ACR 2025 RA Topic Podcasts Compilation 1 Save

This is an ACR twenty '25 podcast coming to you from Chicago. Hope you enjoy it.

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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 IANMO, 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, one hundred and forty four patients with preclinical 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. And 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 one hundred and forty four people in the study, they studied about 100 overall. They did different kinds of studies with different subsets. One subset was thirty six 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 twofold. The other thing that they found was those who had the top 20% 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, but 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. 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 to you today about abstract poster one three five five that 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 got parenteral steroids.

So this wasn't a kind of randomized trial or anything like that. This was just looking at what happened to these patients, what the clinicians were giving them. And then the parenteral group is slightly conceptually different in some way. 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. 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, it didn't matter whether you got oral or parenteral, but that there was significantly less persistent glucocorticoid use in those giving parenteral steroids compared to oral. And 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.

And 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.

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 449 looking at the cutoff for C. Diffeile low disease activity.

Now the C. Diffeile was validated against the DAS 28 ESR and CRP, 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. Diffeile 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, you, John. Thanks for that introduction. I first want to 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 Weinbott 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 of 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 CDI 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 C. I. 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 CDAI 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 C. I. Of six, if you had a patient global and a provider global of zero, would be no more than six swollen or three Three. Swollen Three swollen three tender joints.

So you wanna 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 could you can also look at patient and physician and global. So if you're at 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 solid, now you're at a.

So your CA score in that individual is in the heat. 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. Dye 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 this seat height. 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 swollen 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 going to 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 b and t s d 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, a 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, 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.