ACR 2025 Daily Podcasts Day1c Save

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

I will.

Hi, everyone. I'm doctor Brian Jaros. I'm coming to you live here from ACR 2025 in Chicago. Today, I'll be talking to you about two abstracts regarding the sinonasal or ENT components of ANCA associated vasculitis. For those of us that treat ANCA vasculitis, we know intimately there's a lot of challenges surrounding how we can best approach these patients and get them into clinical remission.

Immunosuppression itself is not always effective alone for these patients, and we heard earlier today actually in a session from Doctor. Lally and Doctor. Zacarak that we really need to partner with our ENT colleagues in order to best treat these patients. So what new data do we have this year about the ENT manifestations and ANCA vasculitis? The first is from Abstract seven twelve.

This is a study of the nasal microbiome in these ANCA vasculitis patients. We know that the microbiome in these folks is altered and there's already been data, for example, that colonization with staph bacteria seems to be a risk factor for relapses in these patients. A group took this a step further. They isolated a bacterial supernatant of two different bacterial strains and then took nasal epithelial cells, some from ANCA associated vasculitis patients and some from healthy controls, three patients in each group. They then exposed these nasal epithelial cells to the bacterial supernatant to evaluate a response using transcriptomics.

What they found is interesting. The ANCA associated patients had a different transcriptional response with certain genes being upregulated, including those in angiogenesis, so blood vessel formation, as well as in the extracellular matrix modification and in cell cycle pathways. As you might imagine, based on the pathophysiology of ANCA vasculitis, there were several genes upregulated that contribute to neutrophil biology, And perhaps most interesting in these ANCA vasculitis patients, genes associated with barrier formation, mucin function, immune signaling were all downregulated in patients with ANCA vasculitis. So the author sort of concluded that there's something to do with an impaired, cell signaling pathway, impaired immune defense strategy in these ANCA patients. They're responding differently to these normal bacteria that all of us are typically exposed to on a regular basis, and that aberrant response is contributing to the inflammatory environment in the ear, nose, and throat.

Now another group took a more clinical stab at this. This is Abstract seven twenty five, Rheumat et al. Noted that having ENT manifestations in ANCA vasculitis is known to be associated with an increased risk of relapse, and that group has previously come out with an aptly named patient questionnaire called SNOT22 that the patient fills out in a variety of different domains to kind of understand their burden of psychologic and ear, nose, throat symptoms. They used this questionnaire adding four additional vasculitic components surrounding crusting, bleeding, and nasal pain and looked for an association of items on the SNOT22 plus with different clinical manifestations.

So they had a huge group

of ANCA patients, this was six sixty three patients, a majority of which had a history of sinonasal disease. The authors found that a higher total SNOT SNOT22 22 plus plus score was more associated with active vasculitis, and even when they looked at the different sub domains within that SNOT 22 plus score, including things like vasculitic manifestations, sleep quality, psychiatric qualities, facial, symptoms, nasal symptoms, all if they had higher scores were more associated with active vasculitis. When they looked which specific features correlated the best with active disease, it appeared to be the presence of severe nasal pain, actually the presence of self reported sadness, and a decreased prevalence of sneezing. Now they also compared these to healthy controls, and even in, quote, inactive vasculitic disease, those folks tended to have higher scores than their healthy control counterparts. So both of these studies give insights into the ENT manifestations of ANCA vasculitis, one from the biologic aspect helping us understand the mechanisms of this disease, another from the patient aspect helping us understand our treatments and the patient reported outcomes.

And both coming together to really enrich our full understanding of how we should approach, these patients. That's all I have for today. Take care.

Hello. I'm Anthony Chan reporting here from ACR twenty twenty five in Chicago. And there have been interesting posters on treatment in axial spondyloarthritis today. And we know that the advance in the treatment with biologics has really revolutionized the treatment in XPA. But there were two posters today that looked at the use of a generic tofacitinib.

And this is really important in countries where, where there might be low income or in more developing countries where the cost of biologics, may prohibit the widespread use of, treatment in XPAR. And the poster was a zero five eight two, and this was a study, of XPAR patients in South India where there are two hundred and ninety patients treated with generic tofacitinib five milligram twice a day. And these patients were followed up for twenty five months. And what they showed was in this group of patients, firstly, they reduced the use of anti inflammatories, and also these patients had an improvement in their disease activity score using the S test. In this study, nine percent of them either achieved inactive disease or low disease activity based on the S test.

It was quite well tolerated. There were some cases of transaminitis and also cases related to fatty liver. But overall, it was well tolerated. Similarly, there was another poster, May, this time in North India, where they also looked at the use of generic tofacitinib five milligram twice a day, and this was followed up for a period of, twenty four weeks. And in this study, they had 100 patients, their long disease duration over eight years, and these patients were treated and with generic tofacitinib.

And what they found in this cohort of patients, seventy one percent of these patients achieved either inactive disease or low disease activity based on their S test score. So there was an improvement of improvement of 1.76 on the S test score and also a drop in the CRP. Both these studies demonstrate to us that in countries where perhaps there is a lower income and or more developing countries, that such therapies such as the generic tofacitinib can be very useful to treat patients with axial SpA and also to improve, the outcomes for these patients in order to prevent long term, mobilities. I'm Anthony Chan reporting here, for RheumNow in Chicago.

Welcome to day one at, ACR Convergence. My name is doctor Elaine Husney, a rheumatologist at the Cleveland Clinic, and I wanted to pick, several abstracts out today on, specialized biomarkers for psoriatic arthritis. I have abstract 111 which is called predicting response to adalimumab in patients with psoriatic arthritis using an epigenetic chromosome conformational signature. So that was a mouthful but what I found this was so interesting is that we all know that TNF is commonly a first line drug used in psoriatic arthritis, but we're not really sure if all patients respond. And wouldn't it be wonderful if we kind of knew ahead of time who was gonna be a better responder to adalimumab and who might not be as good a responder.

So in this particular abstract, saw a cohort about 91 patients that they saw. And what they did is, using ACR response criteria, they looked at a group of what we

call

extreme responders and a group of extreme non responders and they looked at these two cohorts and they were able to find a signature using a very sort of specialized chromosomal assay. So called an EpiSwitch, explorer microarray. And so using this technology in their 22 patients, they were actually able to find or conclude that there's a potential biomarker, for predicting therapeutic, response to adalimumab in psoriatic arthritis patients. So very interesting, more to come. This model, they said, had an accuracy of, 96.4% specificity.

So something that will really help us out to see if we can, rather than kind of just doing, know, trying and trying different ones, maybe ahead of time we can, maybe predict whether or they're going to respond to a TNF class of medication.

Hi, my name is Akhil Sood reporting for RheumNow. Imagine you have a patient with stubborn autoimmune disease. You cycle through multiple biologics and even tried next generation b cell depleters. Initially you see a positive response but within months the disease flares again. You start to wonder why is the patient not responding?

Is it possible that the answer may lie elsewhere such as the lymph node? Abstract 2695 from the Erlogen group looked exactly at that, how different B cell depleting therapies reshape the lymph node environment in autoimmune disease. They performed lymph node biopsies before and after treatment with various treatments including rituximab, obentuzumab, t cell engagers, and CD19 CAR T. Across twenty four patients with various autoimmune conditions, all patients had complete B cell depletion in the blood but what happened inside the lymph node told an entirely different story. CAR T cells achieved complete B cell depletion in every patient and disrupted the lymphoid follicle architecture entirely.

In contrast, protein based therapies reduced B cells but left the follicular structures intact. And here's the kicker, patients with complete follicular disruption after CAR T achieved stable drug free remission while those with residual follicles eventually needed retreatment. And the findings can reframe how we think about B cell depletion. It's not just about how many B cells are gone from the blood, but what's hiding inside the tissues. The lymphoid follicles may act as a reservoir for autoreactive B cells to repopulate after conventional therapies.

And while findings from CAR T studies are exciting, mechanistic studies like this can explain why some patients relapse after B cell depletion. So next time your patient flares, the answer may lie in the lymph nodes. Thank you.

Hi, everybody, and welcome from ACR Convergence in beautiful Downtown Chicago. My name's Professor Peter Nash from Griffith University in Brisbane, and I'm going to review what you should be in the water supply given the data, the GLSGLP1 agonists in rheumatic diseases because there were 14 abstracts on this topic. If you need the numbers of some of the important ones, 41, eight forty nine, ten twenty seven, 2,685, 165, 2,658 and two thirty three. Now a lot of these used huge databases including massive numbers of patients. At least three of them used the TriNetX database.

Now this is a conglomerate of electronic medical record and claims data from 83 different sites in many different countries. And there was another one called the RISE database, the RISE registry, which also had very large numbers of patients. When I say large numbers, I mean a couple of 100,000 compared to say 10 or 20,000. So with those kinds of numbers, it's very easy to make significant differences with small changes. So these abstracts looked at lupus nephritis, they looked at psoriatic arthritis, they looked at total knee replacement, they looked at the incidence of inflammatory rheumatic diseases and infections in patients taking the SGLP1 agonists.

They even had one study where they injected it into the knee joint of an animal model of osteoarthritis. But it's the PSA ones, sorry, just have to mention these studies are all retrospective, observational, they use propensity matching, and at some time we have to talk about Trinetix and the issues of Trinetix which has a propensity score matching program built in. And there's lots of issues with that database, even though it's vast, in data capture, missing data, misclassification, different clinicians deciding on line of therapy and which therapy and recording a date of onset at different times and data garbage in and garbage out make it that you have to take it all with a grain of salt, but the actual numbers are huge. All the studies and this one I'm particularly talking about they followed people for ten years with PSA they compared eighty six thousand patients without PSA with four thousand who had PSA. They all lost weight.

They showed that the patients on the agonists had less CRP dapsa and pain, but they also had, and this is the key, they had less ischaemic heart disease, less acute myocardial infarction, less cardiac failure, less cerebrovascular disease, and even less deaths in the patients on these drugs with active PSA. Now the number needed to treat was in the order of thirty to fifty over this ten year period to prevent one death and to prevent some of those other morbidities that I mentioned. Another study looked at five year risk reduced incidence of knee replacement. Another study looked at diabetics and they looked at seven hundred and ninety thousand diabetics and they compared them with eighty thousand non diabetics and they looked at mortality, dementia, Parkinson's disease and cardiovascular disease with very significant reductions both in the diabetic patients and the obesity patients who are on these drugs. So across the board, they were trying to show that these SGLP1 agonists led to marked and significant benefits as far as cardiovascular risk, particularly in these PSA patients they studied.

They had less cerebrovascular disease, they had less cardiac failure and less deaths. So it looks like it should be in the water supply of all our patients. And the take home message is if you have patients with morbid obesity, BMI over 30, you have to think long and hard about using these drugs and you have to take them off the endocrinologists, think about cost, but also think about the benefits, particularly in a PSA population who have metabolic syndrome, fatty liver, drink too much alcohol and have premature atherosclerosis because all the hard endpoints are significantly improved. It's just a question of how much. Thank you very much.

Hi everyone, it's Mike Putman. I'm a rheumatologist at the Medical College of Wisconsin. I'm reporting to you from ACR Convergence twenty twenty five for RheumNow. Now, today I want to talk about an abstract that is actually coming in a couple days, but in the morning report, Brian England gave an amazing, amazing year end review. And as part of that, he mentioned a drug that I bet many of you have not heard yet, Nirindomilast.

Nirindomilast is a new drug. It's a PDE4B inhibitor that is targeting the lungs for patients with interstitial lung disease. Now they're going to report some of the efficacy data of this on Monday, it's abstract sixteen sixty two, but I want to give you a little preview because you probably don't know much about this drug yet. Now this drug, like I said, was a novel PDE4B inhibitor and it was actually designed specifically to try to target these folks with interstitial lung disease. Now, you may not have heard because we're rheumatologists, but this has already made waves on the pulmonary side.

In October 2025, it was approved for idiopathic pulmonary fibrosis, or IPF. Not a lot of rheumatologists are treating IPF, very difficult disease, very hard to treat and that was reflected in the trial that informed that approval. The trial was called FibroNir IPF and patients in that study who got Nerindoma last experienced maybe 50 to 75 milliliters of less worsening of their FVC over fifty two weeks. Not a lot to write home about if you think about the FVC of the lungs is 2,000 at baseline, so kind of a small difference. That's kind of reflected in the patient's experience.

Didn't seem to improve dyspnea, cough or fatigue scores. You see that and you say that's not very exciting, this is a very refractory, very scary disease. I think because of that we are all grateful for another agent. Thus far the really only other approvals were the anti fibrotic Nintedinib and Prufenadone. Why am I talking about an ILD drug?

At the same time that they ran their IPF study, they also ran a study called Fibronir ILD. That study looked into patients with progressive fibrosine interstitial lung disease and it was open to patients who had autoimmune diseases like us. Fully three twenty five patients in that study had some form of autoimmune lung disease and that study also met its primary endpoint. So this is kind of exciting and I think this is going to be a thing in the field of rheumatology as well. Because of how sick those folks were, they progressed even more and there was actually a little bit bigger of a delta between the people who got the drug, Neurodomolast, the people who got placebo, about 75 of FVC.

Similar to the IPF study, there was no improvement in dyspnea scores, fatigue scores, cough scores, little things here and there but nothing to write home about. So that's all kind of ho right? Another drug, we're sort of excited about that, kind of along the lines of Nantenav and Tefenidone. But in the FibroNir ILD study, they actually observed a relatively large difference in mortality. So the people who got the high dose of the drug, eighteen milligrams, they had a rate of mortality of around six percent, placebo group around twelve percent over one year.

To that in perspective, there are very few things in rheumatology that work that well. Beta blockers and statins and all that stuff, none of that has that high of a mortality benefit over one year. Now, in the paper itself, they didn't bring out the autoimmune people so we didn't really know whether this applied to the autoimmune folks that we're going to be treating. And that's the data that I'm hoping to see in a couple days. It's also kind of peculiar to say that we have a drug that marginally improved FPC, didn't really improve quality of life in any substantial way, but somehow had a large benefit to mortality.

I'm kind of wondering if as we parse this data we'll see that that was maybe not quite as borne out as we would expect, but I would certainly hope so. This is a group of patients that very much needs a new drug and a new mechanism, and if this is better tolerated than the anti fibroidics we currently have and actually has a benefit to mortality, I could see this being a big thing in your clinic. Keep a close eye on this space. I think there's going be a lot coming out in next bit about this. Thanks so much for tuning into our coverage and have a great day.

Hi. Hello. It's doctor Artie Kavanagh coming to you from ACR Convergence in Chicago, ACR twenty twenty five. And I'm at RheumNow, and you're watching RheumNow, the best place to go to catch highlights on many of the important topics happening. So an interesting topic in psoriatic arthritis has been sex.

So now that I have your attention, it's something that we are paying a lot more attention to. Specifically, do many women respond differently to therapeutic intervention? Backing up from that, do they have different baseline characteristics? Even though all patients have psoriatic arthritis, what impact does that have on our approach to the patients and our approach to therapy? So there's a number of ways that have looked at this, and this is something we've seen in psoriatic arthritis maybe more so than in rheumatoid arthritis even, where there seems to be a discrepancy.

Definitely women compared to men seem to have higher levels of disease activity across certain domains, particularly those related to pain. Men may have more severe skin manifestations, and we see this in a lot of studies. It's a super interesting area and one about which we don't have a lot of history. Only recently have we started to look at data according to sex, and once you do, it's very striking that we really need to do that pretty much for all studies going forward. If you had an imbalance in the sex distribution between an active treatment and another active treatment or placebo, that would definitely impact the results.

We're learning that we need to pay attention to this to help us interpret the results of psoriatic arthritis studies. This has not been looked at a lot in rheumatoid arthritis. It's been looked at in ankylosing spondylitis, where we see similar things that you really have to consider in a group of patients the sex distribution to make sense of the baseline characteristics, but more importantly, the response to any particular therapeutic intervention. We're seeing this has become more standard now in the reporting of studies, including some that are present at this meeting. We see a new psoriatic arthritis study, we want to know, is there an impact of the sex difference in the baseline characteristics or in the response to therapy?

Another aspect of that that we have not really considered a lot in psoriatic arthritis relates to change in the hormonal status. I'm thinking specifically of the perimenopausal and postmenopausal status. We've thought of this in rheumatoid arthritis, and there, of course, it makes sense. The average age of the patients being a little higher in rheumatoid arthritis than psoriatic arthritis in general. The sex distribution being many more women with rheumatoid arthritis, whereas the sex distribution, psoriatic arthritis, relatively equal men and women.

But we haven't paid attention to changes in hormones over time. That's something that's getting us a little bit of attention at this meeting, and I think it's something we're going to have to factor. If sex is important, then hormonal changes, and as they occur over time, how that influences the patients, how it influences the activity across different domains of disease, and most importantly, how that influences the response to therapy. So, kind of a newish area, one that very rapidly has become the center of a lot of attention. We need to pay attention to this if we're able to really understand the data that we're seeing from so many of the new studies that are happening.

So, very exciting. Psoriatic arthritis continues to blaze trails and have important new information across multiple areas such as the impact of sex. So, I'm doctor Arty Kavanaugh reporting from the ACR Convergence in Chicago for RheumNow.

Hey, everyone. This is Jeff Sparks, rheumatologist at Brigham Women's Hospital in Boston. I am reporting from RheumNow for RheumNow at ACR twenty twenty five here in Chicago. Great weather here in October, and I'm gonna give you my perspectives on day one for rheumatoid arthritis. In particular, we're gonna be focusing on novel cellular biomarkers.

So I'm gonna talk about four abstracts, and I think this is an overall a big theme related to the revolution of of cellular therapy and cellular biomarkers within rheumatology. Part of this is just related to it's now feasible to actually collect, extract, and measure things in cells, certainly single cell RNA seq. And this is really being enabled us to be able to with huge granularity, actually understand what's going on from a mechanistic standpoint. So the first two abstracts I'll talk about have a similar theme. It's abstract eighty nine and seven seven four.

And these were looking at, particular cells called T peripheral helper cells and T follicular helper cells. If you're not familiar with these yet, these would be pathogenic T cells that, seem to be very important in pathogenesis of RA and even other rheumatic diseases, particularly those that are seropositive. And actually, this was enabled by some studies through the Accelerating Medicines Project where looking at synovial tissue, high levels of T peripheral helper cells were actually in the joints of patients with RA disease. Now we're trying to see whether these cells are actually circulating and whether these blood biomarkers could be novel ways to help diagnose and prevent and look for different treatment pathways. So both of these are characterized by PD one high, also CXCR five either positive or negative, and then ICOS one.

So these are basically cell surface markers that help to distinguish these T cells. The T follicular helper cells and T peripheral helper cells are both basically pathogenic cells. The T peripheral helper cells or TPH cells, again, seem to be very associated with autoimmunity, particularly rheumatoid arthritis. So both of these abstract, number eighty nine and seven seventy four, were looking at this cellular biomarker in people at risk for RA based on seropositivity. The first study, number 89, was looking at clinically suspect arthralgia and looked at people who were, CCP positive and negative, also whether they progressed to RA or not, and then also looking at healthy controls in people with prevalent RA.

And they actually found that both T follicular helper cells and T peripheral helper cells were present in the blood at higher concentrations compared to the non progressors and healthy controls. And that in particular, the T follicular helper cells seem to be most predictive of who would go on to progress to rheumatoid arthritis. So this is data suggesting that these are really important players in the pathogenesis of RA. The second study is seven seven four, and this is a secondary mechanistic biomarker study, using the stop RA clinical trial that I was part of, mostly analyzing the placebo arm. As you probably know, hydroxychloroquine did not affect the future risk of RA, but the hydroxychloroquine could have obscured some of the biologic findings.

So they really looked at placebo arm as sort of a natural history project. And this used multi omics, many different assays to look down to the cellular level to see proteomics, transcriptomics, what is different in the different groups in these patients, all who are seropositive, about who progressed to RA during the trial. And using these non biased approach, they actually found the T peripheral helper cells were, a biomarker that was particularly important. So the T peripheral helper cell, T follicular helper cells, important pathogenesis, perhaps depleting those could be a novel, method to treat RA. The other abstracts I'll highlight are slightly different biomarkers related to cellular mechanisms.

Seven seven five was also a plenary presentation. This was looking at microbial small RNA, within a pre RA cohort, and they found that this, RNA was, present in higher titers in those who progressed to rheumatoid arthritis. They also did some ex vivo studies and said that giving this RNA to, monocytes actually changed the type one interferon pathway. And this is not a pathway we typically think about in RA. And again, I think it does open up the path to particularly new drug targets.

The last I'll talk about is eight thirty two, which is looking at PAD four. We've talked a lot about PAD, peptidyl arginine deaminase as the enzyme that catalyzes citrullination and, of course, CCP is citrullinate an antibody to citrulline. There's been prior studies looking at antibodies against the PAD four enzyme. This actually measured PAD four levels themselves, and these were also at higher concentrations in those who were pre RA compared to healthy controls and also was predictive of who might go on to, progress rheumatoid arthritis. So in summary, we have a new some new biomarkers on the horizon, and I think it's very possible that in the near future we might even think about using cellular biomarkers to help diagnose and treat rheumatoid arthritis.

Beyond just CAR T, these this cellular era is opening up new horizons. So, again, this is my impression for RA from day one looking at cellular biomarkers in rheumatoid arthritis. Thanks so much for your attention. Thank you.

Hi. This is Bella Mehta reporting for RheumNow, from ACR twenty twenty five. We have a lot of interesting abstracts here. One particular one, that I'm gonna talk about is using artificial intelligence for qualitative research, analyzing large sets of qualitative research. The abstract number is zero seven nine four.

This is something that we've studied a lot. Last year, we even came up with a technique to do this. So this is a study looking at patients with lupus who are pregnant and a qualitative study where there's a semi structured interview talking to them about their experiences, their perceptions on how the pregnancy goes. And what we did is that we used some of the new large language models which were open access including ChatGPT, Claude, etcetera, and used three different prompting strategies, few short, zero short, and chain of thought, and came up with themes that were that could be not only translated from the Portuguese language, which was the original language of interviews, but also come up with the same themes translated down to English. So what we found is that few short techniques for prompting are pretty good in trying to summarize these large volumes of data, especially in qualitative research, and can also do it for different languages.

So, again, everything from large language models needs to be validated. Hallucinations should be minimized using some of the better prompt engineering techniques, but it's something that I would recommend a lot of people to try, not only for qualitative research, but even in clinical practice where there's large volumes of data and you wanna do a QI project, for example, just to summarize all this language or conversational data. So with that, again, there's a lot more AI coverage that we'll have here too. And follow me at Bella underscore Mehta on Twitter. And thank you so much.

Hello, everyone. My name is Youssef. I'm reporting live from Chicago to cover the ACR twenty five conference. Today is the official day one of the ACR conference. There were many abstracts presented, and one that caught my eyes was an abstract title number eight zero three.

So, essentially, this abstract was looking at to compare the use of belimumab whether before or after immunosuppressive therapy in SLE. As you all may be aware that in 2024 EULA recommendation guideline, the guideline recommended that belimumab could be used after a failure of antimalarial. However, in terms of other healthcare settings, this may not be cost effective, and many healthcare settings wanting patient to try at least one immunosuppressive therapy. So in this abstract, the investigators use data from five phase three randomized controlled trials of belimumab in SLE. So what they did is they compare two groups.

So one group was belimumab plus no immunosuppressive therapy at baseline versus second group patient who were on immunosuppressive therapy and also on placebo group. And both of these group were treated with antimalarial and also glucocorticoid. So what they found that at the endpoint time, which is about fifty two weeks, they found that patients in the belimumab plus no immunosuppressive therapy group had a better disease activity and also less FLAIR as well as reduced glucocorticoid dose compared to those who are on placebo and immunosuppressive therapy group. Therefore, the investigator mentioned that this study lend support to the EULA recommendation on early use of belimumab. However, when looking back at the abstract, there's quite a few things that need to be discussed, particularly in terms of the group selection.

The investigators assigned the belimumab and no IS group based on the baseline data. So we were not sure whether this patient might have had immunosuppressant before, that's not been disclosed, and also the disease duration also was similar between the two groups. Therefore, it is still an unanswered question whether early use of ilbelimumab after failure to antimalarial and glucocorticoid might be superior than after failure to immunosuppressive therapy. What we do need is that a proper definitive clinical trial of early first line use biologics in this group of patient. But this is still intriguing for us to discuss and also in terms of implication of our clinical practice.

So thank you so much for listening to my summary, and I hope you follow me and also follow all of my colleagues you know, at the room now for further content coverage. Bye bye.

Hi. I'm doctor Janet Pope. I'm here at room now reporting on some cool posters. So this is poster number 0164. We're at ACR twenty twenty five in Chicago, and, the weather's great, and the science is great too.

So here's the question. Do patients with rheumatic diseases weather the storm well? So first of all, why did I choose this poster? A lot of my patients say that they flare when there's a big change in weather. So, both barometric pressure changes as well as temperature changes, especially going colder and damper, seem to make some of my patients flare, certainly not all.

This is a far different question on a ginormous scale. So what the question was here, when there's extreme weather, flooding, and other, disasters that can really, do damage to the patient's home, etcetera, what happens to the patients with rheumatic diseases? So this was a questionnaire, a fairly good response rate, and they found that even after ninety days after an extreme weather event, the flares were occurring. And they thought it could be due to loss of power, loss of heat, medication storage. But here's what I really wonder about, and this they they didn't ask the question in this way.

I wonder if, first, the natural event, might maybe flare your arthritis because it's a big dip in temperature when there's hailstorms, hurricanes, etcetera, or floods. But I wonder if it's ninety days later, if it's nothing to do with the weather of the extreme weather, but actually with the situation. Once you have a lot of chronic stress, I think you're more apt to flare, and these are stressful events when you're going through extreme weather. However, we really don't know the difference, but my patients in my clinic, if they flare by weather, it seems a very, very short lived, whereas this was long standing. So what they said was basically, in extreme weather conditions, expect your patient with a rheumatic disease to have a far higher chance of flaring, especially in the next three months.

Please follow us at RheumNow. Thank you.

Hello. My name is Runaalini Day, and I'm a fellow in rheumatology internal medicine working in London in The UK. I'm here reporting for VroomNow from ACR twenty twenty five here in Chicago, and I'm delighted today to be joined by doctor Barak Kumar, who is a rheumatologist and fellowship program director at the University of Iowa. Thank you for joining us.

So doctor Dave, the pleasure is all mine.

Thank you. So we are actually gonna be discussing a topic that's really taken over ACR this year, and that is artificial intelligence. You can't move for seeing all of the sessions and the posters and the various different abstracts about artificial intelligence. And we're specifically gonna be talking about abstract two one seven four that's due to be presented on Tuesday of the congress at 10:30 in the poster session. We're specifically looking at the use potential use of AI in looking at fellowship applications.

I'm gonna ask doctor Kumar to explain a little bit more about your work.

Sure. So, it's application season right now. It's interview season. It's actually just finished and we're about to make our rank order lists. The problem is that there's so much information in these applications.

In terms of personal statements, in terms of letters of recommendation, in terms of transcripts, etcetera. And it's not always easy to parse all this information and to do it in a very timely and efficient manner. And it's also very hard to do in a standardized way too because one evaluator may see something in one way and another person may see it another way. So this is where artificial intelligence can be really helpful, but it has to be used very carefully. As Doctor.

Jay is mentioning, AI is everywhere, but the more important thing is not developing a tool, but rather figuring out how a tool can be used. So for our project, we did is that we used AI to help evaluate character strengths within personal statements. So character strengths, and we used a framework called the VIA Character Strengths Framework. Character strengths are different aptitudes and attitudes and dispositions that exist within individuals such as honesty, trustworthiness, spirituality, forgiveness, teamwork, etcetera, conscientiousness, etcetera. And so, we developed this large language model and we parsed through all of these personal statements in order to identify the presence or absence of these character strengths within these applications, in particular the personal statements.

In that way, we can more we can have a more nuanced understanding of what people they see themselves as and how they can fit into a program through their own personal statements and through our own mission statement.

Great. Okay. So just talk us through a little bit more about how you developed the the program and the model specifically. Yeah. And what you found.

Yeah. Absolutely. So it was programmed in Python, which is a computer language. And what we did was we looked at that framework, the via character strengths framework. And for each of the framework strengths, we associated with about three to five different adjectives.

Now, the way how this large language model works is it goes through the sentences and looks for specific terms that are associated with these character strengths and also the relationship to other words nearby.

Mhmm.

So, by doing so, you can actually grade personal statement from zero to one for the presence and strength of that character strength in relation to the other character strengths that are there. And in the end, it in outputted this nice little heat map that shows where the character strengths lie within the entire candidate pool depending on their personal statements.

Okay. Fascinating. Okay. And how what what were the what were the sort of top line results that you found when you

So top line top line results is number one, it was very rapid and very quick as compared to a manual screen. Literally took hours to literally seconds to do that. It was pretty reliable in that when we had our human raters look at this, we saw that there was high congruence to what we were seeing. And the other top line actually interestingly enough is that there are two character strengths that are not very well represented. Those are forgiveness and spirituality.

They're strange things to be writing in a personal statement. So it's not too strange about that. But otherwise, beyond that character strengths are highly and readily available to be seen through this algorithm if you parse through the different personal statements.

Okay. I'm curious to know what did your current fellows or what do they think about the use of this model?

Our current fellows and faculty members are enthusiastic about this. There is of course a very good reason to be healthily sorry. Healthily skeptical about the use of AI, you know, to automate And so there's a big belief, and I concur with all of our fellows and faculty members that this should be used as a tool, an adjunct in order to understand what's going on. Now, to give an example of that, when we had seen in some of our pilot data, this is not in our poster, but some of our pilot data that someone had many character strengths, however honesty was somehow lacking in that. That prompted a critical review of those application materials to see if there was evidence of honesty in other places such as the letter of recommendation, etcetera.

So that's how this tool is meant to be used rather than as a substitute for screening people out and deciding who goes there and who goes into another pile.

And I think, to be honest, when we look about look at AI in other areas of rheumatology more broadly, that seems to be the recurring theme at the moment to be, you know, exercising caution and using it as additional tool rather than overreliance. I think that's what we need to be cautioning against here.

Absolutely. So I think program directors will be very relieved to hear that this program will not will not take away your job. You will still be able to read all of these essays and you'll still have the liberty of selecting whoever you would want.

Perfect. Okay. What are the next steps?

So the next steps are actually to see if there is a larger subset of individuals that we can use this for and to see whether there is consequential validity. That is, even if you do see the character strength when they get into fellowship, does that actually translate into the strengths that are exhibited by the individual as observed by different faculty members? So that's kind of the big thing. Those are obviously large steps. It'll take a couple of years to figure that out.

And by that time, AI will have expanded beyond that.

Perfect. Okay. If we can just end with a final thought, what's your view on the just generally AI in rheumatology and how it's being presented at the ACR this year? That's probably a very long question, but perhaps in a few short sentences, you sum it up for us.

So in a few short sentences, I'm very excited about the future of AI in rheumatology. However, we have to be very, very careful. AI should be considered in very advanced predictive or generative tool such as a spell check or grammar check. There needs to be extensive regulation and oversight over any tool whether if it's for clinical use, educational use, research, etc. But nevertheless, AI is really changing the way how we do rheumatology and I'm very grateful to be an age in which we have the advent of AI.

Wonderful. Okay. Well, thank you for going through that all with us today, Doctor. Kumar. If you'd like to know more about Doctor.

Kumar's work, is posted 2174 on Tuesday. You'd If like to know more about what's going on here at the congress, do keep following along the coverage, on RheumNow. Thank you very much for joining us.