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Hello. My name is Rinalini Day. I am a clinical fellow from London in The UK, I am at ACR twenty twenty four in Washington, DC. And I'm delighted to have with me today, professor Elena Maja Sadova, is professor of medicine at Mayo Clinic in The US. Thank you for being with me here today.

So we have just come out of a really exciting and highly relevant session on ageing and aspects in the rheumatic diseases. And first of all, I'd like to get if it's okay, I'd like to get your thoughts, professor Maestadova, on why this session is so necessary. And I believe also that The Lancet Rheumatology has recently published a special edition on this topic. So why do we need to know more about this topic and why it's so important?

Thank you so much for having me. And, I I agree that the session that just ran here at the ACR sheds the light on the understudied and underappreciated topic of aging and rheumatic diseases. The guidelines and the care do not necessarily imply or focus on aging aspects with treatment or screening or general management plans and prevention for patients with rheumatic diseases which needs to be done. The session shed some light on the aspects of things from that standpoint.

You mentioned about the guidelines and I know that was talked about in the final talk of the session. I'd just like your thoughts on that a little bit more. So the guidelines that we currently have don't necessarily meet the needs of our older patients. I think the same could be said of recruitment to clinical trials. What do you think we can do to improve both of those aspects?

What can clinicians do on a practical level when they're seeing patients?

Great questions. Certainly, age is a number that doesn't apply equally to different patients and different aspects of things in terms of, for example, administration of treatments or choice of treatments and guidelines to not necessarily highlight that patients of certain age should or should not receive a particular treatment and it shouldn't really be a barrier in itself. Certainly with age, we accumulate comorbidities and other polypharmacy and that can preclude the use or at least become a worrisome aspect of use of certain disease modifying agents, for example. But other than that, literally treating patients who are older similarly otherwise with the younger patients is probably reasonable.

Thank you. Let's just pick up on the aspect of comorbidities a little bit more. So that also came up quite a bit in this session that we've just been to. The clinics are time pressured for rheumatologists. I work in The UK, you work in The US.

I think the problems are fairly similar from that point of view. How can we best manage and address comorbidities in the clinic setting when we have such limited time with our patients?

One way to do that would be to certainly use teamwork and multidisciplinary care. It's not always feasible and that's where potentially screening instruments come into play such as screening for cognitive impairments, screening for functional impairments, screening for depression, anxiety, and such, and then referring to a particular provider. But certainly, if you have an infrastructure to use multi specialty approach, that probably is an optimal way to do it. Although, that said, rheumatology specialty deals so much with patients who are older, just by the nature of our specialty, that picking up some of these skills is important in itself for rheumatologists, and that's why that essentially justifies the topic of geriatric rheumatology that we are trying to introduce with the session and with the series.

Thanks. One thing that really struck me, I'm just remembering a slide from our second speaker, was that the fact that DMARDs are not prescribed so readily in our older patients. That actually includes the population who have late onset RA, and that really struck me. What more do you think we can do to improve uptake there? And I know a few of the aspects were touched on in the q and a, such as infection risk, for example.

But, yeah, how can we improve that to improve outcomes ultimately?

Yeah. There's definitely hesitancy in administration of immunosuppressive agents as as people age, but that's partially because there's not enough evidence about how these agents work and how they compare in this particular population because older adults frequently, especially multi morbid patients or patients with multiple chronic conditions rather, are frequently excluded from the clinical trials and pragmatic trials, at least in rheumatology, may not be as prevalent at this point. One way to improve things would be to do more interventional static studies that are prospective studies, ideally exploring the ways how to optimize treatments. And not only prescribe, but there's also an aspect of deep prescribing. There's definitely some some balance there.

And I think both of those aspects can be improved and researched more. And that's where we're headed.

Thank you. And I think we could we could talk about this all day, but we don't have unlimited time. Where can people go if they want further information? I mentioned at the beginning that special edition that you've just been involved with. Yeah, if we want to know more, how can we find out more about this topic?

Definitely. Lancet Rheumatology just published a series of papers on aging in rheumatology in patients with rheumatic diseases that include a manuscript on cognition in adults with rheumatic diseases, a paper on geriatric five ms, the five major aspects of older adults care, such as multimorbidity, multi complexity, mind, mobility, and what matters most. Those are the five five m's. A paper on frailty, a paper on palliative palliative care, and there is also a paper on aging. All of these are extremely important, and this could can be a good reference.

We are trying to also grow the awareness and the presence of understanding of geriatric rheumatology as a subfield. Certainly, if you would like more communication, more information, our group, Jerry Rheum, is fairly active on social media, and all of us are very approachable as well.

Thank you so much. Thank you for taking the time to talk to me after that really excellent session. If you'd like to know more, as professor Meis Sedova said, do check out that special edition of The Lancet Rheumatology. And also, there's plenty of other sessions which touch on multimorbidity aspects of aging here at ACR. And if you'd like to know even more, then do check out the RoomNow website, for further information.

Thank you.

Hi, my name is Akhil Sood. I'm reporting for RheumNow here in Washington, D. C. Today I want to talk to you about a premilast in psoriatic arthritis. Suppose you're seeing a patient with psoriatic arthritis for follow-up.

Overall, they're doing great with no signs of active disease. But they mentioned they're having low back stiffness and some joint pain and some stiffness in their hands and feet. What do you do next? Sure, NSAIDs may be the answer, but it carries side effects. What about epremilast?

At ACR, there are a few abstracts that highlight the potential benefits of apremelast in psoriatic arthritis. Abstract fourteen sixty six in the FOREMOSS trial, looked at patients with early PSA, specifically those with early osteoarthritis, they found that apremelast was associated with significant improvement in tendon joints and swollen joints, and there was an improvement in patient reported outcome measures. Then, abstract 2583 found that eprimalist not only helps the joints, but also helps the spine. They found at weeks twenty four and forty eight, there were significant reductions in axial inflammation on the MRI. And here's a surprising benefit: Epremalis may even have metabolic benefits.

In Abject May, patients treated with Epremalis perineur had significant reductions in their body fat on DEXA scan, and this was linked to improvements in disease activity. This suggests that Premise might help more than just the joints and the spine, but also have metabolic advantages as well. So the benefits seem great, but are there any risks? Abstract 2,640 highlight that the increased risk of serious infection was higher among patients on a prevelast in the biologic or targeted, DMAR. But it's important to note, we don't know the underlying factors that may contribute to this increased risk.

So back to our patient. Should you add a prevalast? Ultimately, it's about shared decision making. While it's important to weigh the risks and benefits, it's also important to consider the patient preferences. For some patients, lifestyle changes like diet and physical activity may be the preferred route.

On the other hand, some patients may prefer a quicker response and improvement in their joints, spine, and other benefits, and a premis may be the answer. Either way, it's about creating a plan that fits their needs and preferences. My name is Akhil Suth reporting for now. Thank you.

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 AHPa 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 be very helpful to have very, better accurate criteria, particularly for the classification of patients appropriately for research trials. And then, you know, it's going to be very important, of course, you know, a lot of what they found in the result 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 roomnow.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 excess spondyloarthritis. Firstly, in the whole area of using the scores that we use to measure outcomes. So we traditionally have been using something called the PASCAI score, which is the BAV 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 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 best eye score in comparison to other outcomes such as the s test, the ankylosing spondylitis disease activity score, excess 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. One of the things about coming to these meetings is to kind of think of what we 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 at least 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 that 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 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 of arthritis. So here we are in ASAS 24 with these two abstracts of today, o eight one eight and o eight one nine, which I think will help us inform how we manage our patients with excess point zero zero five going forward.

I'm Anthony Chan reporting for RheumNow here in Washington, ACR twenty twenty four.

Hello everyone, I'm Richard Connolly reporting for RheumNow from ACR twenty twenty four. I'm here to talk to you today about a study presented in the RA ILD abstract session on Saturday. This was study abstract eight zero two from Gregory McDermott and Jeff Sparks group. And this was the SAIL RA study, so multicenter prospective study of patients with early rheumatoid arthritis. So less than two years of disease on recruitment to the study.

There are one hundred and seventy two patients in the present analysis. And the interest of this particular presentation was looking at lung disease. And first things, the numbers with lung disease were quite interesting. So sixteen percent of these patients with early rheumatoid arthritis had RA lung disease. Now, that's just kind of a broad term and included interstitial lung disease, emphysema, and bronchiectasis.

And perhaps one could argue that the second two of those would be rheumatoid related, but could also be related to other things. But it's still a relatively high number. And when they looked at just interstitial lung disease, eleven percent of patients had interstitial lung disease. Now that is a high number compared to certainly some of the more revisionist estimates of how many patients with rheumatoid arthritis get interstitial lung disease. Do remember, again, this is patients with early rheumatoid.

So this is early on in the disease course. Potentially later on, even more of these patients will have interstitial lung disease. So they went and looked and analyzed with a multi variable analysis, but what predictors there might be of patients who do get lung disease. And for rheumatoid lung disease, so the three things, interstitial lung disease, emphysema bronchiectasis, two things we know about, so age and being male. So about twice the risk and with increasing age, four times the risk if you are male.

And then the one which I find really interesting, moderate to high disease activity, four point eight nine was the risk with that. It got even more interesting when they looked at interstitial lung disease and in that alone, so interstitial lung is alone, the moderate to high disease activity, the number was six point one seven for having moderate to high disease activity. So this suggests a couple of things to me. It does seem that disease activity is really important in the development of interstitial lung disease and rheumatoid arthritis. It suggests that maybe there is an amplification of this window of opportunity concept that we have in rheumatoid for these patients.

And it's even more important to really aggressively treat patients who might be falling into these risk groups at the start to prevent the development of interstitial lung disease. And then the thing that I know everybody is waiting for me to say, the ACR guidelines, our recent ACR ILD guidelines. For rheumatoid arthritis ILD, they recommend as their first line treatment options agents that have either very limited effect on disease activity or not as good as other agents we have on on disease activity, so especially mycophenolate mofetil, azathioprine. And this is another piece of evidence and something in support of what I have said from the start. And that really the first thing we should be doing when we're trying to treat people who have rheumatoid interstitial lung disease is controlling their disease activity with whatever agent we need to do that.

And then we can worry about what may or may not be better from the limited evidence we have for the interstitial lung disease itself. So I've been at Richard P. A. Conway on Twitter and follow RheumNow for all the updates from ACR twenty twenty four.

Hello. I'm Jonathan Kaye reporting from ACR Convergence twenty twenty four in Washington DC on day one of this meeting. I am here with professor Ernest Choi of Cardiff, Wales, who presented poster number five sixty about a transcriptomic analysis of blood from patients with a variety of inflammatory rheumatologic diseases treated with a variety of combinations. And the question is, can you identify a subpopulation that is most responsive to specific combinations of therapy or specific therapies that could be used in combination to better treat our patients? So Ernest, tell us a little bit about your poster.

Okay, so as you know, rheumatologists are spoil for choice. We have lots and lots of different classes of advanced therapy, but as you know, most patients actually don't solve your remission, which is the goal of treat to target. So there's a desire to use treat to target, but to find the right combination is not that easy. So we developed this program trying to see whether we can find a logical way to find the best combination quicker before we test any patients. So the program is taking advantage of the bioavailable in Spain.

This patient has a range of different polyexylative diseases treated by lung therapy. So the first step is to identify the genes that may be driving the NAC2 disease even or in a responder. And And then the hypothesis is that to find the right combination means you must find a drug that will suppress this actively expressed genes in the nonresponders. So we prove the result of all the responders to the biologic agent, and we have reasoned that the genes that are suppressed by these treatments, if it mapped to the actively activated gene in the responder, then we should find the best combination. Was surprising in this analysis that we find actually many of the biologic agents have fairly overlapping effects.

So the benefit from combining them will not be great, but we did find one combination which is TNF plus an IL-six inhibitor. Together they seem to have complementary effect in patients with rheumatoid. So the next step for us to do in this experimental study is to do a clinical trial to see whether we can prove

that this is the case.

So this is a different approach from Kospitallis' approach in the R4R trial, where he found that there were three different subtypes of rheumatoid arthritis, which lymphocytic form, a myeloid form, and a fibroblast driven form, each of which probably respond to different therapies that are directed toward that cell type which is most active in that disease subtype. So you're looking at a relatively heterogeneous mix of non responders. Are there any signals that you pick up in terms of transcriptomes which might indicate what cell type is not responding to the current therapy?

Yeah, that was a great question because when we did single cell sequences, most of the response was mapped to the myeloid population. So it is possible that it's the myeloid driven diseases

that are most suitable for this population. Would

you be able to look at a different population or a different way of analyzing this biobank to come up with perhaps an opacitic driven disease or fibroblast driven disease, looking at scleroderma patients or interstitial lung disease to try to come up with a combination that would work better in a fibrotic disease.

So that's part of

cost collaboration.

I think for myeloid disease it's possible to classify the lymphomas. So, yeah, so it's something that we're gonna move forward to. I think the results are complementary. I completely sign up to the fact that we need to have Francis's hepatitis.

So this work suggests that the next era of biologic therapy will be looking at combinations of biologic therapy. Gastroenterologists are already ahead of us in that they're looking at Vedalizumab in combination with TNF inhibitors, finding that the combination is superior to either alone. So this is very interesting work. As always, you're doing great work at the cutting edge. Thank you so much for talking with us about this.

For more about ACR convergence twenty twenty four, I'm Jonathan Kaye for RheumNow. Go to rheumnow.com.

Hello. I'm Marina Magre, the division chief of rheumatology at University Hospitals and professor of rheumatology at Case Western Reserve University. And 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 gonna walk you through some key highlights of today's meeting. So, you know, the ASAS consensus definition for difficult to manage axial spondylo arthritis 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 in 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 Amagre, professor of medicine at Case Western Reserve University, division chief of rheumatology at the University Hospitals Cleveland, once again reporting for RheumNow from ACR twenty twenty for 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, the 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. You know, 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. 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 b twenty seven positivity was also associated with difficult to manage axSpA suggesting maybe there is a genetic role into it. Thank you so much.

I'm Anthony Chan reporting here at ACR twenty twenty four for RheumNow. And one of the key highlights of, today was the new preliminary ACR guidelines on the use of ultrasound in both rheumatoid arthritis and also psoriatic arthritis. I wanted to focus on the psoriatic arthritis area because it's one of the areas that I find clinically quite challenging to assess patients, especially when they don't always present with very straightforward clinical signs, and ultrasound will be a benefit. And I'm very happy that I can be joined by the lead author from this morning's presentation, doctor Catherine Bakewell from Salt Lake City. Yes.

And she presented the work today. So welcome.

Thank you so much for having me. It's a pleasure to be here.

So the tell us about the the work that you've been doing regards to developing these preliminary guidelines.

Absolutely. So this has been a labor of love. As you heard this morning, it's been about project. On the psoriatic arthritis side, I can tell you we had convened first with 13 different experts in addition to the core panel that developed a series of what we called Quick Go Questions. And the idea was to ask how can we better use musculoskeletal ultrasound and psoriatic arthritis both for diagnosis, contextualizing findings, determination of treatment escalation, and remission.

We then went through the literature. There's the real labor of love. It was over 3,800 articles that we came up with for ultrasonic psoriatic arthritis. And a series of 19 different literature reviewers whittled it down to just over 150 documents, and then we had a voting panel of 10 folks who were able to ring forward with a 70% consensus, 20 different people statements or guidance statements that you heard this morning,

and thank you for coming on this evening.

It was a very stringent methodology. Yes. Lots of review and lots of people getting involved in it. So just tell us what what is the main difference compared to the twenty twelve guidelines? So ten years down the line, what's different this time?

So for better, for worse, truly for better, but it made this a challenging project. There has absolutely been an explosion in the number of papers published, in the field of musculoskeletal ultrasound since the 2012 guidelines were published. A big difference just in the structure of what the output will be is that in 2012 it was looking at the application of musculoskeletal ultrasound across the field of rheumatology, stating various areas where it was reasonable musculoskeletal ultrasound to evaluate for inflammatory disease and making statements like, for example, that SI joints would not be an appropriate location in absence of the availability of other imaging modalities. But this is truly focusing on rheumatoid arthritis, psoriatic arthritis, and narrowing it down to clinical application and day to day practice for the everyday rheumatologist. It's not meant to be just in clinical trials.

So these guidelines are, you know, many ways set the standards for us for what we should be looking for. But also, I was very, attracted to, you know, how do we use this practically in clinic. So if you could share with us some of your thoughts about how we're gonna translate this into clinical use.

Absolutely. So first and foremost, when we talk about diagnosis, we talked this morning about the concept of ultrasound enhanced Casper classification criteria. So can we use musculoskeletal ultrasound to determine who we would even put through the classification criteria? Who can we confirm inflammatory articular disease? So joints, and theses, or spine are kind of the three categories that this has far refers to.

So there's looking at diagnosis. We talked a lot about not only escalation of therapy but determination of flare and what constitutes flare. And we talked about the concept that clinically normal joints can have ongoing synovitis and clinically swollen joints can have full residual fibrotic synovium. So you put the ultrasound transducer on and there may be no dropper signal because somebody actually has burnt out

or has some disease on

their skin. Feel that it's still swollen. And so one of the statements was MSUS can confirm the presence of FLAIR. And that is also helpful in that patient provider discordant situation. So a patient comes in and they may have significant synovitis on exam, but they're saying, look, doctor, I really only want to use my doTERRA oils.

I really don't want these. I've read the package it's served that this medicine concerns me. And it's so helpful to be able to put on the transducer, show them the Doppler signal, multiply fire, or you may have a large aversion and they say, Oh, this is really causing damage. This has a different risk benefit ratio than I was thinking. Or the opposite is also true to the patient with psoriatic arthritis not your choice of arthritis that is flaring.

Let's talk about other ways to handle your pain.

I mean,

that to me is one of the, the key highlights from your presentation this morning of how you can take a guideline and then put into clinical practice. My shot of it is telling the sub what what for us is a very subjective assessment, doing objective assessment. Yes. You know, so the subjective becomes objective because of MSUS. That's And I think the big area that we maybe struggle is antisis, antisitis, because they're quite hard to sometimes assess.

Yes. So maybe a few words about maybe how we can take that kind of forward with this new guidelines with the use of MSUS, because you did show us some very nice work there.

Thank you. And this is such a key element or domain to assess and think it's really important that up? Because all of the agents that we are shown now that say, Hey, look, this works for enthesitis. We're talking about clinical endothelicis where the provider presses, the patient says, Ouch, that's counted as enthesitis. If they don't say, Ouch, counts as no enthesitis.

So again, your patient with fibromyalgia all of a sudden has enthesitis, and your patient with subclinical inflammation who doesn't say ouch but is still inflamed doesn't even get counted towards the TALI. So there really is a need for that objective assessment that ultrasound provides us. And we talked about the elementary lesions of empathicitis and how this can be used especially for diagnosis but also monitoring of treatment and remission.

I think that's really excellent. It kind of takes us to a different level. So just to wrap up, what would you say for our audience that key take home from your session today?

If you have not started scanning yet, now is the time to get into it. And I think we all are so busy in our day to day practices. I completely understand both the cost and the time limitation. But I do believe that this is a powerful tool. It just gives us more information to work with and base our clinical decisions off of.

And I really do consider it my stethoscope in day to day practice. Get So out there, buy one, it's worth it.

Alright there. Start scanning. Start going. Start looking at it. So, you can refer to the the video or the slide from today's presentation.

It gives you the outline of the preliminary guidelines and I think this is something that will certainly help us in our clinical practice. So, Catherine, thanks very much for your time, and this is Anthony Chan reporting here from Washington at ACR twenty twenty four.

Hi. It's doctor Artie Kavanagh coming to you from ACR Convergence twenty twenty four in Washington DC for RheumNow. Lot of interesting abstracts. Now, I'm looking at things in psoriatic arthritis or related to, and let's start out with a couple things that are related to. There was a nice seminar on uveitis, and of course, uveitis is important across a number of rheumatic diseases, but I think it's especially relevant in psoriatic arthritis.

We see patients who have uveitis, and that can influence the treatment decisions. There's a seminar, Jim Rosenbaum gave a nice presentation, and there's a Doctor. Lerner gave a presentation on the pediatric aspect of uveitis, which was similar, although distinct. Anyway, there's a lot of data now in uveitis, and it's very exciting that it looks like we do have some options. TNF inhibitors are a natural, but there are other mechanisms that have had some interesting data that will help us manage patients for whom this is really an important comorbidity.

So, another, when we talk about psoriatic arthritis, and that was the seminar, let's look at some of the abstracts. We talk about psoriatic arthritis. We always talk also skin psoriasis. And I think an abstract that was very interesting was three zero three, was an oral TNF inhibitor. This is a Janssen drug, and I think the whole concept is very exciting.

The TNF inhibitors have been with us since the late '90s, and we've been using them in psoriatic arthritis since the early '00s, for sure, and they really have established a central role in the treatment of psoriatic arthritis. Unlike our colleagues in skin psoriasis, where they now have better results with other mechanisms, such as IL-twenty three and IL-seventeen, in the joints for psoriatic arthritis, TNF inhibitors still have a central place and the most experience. We've always assumed they would be parenteral, but this is a fifty two week follow-up, long term extension study, dose finding study of an oral version of TNF inhibitor. Is it going to be just a pill with all the same attributes as the TNF inhibitor? Will there be differences?

We have to see. But it's very exciting. And then one more abstract, a couple of hot topics, and that's abstract two twenty three. Hot topics meaning the use of ultrasound, and also difficult to treat psoriatic arthritis. So this was from Ottawa, where they took patients and divided them using the EULAR assessment for difficult to treat RA, so not exactly the same, but I think it works well in psoriatic arthritis.

And they looked at the patients who had difficult to treat psoriatic arthritis compared to those whose psoriatic arthritis was not difficult to treat. Interestingly, they did not find many clinical differences in the readouts that we might think would be different, such as number of swollen joints. The ultrasound also was not different between the groups. So I think this really highlights the fact that there are other factors that go on as we're thinking about patient assessments, which are of course very important to our overall treatment approach to patients, and difficult to treat is complex. It's a complex construct which includes a number of different facets, not all of which are amenable to easy analysis like with the ultrasound.

So a lot of great presentations so far. We're just starting ACR convergence. This is Arti Kavanaugh from RheumNow.

Hello. I'm Jonathan Kaye reporting from ACR convergence twenty twenty four in Washington DC. I'm here with doctor Cecile Georgie Villara from Nimes in France, who has presented poster number three sixty about shared decision making in patients who have been prescribed targeted therapy. Most of the guidelines for rheumatic diseases, rheumatoid arthritis, axial spondyloarthritis and others, talk about shared decision making. The question is, do the patients agree with the physicians that they've shared in that decision process?

So, Doctor. Aujou Viola, you studied patients who were prescribed targeted therapy and interviewed or provided a questionnaire to both the physicians and the patients. And what did you find among responders compared to non responders?

Thank you so much. It's a very important point to consider. We have asked the patients, will you participate as much as we want in the decision, in the choice of the therapeutics and of the treatment? And the answer was on five point scale. We consider the patients completely agree with this point as good shared decision making.

And you have asked the nearly same question to the physician. Have you practiced shared decision making and completely what the best point to consider a very shared decision making. It's very interesting to note that in patients with good adherence to the treatment, the answer, the confidence between the physician and the patient perception on the chair decision making are very close. But in the patients who never adherence to the treatment, there were a disconnection in the perception, a discordance between the the physician who thinks that the patient is happy and the decision is shared, and the patients who only 20% think that was a great shared decision making. So I think that's really a point to consider to improve adherence of the treatment.

Do you find any specific differences between the non adherent patients who felt that they had not participated in shared decision making compared to those that did feel that they had participated?

No, but I think the most interesting and maybe something I think I'm not happy with this result because the physician have not this perception. They think that the patient is happy with the decision and they think, we have made a great shared decision making. And it was not the perception of the patient at all, and they don't precise these these facts.

So what would you suggest that physicians do to change this perception?

Maybe ask a more open question. What do you think? Not just you are agree. Okay. That's fine.

Just what do you think? What's your expectation? What's your what's the goal of your treatment for you? Maybe something more open, more cooler, maybe. It could be a great point to avoid this perception, this disconnection in the perception.

Decision making is not I explain you, it's that, it's that, it's that's a good way. You are me, you're okay, okay. I have made a great decision, a chair decision making. No. It's not like that.

So this is very important because although we think that we're sharing the decision making process with the patient, patients don't necessarily perceive the same. Shared decision making is an important approach to the physician patient relationship, And this abstract number 360 highlights that there's still room to go in improving this. So is shared decision making really shared? Not necessarily, but let's improve that. This is Jonathan Kaye reporting from ACR Convergence twenty twenty four in Washington.

For more on the ACR Convergence twenty twenty four meeting, tune in to roomnow.com. Thanks.

Hey, everyone. My name is Brian Jaros, and I'm reporting to you live from ACR Convergence twenty twenty four Washington, D. C. I'll be telling you about abstract number thirteen sixty two. So as we all know, as rheumatologists, rheumatoid arthritis is one of our bread and butter conditions that we treat, and one of the most common diseases that we see in rheumatology.

We're lucky enough now that we've developed really an arsenal of treatments that we have to offer patients with rheumatoid arthritis. That leaves us with the question of always which medications will be the most effective. Several groups have sought out to answer this question, and one group in particular is trying to see is there a particular type of JAK inhibitor that's more effective for rheumatoid arthritis compared to the others? And of course, this is really relevant to our patients. If we can pick a JAK inhibitor that we know upfront has better data, has better success for putting people into remission, it'll hopefully decrease the amount of time we spend cycling through meds and getting patients to an area where the disease is quiet.

This abstract is from Peter Taylor, et al, and they used real world data to complement trial data that's been shown in the past regarding this question. They had a really clever design to try to increase the power of the study where they sent out surveys to rheumatology practices internationally throughout North America, Europe, Japan, many countries being involved, and they included patients who had rheumatoid arthritis and had been treated with any kind of JAK inhibitor for at least six months. Now, when they sent out these surveys, they were asking physicians to report on outcomes of these patients, specifically DAS28 scores, outcomes of pain and fatigue, and outcomes of compliance to the JAK inhibitor that the patient was prescribed. They then took all of this data back and tried to look for significant differences between the different types of JAK inhibitors. Ultimately, they accrued a pretty good sized population of 1,400 patients, a majority of whom were taking upadacitinib, fifteen milligrams, and some other patients taking mostly tofacitinib or baricitinib.

This data, they found that patients on the upadacitinib fifteen milligram compared to the other JAK inhibitors were actually more likely to achieve DAS28 remission in comparison, and this was on the order of about fifty four percent of patients on upadacitinib achieving DAS28 remission compared to an average of forty four percent on the other JAK inhibitors. An absolute difference of 10 between medications is significant, both statistically and clinically, for when we're treating our patients. There are other outcomes in terms of patient reporting fatigue and pain mirrored this DAS28 response. They saw that patients on upadacitinib had less fatigue, higher rates of decreased pain, and actually higher rates of compliance, which is of course multifactorial. It might suggest that the patients have less side effects or maybe just also suggests that the patients have more success with the medication, were feeling better, and were more likely to stay on it.

This study is really important because we've had meta analyses of phase three trial data which have suggested that numerically upadacitinib might be more effective compared to other JAK inhibitors in RA, but this is one of the first studies to look at real world practice data, and again internationally representing a huge body of patients, and further demonstrate this finding. For me, I might now reach for upadacitinib a little earlier compared to other JAK inhibitors given the choice in treating patients with rheumatoid arthritis based on this data complementing the trial data, again these post hoc analyses showing that upadacitinib might be more effective in putting our patients into remission. That's all I have for now. Thanks for listening and keep tuning into RheumNow.

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 eight twenty 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 spondyloarthritis. 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. Right. 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 of 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. Okay. 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 fifteen 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.

Uh-huh.

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 in favor of ankylosing spondylitis versus nonspecific fat 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 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 nonspecific back pain control.

Okay. So wow. That's that's very good. And 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. 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.

Know, occasionally it may be 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 spondyloarthritis. 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 bone, sorry, three erosions, three lesions, erosions, and then four bone marrow edema lesions, 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 a 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, 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, 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.