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

Hi, everyone. Jack Cush here at ACR twenty twenty five. ACR Convergence, we're in Chicago. It's the first morning of the meeting. This is my first video.

I hope I get better as time goes on. I just left the plenary session. Interesting plenary session. Good, reports from Michelle Petrie on lupus biopsies and new insights there. Follow-up study to the Select GCA study, using OOPA in GCA, two year results.

I'm gonna talk about the results of the STOP RA trial. Abstract seven seventy four from IANO, IANO, et al, and Kevin Dean's group at the University of Colorado. They did longitudinal analyses, multi omic analyses, looking at cell sequencing, cell cytologies, surface proteins, cell subsets, serologies, all as predictors for the STOP RA study. So again, University of Colorado under Kevin Dean, published the STOP RA, a hundred and forty four patients with pre clinical seropositivity who were have some risk of developing RA, maybe a thirty percent risk. They all were seropositive going in, right?

So in the trial, they either got hydroxychloroquine or placebo, and it didn't work. It didn't prevent anything. The outcomes were sort of, disappointing, and that's the end of it. But that's not the end of it. They have a number of different analyses that they have done.

In this analysis, they looked at, whether you could predict who's going to convert, from having just preclinical arthralgia CCP, to actually having RA. So a 144 people in the study, they studied about a 100 overall. They did different kinds of studies with different subsets. One subset was 36 patients, another subset a 100 patients. And they found a few things that were interesting.

One is that they could identify cellular subsets that were enriched for or increased, at baseline and then throughout the development period in those who became the converters. And the main thing is that peripheral helper t cells were enriched. The number is low. It's like two and a half percent, but it's increased at baseline and also in those that ultimately converted. The second thing is they found was again the importance of CCP and higher levels of CCP.

In the end, when you got into what predicts progression, they did different modeling and they showed that number one, that the combination of those two, CCP three being elevated and, an increased number of peripheral helper T cells, increased the odds of those that were gonna progress by roughly two fold. The other thing that they found was those who had the top twenty percent elevations of t helper peripheral helper t cells and the top twenty percent of CCP had an earlier time to develop RA. So that was faster and shorter as far as progression. So the question is, what's the added advantage of the cellular subsets, those peripheral helper t cells in predicting more than what you would get, CCP and rheumatoid factor, it's a little bit. The a AUC went up.

I had it on my phone, I can't get it on my phone. Here we go. The AUC went up, let me see. I'm gonna give you the numbers right here. If you just looked at usual things, CCP, RF, and age, the AUC was point five one.

If you added in the helper t cell subset, the AUC went up to point seven three. So it went up, you know, a modest amount, but not enough I think to be worth doing in practice in clinic. A very good, presentation, really involved research that I think tells us more about what's going on pathogenically in people who are going to progress from this clinically suspect arthralgia to actually overt inflammatory arthritis. But the clinical utility of this still is CCP, especially high titers. That's it from ACR.

More to

come. Hi.

It's doctor Janet Pope. I'm here at RheumNow at ACR twenty twenty five in beautiful Chicago. I wanna really know is AI smarter than a doctor and maybe me in particular. So I went to the session on AI in medical education. It was Jonathan Hausman talking.

He's a physician, and he publishes in AI and does RCTs in AI. It was session number 26 s one seven. So there's a few take home messages. Number one, he said, don't plan for superintelligence in AI. He said plan for knowing things, and we might be dumber than AI eventually, but we need to actually have cognitive, ability to actually do what we need to do as a job.

Number two, he said that large language models can have virtual tutors to help train medical students to actually do better on their OSCEs. And in an RCT, there was satisfaction, and the OSCEs were done better by these students that were randomized. And in fact, the OSCEs were graded better by AI. Number three is that something kinda telling. If you do an RCT of AI giving the answer on a medical case versus the physicians and they can look up stuff, we kinda screw it up, and we have innuendos, ifs, ands, or buts.

And so AI can do better than us, but not always. In particular, it can do better than us on soft skills such as, should I apologize to the patient? How do I introduce the idea of medical error? Which should I, counsel the patient on in this area where a drug could give benefit but risk? So I think right now, doctors are pretty smart as are other health care providers.

AI is pretty smart, and I think we'll work together and really solve a lot of problems. Thanks. Follow me at Janet Burdeau. Thank you.

Hi, everyone. My name is Mike Putman. I'm a rheumatologist at the Medical College of Wisconsin, and I'm reporting to you from ACR Convergence twenty twenty five for RheumNow. Now today I'd like to talk about an abstract I thought was particularly interesting from the ANCA associated vasculitis session. This is abstract seven twenty one, pulmonary manifestations of granulomatosis with polyangiitis or GPA and microscopic polyangiitis or MPA.

These are the two variants of ANCA associated vasculitis that we are all familiar with. Now this was an analysis of the VCRC, that's the Vasculitis Clinical Research Consortium longitudinal cohort study. This is an observational study of these two types of vasculitis. Huge effort from the vasculitis community. It covered a lot of different centers.

This particular poster discussed the pulmonary involvement that was observed in that study. Really important of ANCA associated vasculitis and I want to highlight a couple really important teaching pearls from that today. The first is that about over seventy percent of patients with ANCA associated vasculitis had some pulmonary involvement at baseline. Over the course of that study, went up to a GPA almost eighty five percent of people nearly had some pulmonary involvement. The lungs are one of the most important manifestations for this disease.

Obviously, kidneys and others, but think about the lungs. Some of what they saw is what I would expect. There was a big difference in nodules. Waxing and waning pulmonary nodules is a classic feature of GPA and they saw that in sixty three percent. Not quite so common for MPA or microscopic pine jars.

Only twelve percent had pulmonary nodules in that group And that jives with my clinical experience. I actually wonder if some of those MPA people were actually GPA all along. Now there were smaller differences in some of the scary pulmonary manifestations, so diffuse salveolar hemorrhage, and those actually favored microscopic Pongiitis or MPA, more common with MPA. So sixty one percent of people with MPA had diffuse alveolar hemorrhage versus thirty one percent with GPA. Respiratory failure was a little more common than microscopic Pondyitis group as well, seventeen percent versus six.

So when you see patients with GPA, expect nodules, maybe some of the scary stuff. Microscopic crongitis, expect more of the scary stuff, less nodules. Now a couple things that you may not have expected. And these are some rarer manifestations of ANCA associated vasculitis that think everyone needs to know about. The first one is interstitial lung disease.

We're increasingly recognizing interstitial lung disease among patients with microscopic fungitis. In this cohort they saw eleven percent of their patients with MPA having ILD compared to one percent with GPA. This is a really important thing. When you see people with microscopic fungitis, ask yourself, are they developing any signs of interstitial lung disease? The other thing that I can't talk enough about is endobronchial involvement.

These patients with tracheal stenosis, this is a very difficult manifestation that often drives flares, long term morbidity for people. About twelve percent of people with GPA had that kind of involvement, only two percent for microscopic polyangiitis. You're thinking what are these long term ramifications of disease? GPA, worry about the tracheal endobronchial involvement. For the MPA, think more interstitial lung disease.

What brings that all together? Why are these so different? I actually think it's in the name. The granulomatous manifestations that go along with GPA, that causes those lung nodules, all your crusting up top. Then the capillaritis that we see with microscopic pinegitis, that's where you're getting this diffuse alveolar hemorrhage, probably some low level inflammation that's driving interstitial lung disease.

Really nice report. Verifies a lot of what we expected and highlights some under recognized findings in this disease. Thanks so much for tuning in. Be sure to follow along with all of our coverage at ACR Convergence 2025.

Hi everybody, we're in the Windy City Of Chicago for ACR twenty twenty five. This is our first day and I have here Doctor. Sebastian Setui from University of Pittsburgh to talk about abstract number ten seventy two, which is to evaluate the age gap in rheumatology. So the population is aging globally and that means as rheumatologists, we're progressively caring for an older adult population. And Doctor.

Sattui is answering the question, do we actually know how best to treat for this population? So Doctor. Sattui, can you tell us what motivated you to study this and how you actually looked at and what you found?

Well, you so much for the interest in our abstract. And as you pointed out, we know at this point that our population is aging. And with that in mind, we need to understand how the therapies that we have and the treatments that we have are really applicable to our population, which we know that with RCTs being the higher level of evidence dictating care, dictating our guidelines, we need to understand how representation of older adults is in clinical trials and understand in order to really kind of apply our therapies and in daily clinical care. So with that in mind, what we did, which has been of interest in many fields, is looking into how older adults are represented across clinical trials for rheumatic diseases, and that's kind of the main idea behind this systematic review meta analysis.

And what diseases did you look at for the

So we did, this was a massive gargantuan effort, I'm speaking this on behalf of all my co authors, which included rheumatoid arthritis, axial spondyloarthritis, including axial spondees, and of course psoriatic arthritis as well as reactive arthritis, ANCA vasculitis, GCA, PMR, myositis and scleroderma. So we looked into over, around like thirteen years of trials, pharmacologic trials starting at phase two onwards for all of these diseases with the specific criteria for inclusion, ended up with 5,000 trials going down to all the trials that were included at the very end. Expected, most of the trials, rheumatoid arthritis, lupus were the biggest group of trials, But we included trials for all of the diseases, calculating, looking specifically into the mean age, the population of older adults, representation of older adults, individuals over the age of 65, where these trials were happening, who were running these trials, and that was a part of the systematic review analysis. In order to actually allow for a comparison with some limitations of more of how the trials and the population trials really represent or compare with real world data, what we use is a cross sectional data cut from the RISE Registry that as many people know includes over thirty percent of the rheumatology providers in this country to understand how for each of these diseases, what is the mean age and what is the proportion of older adults as well and therefore allow a degree of comparison from our results of the systematic review meta analysis.

I see. So it seems like it's fair to say this is probably one of the largest comprehensive evaluations done for seven rheumatic diseases of clinical trials, and what you did was compare the age of enrollment in clinical trials that actually and inform our compare it to real world population and to see if this reflected.

Exactly.

And so what did you find? Are we doing a good job?

Sadly no. We actually found quite a difference between, I think, first, so from the systematic review of meta analysis, as expected, we found an older age with GCI PMR, which again reflects what we would expect from a clinical population, then followed by ANCA vasculitis and other conditions. The proportion of older adults as well was unfortunately still lower when we looked specifically at the trials. But when comparing to the real world data, we actually saw a significant gap in most of the diseases. Certainly, again, going from a smaller gap in GCA and PMR trials to even larger gaps in diseases like lupus, rheumatoid arthritis, or the spondyloarthritis as well.

And the proportion of older adults also kind of having quite a substantial gap from diseases where in lupus for example, only one percent of individuals were over the age 65 in trials, the real world data showed that at least twenty percent or more are within that age group. So I think we have a lot of work to do in order to actually understand what are the barriers for this and how we can improve and make the population of patients who are participating in trials who are informing our care, who are informing our guidelines, who are informing our decision making from patient care to really reflect the patients that we care for in the real world. So the future steps for sure are to better understand what these barriers are and how to take from other fields ways and kind of implementation methods to improve recruitment of older adults in clinical trials.

I see, thank you. I remember seeing at ACR twenty twenty five, there's a patient perspective poster that actually says they didn't expect to age with all these diseases, but then they are and they're trying to figure it out. It shows that we as a community need to do a better job because I think like you said for RA, there's a difference even up to a decade. Like clinical trials enroll people in their mid fifties, but in reality we're caring for people in their sixties. So there's a long road ahead that we need to do.

Even from the IRON review, they said the science we develop is only as good as the data. I really appreciate you and your team raising the awareness about the gap, the age gap that we exist in rheumatology and about how we can address this moving forward. So thank you for that.

Thank you. Thank

you This for is Chih Lee reporting for RheumNow in Chicago.

Greetings from Chicago. My name is Doctor. Al Kim, an adult rheumatologist at Washington University School of Medicine in St. Louis, Missouri. Welcome to RoomNow, the video series that provides updates for American College of Rheumatology Convergence twenty twenty five conference.

So I'm the faculty lead for the CAR T and T cell engager group and the poster, the abstract I'm going to be selecting today is actually abstract number one entitled XM AB six fifty one, a CD19 by CD3 T cell engaging bispecific antibody for autoimmune disease. Now this is a preclinical poster. Typically we don't cover these but I think one of the issues with T cell engager data in the past such as compounds such as blinatumomab is that they haven't been as efficacious as we want them to be compared to CAR T cells and this may be due to the fact that they are not as potent. They don't deplete B cells out of tissues. So again, this is a preclinical poster examining this compound XM AB five XmAb651.

This is another three by 19 T cell engager and what they do is some ex vivo RA and lupus PBMC killing assays which it does very well. Then they actually moved into in vivo in non human primates and this is where it gets a little interesting. So not surprisingly after a single dose you get rapid depletion peripherally I. E. In the blood of B cells.

Now what they did was they actually looked in the bone marrow and lymph node and saw equally good depletion in those compartments. This is new and different. Georg Schetz Group and Erlagen had previously published that when using first generation, t cell engagers like blinatumomab, you can't deplete out of the lymph node. But this one can at least in a non human primate. This is going to be important because this can translate into more durable clinical responses.

You can restore potentially pre disease b cell compartments and homeostasis which appears to be required for that durability of response that we're seeing with the CAR T cells. Know so the advantages for T cell engagers compared to CAR T cells are quite numerous. No need for lymphodepleting chemotherapy, easier access, particularly if they can formulate a successful subcutaneous delivery approach. So if we can get these T cell engagers to be more effective without creating increased toxicity, this may be an interesting future for our patients instead of CAR T therapy.

Hi. I'm Sheila Reyes from The Philippines, and I'm reporting live for RheumNow in Chicago for the ACR convergence twenty twenty five. It's a beautiful, bright, sunny day, and I just attended an interesting and well attended session on the ACR on the rather, on the 2025 ACR guidelines for SLE. And I would like to share some important points from the session in this video. Doctor Ali Duarte Garcia discussed the recommendations for lupus pleural pericarditis, and according to him, the recommendations intentionally used colchicine and recommended the use of colchicine and NSAIDs over glucocorticoids.

However, special circumstances still exist where glucocorticoids are needed in patients with pleural pericarditis, especially when there's concomitant active systemic disease. Our patients do have contraindications in the use of colchicine and NSAIDs, including possible drug interactions when taking colchicine and NSAIDs with concomitant C and Is probably, and also in cases where there is late pregnancy. And in terms of DMARDs, mycophenolate was recommended to be used over azathioprine. Now for cutaneous lupus, it is generally and recommended that all patients receive hydroxychloroquine unless contraindicated. Glucocorticoids may be used, but again, using the lowest possible dose and the shortest duration necessary.

And when patients become refractory to initial treatment, escalating therapy is the next step bearing in mind disease activity. So for moderate disease activity, conditional recommendations are to add immunosuppressants like your methotrexate or your mycophenolate or a biologic like your belimumab or anifrolumab. Doctor. Worth also highlights the importance of medication review, when lupus patients present with new rashes in the absence of active disease and to consider drug induced SLE in these classification or in these group of patients. For lupus arthritis, similar recommendations exist as that of cutaneous lupus emphasizing the need for early immunosuppressive treatment so as to spare glucocorticoid use or its complications.

And in certain specific clinical scenarios, there were also conditional recommendations like for methotrexate, it should be considered as first line, especially when the predominant feature is arthritis and there is the absence of organ, other significant organ involvement. Mycophenolate, if there is a history or there is current active systemic involvement on top of the arthritis. Adding anifrolumab or belimumab versus initial therapy was conditionally recommended for cases of inadequate response. Now additionally and interestingly, there was really no recommendation on how to manage Jack Cush, taking into account or requiring further research in this area. Now then again, the main message here is that treatment should always be individualized, taking into account patient preferences and availability of these treatments in the countries that these patients are being treated in.

Follow me on x at RheumOrampo, and tune in to RheumNow for more updates on ACR twenty twenty five.

Hi. This is doctor Arti Kavana, University of California San Diego. Very happy to be here at the ACR Convergence in Chicago twenty twenty five at RheumNow. Of course, the greatest coverage of the meeting. And you took on a hot topic, hot topic in psoriatic arthritis, and that is imaging.

And imaging, of course, as one of the forms of inflammatory arthritis, we looked imaging as a measure of damage to the joint, and we extrapolate what we had learned early in rheumatoid arthritis to psoriatic arthritis. But over the years, we've seen, as has been seen in rheumatoid arthritis, it's really hard to discern a therapeutic effect at inhibiting structural damage using plain x rays because the patients are not progressing to the degree that they used to before we had so many therapeutic interventions. Now we see progressions of just a couple of units in the Sharp modified van der Heide score, and whether or not that has any clinical relevance is a subject of intense debate. What that has done in psoriatic arthritis is drive interest in other forms of imaging, particularly ultrasound. It's come a long way in ultrasound, and ultrasound has a number of benefits in imaging peripheral arthritis and psoriatic arthritis.

Also, is able to image the entheses, which are not visualized well by other techniques such as plain x-ray. In addition to being able to find damage, the ultrasound is able to look at inflammation. Very important. So the question, how do we best do ultrasound, is one that's been actively studied. There's a study called DUET that collected data from ultrasonographers on PSA patients, from multiple investigators around the world to try to create a scoring system by which we could accurately quantify the important aspects aspects of inflammation and also structural damage in patients with psoriatic arthritis.

In addition to that, there are a number of other ways that we can look at the joints. Big interest in using quantitative CAT scan, which can image bone in a much greater detail than plain radiograph can and give important information, for example, on the potential healing of erosions that we see in inflammatory peripheral arthritis, including psoriatic arthritis. Then fancy techniques, would call them, like the PET scan, positron emission tomography with the CAT scan, can look at inflammation. I think, like MRI, can offer us valuable information on many of the domains of involvement, the peripheral arthritis, enthesitis, dactylitis, also the axial disease. And then MR, how best do we use MR?

If it was widely available and had no downside, will we do it on all the patients all the time? Quite possibly. And I think there's a lot of work in MRI looking at novel ways to both set up the exam and then to interpret it. So what's being looked at are the higher strength magnets and beyond the three Tesla magnet, and also novel sequences like the ultra short time echo recovery sequence. So imaging, super hot topic in psoriatic arthritis.

Historically, had plain x rays, and they showed us a lot of good information, but I think more exciting is the future with novel methods to assess the joints. It's doctor Artie Kavanaugh from ACR in Chicago, and you're watching RheumNow.