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

Hi, guys. This is Aureli Naj. I'm from Glasgow live from ACR twenty twenty five in Chicago. I am having a great time. I'm super excited.

I was just hanging out in the poster area, and it was just really cool to see all of these physical paper posters back again after this kind of digital era where we had to push buttons and screens and all that stuff. So it was just really nice. And as I was just walking there, I came across this really cool abstract. It's zero one eight nine. And it was looking at our practice, which, like, there's not that many scientific work looking at what rheumatologists do.

And it was about AI and it's very popular topic, but it was looking particularly about AI scribes. And I don't know if you've implemented that in your practice or not, but certainly this is something I've been looking into. I personally don't really like it and this is how it was so surprising for me to see that in this study from UCSF, they implemented AI Scribe for their ambulatory clinics. So it was across many, many specialties. And they looked for six months across 2,500 physicians that are conducting clinics in these hospitals.

And they offered every physician the possibility to use AIScribe. So first of all, the intake. So I was actually not that surprised to see that intake wasn't massive. It was like 37% overall and rheumatologists were not much higher than that. It was like 40%.

So it was really the tense adoption rate across internal medicine specialties. So until then, nothing really surprising. However, it turns out that rheumatologists seem to love it. The retention rates over the many months was a 100%. So whoever adopted it kept it.

And also they just were using it more often in about eighty percent of the case all the time compared to any other specialty. And the percentage of high utilizers across rheumatologists was about eighty percent. And what's even more interesting because I was curious to understand why it was so popular. It was not even saving that much time because the time saved on average per day for electioning health records related activity was one minute. So really clearly not much.

So I had quite a few conversations with the the the the presenter, the person who was presenting the the and we were both quite curious about why rheumatologists would like it so much. Certainly, we know that in rheumatology there's a lot of conversation around, you know, PROs and and all that. And so I think it's definitely a plus that it can be captured in real time by AI scribes, but also I would be quite interested to know why in particular rheumatologists like it so much. They are now conducting focus groups. So hopefully we're gonna hear the answer to that next year.

I would be super interested to know what your practice is, if this is something you've already implemented or if you don't like it. But yeah. This was certainly quite a bit of a surprise for me. I suggest that you tune on RheumNow for more content and follow me on Twitter at OrelieRomo. See you guys around.

Hi. I'm doctor Janet Pope reporting here at RheumNow at ACR twenty twenty five in Chicago. I wanted to talk about something that might be an ACR best. So it's really asking about hospitalizations in people with Still's disease, and is it Still infection? So why did I choose this abstract?

This was a nice poster. It was number, 0163. And, basically, what it looked at was a national inpatient database where there were lots and lots of hospitalizations for people with Still's disease. So there were eighteen hundred twenty seven unweighted and nine thousand one hundred and thirty five weighted American hospitalizations from this very large database. So first question was, why are these people hospitalized?

The main reason for hospitalization was infection, but we have to remember that often when someone's flaring their Still's or being diagnosed with Still's, they have high fevers, they have rash, they have high inflammatory markers, a high ferritin. So Still's can mimic an infection. So I would say, is it misclassification? Because, of course, at this level, they didn't have all the positive blood cultures or what was negative, etcetera. The next thing that's important was the, mortality was low, but it was about two, two and a half percent of these hospitalizations for people with stills.

Who did worse? So you did worse if you had, male versus female, a black race, or if you were on Medicaid versus private insurance, and Medicaid would be people often with, less socioeconomic status, maybe poor health related behaviors. However, what I think is most important is when my patient has known adult onset Still's disease, if they have a high fever and they're sick enough to come into hospital, I think we always have to rule out infection. But sometimes if we can't grow any, positive cultures and we've treated for infection and they still have fevers, look at the characteristic of the fevers because it still could be stills. Thank you, and please join us for more reporting.

It's at Janet Broudhope. Thank you.

Hi, David Lee from Melbourne Australia here at ACI twenty five in Chicago reporting for RheumNow. It's been a big first day. I want to focus in a bit on some GCA abstracts and particularly what they might mean in terms of thinking about upadasidenib and cardiovascular risk in GCA. So I think in general people have been a little bit concerned about upadasidenib in GCA even though there's clear evidence from the SELECT's GCA study and there's an indication now for giant cell arteritis here in The US. I think perhaps some of those concerns have come about from what we know from oral surveillance and the subsequent regulatory warnings that we've really extrapolated from rheumatoid arthritis and taken to other diseases like GCA.

In particular, we're concerned in GCA maybe because we're looking at an older population, GCA inherently is an older population and we saw some data from the abstract before which did show that people do bring cardiovascular comorbidities into GCA as well, so that's completely understandable. There are a few things that might mitigate things the other way though when we think about upadacitinib in GCA which were really highlighted on the poster floor. Firstly, of course, we know steroids are a problem when it comes to cardiovascular risk in GCA. Arguably they're what drives cardiovascular risk. Well, certainly it's up there perhaps the most in GCA.

It's really steroid driven. So the more that we can steroid spurt there, the more effectively we can steroids there, the better we are in terms of cardiovascular risk. I think that was fairly clear from what we saw in terms of the steroid sparing capacity in select GCA. But more importantly, we saw some biomarker data presented here, abstract seven fifty one presented by Lisa Christ, looking at interferon gamma and the effect that upadacitinib has on those signaling pathways. What we could see is that upadacitinib doesn't just affect IL-six related pathways, it also affects interferon gamma related pathways CXCL9, ten, eleven as well.

And we know from that that actually those are really important in the vascular complications that we see in GCN. Now we've got this direct biomarker evidence as well, is every single plausible benefit from managing the interferon gamma side of things where we manage GCA. So if we accept that steroids and disease activity are a big part of cardiovascular comorbidity in GCA, it's a very different paradigm than rheumatoid arthritis when we're thinking about upadis syndrome. It's a bit of a double edged sword and while we have those concerns which have extrapolated from oral surveillance, at the same time we've got potential benefits that might exist from the mechanism of action dealing directly with interferon gamma. For plenty more on vasculitis and everything here at ACI twenty five, you know where to go, rheumnow.com.

Hello, everyone. I'm Richard Conway from Dublin, Ireland, and I'm reporting for RheumNow from ACR twenty twenty five in Chicago. I wanna talk today about abstract poster one three five five and it was presented at Monday's poster session. And this was by RheumNow's very own Janet Pope and colleagues. This was a study based in the CATCH early arthritis inception cohort in Canada, and it was asking the question of what happens depending on what route you might give patients with early arthritis glucocorticoids.

And so this has been a topic of interest recently. When I first started out in rheumatology, which was, God, twenty years ago now, we used to do quite a lot of intramuscular glucocorticoids to treat patients for flare ups and to treat patients who are newly presenting with arthritis. And then it kind of fell by the wayside a bit, and it just seemed easier to give oral steroid tapers, just give a script and the patient goes off and takes it in their own time rather than going through the whole injection process. But the kind of debate and consideration of this was reignited by a study that Michel Petrie did in SLE. And that showed that if you give the glucocorticoids intramuscularly compared to orally, that in SLE patients, they seem to be able to get off the steroids easier and have less side effects.

And SLEEP has always been a particular difficulty with getting people off steroids and how well that translates into our other conditions such as rheumatoid arthritis, it hasn't been entirely clear. And I think that this current study helps answer that question. So this was looking at an overall population of two thousand two hundred and twenty two patients with early rheumatoid. There were four twenty one of those who got oral steroids and one hundred and twenty one who got parenteral steroids. So this wasn't a kind of randomized trial or anything like that.

This is just looking at what happened to these patients, what the clinicians were giving them. And then the parental group is slightly conceptually different. This wasn't just intramuscular steroids, there was no intravenous steroids, but it was kind of a combined intramuscular and intra articular steroid administration group. And so combining those two groups together and comparing them to oral steroids. And what they found was that after a year of follow-up, there was no difference in the need for advanced therapies between these two groups, so it didn't matter whether you got oral or parenteral, but that there was significantly less persistent glucocorticoid use in those given parenteral steroids compared to oral.

This was twenty six percent versus forty seven percent, so approximately half. So to me, that seems like a good idea. It seems these people are in some sense achieving better outcomes, Either they are doing better and not needing the steroids, or they're not becoming dependent on steroids like can sometimes happen, probably because of the smoother off of the parenteral steroid effect. So for me, this is kind of reinforcing a change I'd already started to make in my practice and shifting back towards more intramuscular and more intra articular steroid administration and trying to minimize the oral steroids wherever possible. So I'm Richard Conway.

Follow me on Twitter at Richard p I Conway, and tune in to RheumNow for all the coverage from ACR twenty twenty five.

Hi, my name is Akhil Sood reporting for RheumNow. As rheumatologists, we commonly see patients with chronic low back pain, and the key question we get asked, is it inflammatory or noninflammatory? Early detection of axial spondyloarthritis is critical. Delays in diagnosis can lead to irreversible structural damage and abstract 2,635 takes an ambitious approach to capture this condition early through the space cohort. This cohort includes individuals under the 45 with chronic low back pain defined as at least three months less than two years.

Each participant was diagnosed by rheumatologists as having ACSPA or no ACSPA. In over two years, the investigators tracked imaging changes on radiographs and MRIs. So what did they find? On conventional radiographs, there were no significant changes but on MRI, they observed a significant increase in fat lesions suggesting that MRI may hold early clues of axial spondyloarthritis. And this raised an important question, should we be ordering MRIs for all our patients with chronic low back pain?

While these findings are intriguing, the study doesn't tell us which patients are most likely to develop these lesions. So more research is needed before we consider changing our, screening approach. Meanwhile, abstract 2,636 takes another exciting angle, a potential blood biomarker for early detection of BaxSpA, the fourteen thirty three antibody. This serum marker shows high sensitivity and high positive predictive value, exceeding the spartan target threshold. When combined with age, sex, and CRP, the biomarker can distinguish who has XBAW and who does not.

And this is a promising step towards a simple diagnostic tool. And of course, these findings still need validation in larger and more diverse cohorts. So what do you take from this? While we're moving closer to better diagnostics for early XBA from MRI based detection to serologic biomarkers, the next step will be identifying which patients are at highest risk and determining the least invasive, most cost effective approach to early diagnosis. This is Ecclesioude reporting for RheumNow.

Thank you.

Hello. I'm Jonathan Kaye reporting from ACR Convergence twenty twenty five in Chicago. I'm here with Joel Kremer, who is president of the Corona Research Foundation, who's done amazing work from that registry. And at ACR Convergence twenty twenty five, he presented poster number four four nine looking at the cutoff for Cdai low disease activity. Now the Cdai was validated against the DAS 28 ESR and CRP, and levels of disease activity, low, moderate, and high disease activity as well as remission were developed with cutoffs comparing it to the DAS 28.

The cutoff for C. Diffeye low disease activity is 10, and that is a target for treat to target. Now the question comes up, is that low enough? And you looked at the outcomes of patients from the corona registry, who had CDAs of 10 or less, and what did you find?

Well, thank you, John. Thanks for that, introduction. I first wanna say that we use about 7,000 patients across more than a 100 sites, academic and private, multi specialty, etcetera. So we think we have a good representation of what's happening in The US. And the whole idea for this study was spurred by a study that was presented last year at this meeting by Mike Weinbrott using the BRASS Registry.

And the BRASS Registry, which is tertiary health care center, of course, at the Brigham, found that there were indeed differences in outcomes between patients in so called low disease activity between a score of two point eight and six versus six and ten. So we wanted to replicate that in a very large registry. What we found that indeed there are dramatic differences. When you look at baseline CDA scores versus scores of one year and two year, starting different interventions, if you have what I'm calling very low disease activity, a CDA between two point eight and six, your likelihood of remaining in LDA at one in two years is fourteen percent. If however you have a baseline CDA at between six and ten, you're likely at a remaining LDA at one and two years is about one third.

Now how does the change in therapy that is initiated based upon the CDAI score, how does that impact the outcome? Are people

That's a very good question. We looked across all interventions in thousands of patients, validating the legitimacy of the CDI across different interventions. So it it really begs the question as to what should our targets be. I mean, remission is great, 2.8 or less, but not everybody can do a remission. So if you have a C.

D. I. Score between two point eight and six, that's better. Turns out to be infinitely better for this lifelong disease than between six and ten. So why are we creating an LDA between 2.8?

Why are we saying it's monolithic? It's LDA. And we should be making, I believe, treatment decisions, whether we change or add treatments based upon LDA scores that are 2.8 versus six and of course remission versus six to 10, there's just not a stable low disease.

So as a practicing rheumatologist, calculating a score isn't that hard, but it takes a little bit of time. But in clinical practice, a score and CDI of six, if you had a patient global and a provider global of zero, would be no more than six swollen or three swollen and tender joints. So you want to make sure that you have fewer than three swollen and tender joints. So that in and of itself is a good outcome measure to target. Yes.

That's a good point. But you can you can also look at patient and physician and global. So if you're at a two on a 10 scale, and you're at a two patient and physician global, that's four. And you're at two tender and two swollen. Now you're at eight.

So your CA score in that individual is in eight. Is that good enough to treat this disease? Is a fasting glucose of one thirty three good enough? So we're drilling down a bit and we're finding and again, reproducing what we what was originally reported in brass by Michael Weinblatt that there are indeed significant implications of lower LDA scores versus higher LDA scores that we believed should be associated with decision making how aggressively we treat these people.

So in your analysis of the patients with C. DIE scores of less than six, how many of them had one or no swollen and tender joints? Well,

you're asking a very good question. We have not yet broken down the components of the C. Dye. We will do that. And I think it's a very legitimate question.

But and it's a it's a question I've parenthetically been very interested in. But I think you gotta do a metric. And there's all kinds of metrics. But tender and small joints physician and patient global, do a C. Dive.

Right. If you're in this category, think about what you're hearing from your patient. Think about what is a legitimate metric for measuring disease activity and what is a perhaps more shaky metric with the implications for accelerating treatment.

So as a rheumatologist, when I'm seeing a patient, I try to get it so that the patient has no swollen and tender joints. And if I can't achieve that, I will settle for one swollen and tender joint. And that pretty much is gonna be a very low disease activity patient. So in clinical practice, one could already start applying the finding from your your poster, your your study

Well. By aiming for that. Yes. Well, thank you. We're we're writing up the manuscript.

Hope to have it submitted by year end. You know, we've been doing things the same way for so long that in many areas of human activity, it's difficult to accept and embrace a more refined manner of looking at any outcome. And that's just human nature. But so you need evidence. And this is a very large number of a very heterogeneous group of practices.

So I think it would be nice to see this performed in a European registry. The difference is in Europe, of course, they use far fewer BNTSD mods. So these findings are particularly germane to a US population because the Europeans, they have cutoffs. You're not eligible in The UK unless you have a DAS. I believe it's 5.1.

So these findings should be confirmed in European populations or far eastern populations. But I think for a US registry, we'll probably it'd be very difficult to have similar findings because there's no big registry that collects these kinds of metrics other than what we do Right. In the Corona Research Foundation.

This is yet another example of very important findings coming out of the Corona Registry with major implications for practice. So when you're seeing a patient with rheumatoid arthritis aiming for low disease activity, aim for very low disease activity, C. I. Of no more than six. Try to get it down to zero swollen and tender joints or at most one swollen and tender joint.

And, Joel, thank you very much for Thank you much. Talking to me about this study, but the important findings that you're presenting.

Thank you very much. Pleasure.

I'm Jonathan Kay here from ACR Convergence twenty twenty five in Chicago. For more on this and other topics from this meeting and elsewhere, go to roomnow.com.

Hello, everyone. I'm, Richard Conway reporting for RheumNow from ACR twenty five in Chicago. I want to talk to you today about a poster that was presented at, Sunday's poster session. This was poster five sixty eight, by Daman at all. And this is an interesting poster to choose was about drug withdrawal when people are in remission, which is a pet hate of mine and we work so hard to get these difficult to treat diseases under control And then once we achieve that, maybe spending a year or more doing it, we decide, oh, let's change things again.

Let's try and take away the treatments that are working and see what happens. And we've had lots of studies like that in our diseases, and most of the time it just doesn't work. Things like rheumatoid arthritis, axial spondyloarthritis, best case that we've seen you get to about a year, might have fifty percent of people still okay off the drug, but as time goes on, pretty much all of those people fall off the wagon and everyone seems to end up needing to go back on their treatments. And yes, most of them do fine. Ninety percent recapture when they restart the treatment, but that means ten percent don't.

Then what happens to those people and maybe they need to cycle through multiple other agents to regain disease control. So I've never been a fan of it. However, this study suggested that maybe that taking the drugs away is always not the wrong thing to do. So this was a ten year follow-up of a study called CRESPA, and CRESPA was a study in peripheral spondyloarthritis, so early peripheral spondyloarthritis. And what they did in that study was they treated people with galimumab essentially.

They had 60 people in the original study and after a year they stopped the treatment. Forty nine of the original sixty people were in remission at one year. So they then followed these forty nine patients up for the next ten years. And at the ten year time point, eighty two percent of the patients were in remission. And most impressively, thirty eight percent were in drug free remission.

So that says that maybe a reasonable percentage of these people can get away with taking treatment away. I think that may be applies to these kind of slightly less common diseases we see, for want of a better word. So early peripheral spondyloarthritis is a slightly less common condition, and it seems to be that many of these people, may achieve a drug free remission for a sustained period. So I'm Richard Conway. Follow me on Twitter at Richard p a Conway, and tune in to RheumNow for all the updates from Chicago.

Hello. I'm Anthony Chan reporting for RheumNow here at ACR twenty five in Chicago. And here we are talking today about the difficult to treat and difficult to manage axial spondyloarthritis, a key area that has come out as a result of the new definition of this condition. And I'm here today joined by doctor Rodrigo Garcia Salinas from La Plata, Argentina, who has presented a poster today, poster five eight four on this very topic. So, Rodrigo, welcome to the session.

Thank you, professor.

I wonder whether you could take us through the your findings from your abstract this morning.

Thank you very much. Fundamental in our poster was we had a cohort of axial SPA with more than 100 patients. Of those, only eight percent fulfilling the criteria of axial SPA difficult to manage. Do you remember maybe it's failure two, different mechanism of action this is activity or radiological progressions and only eight percent is a low prevalence of difficult tumor. But I believe the most important thing of this is the baseline characteristic of the patient who fulfilling the criteria.

Yes, so could you describe to us what were the important patient characteristics in this eight percent of your patients who you classified as difficult to manage?

The characteristics always is the disease activity. The disease activity in Western when you know you achieve the remission early, the chance to develop difficult to read is more. And in our case, for example, Basti, Basti and ASDAS two was the important characteristic. But when you see all the another publication or another cohort of difficult to manage, the smoking smoking is one of the important factor and psoriasis too. But in our cases and in all Latin America, the peripheral manifestations, joint, inflammatory joint or or enthesitis, was a important characteristic to develop difficult tumor lab.

We believe that it's a phenotype in Latin America, the patient who has axial disease and peripheral diseases.

Yeah, so two different subgroups there. But within that group, how many of your patients who are what we class treatment resistant, as in there were still objective signs of inflammation, but they fell within the difficult to manage group?

Yes, that is very important point, but because just four patients in our cohort were in refractory treatment, two with CRP and two with active disease in in Sacroiliac MRI.

So their number was actually quite small from your cohort of patients that are difficult to manage. So what were the other factors you think that could have pushed them to having higher best die scores or other objective measures if they are not so treatment resistant? Could they be comorbidities for example?

Yes. I believe that the pain is one of the most important factor. Maybe no capture the pain isolated, we capture the pain in bust eye, in bust V and Asthat's too, but I believe that is one of the most important factor of the pain. For example in our cohort, the woman more frequent or difficult to manage than the men, but with no statistic difference, but numerical difference was more women had difficult to manage. I believe that, for example, another mechanism of pain, like a fibromyalgia or whatever.

And then I believe the comorbidity too, we now record systematically the comorbidity but it's one of the most important factors. So

where does this take you now in terms of your future plans about understanding this a bit more from this cohort that you have?

Yes, I believe one of the points difficult to manage is the relation between the patient and physician and the agreement between the patient that the patient is nowadays difficult to manage. Maybe in some cases we don't have agreement between if the patient is or not difficult to manage in that case, but it's one of the most important, or one factor to study in the future, maybe one, I don't know, a patient report or whatever to measure that relation between the physician and patient. But yes, I believe that we follow-up on our cohort that patient who failure to different mechanisms of session than what will be something new treatment that we need.

Yeah, so there's this idea of a patient discordance or patient physician discordance. I think that only can be met by shared decision making between physician and the patient and identifying these many factors. So thank you very much for your presentation. And this is one of many publications that we are seeing emerging in the whole area of difficult to manage expert. And thank you very much, Rodrigo, for sharing with us your work.

Thank you very much.

Excellent.