Day 3 Recap: ACR Convergence 2026

Hi everyone, I'm David Lou and welcome to the RheumNow daily recap ACR Convergence 2026 Orlando. We are now well in the depths of the meeting. Uh everyone's a little bit weary but um there is just so much good stuff out there. So we're very glad to bring it to you. I am just going to go around the uh the virtual table here, get everyone to introduce themselves and then get stuck into some of the great content.

So, um, why don't we go around the table, Sheila? Hi everyone. I'm Sheila Reyes from the Philippines and I'm here in Orlando reporting for ACR 2026. Fantastic. Bella. Hi, I'm Bella Meta. I'm from New York and I'm enjoying the hot weather while I can in Orlando. Yeah, you know, kind of warmer than New York, right? For sure. For sure. Brian. Hey everybody. I'm Brian Jaros. I uh am from Chicago, of course. Also here uh reporting from Orlando in I guess you know the home stretch of this meeting, but excited to be here with all of you. And Henrik. Hey. Hey guys. I'm Inhika. I'm a Brazilian rheumatologist here in Orlando with everyone and I'm very glad to be with you reporting for ACR 2026.

Fantastic. Well, um why don't we start with you Bella? Tell us about uh what you what big thing you saw out there today which caught your attention. I think the OA treatment guidelines uh management and treatment guidelines which I think uh you know it's an update from 2019. So it's been six or seven years. There's a lot of work that went into it and I want to say just the key key things like again OA is a disease millions of patients have it uh and you know we don't quite have a lot of drugs yet uh but um some things that I I think they um you know added they were emphasizing a lot more on NSAIDs this year on these guidelines um saying that use NSAIDs it can help you out with pain symptoms. Um again do it safely.

Um the second thing which was interesting is that you know exercise is something that we've always recommended for OA. What they added this year was walking. So recommend patients uh to walk um and now they've put it in the ACR guidelines. I think especially in the plus 65 you know sort of um patient population it's something that they can easily do without equipment uh without too much training. Uh so I think they emphasize to add that in the guidelines.

Um sort of now going into a little bit of a controversial territory here. So uh ACR guidelines recommend against supplements. Uh chondroitin um you know uh most of the supplements there's not very good data. There have been good placebo control trials. Um and I think ACR stands with the same saying glucosamine chondroitin supplements do not help. Uh I know in practice there's people who do it. Uh but the data is not very convincing that it works. Um and then the bigger one is PRP injections. Um now um again it's pretty popular uh amongst uh some of the other specialty colleagues but um ACR holds its stance uh and recommends against uh using PRP. Again, the level of evidence is um pretty good to show at least the RESTORE RCT um a couple of years back and that's what they referenced to saying, "Hey, this was a well done study um with a good control arm and said PRP was no better than saline."

So this is a stand which is going to uh you know we we're going to fight with the surgeons a little bit when we go out there because the AAOS guidelines uh say that it's um it's okay conditionally okay to use it they don't strongly recommend it but like when people take away these things like oh AAOS recommends it ACR doesn't I mean that's not completely true all the data that even they had and you know the AAOS guidelines which is the surgical guidelines came in 2021 before the RCT was published.

So um and then the last one I want to say is methotrexate uh for hand OA. It's now conditionally recommended. Again very little data out there but you know they wanted to err on the side of um you know saying use it when you need it because erosive osteoarthritis in theory I mean even the small data that they have we have shows that it may help. Uh I think these are the key takeaways. I I I think from the OA guidelines, I mean, we're going to keep using uh we we you know, all rheumatologists are going to see OA in some uh form or the other. So, it's good to uh know what's out there. Patients are going to ask.

Yeah. I never thought I'd see — well, I didn't think that we'd get to the point where the OA guidelines would be so um heavily anticipated or even a little bit controversial. Remember when I was a trainee uh one of my bosses said if you solve osteoarthritis that's when you get your private jet and we all laughed but it's almost — if you don't even have to solve osteoarthritis to get your private jet you can just pretend to solve osteoarthritis you get your private jet. Well the TRIUMPH study I mean they also added GLP-1s uh as recommended for OA which was new this year and like the TRIUMPH study which was two two days back um if you see the pain curves they go like this I mean it works weight loss works in — oh sorry weight loss works in OA uh and you know these are you know 20% reduction in weight and 20 to 30% reduction in pain those are not ignorable results so they did add GLP-1s too.

Now I I I do want to go around the group and get people's thoughts on this because it is so provocative but Bella let me kind of push push on this. So, we've got here now, I mean, obviously a lot of recommendations dealing with things that don't work. I think it's really important to to steer people away from um false hope, wasting money, but kind of the actual real safety impacts, lost time from that kind of thing and and lost bandwidth really. But we're in a situation now where um we've got methotrexate on there all of a sudden. We've got um GLP-1 receptor agonists on there. We've got pharmacotherapy that's not just simple pain relief on the osteoarthritis guidelines. Are we close to having a disease modifying osteoarthritis drug, a DMOAD? What do you think about this trend? And and does this mean that we're going to have to come up with new guidelines in three or four years time?

So this year it's interesting this year I mean I've seen so many phase 2s uh including gene therapy in a way and by the way there's a new terminology instead of DMOADs disease modifying osteoarthritis drugs the term is T-MOADs which is tissue modifying because disease modifying may be too broad and like it's been tough in clinical trials so it's going to be tissue modifying osteoarthritis drugs. I I don't know I mean for me I mean as a clinician I don't care what you call it just solve it uh to be fair but GLP-1s I I think even in clinical practice like we've you know again I work in New York there's a lot of people who are taking this I don't know how they get access to it but they do and it does work. Weight loss we've known it has been working in a way since I don't know 1980s it was just always difficult to do it now we have an agent which does it so even methotrexate in hand OA which is erosive I think it's a very fair sort of choice. We're used to it. They're not asking — but but you know OA is treated by all kinds of clinicians. Uh but for giving methotrexate they still recommend that a rheumatologist should because it comes with a certain amount of monitoring or um somebody who does it needs to be a little um educated on it which is fine.

I noticed you managed to dodge answering whether it's tissue modifying or not which I feel like is definitely the right type of approach. It's it's very hard to know isn't it? Uh there's a lot of excitement out there and I guess questions about how much is mechanical offloading versus not. We talked about it a bit on day one, but seeing these guidelines has really put it in stark contrast. Um I mean Brian, you know, from your Chicago perspective, I guess have you seen um some of these trends move into into your clinical practice and what your patients are talking to you about?

Yeah. Yeah, definitely. And I have to say out of out of all of the the the guidelines you talked about, I'm most kind of interested and surprised about the the methotrexate uh recommendation and I I'm like grappling with that in real time how I feel about it. You know, these erosive hand OA people, you know, on one hand it's awful, right? You don't have much to to do for them. You know, Voltaren and occupational therapy. And so in people who have that kind of inflammatory phenotype, I have um tried uh you know hydroxychloroquine or methotrexate as sort of a hail mary. Um, but I do wonder if this will open up, you know, a pretty big population of patients that would potentially be eligible for treatment and what that looks like for us, you know, workforce wise and, uh, you know, rheumatology wise because, frankly, you know, I don't typically follow hand OA people um, at least in my clinic. Um you know maybe they see us once to make sure that there's no other inflammatory process and then kind of send them on their way but I'm curious other people's approaches and if that's something they do.

Yeah. And I mean look the data behind it is that phase 2b actually it's from uh from back in Melbourne Australia um uh the METHOD study looking uh at really patients with um with synovitis on MRI. So it's really a very — it's a small subsection of the overall hand osteoarthritis cohort you know that's um actually just going to identify those patients um is that the right kind of stratification and then if you look at the effect size well I don't know everything's been thrown by um by retatrutide but um you know the magnitude there and you know we've got what have we got better for hand osteoarthritis not a heap so I think that's I wonder whether that's part of what's driven it but um well Sheila I'm kind of interested in the kind of global perspective as well. Osteoarthritis is clearly very much universal. Um interesting to see how some of these trends have been um playing out around the world. Sheila I might start with you. How much of this have you been seeing in your practice in the Philippines?

Yeah. So um I mean osteoarthritis is really one of the most common reasons why patients would come to clinic and um it's sometimes it's really frustrating not to not give um the the proper or not give anything that really works you know or tell your patient that um oh your uh your osteoarthritis will improve like — like just giving um just like with rheumatoid arthritis in case you have your other treatment options. So, um, in terms of the GLP-1s, um, I think it's already starting to, um, pick up, although um, just like Bella said, there are, um, I I know people um, even patients who are already on GLP-1s, but basically for the um, indication of obesity and I think that's what the guidelines have also um, emphasized that giving the GLP-1s um, are for obese patients with osteoarthritis to help them lose weight. So yes, I'm excited to really look into the potential um effects of um GLP-1s in osteoarthritis.

And with regards to methotrexate, if I'm not mistaken, I think before it was already a um it uh it was a recommendation for the ACR but um against uh if I'm not mistaken. So yeah, it it also came as a surprise for me that you know it went to um becoming conditionally recommended although I think when you look at OA um if there is anything that you can give the patient we will try.

So I guess yeah Henrik any kind of other perspectives I don't know you seeing much uh um GLP-1 RA into practice in Brazil and I think as well I mean how much do you think that your patients are going to listen to guidelines from you know uh well these type of guidelines from the US. Yeah it's interesting to say that that here in Brazil a lot of patients came to the rheumatologist already using the GLP-1 medication because another doctor had already prescribed to them. Well, I'm seeing in my practice I started to prescribe a lot of GLP-1 especially for knee osteoarthritis. The results that we are having it's something very very good especially when they lose weight. Uh it's something that is already reality here in Latin America, especially in Brazil. And I'm very glad that we finally have something — I know that the the objectives of the studies were to reduce pain but reducing pain is something very important for the patient and for us rheumatologists that before we haven't had tools to treat these patients uh especially for methotrexate this is something that I'm not seeing already especially for erosive osteoarthritis but it's something that we are going to change and I myself as a rheumatologist, I'm going to change.

Yeah, absolutely. I mean, sorry. Sorry. I was just going to say, I mean, we're all for it. This is a magic drug. Uh, in some sense, the GLP-1s, but sarcopenia is a real risk and problem. And especially, we know knee OA um if you don't have muscle, knee OA gets worse. So, we'll have to see. We're going to — I mean, people are using this on a massive scale already. And we'll see. Hopefully. I mean, in a few patients, we're probably going to do harm if we're not recommending exercises. Mhm. Absolutely. Oh, well, I think more than a few.

So, um and I think that's obviously something um we're going to have to adjust to, but and the guidelines to some extent, like often happens, have to play catch up a little bit. Um like we said, I think the practice around the world pretty clearly has um overtaken where the guidelines are and probably um is in the same direction as the data but uh has preceded it. Plenty to watch there. You suspect that we might be getting more um updates for osteoarthritis in the very near future like you say Bella. Um so Sheila maybe let's go to you next. Um what did you find good out there today?

Okay. So, um there was a very um well attended session about um the application of the um SLE guidelines um on NPSLE. Um and this was a talk by Dr. Maria Dall'Era. And so she gave a really um insightful talk because um well personally for me when you when you talk about or when when we think of NPSLE it's one of those very challenging um conditions because it really makes you feel — or it it makes you feel like you're really the rheumatologist. You know, um there are still a lot of um gaps that we need to address, but um I like how um the session was approached with how to evaluate for possible CNS lupus. So just um breaking into like considering what the main um CNS manifestation of a patient is when you approach it. Is it like affecting the vasculature or is it the brain parenchyma and then um highlighting the importance of really ruling out non-lupus etiologies because there would be lots. So um consider infections, metabolic abnormalities, even drug toxicities, toxins and all those things and um really asking the question of whether is this really lupus or is this um part of damage.

So particular especially in patients with acute psychosis you know there are uh you have to really rule out other etiologies and then consider if this is really active disease or just part of chronic damage and um there was also a part there where um Dr. uh Dall'Era also um mentioned that um you know there's really no specific laboratory or imaging study that would really help you diagnose um NPSLE. So it really boils down to the importance of um you as a rheumatologist, your critical thinking skills, your clinical acumen um and really just um making sure that you attribute correctly what you see in the patient.

And um and then she goes into um making mention of the 2025 ACR guidelines for severe neuropsychiatric lupus and um unfortunately because there is still lack of um RCTs on on what uh on additional better treatments. So it's just like cycling around giving um high-dose steroids and then giving the options of either cyclophosphamide, mycophenolate or rituximab and just those options really and not like a step-wise approach just because um there's really still lack of evidence but these are what we have and um and she just um goes on mentioning that you know actually there are only two RCTs um that have been done for severe manifestations of SLE and um again there there lies the problem. So future directions in terms of treatment.

Um and lastly, I think this is one of the most important things also that clinicians and rheumatologists like us um have to consider when um when uh diagnosing or treating NPSLE is um considering mimickers or being aware of mimickers. So we have your PRES or your posterior reversible encephalopathy syndrome because that entails a different type of treatment particularly in patients in the setting of lupus nephritis and also um the presence of for example transverse myelitis with or without optic neuritis consider lupus but also consider a possible NMOSD spectrum disorder or the MOG antibody associated diseases. Um and uh important just highlighting the fact that for example the importance of um CSF analysis is really to rule out an infection and that um she also mentioned about um oligoclonal bands being can be present in the CSF of patients with lupus um but it is not present in um NMOSD or the MOG and um just giving I I like what um what Dr. Dall'Era um said as a closing statement or like a very important pearl which I think it is also applicable in the treatment of other um conditions associated with lupus is that you do your best you treat the patient and then you monitor and you reassess.

So let me just ask you and I think you know it is — everything else in lupus uh we can put our hands on we can see we can see under a microscope easily uh we have a marker to be able to track which is a pretty good uh biomarker. This is one of the things which we've really struggled with. What is inflammation? What is cognitive um dysfunction that would — which would actually maybe be worsened by um heavy immunosuppression? What's a mimicker? It seems to me did did did they mention much about kind of how we move forward on this? It seems like phenotyping still despite everything that we've talked about and despite new biomarkers and everything we've struggled to get the phenotyping that's required to get the to get the um treatment pipeline that we might want.

Yeah. So there was actually a question raised about the use or um the utilization of biomarkers although it was not really part of the um discussion but yes someone asked about it and uh yeah there were um I think there are potential um directions um going using uh taking looking into biomarkers and also um like uh for the use of MRI like MRI but using with a different modality or like a different um like still using MRI but on a different uh approach um in establishing um diagnostic I mean diagnosis for NPSLE because I mean at least like 30% if I'm not mistaken of patients with MRI 30 to 40% only 30 to 40% um test positive on MRI and so yeah we don't really know all the tests are not great right. Correct. Correct. There's really no specific so yeah.

Let me ask kind of around the group does anyone kind of I mean I think this is something that we globally struggle with can anyone see a pathway out of this. I mean quiet around the group. I feel like that's probably — that's probably it's a tough one it's a tough one you know sometimes you don't know if it's lupus or a super infection and like you know has meningitis. It's like a it's a tough one. Yeah. Well, and I feel like um you know autoinflammatory conditions have obviously gone through a bit of a — you know your kind of home turf has gone through this real evolution where maybe once upon a time it was all a bit as mysterious as NPSLE and we move to a situation now where we're getting very precise. Maybe it is easier to understand the drivers there now, but it's always easier when we look back and know what's going on. Anyway, I think that's something — I'm glad that we have the likes of um Dr. Dall'Era working on this kind of stuff because uh there are um I continue to look to those experts for um advice on what to do when those patients land um in your care.

All right, Brian, what have you found that's good out there today? Yeah. So, uh I attended um the vasculitis session. It was a beyond the guidelines session by three um really awesome experts. Uh Dr. Chung, uh Dr. Dua is my own mentor. Um and then Dr. Carmona. So, I thought I would bring a few. I mean, there were so many pearls from it. I thought I would bring at least just a few for us to kind of talk about.

Um Dr. Chung went first. She talked about uh GPA and MPA and kind of addressed two major points. Um the first being, you know, the avacopan of it all, which is something at this meeting that's had a lot of data actually if you look at the vasculitis ANCA abstracts like a good third of them, you know, are real world evidence of avacopan. And I think the question for all of us, right, is like how does this drug in the current environment and even depending where you're practicing, you know, internationally fit into our practice anymore? Sure. And maybe I'll just give background for the general audience. Two main issues with the avacopan. Firstly, this liver signal that we've primarily — vanishing bile duct syndrome we've primarily seen in Japan and then possibly some uh uh GCP um trial conduct issues which have led to the NEJM paper being withdrawn and then jurisdictions around the world responding. It's been a big issue at this meeting.

Tell us Brian what what was the word in this discussion? Where were people getting at? Is a lot of — you know a lot of people believe this drug is — it's going to go away? I'm still using it. Exactly. And I think that was, you know, like she summarized the exact data you're talking about, David, you know, the hepatic toxicity and then the trial conduction concerns and and I actually quoted her sort of takeaway statement which was starting avacopan at this time and in this environment is extremely challenging. And she put that into a few lenses. One is access, which we've all alluded to, right? If we start someone on the drug tomorrow, will it be pulled and then we'll kind of just say, you know, where are we left with things, you know, and the other is the shared decision making about, you know, the potential risks and the changes, you know, from the data.

What I liked is that she also focused in that talk on falling back on the PEXIVAS and the LOVAS tapers. So kind of framing it, you know, look, if avacopan's off the market, if this isn't going to be an option anymore, what are the sort of like tried and true, you know, uh, steroid tapers, we should be looking to PEXIVAS and people who have, you know, especially severe disease, renal disease, alveolar hemorrhage, which was a population that was excluded um, in the LOVAS trial. So I thought that was um, a nice kind of review and touch point.

Um she also talked about which I was super curious about you know this population of GPA MPA patients that is quite controversial in how to treat which is the severe kidney folks. She had a very nice chart that compared the ACR guidelines which are pretty in line with the EULAR guidelines which are very — all very different from the KDIGO you know the kidney folks guidelines. Um and really the the question is in people who have a creatinine you know four or greater these severe patients they were excluded from RAVE which was the landmark trial of course where rituximab was you know comparable to cyclophosphamide um and so how should we be treating those severe kidney patients — are even though they weren't in RAVE should we be giving them rituximab monotherapy should we be giving them dual therapy should they get cyclophosphamide and she started the presentation with a poll um of what you know the audience approach was and it was it was varied you know rituximab monotherapy with or without glucocorticoids I should say um but not to say there wasn't you know a good 10 to 15 to 20% for for the other options.

Um she you know reviewed in her talk that when we think about rituximab alone versus rituximab combination therapy with cyclophosphamide. There actually is no randomized control data that answers that question. Um there's um RITUXVAS which was the cyclophosphamide uh versus cyclophosphamide and rituximab combination but we don't have uh prospective data um answering the question. And so ultimately on the basis of it her approach um is that she does still start with rituximab um on its own without cyclophosphamide um and and even in patients with severe um renal disease and only um adds cyclophosphamide on board uh if there's you know an issue they're not responding there — you know infections other mimics and you feel like you still need something else. Um and some of that came from um uh observational data that really sort of pointed out the — which we are all kind of theoretically aware of but pointed out the additional additive risk um particularly with infection once you start adding cyclophosphamide into the mix.

Um those patients — isn't it hard to — the risk hard to phenotype the risk of therapy versus the risk of the disease. And she had another great quote that I wrote down here. She wrote — what you know sometimes I ask myself she says what is worse for my patients cyclophosphamide or glucocorticoids you know and you're like weighing will the cyclophosphamide addition help you get off the steroids or are we just throwing more you know toxicity into the mix. If only we had something that could replace prednisolone in the treatment of acute ANCA-associated vasculitis right.

Um and then I think in that session Tanaz Carmona as well talked a little bit about GCA and um steroid-sparing agent therapy duration really kind of one of the hot topics within GCA. How long do you keep on treating? And that's right. Yeah. How long is that string? That's that's exactly right. You know, I think a lot of us, you know, proverbially I've known for a while, right? Like, you know, these trials for GCA start — is a year. Is a year long enough? I think we can pretty confidently with a growing growing evidence say no.

Um she presented that um SELECT-GCA extension data. So after the first 52 weeks, people that were in remission were randomized to either stay on ixekizumab or go to placebo. And you just look at that chart and it it's jarring, you know, how many people that get put on placebo after a year um relapse. Um and in you know knowing that we probably need to treat these people longer than a year. Um she also kind of reviewed the uh METEORIC study whether methotrexate is maybe uh like an escape strategy from tocilizumab if we're trying to you know kind of wean people down off therapy. Um and it kind of seems like no it's not great. Um they — each individual person had less relapses if they were on methotrexate, but the time to relapse between being tapered to methotrexate versus coming off, you know, to placebo wasn't very different.

So, she sort of framed the discussion in risk factors. Um how bad's their damage? Are they a person that's had vision loss and you're trying to preserve that other eye and you're really saying, you know, the risk of you having a relapse is so high, we should keep you on treatment longer. Um, are you a person that has large vessel involvement, that being a risk factor for relapse? And then ultimately, you know, like we all know as rheumatologists, that shared decision-making for each patient and their preference, what feels right to them, weighing the sort of risks and benefits.

Yeah. I mean, these are — and once again, I think hard — these are rarer conditions. How do you phenotype to get the therapy exactly right? How you design — are you designing studies that are going to fit the patient in front of you? Can I just quickly poll this group? Um I mean how many people uh using steroid sparing therapies if you got access to steroid sparing therapies for GCA? How long — how many are going more than a year for GCA in treating GCA? Brian? Bella? And then you know Sheila. Yeah I think I mean and obviously then I guess beyond two years beyond three years sometimes. Yeah. Sometimes you're stuck what can you do? It evolves also. I think it starts with something and then — yeah. Uh depends on the manifestations of this patient. Yeah, absolutely. That's right.

All right, Henrik, tell us what's uh what was good and great for you on the floor today. Well, they've been bringing some rheumatoid arthritis now. The the area that I like the most. So uh Professor Josh Baker at plenary today brought us one new treatment target. It's something important to us. Why? Because some patients with RA — it's our practice we see every day — had some problems like fibromyalgia had some problems like central sensitization and another kind of pain. So we lose sensitivity with our treatment targets that we use every day. So Professor Josh Baker brings us something new. He calls something like RALIA or RA low inflammatory activity. It's interesting to say because he took out the patient global evaluation and he took out the uh tender joints. So basically what it brings to us is the following: joints and the the CRP. So uh everything that we have that is objective that we see that these patients is — is on activity.

It's interesting to say Dave uh that this new treatment target brought us some results similarly to DAS28 without uh any progression of X-ray or MRI in patients with remission in DAS28. So it is in my opinion it's very interesting to say that some clinical studies especially for who does clinical research is important because it can be a new treatment target in studies because we took out some of that fibromyalgia complaints in these patients and we can see in a in a very objective way what the patient really have of inflammation what the joints are telling us in fact. So I think it was one of the best abstracts and it was presented at plenary. So I think it was one of the best of all the congress.

Because I mean let me ask you this you know talking I guess about the limitations of DAS28 and I mean this is a real problem it flows through — you can't help but think that maybe when we look at rheumatoid arthritis studies and everyone gets the same outcomes we have a 60-20 rule and that flows through to PsA thing — all these — you have to wonder is DAS28 really being able to adequately differentiate, does it discriminate the small amount especially when it comes to outside a classical rheumatoid arthritis situation from 30 years ago from someone who smoked 50 pack-year history and who's you know kind of got floridly seropositive rheumatoid arthritis with inflammation all over the place. So this um this RALIA isn't it — RA low inflammatory activity. Where do you think Henrik this is going to end up landing in terms of how we're going to apply it? Is there a role in studies um I guess maybe phase four studies even kind of development pipeline studies clinical practice? Do you see it landing there?

Yeah, I'm seeing these in phase four studies especially after commercialization. So it's something that is important to say — a new drug that does these studies uh adds something new for our practice. So I think it's important to say uh another thing that is important I think every uh rheumatologist that has residents around the world needs to bring this new information to them to try to put this new RALIA into reality into our clinics into our RA patients. It's interesting to say that uh we know we have a lot of patients that have this pain that is not related to RA and we go to another TNF inhibitor and we go to another JAK inhibitor thinking oh this is RA that is uh that is active this is RA that the patient has some inflammatory state so it is to say that we have these two ways — into phase four studies into real world evidence and in our everyday uh practice in rheumatology and of course our residents need to know. I think it's something that ACR 2026 brings to them that we need to share around the world.

Yeah. And at the moment I suspect this stuff is captured in GDA but actually to try and standardize and maybe capture in studies. I like your bring RALIA into reality kind of uh catch cry there. There's something for us to kind of work at.

Um I'm going to briefly mention um one thing that caught my attention today and then we'll go around and get people's hot takes on some quick hits. Um I you know there's been a bit of discussion about — I don't know maybe generated all by me but others as well — about generic tofacitinib now available in the US been available in Canada for a while been available in India for a long time uh coming to a jurisdiction near you if you weren't already mentioned. So what do you use it for? Well, I think one thing that I've been hyping on for a while about, but I think uh is fairly clear a use case is in a newly diagnosed PMR. Um a while back we saw the EAST-PMR study from Hzo in China small um uh randomized control trial um I guess a 2A trial of about 30 patients in uh each arm which showed that basically it was steroids versus tofacitinib and they did exactly um had exactly the same outcomes. So tofacitinib replaced steroids.

Um so what we saw is essentially the follow on I guess a 2B — maybe you might say probably uh 2B — it's open label RCT N equals 104 from the same group um four-week steroid taper in the tofacitinib arm so just kind of get that little bit up front get get on control quickly and you know if anything the tofacitinib — I mean they're they're um they perform just the same as each other. If anything, the trend was that the tofacitinib arm did better than steroids. I think um if you had to ask me one place where um some uh some cheap tofacitinib might do a lot of good, I feel like that might be the place.

All right, let's go around the table again. And sorry, Bella, unless you wanted to kind of make comments. No, no, I was I thought you'd talk about JAKs and you know there was this propensity matched study that they talked about how MACE events are not as common. So sort of you know harping on the same thing that we've been talking about for the past year or so. Uh but there's more and more data that we can use it if it's cheap and available use it.

Yeah. I agree because there have also been um some abstracts on JAK inhibitors like um the FAST-LANE study um it's used in early axSpA and there was um although uh I think it's a it's a study also by um Dr. Marina Magri on the MACE events. Um but they did see that uh patients on JAK inhibitors — um these are PsA patients who were um treated with either JAK inhibitors or your other TNF uh biologics and IL-17s and um the risk for MACE and VTE were still higher in those patients treated with JAK inhibitors. I guess we really have to strike the balance and stratify patients who will really benefit from giving JAK. Yeah, these are the questions we can ask now.

All right, let's quickly go around the uh the table. Tell me what you — a quick couple of lines on what you liked. Um Bella, what did — what what else? So there was this again going on the same theme of like um pain um there was an OA pain abstract 1569 uh talking about you know all these patients with knee osteoarthritis have pains from four to eight uh pain scales and you know we think this is all coming from the knee or the joint that we're talking about but there's a lot of — at least 80% of these patients either had depression uh fibromyalgia or some sort of central pain sensitization I mean sort of going on the same theme that you're not treating one joint and one tissue in one joint. This is an overall patient. There's many many mechanisms to uh pain. Uh so I I don't know for me as a clinician we need to make sure that we are thinking about a lot more than just one thing. Yeah absolutely.

Uh Sheila. Yeah. So I found um the abstract 2227. So it's about um unsupervised glucocorticoid dose adjustment in SLE. So I really found it just interesting because um I have patients who dose adjust by themselves and so that um this is based on a survey the LOOP — uh it's the lupus survey LUPUS and um they found that at least 30% of those um who answered the survey reported independent modification of um glucocorticoid doses and so I think it's the same um it's the same setting or it's the same environment across um the world like um patients uh feel empowered they become — or it's the perceived self-confidence of them being able to address their disease. Um just the takeaway message of you know um as rheumatologists we really need to educate our patients start that conversation continue that conversation of yes we want to empower them but we want to empower them correctly and safely.

Yeah, I think if you think that your um patients aren't um self adjusting uh — you don't have any patients self-adjusting steroids — you're probably either too intimidating to tell the truth to or you're not asking the right questions.

Brian, what what what did you like out there? That's well said. Um yeah, I was uh impressed about the results from um the BE BOLD study. They presented this at the plenary today. So, this was um results through 24 weeks, the head-to-head, which like whenever we get a head-to-head trial, I am like over it. Um because we have options now and we're like, you know, privileged enough to say that, but then you want to know like what is our order of operations, what should we be starting with, you know, what's better for what folks. So, this is uh bimekizumab um is IL-17A and F versus risankizumab which is IL-23. And the long and short of it is uh whether it's cut at week four uh week 16 or week 24 uh bimekizumab outperformed uh risankizumab in their primary outcome which was the ACR50 response. Um which I found quite impactful. Um I I think this is definitely practice informing. You're kind of hard-pressed if you have someone with severe joint disease in these results um to not follow along. Um so I I I was really impressed by this work.

Yeah. And I think it's one thing to cut it at week four when it's early and and bimekizumab might be kicking in more quickly, but 24 — when I think you you you'd expect risankizumab to be getting close to where it's going to land — it is very impressive data.

Henrik. Yeah. I think that — I think we're getting some issues with the connection. Another another study I'm going to talk about the abstract 2673 uh from the LEEDS cohort. I think it's all right. I think — are you hearing me? Henrik, you might want to turn — you might want to turn your camera off and then leave your audio on. Yeah, I I can hear you, but I think the connection's not great. Maybe we'll just uh — this is the problem with hotel room Wi-Fi in a place like Orlando. It's tough. Oh, just try again. I just try one more time. Oh, are you hearing me right? Yeah, go ahead. Video. Yeah. Final. Oh, it's the hotel here. It's the Hilton Hotel. Oh.

So, I'm going to talk about another abstract that was presented at the plenary. It's the abstract 2673. It was made by the LEEDS cohort. Uh they bring a curiosity. They bring new information for us that is different from one thing that we always thought was real. What they bring to us? They bring information that arthralgia is worse than arthritis in patients with use of uh immune checkpoint inhibitors because we thought patients with arthritis are having more trouble or have more inflammation. They have even a worse prognosis but it's not true. Patients with arthralgia had worse prognosis than patients with arthritis.

This is something that — we can think that these patients with arthralgia and not arthritis are having less effect of use of immune checkpoint inhibitors or these patients have pain because of other things. All these patients have more advanced cancer with metastasis that brings more pain. So it's different. It's new information that when we see a patient with arthralgia don't think that it's nothing. This patient can have a worse prognosis than patients with arthritis. When we see arthritis it is easy. We see a swollen joint. We see an ultrasound with inflammation. But remember the patient with arthralgia — they had the worst prognosis in the LEEDS cohort.

Yeah. And I think the uh you know it's obviously someone whose era this is. I think um two things. I think in these checkpoint inhibitor treated patients uh inevitably the thing that's more likely to kill you is is by far the cancer not the the arthritis and that — I guess even though it's slightly controversial still I think the um all the suggestions are that maybe having an irAE uh like inflammatory arthritis probably does portend a better — you're getting a better inflammatory response attacking the cancer so maybe that does give better survival so interesting to break it down like that um always good to see that data from LEEDS.

Thank you team. It's been great having this conversation uh near the tail end of a very long meeting. Um but for those of you still here tomorrow, um I always feel like the best stuff is saved for last. I love the late breakings and we're going to have fun tomorrow. But to the four of you here, thank you so much. Thank you, Bella, Sheila, Brian, Henrik, and thank you everyone out there. Have a great night. Awesome. Thank you.