question to ask because our most recent guidelines out of EULAR and ASAS suggests that after failing NSAIDs either TNF inhibitors or IL-seventeen inhibitors in addition to JAK inhibitors may be used for refractory symptoms, not providing specific guidance whether TNFs are preferred first or IL-seventeen agents are preferred first owing to a lack of head to head data about these agents. And so this study might be interesting to tell us a little bit more about patients who fail TNF inhibitors first line, whether it's beneficial to class switch and go to a different agent like IL-seventeen or to stick with the TNFs.

So let's get into the data of the study. And so as I mentioned, they used about 13 registries. They excluded patients who had been on other biologics besides TNF inhibitors or IL-seventeen inhibitors and their primary outcomes were the time it took for the patient to achieve low disease activity or I'll refer to it as LDA and they defined this as an egg spa disease activity score of less than 2.1. The other primary outcome was looking at durability and so once people achieved low disease activity, how long did they stay in low disease activity until a subsequent visit where they became active? So in total they had over fifteen thousand patients who initiated TNF inhibitors and over two thousand patients who initiated IL-seventeen agents, largely with similar baseline characteristics between the groups, although with more biologically naive patients in the TNF group.

The results are really interesting. So they showed that the mean time to achieving low disease activity increased based on the number of exposures patients had had to TNF inhibitors previously. It was shortest if they'd never been exposed before and that was around an average of thirty three weeks for the TNF agents and thirty seven weeks for the IL-seventeen agents and increased all the way up to fifty one and forty six weeks respectively if they'd used two or more agents. In some ways this is not surprising, it might suggest that people who have failed a previous treatment have more refractory disease or a more severe phenotype in general, but it was interesting that both TNF inhibitors and IL-seventeen inhibitors suffered from this delayed LDA in those that had tried just a TNF before. Now, the other outcome that I mentioned was the duration of the low disease activity.

So how long it actually lasted once they achieved and this finding was even more interesting. It showed that the patients who were switched to IL-seventeen therapy actually had shorter durability of low disease activity in the patients who had previously trialed TNF inhibitors. And this was different than the patients who were prescribed a new TNF inhibitor and actually maintained durability. And I thought this was quite surprising. Know, oftentimes we think about patients failing agents and the idea of class switching, which is switching to an agent that has a different mechanism with the idea of trying to target inflammation, trying to target different disease from a different way.

But this study actually suggested people who stayed in the same class, who stayed in TNF inhibitors performed better in terms of staying in that low disease activity. So in some ways this gives us a little bit of insight into maybe using additional TNF inhibitors before switching to IL-17s but I think it also is one of those studies that actually raises more questions than maybe it gives answers. It'd be really interesting to see if the group went back and sorted these people from primary failures, which is, you know, no response to the TNF upfront versus secondary failures where they responded to the TNF and then had a, you know, wearing out effect over time to see whether the class switching to IL-seventeen had a more profound effect in those with secondary failures since this is something that we often think about when we're making our clinical decisions in practice. That's all I have for you today. Tune into RheumNow for more.