EULAR 2026 Rheumatology Round Up Save
Transcription
Welcome to EULAR roundup. This is the 2026 edition of the roundup we do after each meeting. This one is from EULAR, which used to stand for the European League Against Rheumatism and now we know it's the European Alliance of Associations of Rheumatology, held in London last week. I'm Jack Cush from Dallas, Texas. Arty Kavanaugh from San Diego. In this session, we're going to be discussing abstracts and presentations of interest from the meeting that we thought were of high quality and high impact on practice and rheumatology. There were many live sessions that were attended, a lot of in-person paper posters and that was a big hit. There's a lot to cover.
Arty, why don't you start us off? All right. Well, thanks and welcome to our audience. Some of you may be thinking, well, boy, I already dressed pretty casually today. But what I'm doing is kind of advertising. Those of you in the know recognize this as a memento of RheumNow Live 2026. So you'll hear a lot of what we're going to discuss now and a lot more at RheumNow Live 2027 and maybe even get a sweet t-shirt like this.
So anyway, I love going to the meetings and I think I like when I really learn a bunch of stuff, and one of the abstracts I think that prompted that was OP120. And this is mosaic loss of the Y chromosome may differentiate giant cell arteritis from polymyalgia rheumatica across the GCA PMR spectrum. There's a bunch of stuff that was in here. Actually the abstract itself was sort of promissory. They had done some work in the past which is interesting and I think it's a very interesting future.
The idea is that we've learned a lot in recent years about somatic mutations. Now these are genetic mutations that don't occur in the germ line. So you're not born with them — they occur during the course of our lives. Generally happen in older persons. Men seem to be more susceptible than women. And we've learned about a number of these conditions. VEXAS, where there is a genetic defect in UBA1, IDH1 and 2, even the whole category called CHIP, or clonal hematopoiesis of indeterminate potential. What these have in common is they're somatic mutations in a line of cells, generally myeloid cells, and they come to rheumatology and hematology because they have a number of musculoskeletal type issues and also they have myeloid issues like deficiencies in various cell lines. Think of VEXAS.
So this actually — I did not realize this — the most common defect in men is the loss of the Y chromosome. And up to 40% of men who are over 70 lose the Y chromosome in certain cell lines. And think of the disease population we're talking about. We're talking about older persons with inflammatory arthritis and inflammatory systemic conditions. So you think of those conditions like polymyalgia rheumatica and giant cell arteritis.
In this analysis, they looked in their center and looked at people who only had PMR and only had GCA. And what they found is that the number of people who had the mosaic loss of Y was negligible in the PMR population, but definitely present in a subset of the GCA population. Previously they had looked at the relapse of GCA and found a similar over-representation of mosaic loss of Y among those persons who had relapsing disease. So I think it throws open an entire new consideration of these somatic mutations that we see in various cell lines. In some cases we have specific treatments that can address them. But I think it's super interesting scientifically and something that we need to watch for clinically.
So again, these CHIP studies, the clonal hematopoiesis studies, have shown up before — they're often positive with aging, it's a part of immunosenescence, but it has disease associations as you say in rheumatology and hematology. It's got a lot of associations in vasculitis, and what's really intriguing about this study is it showed this nice distinction between PMR — the disease we prefer — and GCA, which had all somatic mutation activity. And could that be a factor where you could tell people may be at risk? It may have a clinical utility. This is going to need to be, I think, redone with larger populations. There was a really good-sized population for GCA, a smaller population for PMR. But I think this is really intriguing and its utility for the future.
You know, when I look at these clonal hematopoiesis studies, and we've covered them in the past, I often think this is really cool, but I don't know what to do with it. This might be what we do with it.
Yeah. And if there was a star at this year's EULAR, PMR would be in the running. A lot of material in lupus, a lot of material in PsA, but PMR was really a star. Think of many ACRs and EULARs in the past — nothing about vasculitis, nothing about polymyalgia rheumatica. Now there's a lot of great stuff on that, and this highlights it and it's a fascinating question. They are overlapping. We know that the symptoms and signs can overlap but they're also distinct, and
that we're seeing that with therapeutic approaches as well. So a fascinating abstract I thought.
Yeah and I I agree with you that it was a little bit of a fire hose on PMR and GCA at this meeting. There were guidelines put out by EULAR about the management and assessment of patients with PMR, GCA and they threw in Takayasu's for some reason and it was an odd sort of uh grouping but I think the audience will appreciate the the new guidelines in PMR and GCA and that's been covered on RheumNow but I'm going to present a a PMR um study was called REPLENISH uh it was um presented at the meeting um um and it was also at the same time published in New England Journal.
Um this is a phase three double blind randomized control trial of 381 PMR patients with relapsing disease. And I think that's something to be uh to note from the start when you look at PMR studies are they brand new onset patients which is a different can of worms than is the relapsing patients and you know more than 50% of patients are going to relapse when you start taking away their steroids.
Um and again the important prelude to this is a few years ago um secukinumab was studied in GCA in a phase two trial the TITAN study and looked really good and then they did a phase three trial and it didn't meet its primary endpoint and now even though you know IL-17 Th17 cells are thought to be involved in PMR and GCA you know what happened why did that not happen well here comes the REPLENISH study showing that secukinumab the IL-17A inhibitor does work in relapsing PMR.
So again, it was patients with relapsing disease. They either got um one of two doses of secukinumab or placebo um and they had data out to I guess it was a year. Um the primary endpoint was at week 24. Both doses of uh secukinumab uh were were superior uh with over 40% what was it um response rates uh and to compared to placebo was about 20%. And the primary endpoint was sustained remission. It's a very stringent endpoint. It's what was used in the SAPPHIRE trial was also in New England Journal on um um the other — not a JAK inhibitor — which one already um blanking on it. SAPPHIRE study was sarilumab. Yeah, sarilumab. Sorry, not JAK inhibitor. Sarilumab. And um they use the same end points um and had the same kind of results here.
But the again sustained remission is being in remission from weeks 12 to 52. So there's no room for error there. It you needed to respond by week 12 and stay in response and be in remission. That was achieved in twice the number on drug compared to those on placebo.
Um it also turned out using the IL-17 inhibitor, not an IL-6 inhibitor, that you actually use less steroids, 500 to a thousand milligrams less than the placebo population. And because these people were of the relapsing variety of PMR, it was not uncommon that they would uh relapse later on in the study, except the relapses were much more in the placebo population than they were on the than the IL-17 treated population. So this is exciting data. Uh I think this paves the way for possibly an indication in the future.
Yeah, super exciting data. Well, super exciting to have data in GCA and PMR in recent years. Uh this is uh very exciting and one exciting aspect is the potential safety. Uh and this has been talked about the IL-6 inhibitors have been great and they could and certainly well tolerated medicines in general but you always think about bowel perforations. Uh we don't know exactly why there's a bowel perforation issue with IL-6 inhibition but there was another abstract that showed that it appeared that it was GCA more than PMR making you think that it's a a combined impact of steroids but uh having something like an IL-17 inhibitor uh would be great it'd be great to have another option and we have I think a good understanding of the safety profiles of the IL-17 inhibitors.
In this study as you said the interesting — there was no dose benefit. The 300 was not better at least by appearances than the 150. So you wonder what about a 75 milligram dose which has been looked at in other diseases with for example in some of the AS studies with secukinumab. So might you be able to get away with even a lesser dose?
But uh as you said Jack these studies are they're they're tough because in GCA and PMR steroids are the treatment of choice. So you have to treat with steroids and then you wonder how much did you use, how fast did you taper it and that's one of the first things we look at when we look at study design is what is let let's look at that and that maybe study design issues were some of the reason why it failed in GCA.
Yeah, there was another one that uh the JACK SPAR study of baricitinib in new onset PMR and that was very successful. That was a late breaking 00005. Um and it's different though. They gave the the JAK inhibitor right quick uh with a rapid 11 week or 8 week steroid taper and they showed really significant results. So again, we want to get away from steroids. We can't get away
from steroids in these two disorders. But if we have effective therapies that are really steroid-sparing, we can now start to think about where we're going to put them. Yeah, it's a boy, it's exciting. We have a brand new area with so much new data to pour over.
So my next one, I think we always like positive studies like the replenish and you just talked about, super exciting. But sometimes we learn and we have to address negative studies. And one big negative study I think is POS0063 and this is from Johan Askling's group in Sweden and it looks at time trends of malignant lymphoma risk in rheumatoid arthritis.
So this is an old story back to the initial times when TNF inhibitors were new. One of the things that we saw is that there were side effects among the people with TNF inhibitors including infections but including also the risk of lymphoma, particularly diffuse large B-cell lymphoma. Looking at the patients who were treated, it kind of made sense because we've known even before the TNF inhibitors that the association between rheumatoid arthritis and lymphoma was driven very much by those with the most severe, the most active disease at the onset — that's who got TNF inhibitors. So it was a real confounding by indication kind of a bias, that you're treating those people who are meant to have those side effects. So we thought, well, you know, you're treating people who are at a greater risk, you're going to see this.
But really, we always had in the back of our minds that eventually if we do better with treatment of rheumatoid arthritis, that risk should go down. And we've seen that with other aspects of disease. You see that with — we're doing better in RA, we need fewer joint replacements, overall we see fewer extra-articular manifestations. These days, if I see a patient in the clinic with rheumatoid nodules, I go get the medical students and show them because we don't see rheumatoid nodules and all those manifestations quite as much. So the idea was that eventually the incidence of lymphoma would go down.
So this study — and we walked up and talked to Johan Askling and said, "This is kind of depressing." And he said, "Yeah, this is depressing," because what they found in their Swedish database comparing the rheumatoid arthritis patients over time to the general population, the rheumatoid arthritis patients retain their increased risk of developing lymphoma even though the population use of biologic agents has gone way, way up over the time period. They look from 2005 through about 2025, they don't find a difference. So there's — what else is going on?
And it raises some interesting questions. And in our discussions, people said, "Well, what about methotrexate? What about maybe the TNF inhibitors — they're lowering the inflammation, but they're contributing." We don't know. We don't know. But it still could be that over longer periods of time we keep doing better with RA. If we look at people by remission — and this is a population study, so you can't look at disease activity — but instead, I think we were all rooting for this to be positive, and it wasn't.
Yeah. Another interesting conversation I had on this was — first of all it was very deflating. I thought for sure that if you control inflammation, you'd lower risk, and that's not the case. And they show this very well. Those of you who are just listening, imagine the population risk of lymphoma — just the general population running along the baseline and varying year to year — and then the RA risk line is above it, you know, like 50–60% higher. It was like 10 per — what was it, 100,000? — versus the rate, I can't remember. It was 10 versus six, RA versus — and it stayed that way over time even though they got more aggressive therapies.
But I think a nice argument that I heard might be that that risk of lymphoma is not driven by, let's say, the CRP and sed rate inflammation. It may be driven by the chronic dysregulation of immune response — that years of dysregulated T-cell B-cell activity now sets you up for this. And if you're doing that RA for two or three or four years, that's what gets you into the lymphoma risk category that you can't quite get out of. And that — that's my new hypothesis that someone else is going to have to shoot down.
But what I do like about this is the data proves the point that the drugs that have the lymphoma risk in the warning section of the package insert — these drugs don't cause lymphoma. This study, while it showed that inflammation didn't get better and the risk didn't get better, it also showed increased use of these drugs didn't drive up the risk of lymphoma. And it's okay though that you warn your patients about a lymphoma risk because it goes with RA. You want to blame it on a drug, fine — I think that's a mistake, but that's up to you to decide. The good news is you have a lot of other choices. So if you don't want to use
any like a TNF inhibitor for instance, you have many other choices. But I think they're also at the same risk of lymphoma by having chronic RA. So if it is immune dysregulation early in the disease, what about something like CAR T in rheumatoid arthritis, Jack?
Yeah. Well, that's a good tee-up for the next one. This was an important presentation. See if I can find the number. It's OP8, presented in Plenary Hall. CD19 CAR T-cell therapy in seropositive active refractory rheumatoid arthritis. This was the COMPARE study, and they've developed a CAR T-cell preparation. It was an early phase one, phase two. They reported on six patients. They have 12 others in trials. They've developed something called MIV cell autologous fully human anti-CD19 CAR T-cell therapy.
Patients were very refractory, having failed four to seven biologics and targeted synthetics going in, very active, and they were all strongly seropositive with mean DAS28 scores of greater than six, ranging from four to 7.1. They all were pre-treated with lymphodepletion by fludarabine and cyclophosphamide, and then received one infusion of CAR T-cell therapy. They stopped their DMARDs; they're on no other background therapies. And when you looked at the graphs, you saw a lot of the things you want to see — CD19 or B cells going boom, just down and gone — and it stayed down for a while, although there was some repletion after time. Most of these people became neutropenic, most of them became hypogammaglobulinemic, rheumatoid factor and CCP dropped although not completely, and some at a very steep decline, others kind of slow and waffling.
And then from the podium, the author said, "And the good news is that they all went into remission." And if he had stopped there, that would have been the headline in the press: CAR T-cell therapy puts everybody in remission in RA. Not so fast, Bubba — in that when you look at the ACR 20/50/70 scores at different time points, week 12, week 24, it wasn't so good. I mean, it wasn't as great as you think. The ACR20 response rate at week 12 was only 50%, and greater response rates approaching 80% were seen when you went out to week 36 and 48 or 50 and things like that. So there was a good response, not fabulous.
It wasn't — we were kind of hoping that in RA, cellular depletion therapy, especially CAR T-cell targeted therapy, might do what it did for lupus as reported by Gayord Shett, but I don't think it's as magical as that. I think there might be some role for it, but maybe this says something about the pathogenesis of RA — that B cell activity is an important part of what's going on there. We certainly have autoantibodies that are distinctive for the disease and may be involved in the pathogenesis, but it's not quite as clear as it is in lupus, where double-stranded DNA, Sm, what's going on in the kidney — you can really connect the dots much better — and maybe that's why we've seen better responses.
So there's a lot of excitement about this. It got a lot of press. I think it's positive, but it's not, in my opinion, a magic bullet. Not yet.
No. I mean, it was surprising because those of us with gray hair remember using cytoxan — cyclophosphamide — in RA, where it works actually really well, but of course it's very toxic. Also fludarabine, 2-CDA — another chemotherapy that is effective in rheumatoid arthritis — given those as conditioning, you thought, boy, you'd really think that you would have had a good response even besides the CAR T. So I think you hit it right on the head, Jack. I think what this tells us is that all RA is not driven by B cells. And it's not a question of if only we could eliminate more B cells — which I'm not sure that's the case in lupus, but it's certainly much more the case than it is in rheumatoid arthritis, right?
And that fits in. We did a study years ago called ARISE, and we looked at synovial biopsies, and it turned out that the clinical response was not predicted by anything you saw in terms of changes of B cells in the synovium. So it's not the whole story in RA. And given the other issues with CAR T, especially the cost, the potential for side effects — they didn't get into it much — and these CAR T studies always make me chuckle a little bit. In this one, there were six patients and 35 authors. So I mean, is that something that the practicing rheumatologist is going to go for? I don't think they're going to go for it in RA.
Now, maybe as you're seeing in lupus, these other offshoots — the bispecific and trispecific T-cell engaging sort of therapies, which may not need the conditioning, may be simpler and cheaper — maybe they will have a place. But boy, I thought the data were really quite disappointing.
Yeah, I agree. So, lot — PSA — I'm gonna, there's a
couple now usually our listeners know Jack and I try to find the the the uh the real pearls among the abstracts, but there were a couple of PsA posters that were so impactful we think most people are probably aware of them, but I think everybody needs to be aware of them because the patients are certainly going to be aware of them. This one is OPO69 and it's called TOGETHER PsA and it's actually been published and what it is is a study of a combination of uh IL-17 inhibitor ixekizumab with a like a GLP-1 uh family of medication that is tirzepatide for obese or overweight patients with PsA talking about this in in uh for years now the importance of obesity as a comorbid condition in PsA say obese persons don't do as well. They have more refractory disease. It's bad, bad, bad, bad. Those of us in practice know we talked to nine out of 10 patients who come through your door, you're talking about weight loss. And we've not had therap we've not had a great way to have people lose weight. But now we do. So what impact is that going to have? This was a randomized study. Um average BMI was uh 38. So a big group of patients. uh lot of them were biologic DMARD experienced the primary endpoint and you could say well well oh well geez they kind of you know biased it a little bit it's ACR50 and that's appropriate for a head-to-head study of two active therapies plus 10% or more weight loss at week 36 um most of the patients finished the the study adverse events were what you would have thought of GI stuff with the GLP not really much with the IL-17 and they blew it The primary endpoint was 35% or so with a combination treatment and almost zero with a placebo. The weight loss of course gigantic in favor of tirzepatide. But it's interesting the I the ACR50 alone was significantly better with the combination therapy. The CRP was perhaps the most dramatic difference in the active treatment versus the placebo. uh the it kind of was stable increased a little bit in the placebo group went down in the combination therapy. So this the combination of a GLP-1 and IL-17 inhibitor work great weight loss improvements across the domains of psoriatic arthritis. I think if the patients haven't come to you about this, they're gonna. So, I think, you know, because of access issues, I think we've sort of not done as much with the GLP-1s, but I think that's going to be coming. It's going to be part of something we're going to be able or or really take on the responsibility for prescribing.
So, my first question to you is um how can you in that I think the most interesting bit of data is the ACR50 alone, not the combined endpoint. Um and it was really if you look at the bars it's like high for the combination and very little for um ixekizumab by itself. Um how do you know that the uh great ACR50 response was something due to an added immune or anti-inflammatory effect of IL-17 of the of the GLP-1 versus just the weight lowering effect? Well, yeah. And I don't know that you can and of you know it's it's funny in PsA we've been studying it for 20 almost 30 years and we always worried that there was unmasking. So if your skin psoriasis is better you know you're not on the placebo. In this study the difference in uh 10% or more weight loss was like 85% with the active treatment I mean with the combo treatment and 5% less than 5% with the IL-17 alone. So the patients knew the if they're losing weight, they know and of the ACR50 is a great outcome measure, but it's driven in some part by patient reported outcomes. So does that bias it in a way? So that I I think that's always possible, but you know what? We don't care. I mean, your patient loses weight, they feel better, that's great. Don't care why. I tell people that all the time. It's like, you know, your first dose of whatever medicine you think you're cured, it's in your head. But you know what? That's fine. you you go ahead and believe that and that's why I think the the CRP data is really compelling. You can't you can't placebo your placebo response your way to a lower CRP.
So I I I in the last um year or two I've had conversations with some leading rheumatologists about who have weight loss clinics operating inside of their rheumatology practices um saying oh you got to do that you got to get data on it. You gotta, you know, it's getting to the point now that this is low-hanging fruit for rheumatologists. You should have a weight loss arm of what it is that you deliver. It could be run by APPs and very protocolized, you know, um this this whole thing, you know, this is combination therapy. Who's going to pay for the GLP-1 and the IL-17? Well, that's like other combination therapies. One specialist writes for one, the other specialist writes for the other. So maybe your patients do have to see an endocrinologist, weight loss specialist to get the the GLP-1, you know, old generation, new generation preparations because they're going to get better and better. But to uh we need to really invest in this I think going
forward because we're going to see a lot more of these studies and unlike CAR-T which is teasing us endlessly with fabulous responses but no control data, we're going to start seeing control data that's going to end up in new indications, especially for our patients. Remember the data is very strong for GLP-1s in OA, RA, gout, what else am I forgetting? PsA, PSO, and we haven't even begun to scratch the tremendous benefit on cardiovascular risk and death, which is enormous. So OA and gout are very exciting.
The OA patients — we don't really have anything specific to offer, but if they're overweight that is something very important that can be offered. And gout — I remember quite a number of patients over the years who lost five or 10% body weight; they're still overweight but the gout did so much better, and now we have something to be able to offer them to help assist with that. So it's very exciting.
There are a lot of — again, as Ari already says, we like to find these really cool abstracts — and I have a bunch of really cool abstracts and posters I want to present, but there are several that were big time that we got to talk about. And one was BE BOLD. BE BOLD was a late breaker presented on the last day by Joe Merola from UT Southwestern, LB0001. It's a head-to-head trial of bimekizumab versus risankizumab — the dual IL-17A and F inhibitor versus the IL-23 inhibitor — in adults with active psoriatic arthritis, n=553. The primary endpoint was an ACR50 at week 16. This was, as you know, covered by RheumNow as a press release and then as a pre-publication release, and now they presented not only the week 16 data but the week 24 data, and it still holds up.
What's interesting is that the primary endpoint, ACR50, was significantly different: 49% for bimekizumab versus 38% for risankizumab. And then when they carried that out to week 24, it's still significant — an 11-point difference, 55% versus 44%. And then this is where things get interesting. There were a lot of secondary endpoints, and whether it was at week 16 or week 24, they were numerically better with the IL-17 inhibitor, but they weren't significantly better. That included the MDA, minimal disease activity, DAPSA, and PSSI 100. So that was all good. There were no unexpected safety signals, as expected with IL-17. There were more non-serious candidal infections.
Again, this was a positive trial. My biggest question — since I can't ask this of Dr. Merola because he's not here — I'll ask you, Ari. Why did this head-to-head work in PsA while all other head-to-heads or comparisons don't seem to matter?
Well, we love the head-to-head studies. We hate comparing an effect size from one study to a completely different study done in different people and maybe even a different time period. So we love the idea of the head-to-head. There's not that many of them. There's actually a ton in skin psoriasis, and bimekizumab has been honestly kind of mopping up in the psoriasis studies and has been proven to be more effective than a couple of the other comparators, including the TNFs and other IL-17s and IL-23s. So in that way it's not necessarily unexpected.
I guess the question — if you polled rheumatologists — I think the bias, not based on data but bias before this, would have been that the IL-17s are probably better for the joints than the IL-23s, based on nothing, based on no data for that, but that's kind of the bias. And this I think almost feeds into it. As you said, the skin manifestations — these are both great ways to treat skin psoriasis and they approximate each other the longer you go out. The joint manifestations stay different, and maybe both can be good. Of course, the IL-23 inhibitors have been proven effective for musculoskeletal manifestations in PsA. Maybe there is a difference in IL-17 inhibition, at least with the A and F inhibitor. Maybe that is superior in the musculoskeletal manifestations. It's super interesting data, and the question is which is better, and I don't know how to judge that. I mean, this study says well, in this instance, this design, it's better.
Another way of looking at it is what's better in, as you said, psoriasis skin-only disease — again bimekizumab looks good and the IL-23s also look very good. Which is better according to who's spending more in direct-to-consumer advertising on TV? Well, all these companies, including the IL-23 makers and the IL-17 makers, are spending a lot of money on television. And which is better as far as sales? It turns out that risankizumab is doing, I think, the best in psoriatic arthritis right now as of June 2025, but again these are subject to advertising, market research, etc. So I like the competition. I like that this area is going to get hot here. I think patients will benefit.
Yeah. I think if it was based on who had the better jingle,
Risen Kismap would have won. Um, but, you know, that's not something we're supposed to consider in our scientific discussions. I agree.
Well, um, a poster that, uh, well, two posters, one I want to cover and one very close to it, um, deals with something that, uh, it used to sound like a fringe thing, um, but I think it's going to be more and more important. That's high resolution peripheral quantitative CT scan. So, uh, we know, we've talked before and in past meetings, why do we still do X-rays? The amount of change that you see on plain X-ray films is so small. Uh, and if you think in RA it's very small, in PsA it's incredibly small, and you have Sharp score changes of one minus .3 and it's statistically significant, woohoo. Um, but it doesn't tell us uh enough. I don't think so.
There is a technology, uh, high resolution peripheral quantitative CT. It's not a ton of radiation. There are small devices, kind of tabletop, that you put your hands in and get quantitative CT scan uh of peripheral joints. Um, I think it may be coming because I think it's maybe a better technology. It actually gives us more information.
There are a couple abstracts. One is uh poster 1267. The other is poster uh 1263. Uh, the 1267 uh was very interesting to me personally. We have great radiologists here at my university, very interested in musculoskeletal disease. They find lots of erosions that a typical radiologist might not find, but not all erosions are pathologic. And that was the goal of this. They looked at 247 RA patients with a 78 age and sex matched controls. They found a lot of small erosions in both populations. Mostly they didn't progress. Bigger uh erosions over five millimeters or five cubic millimeters compared to less — the small would be less than one cubic millimeter, large would be greater than five, and the rest were intermediate. The large ones were only seen in RA, really not in the normals, and they could progress. Not all of them did, but they could progress. The small ones never did.
Um, the other abstract, which was using the same technology, is 1263. And at first when you read it you say, you know, so what. Um, what they found was that erosions measured by the high resolution peripheral quantitative CT correlate with functional status. And you say, well yeah, X-ray change correlates with functional status, but in plain films it's only joint space narrowing that drives almost all of that correlation with functional status. Here, and it makes sense, the more disease you have, the more likely you are to have periarticular erosions that correlates with functional status. So I think it's the real deal.
Um, we have to see costwise and availability wise, but I think plain X-rays are going to be a thing of the past. Uh, I think you you you won't even get Claude to read them anymore. He'll be like, "Hey, what are you doing this for? Go to high-res peripheral QCT." Uh, but I think it's a thing to keep an eye out for.
Uh, you know, I'm uh I'm not popular with a bunch of my friends who like imaging because I've always said um imaging is important at diagnosis to know whether they're erosive or not. Um, but repeat imaging, what are you doing that for? You know, MRI at the drop of a hat. What are you doing that for? I'll do MRI, you know, in an RA or PsA patient when I'm asking a hard question, uh, and let MRI — but so which means I do two or three a year. But the my main gripe on imaging is um it's going to be read by someone who's not an expert musculoskeletal radiologist. No fracture present. Hello. And um, and then if you read it and you're good as a rheumatologist, um, you're not going to have the old ones and you don't know how to score them.
And all this to say I'm changing my mind, because now there were a number of presentations at the meeting about the use of AI and machine learning to read um you know MRIs of SI joints and pelvis, you know, to read peripheral joints, to read CT scans and whatnot, and their accuracy is you know really really really high, such that now all the new machines that are coming out they're coming in with AI software uh and that's how they're going to be read. And now you as a rheumatologist can get a report that is both qualitative and quantitative and show serial change, and now I think that becomes a useful tool in practice, especially if we use something like uh um you know high-res QCT that can be done maybe a little more easily um and reproducibly. Again, the patient's going to win.
Yeah, I think you're very spot on. All right. So, another big one um and and then I'm going to get to some posters after this — is the RA BRIDGE study. Um, this was a post-regulatory commitment uh where the FDA um requested that uh the makers of baricitinib do a long-term safety study on baricitinib and its risk of venous thromboembolic events, VTEs, meaning uh DVTs and pulmonary emboli. Um, and again this study was designed um to be enriched for people who would get these events. So the inclusion criteria were RA patients who
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Arty, why don't you start us off? All right. Well, thanks and welcome to our audience. Some of you may be thinking, well, boy, I already dressed pretty casually today. But what I'm doing is kind of advertising. Those of you in the know recognize this as a memento of RheumNow Live 2026. So you'll hear a lot of what we're going to discuss now and a lot more at RheumNow Live 2027 and maybe even get a sweet t-shirt like this.
So anyway, I love going to the meetings and I think I like when I really learn a bunch of stuff, and one of the abstracts I think that prompted that was OP120. And this is mosaic loss of the Y chromosome may differentiate giant cell arteritis from polymyalgia rheumatica across the GCA PMR spectrum. There's a bunch of stuff that was in here. Actually the abstract itself was sort of promissory. They had done some work in the past which is interesting and I think it's a very interesting future.
The idea is that we've learned a lot in recent years about somatic mutations. Now these are genetic mutations that don't occur in the germ line. So you're not born with them — they occur during the course of our lives. Generally happen in older persons. Men seem to be more susceptible than women. And we've learned about a number of these conditions. VEXAS, where there is a genetic defect in UBA1, IDH1 and 2, even the whole category called CHIP, or clonal hematopoiesis of indeterminate potential. What these have in common is they're somatic mutations in a line of cells, generally myeloid cells, and they come to rheumatology and hematology because they have a number of musculoskeletal type issues and also they have myeloid issues like deficiencies in various cell lines. Think of VEXAS.
So this actually — I did not realize this — the most common defect in men is the loss of the Y chromosome. And up to 40% of men who are over 70 lose the Y chromosome in certain cell lines. And think of the disease population we're talking about. We're talking about older persons with inflammatory arthritis and inflammatory systemic conditions. So you think of those conditions like polymyalgia rheumatica and giant cell arteritis.
In this analysis, they looked in their center and looked at people who only had PMR and only had GCA. And what they found is that the number of people who had the mosaic loss of Y was negligible in the PMR population, but definitely present in a subset of the GCA population. Previously they had looked at the relapse of GCA and found a similar over-representation of mosaic loss of Y among those persons who had relapsing disease. So I think it throws open an entire new consideration of these somatic mutations that we see in various cell lines. In some cases we have specific treatments that can address them. But I think it's super interesting scientifically and something that we need to watch for clinically.
So again, these CHIP studies, the clonal hematopoiesis studies, have shown up before — they're often positive with aging, it's a part of immunosenescence, but it has disease associations as you say in rheumatology and hematology. It's got a lot of associations in vasculitis, and what's really intriguing about this study is it showed this nice distinction between PMR — the disease we prefer — and GCA, which had all somatic mutation activity. And could that be a factor where you could tell people may be at risk? It may have a clinical utility. This is going to need to be, I think, redone with larger populations. There was a really good-sized population for GCA, a smaller population for PMR. But I think this is really intriguing and its utility for the future.
You know, when I look at these clonal hematopoiesis studies, and we've covered them in the past, I often think this is really cool, but I don't know what to do with it. This might be what we do with it.
Yeah. And if there was a star at this year's EULAR, PMR would be in the running. A lot of material in lupus, a lot of material in PsA, but PMR was really a star. Think of many ACRs and EULARs in the past — nothing about vasculitis, nothing about polymyalgia rheumatica. Now there's a lot of great stuff on that, and this highlights it and it's a fascinating question. They are overlapping. We know that the symptoms and signs can overlap but they're also distinct, and
that we're seeing that with therapeutic approaches as well. So a fascinating abstract I thought.
Yeah and I I agree with you that it was a little bit of a fire hose on PMR and GCA at this meeting. There were guidelines put out by EULAR about the management and assessment of patients with PMR, GCA and they threw in Takayasu's for some reason and it was an odd sort of uh grouping but I think the audience will appreciate the the new guidelines in PMR and GCA and that's been covered on RheumNow but I'm going to present a a PMR um study was called REPLENISH uh it was um presented at the meeting um um and it was also at the same time published in New England Journal.
Um this is a phase three double blind randomized control trial of 381 PMR patients with relapsing disease. And I think that's something to be uh to note from the start when you look at PMR studies are they brand new onset patients which is a different can of worms than is the relapsing patients and you know more than 50% of patients are going to relapse when you start taking away their steroids.
Um and again the important prelude to this is a few years ago um secukinumab was studied in GCA in a phase two trial the TITAN study and looked really good and then they did a phase three trial and it didn't meet its primary endpoint and now even though you know IL-17 Th17 cells are thought to be involved in PMR and GCA you know what happened why did that not happen well here comes the REPLENISH study showing that secukinumab the IL-17A inhibitor does work in relapsing PMR.
So again, it was patients with relapsing disease. They either got um one of two doses of secukinumab or placebo um and they had data out to I guess it was a year. Um the primary endpoint was at week 24. Both doses of uh secukinumab uh were were superior uh with over 40% what was it um response rates uh and to compared to placebo was about 20%. And the primary endpoint was sustained remission. It's a very stringent endpoint. It's what was used in the SAPPHIRE trial was also in New England Journal on um um the other — not a JAK inhibitor — which one already um blanking on it. SAPPHIRE study was sarilumab. Yeah, sarilumab. Sorry, not JAK inhibitor. Sarilumab. And um they use the same end points um and had the same kind of results here.
But the again sustained remission is being in remission from weeks 12 to 52. So there's no room for error there. It you needed to respond by week 12 and stay in response and be in remission. That was achieved in twice the number on drug compared to those on placebo.
Um it also turned out using the IL-17 inhibitor, not an IL-6 inhibitor, that you actually use less steroids, 500 to a thousand milligrams less than the placebo population. And because these people were of the relapsing variety of PMR, it was not uncommon that they would uh relapse later on in the study, except the relapses were much more in the placebo population than they were on the than the IL-17 treated population. So this is exciting data. Uh I think this paves the way for possibly an indication in the future.
Yeah, super exciting data. Well, super exciting to have data in GCA and PMR in recent years. Uh this is uh very exciting and one exciting aspect is the potential safety. Uh and this has been talked about the IL-6 inhibitors have been great and they could and certainly well tolerated medicines in general but you always think about bowel perforations. Uh we don't know exactly why there's a bowel perforation issue with IL-6 inhibition but there was another abstract that showed that it appeared that it was GCA more than PMR making you think that it's a a combined impact of steroids but uh having something like an IL-17 inhibitor uh would be great it'd be great to have another option and we have I think a good understanding of the safety profiles of the IL-17 inhibitors.
In this study as you said the interesting — there was no dose benefit. The 300 was not better at least by appearances than the 150. So you wonder what about a 75 milligram dose which has been looked at in other diseases with for example in some of the AS studies with secukinumab. So might you be able to get away with even a lesser dose?
But uh as you said Jack these studies are they're they're tough because in GCA and PMR steroids are the treatment of choice. So you have to treat with steroids and then you wonder how much did you use, how fast did you taper it and that's one of the first things we look at when we look at study design is what is let let's look at that and that maybe study design issues were some of the reason why it failed in GCA.
Yeah, there was another one that uh the JACK SPAR study of baricitinib in new onset PMR and that was very successful. That was a late breaking 00005. Um and it's different though. They gave the the JAK inhibitor right quick uh with a rapid 11 week or 8 week steroid taper and they showed really significant results. So again, we want to get away from steroids. We can't get away
from steroids in these two disorders. But if we have effective therapies that are really steroid-sparing, we can now start to think about where we're going to put them. Yeah, it's a boy, it's exciting. We have a brand new area with so much new data to pour over.
So my next one, I think we always like positive studies like the replenish and you just talked about, super exciting. But sometimes we learn and we have to address negative studies. And one big negative study I think is POS0063 and this is from Johan Askling's group in Sweden and it looks at time trends of malignant lymphoma risk in rheumatoid arthritis.
So this is an old story back to the initial times when TNF inhibitors were new. One of the things that we saw is that there were side effects among the people with TNF inhibitors including infections but including also the risk of lymphoma, particularly diffuse large B-cell lymphoma. Looking at the patients who were treated, it kind of made sense because we've known even before the TNF inhibitors that the association between rheumatoid arthritis and lymphoma was driven very much by those with the most severe, the most active disease at the onset — that's who got TNF inhibitors. So it was a real confounding by indication kind of a bias, that you're treating those people who are meant to have those side effects. So we thought, well, you know, you're treating people who are at a greater risk, you're going to see this.
But really, we always had in the back of our minds that eventually if we do better with treatment of rheumatoid arthritis, that risk should go down. And we've seen that with other aspects of disease. You see that with — we're doing better in RA, we need fewer joint replacements, overall we see fewer extra-articular manifestations. These days, if I see a patient in the clinic with rheumatoid nodules, I go get the medical students and show them because we don't see rheumatoid nodules and all those manifestations quite as much. So the idea was that eventually the incidence of lymphoma would go down.
So this study — and we walked up and talked to Johan Askling and said, "This is kind of depressing." And he said, "Yeah, this is depressing," because what they found in their Swedish database comparing the rheumatoid arthritis patients over time to the general population, the rheumatoid arthritis patients retain their increased risk of developing lymphoma even though the population use of biologic agents has gone way, way up over the time period. They look from 2005 through about 2025, they don't find a difference. So there's — what else is going on?
And it raises some interesting questions. And in our discussions, people said, "Well, what about methotrexate? What about maybe the TNF inhibitors — they're lowering the inflammation, but they're contributing." We don't know. We don't know. But it still could be that over longer periods of time we keep doing better with RA. If we look at people by remission — and this is a population study, so you can't look at disease activity — but instead, I think we were all rooting for this to be positive, and it wasn't.
Yeah. Another interesting conversation I had on this was — first of all it was very deflating. I thought for sure that if you control inflammation, you'd lower risk, and that's not the case. And they show this very well. Those of you who are just listening, imagine the population risk of lymphoma — just the general population running along the baseline and varying year to year — and then the RA risk line is above it, you know, like 50–60% higher. It was like 10 per — what was it, 100,000? — versus the rate, I can't remember. It was 10 versus six, RA versus — and it stayed that way over time even though they got more aggressive therapies.
But I think a nice argument that I heard might be that that risk of lymphoma is not driven by, let's say, the CRP and sed rate inflammation. It may be driven by the chronic dysregulation of immune response — that years of dysregulated T-cell B-cell activity now sets you up for this. And if you're doing that RA for two or three or four years, that's what gets you into the lymphoma risk category that you can't quite get out of. And that — that's my new hypothesis that someone else is going to have to shoot down.
But what I do like about this is the data proves the point that the drugs that have the lymphoma risk in the warning section of the package insert — these drugs don't cause lymphoma. This study, while it showed that inflammation didn't get better and the risk didn't get better, it also showed increased use of these drugs didn't drive up the risk of lymphoma. And it's okay though that you warn your patients about a lymphoma risk because it goes with RA. You want to blame it on a drug, fine — I think that's a mistake, but that's up to you to decide. The good news is you have a lot of other choices. So if you don't want to use
any like a TNF inhibitor for instance, you have many other choices. But I think they're also at the same risk of lymphoma by having chronic RA. So if it is immune dysregulation early in the disease, what about something like CAR T in rheumatoid arthritis, Jack?
Yeah. Well, that's a good tee-up for the next one. This was an important presentation. See if I can find the number. It's OP8, presented in Plenary Hall. CD19 CAR T-cell therapy in seropositive active refractory rheumatoid arthritis. This was the COMPARE study, and they've developed a CAR T-cell preparation. It was an early phase one, phase two. They reported on six patients. They have 12 others in trials. They've developed something called MIV cell autologous fully human anti-CD19 CAR T-cell therapy.
Patients were very refractory, having failed four to seven biologics and targeted synthetics going in, very active, and they were all strongly seropositive with mean DAS28 scores of greater than six, ranging from four to 7.1. They all were pre-treated with lymphodepletion by fludarabine and cyclophosphamide, and then received one infusion of CAR T-cell therapy. They stopped their DMARDs; they're on no other background therapies. And when you looked at the graphs, you saw a lot of the things you want to see — CD19 or B cells going boom, just down and gone — and it stayed down for a while, although there was some repletion after time. Most of these people became neutropenic, most of them became hypogammaglobulinemic, rheumatoid factor and CCP dropped although not completely, and some at a very steep decline, others kind of slow and waffling.
And then from the podium, the author said, "And the good news is that they all went into remission." And if he had stopped there, that would have been the headline in the press: CAR T-cell therapy puts everybody in remission in RA. Not so fast, Bubba — in that when you look at the ACR 20/50/70 scores at different time points, week 12, week 24, it wasn't so good. I mean, it wasn't as great as you think. The ACR20 response rate at week 12 was only 50%, and greater response rates approaching 80% were seen when you went out to week 36 and 48 or 50 and things like that. So there was a good response, not fabulous.
It wasn't — we were kind of hoping that in RA, cellular depletion therapy, especially CAR T-cell targeted therapy, might do what it did for lupus as reported by Gayord Shett, but I don't think it's as magical as that. I think there might be some role for it, but maybe this says something about the pathogenesis of RA — that B cell activity is an important part of what's going on there. We certainly have autoantibodies that are distinctive for the disease and may be involved in the pathogenesis, but it's not quite as clear as it is in lupus, where double-stranded DNA, Sm, what's going on in the kidney — you can really connect the dots much better — and maybe that's why we've seen better responses.
So there's a lot of excitement about this. It got a lot of press. I think it's positive, but it's not, in my opinion, a magic bullet. Not yet.
No. I mean, it was surprising because those of us with gray hair remember using cytoxan — cyclophosphamide — in RA, where it works actually really well, but of course it's very toxic. Also fludarabine, 2-CDA — another chemotherapy that is effective in rheumatoid arthritis — given those as conditioning, you thought, boy, you'd really think that you would have had a good response even besides the CAR T. So I think you hit it right on the head, Jack. I think what this tells us is that all RA is not driven by B cells. And it's not a question of if only we could eliminate more B cells — which I'm not sure that's the case in lupus, but it's certainly much more the case than it is in rheumatoid arthritis, right?
And that fits in. We did a study years ago called ARISE, and we looked at synovial biopsies, and it turned out that the clinical response was not predicted by anything you saw in terms of changes of B cells in the synovium. So it's not the whole story in RA. And given the other issues with CAR T, especially the cost, the potential for side effects — they didn't get into it much — and these CAR T studies always make me chuckle a little bit. In this one, there were six patients and 35 authors. So I mean, is that something that the practicing rheumatologist is going to go for? I don't think they're going to go for it in RA.
Now, maybe as you're seeing in lupus, these other offshoots — the bispecific and trispecific T-cell engaging sort of therapies, which may not need the conditioning, may be simpler and cheaper — maybe they will have a place. But boy, I thought the data were really quite disappointing.
Yeah, I agree. So, lot — PSA — I'm gonna, there's a
couple now usually our listeners know Jack and I try to find the the the uh the real pearls among the abstracts, but there were a couple of PsA posters that were so impactful we think most people are probably aware of them, but I think everybody needs to be aware of them because the patients are certainly going to be aware of them. This one is OPO69 and it's called TOGETHER PsA and it's actually been published and what it is is a study of a combination of uh IL-17 inhibitor ixekizumab with a like a GLP-1 uh family of medication that is tirzepatide for obese or overweight patients with PsA talking about this in in uh for years now the importance of obesity as a comorbid condition in PsA say obese persons don't do as well. They have more refractory disease. It's bad, bad, bad, bad. Those of us in practice know we talked to nine out of 10 patients who come through your door, you're talking about weight loss. And we've not had therap we've not had a great way to have people lose weight. But now we do. So what impact is that going to have? This was a randomized study. Um average BMI was uh 38. So a big group of patients. uh lot of them were biologic DMARD experienced the primary endpoint and you could say well well oh well geez they kind of you know biased it a little bit it's ACR50 and that's appropriate for a head-to-head study of two active therapies plus 10% or more weight loss at week 36 um most of the patients finished the the study adverse events were what you would have thought of GI stuff with the GLP not really much with the IL-17 and they blew it The primary endpoint was 35% or so with a combination treatment and almost zero with a placebo. The weight loss of course gigantic in favor of tirzepatide. But it's interesting the I the ACR50 alone was significantly better with the combination therapy. The CRP was perhaps the most dramatic difference in the active treatment versus the placebo. uh the it kind of was stable increased a little bit in the placebo group went down in the combination therapy. So this the combination of a GLP-1 and IL-17 inhibitor work great weight loss improvements across the domains of psoriatic arthritis. I think if the patients haven't come to you about this, they're gonna. So, I think, you know, because of access issues, I think we've sort of not done as much with the GLP-1s, but I think that's going to be coming. It's going to be part of something we're going to be able or or really take on the responsibility for prescribing.
So, my first question to you is um how can you in that I think the most interesting bit of data is the ACR50 alone, not the combined endpoint. Um and it was really if you look at the bars it's like high for the combination and very little for um ixekizumab by itself. Um how do you know that the uh great ACR50 response was something due to an added immune or anti-inflammatory effect of IL-17 of the of the GLP-1 versus just the weight lowering effect? Well, yeah. And I don't know that you can and of you know it's it's funny in PsA we've been studying it for 20 almost 30 years and we always worried that there was unmasking. So if your skin psoriasis is better you know you're not on the placebo. In this study the difference in uh 10% or more weight loss was like 85% with the active treatment I mean with the combo treatment and 5% less than 5% with the IL-17 alone. So the patients knew the if they're losing weight, they know and of the ACR50 is a great outcome measure, but it's driven in some part by patient reported outcomes. So does that bias it in a way? So that I I think that's always possible, but you know what? We don't care. I mean, your patient loses weight, they feel better, that's great. Don't care why. I tell people that all the time. It's like, you know, your first dose of whatever medicine you think you're cured, it's in your head. But you know what? That's fine. you you go ahead and believe that and that's why I think the the CRP data is really compelling. You can't you can't placebo your placebo response your way to a lower CRP.
So I I I in the last um year or two I've had conversations with some leading rheumatologists about who have weight loss clinics operating inside of their rheumatology practices um saying oh you got to do that you got to get data on it. You gotta, you know, it's getting to the point now that this is low-hanging fruit for rheumatologists. You should have a weight loss arm of what it is that you deliver. It could be run by APPs and very protocolized, you know, um this this whole thing, you know, this is combination therapy. Who's going to pay for the GLP-1 and the IL-17? Well, that's like other combination therapies. One specialist writes for one, the other specialist writes for the other. So maybe your patients do have to see an endocrinologist, weight loss specialist to get the the GLP-1, you know, old generation, new generation preparations because they're going to get better and better. But to uh we need to really invest in this I think going
forward because we're going to see a lot more of these studies and unlike CAR-T which is teasing us endlessly with fabulous responses but no control data, we're going to start seeing control data that's going to end up in new indications, especially for our patients. Remember the data is very strong for GLP-1s in OA, RA, gout, what else am I forgetting? PsA, PSO, and we haven't even begun to scratch the tremendous benefit on cardiovascular risk and death, which is enormous. So OA and gout are very exciting.
The OA patients — we don't really have anything specific to offer, but if they're overweight that is something very important that can be offered. And gout — I remember quite a number of patients over the years who lost five or 10% body weight; they're still overweight but the gout did so much better, and now we have something to be able to offer them to help assist with that. So it's very exciting.
There are a lot of — again, as Ari already says, we like to find these really cool abstracts — and I have a bunch of really cool abstracts and posters I want to present, but there are several that were big time that we got to talk about. And one was BE BOLD. BE BOLD was a late breaker presented on the last day by Joe Merola from UT Southwestern, LB0001. It's a head-to-head trial of bimekizumab versus risankizumab — the dual IL-17A and F inhibitor versus the IL-23 inhibitor — in adults with active psoriatic arthritis, n=553. The primary endpoint was an ACR50 at week 16. This was, as you know, covered by RheumNow as a press release and then as a pre-publication release, and now they presented not only the week 16 data but the week 24 data, and it still holds up.
What's interesting is that the primary endpoint, ACR50, was significantly different: 49% for bimekizumab versus 38% for risankizumab. And then when they carried that out to week 24, it's still significant — an 11-point difference, 55% versus 44%. And then this is where things get interesting. There were a lot of secondary endpoints, and whether it was at week 16 or week 24, they were numerically better with the IL-17 inhibitor, but they weren't significantly better. That included the MDA, minimal disease activity, DAPSA, and PSSI 100. So that was all good. There were no unexpected safety signals, as expected with IL-17. There were more non-serious candidal infections.
Again, this was a positive trial. My biggest question — since I can't ask this of Dr. Merola because he's not here — I'll ask you, Ari. Why did this head-to-head work in PsA while all other head-to-heads or comparisons don't seem to matter?
Well, we love the head-to-head studies. We hate comparing an effect size from one study to a completely different study done in different people and maybe even a different time period. So we love the idea of the head-to-head. There's not that many of them. There's actually a ton in skin psoriasis, and bimekizumab has been honestly kind of mopping up in the psoriasis studies and has been proven to be more effective than a couple of the other comparators, including the TNFs and other IL-17s and IL-23s. So in that way it's not necessarily unexpected.
I guess the question — if you polled rheumatologists — I think the bias, not based on data but bias before this, would have been that the IL-17s are probably better for the joints than the IL-23s, based on nothing, based on no data for that, but that's kind of the bias. And this I think almost feeds into it. As you said, the skin manifestations — these are both great ways to treat skin psoriasis and they approximate each other the longer you go out. The joint manifestations stay different, and maybe both can be good. Of course, the IL-23 inhibitors have been proven effective for musculoskeletal manifestations in PsA. Maybe there is a difference in IL-17 inhibition, at least with the A and F inhibitor. Maybe that is superior in the musculoskeletal manifestations. It's super interesting data, and the question is which is better, and I don't know how to judge that. I mean, this study says well, in this instance, this design, it's better.
Another way of looking at it is what's better in, as you said, psoriasis skin-only disease — again bimekizumab looks good and the IL-23s also look very good. Which is better according to who's spending more in direct-to-consumer advertising on TV? Well, all these companies, including the IL-23 makers and the IL-17 makers, are spending a lot of money on television. And which is better as far as sales? It turns out that risankizumab is doing, I think, the best in psoriatic arthritis right now as of June 2025, but again these are subject to advertising, market research, etc. So I like the competition. I like that this area is going to get hot here. I think patients will benefit.
Yeah. I think if it was based on who had the better jingle,
Risen Kismap would have won. Um, but, you know, that's not something we're supposed to consider in our scientific discussions. I agree.
Well, um, a poster that, uh, well, two posters, one I want to cover and one very close to it, um, deals with something that, uh, it used to sound like a fringe thing, um, but I think it's going to be more and more important. That's high resolution peripheral quantitative CT scan. So, uh, we know, we've talked before and in past meetings, why do we still do X-rays? The amount of change that you see on plain X-ray films is so small. Uh, and if you think in RA it's very small, in PsA it's incredibly small, and you have Sharp score changes of one minus .3 and it's statistically significant, woohoo. Um, but it doesn't tell us uh enough. I don't think so.
There is a technology, uh, high resolution peripheral quantitative CT. It's not a ton of radiation. There are small devices, kind of tabletop, that you put your hands in and get quantitative CT scan uh of peripheral joints. Um, I think it may be coming because I think it's maybe a better technology. It actually gives us more information.
There are a couple abstracts. One is uh poster 1267. The other is poster uh 1263. Uh, the 1267 uh was very interesting to me personally. We have great radiologists here at my university, very interested in musculoskeletal disease. They find lots of erosions that a typical radiologist might not find, but not all erosions are pathologic. And that was the goal of this. They looked at 247 RA patients with a 78 age and sex matched controls. They found a lot of small erosions in both populations. Mostly they didn't progress. Bigger uh erosions over five millimeters or five cubic millimeters compared to less — the small would be less than one cubic millimeter, large would be greater than five, and the rest were intermediate. The large ones were only seen in RA, really not in the normals, and they could progress. Not all of them did, but they could progress. The small ones never did.
Um, the other abstract, which was using the same technology, is 1263. And at first when you read it you say, you know, so what. Um, what they found was that erosions measured by the high resolution peripheral quantitative CT correlate with functional status. And you say, well yeah, X-ray change correlates with functional status, but in plain films it's only joint space narrowing that drives almost all of that correlation with functional status. Here, and it makes sense, the more disease you have, the more likely you are to have periarticular erosions that correlates with functional status. So I think it's the real deal.
Um, we have to see costwise and availability wise, but I think plain X-rays are going to be a thing of the past. Uh, I think you you you won't even get Claude to read them anymore. He'll be like, "Hey, what are you doing this for? Go to high-res peripheral QCT." Uh, but I think it's a thing to keep an eye out for.
Uh, you know, I'm uh I'm not popular with a bunch of my friends who like imaging because I've always said um imaging is important at diagnosis to know whether they're erosive or not. Um, but repeat imaging, what are you doing that for? You know, MRI at the drop of a hat. What are you doing that for? I'll do MRI, you know, in an RA or PsA patient when I'm asking a hard question, uh, and let MRI — but so which means I do two or three a year. But the my main gripe on imaging is um it's going to be read by someone who's not an expert musculoskeletal radiologist. No fracture present. Hello. And um, and then if you read it and you're good as a rheumatologist, um, you're not going to have the old ones and you don't know how to score them.
And all this to say I'm changing my mind, because now there were a number of presentations at the meeting about the use of AI and machine learning to read um you know MRIs of SI joints and pelvis, you know, to read peripheral joints, to read CT scans and whatnot, and their accuracy is you know really really really high, such that now all the new machines that are coming out they're coming in with AI software uh and that's how they're going to be read. And now you as a rheumatologist can get a report that is both qualitative and quantitative and show serial change, and now I think that becomes a useful tool in practice, especially if we use something like uh um you know high-res QCT that can be done maybe a little more easily um and reproducibly. Again, the patient's going to win.
Yeah, I think you're very spot on. All right. So, another big one um and and then I'm going to get to some posters after this — is the RA BRIDGE study. Um, this was a post-regulatory commitment uh where the FDA um requested that uh the makers of baricitinib do a long-term safety study on baricitinib and its risk of venous thromboembolic events, VTEs, meaning uh DVTs and pulmonary emboli. Um, and again this study was designed um to be enriched for people who would get these events. So the inclusion criteria were RA patients who
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