ACR 2025 PsA Topic Podcasts Compilation 5 Save

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

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Hello, my name is Atul Devdar. I'm a professor of medicine at Oregon Health and Science University in Portland, Oregon. My research interest is in spondyloarthritis and psoriatic arthritis. And today, I'm joined here by Doctor. Mohammad Bittar, who is also an assistant professor at Oregon Health and Science University.

Doctor. Bittar's research is very novel, and this is a big trend that actually I'm noticing in this particular conference as well and that's why I thought I will bring him here to discuss his research but just in short what we are finding is that nowadays in inflammatory arthritis, axial spondyloarthritis included, the morbidity is not because of the inflammation. We are pretty good at controlling the inflammation of our patients with our biologics. Leftover pain, leftover pain, leftover fatigue is the reason why people are becoming disabled. And so Doctor.

Bittar has some very novel research ideas. He had a poster here. He also was chairing a session on this particular entity of leftover pain. So Doctor. Bittar, take it from here.

Tell us a little bit more about this leftover pain and how can we measure it and what can we do about it?

Thank you so much for having me and this is an extremely important topic that has been neglected in rheumatology. As you mentioned, we always focus on treating inflammation, inflammation, but we forget about the leftover pain, which is driving the patient's disability and the symptom and the burden of the disease, and that's why it's time for us to focus on studying pain and rheumatic diseases. So I'm very happy to share that in this conference at the ACR we've seen a lot of new work on pain in rheumatic diseases, whether in rheumatoid arthritis, in psoriatic arthritis, and of course in axospondyloarthritis, our research interest. I can talk to you a little bit about the project that we've done is where we are trying to look into the brain imaging and the CNS, central nervous system, dysregulation in patients who have axial spondyloarthritis because this can explain why patients continue to have chronic pain without having inflammation. So in particular we're interesting at looking the resting state connectivity on how different parts in the brain connect to each other and also how the brain responds to a painful stimulus.

So for example, the project that we've done on axSpA patients that showed that axSpA patients respond differently to a painful stimuli compared to healthy controls. For example, mainly we got two signals from the default mode network and the salience network. Default mode network, it's usually is active when we are in a relaxed state. Whenever we get an input or an insult, this should be inactivated. Our study showed that in patients who have AXPA, actually default mode network got activated, which is abnormal.

That means patients are focusing on the brain, is focusing on pain, that's why they go into a chronic pain state. Also the salience network, it got exaggerated responses in Salience the network. And axSpA compared to healthy controls. So we got signals that different parts of the brain are working differently in axSpA patients who have chronic pain.

Yeah. So there were some abstracts yesterday, and you were chairing that one session, where some similar work has been done also in rheumatoid arthritis and in psoriatic arthritis. Do you want to tell us about that?

Definitely. And there was a very interesting oral abstract that was presenting yesterday on rheumatoid arthritis where patients had, I believe it was twenty seven patients who had functional imaging of the brain, and a task was an input or a painful stimulus was done on rheumatoid patients and the rest and it showed activity in the insula and the brain which is part of the salience network. Similarly, there is another session on psoriatic arthritis but this was mainly on fatigue and that showed that Insulet played a role in it. So we are seeing a different mechanism that are non inflammatory playing a role in rheumatoid and PSA and axSpA. So we need to start looking at these pathways.

Yeah,

This is going forward. We are going to be looking at more and more research as well as abstracts at annual meetings. And and we will hopefully one day find the differences of how the brain works with nociceptive, and nocplastic and neuropathic. Those are the three different different types of pain, which parts of the brain get activated, and how we can intervene to prevent this. I think this is something that I would suggest, the viewers should be aware of and keep an eye on.

This is a very exciting new area in the field of rheumatology.

Hi, welcome to day one at the ACR. So excited to be here. I've been assigned, the area of psoriatic arthritis and I decided to think about the themes of some specialized biomarkers. I wanted to go over one of the first abstracts. My name is Elaine Husney, and really glad to be here at RheumNow talking about specialized biomarkers and PSA.

I have abstract five twenty nine, which I thought was really interesting today, that is called the anti peptidyl arginine deaminase two or anti PAD two autoantibodies in psoriatic arthritis. So for this particular abstract, why I thought it was interesting, it was looking at a very specialized autoantigen in psoriatic arthritis. And what they did was take a look at a cohort of psoriatic arthritis patients that fulfilled a criteria, a Casper criteria, and interestingly they found in this specialized cohort, they had about forty four out of one hundred and twenty four patients with some interesting biomarker assay. So they discovered that PAD two auto antibodies that are found in psoriatic arthritis, that twenty nine percent were positive for this anti PAD two. And what was more interesting is that these were associated more with patients with active joint disease as opposed to active skin disease and the clinical significance of this is that the anti PAD2 may be a biomarker for us that can possibly distinguish specific phenotypes within psoriatic arthritis.

Hi. Welcome, everyone. It's doctor Janet Pope. I'm here tweeting at our lovely RheumNow booth. I'm at ACR twenty twenty five in Chicago.

I just attended a session that was on secrets and pearls in rheumatology, and I wanted to just tell you a few that I actually learned at this session. So the first one is if you're working up a patient, say she has inflammatory arthritis, she's RF and CCP negative. Obviously, we know to look at nails. We know to look at the scalp and at the back of the neck, the nape of the neck for psoriasis. But something I learned was that if you look basically at the IP of the toe, not m t not first MTP.

It's not crystal. IP of the toe commonly involved in early, axial Spall with peripheral arthritis or early PSA. So that's a good take home for me. And I think for trainees listening, always examine the feet and and all our patients and, in particular, seronegative patients. K.

The next thing is that patients with PSA often report SICA, dry eyes, dry mouth. I'm not sure why that is. I had noticed it in my practice, but I'd never really formalized it. So if they're reporting SICA, I'm not necessarily going to do an anti Roe or LAW antibody unless if I think they're an overlap. What's the next thing?

This was one that a tip that I didn't know about at all. Patients that present with POTS could be having autoimmune neuro neuropathy problems, but that could be a first presentation of Sjogren's disease. So when you're working up someone with POTS, as we are seeing them sometimes in rheumatology clinics, don't forget to do ANA. And if ANA is positive, think of ENA. And if ANA is negative, you can still think of doing the ROH antibody.

The next thing is IgA vasculitis. If you have an older person presenting with IgA vasculitis, don't just think about HSP, hemoxylamine purpura. It might be cancer associated. So I think the take home from this session is that if we really think about the history and the physical, then it really can help us in understanding what the patient might have, and these little secrets and pearls can give us clues to what's going on. Thank you, and please follow me at Janet Burdope.

Hi, everyone. Presenter Peter Nash reporting for RheumNow from ACR Convergence in Chicago. This is gonna be an overview of the PSA axSpA abstracts that I found interesting. There's not a lot of fantastically new stuff, so I'll just give you the bottom line from my point of view. There's a couple of papers on the difficult problem of patients with ongoing fibromyalgia type pain once you've got their inflammation under control And they showed in one paper from the Desirea cohort that if this is the case it interferes with the assessments of disease activity and the scores and the people most likely to get this kind of issue turn out to be females with enthesitis and there's a fibromyalgia rapid screening tool that they use.

Another abstract looked at whether upadacitinib and the JAKs seem to have a separate pain control element, whether upadacitinib could improve some of this fibromyalgia ness seen in this patient population and the answer was yes it can and this may be because of a peripheral effect on GM CSF and IL-six in the peripheral tissues to assist with pain control. I've always been concerned that what we call fibromyalgia when you can't find any inflammation, no joint swelling, normally SRCRP, these patients are prone to have a lot of enthesitis and we should examine some of these enthesial points and not write them off as having fibromyalgia and give them Pregabalin, amitriptyline, physiotherapy, and when some of them might respond to, adequate medication for their underlying inflammatory disease, upadacitinib was mentioned as an option. The other thing of interest was the oral twenty three inhibitor Icotrokinra worked very nicely in psoriasis. The psoriatic arthritis trials are underway. It worked very nicely compared to placebo.

The IGA was the primary endpoint and something like fifty seven percent response to six percent with placebo. And these were, a couple of the studies looked at different aspects. One of them looked at those difficult to treat areas like scalp, genitals, hands and feet. It worked very nicely for that and another abstract looked at biomarkers and showed that it very nicely turns off IL 17, IL 17 ANF, as well as nineteen and twenty two. There was a paper, following up the foremost APREMALA study, which really showed that early disease is less than four joints in over two thirds of the patients that you and I are going to see and that it stopped the progression from porcie to polyarthritis and the people who had the most risk of progressing were females, those who had no background standard of care when the trial started and those with a lot of emphasitis.

We've already mentioned a number of papers looking at the GLP-one agonists in reducing MACE in psoriatic arthritis, in reducing a lot of inflammatory rheumatic disease, lupus nephritis, etc. That's in a separate video. One of the questions very quickly asked from the gastro's is should you use NSAIDs in patients with inflammatory bowel disease? A paper looked at hospitalization rates and showed that if you use an NSAID, you're much more likely to be hospitalized, so it's not recommended. Another very nice paper from, Chris Richland looked further into the mouse model that he has and he injected it with sera from patients with PSA and lo and behold he could transfer the development of axial PSA and the development of classical changes in this mouse model from transferring blood and PBMCs from patients with disease to the mouse model.

What's in the serum and the PBMCs that can cause disease is the question that needs to be asked. These were bio naive patients who had their sera and PBMCs transferred. Very interesting, watch this space. There was a head to head, we need head to head, this one was against secukinumab versus ustekinumab in active PSA and lo and behold the secukinumab was superior for PASI, HAC, MDA and ACR responses when you compare the two head to head. There was a very intriguing paper and the meta analysis recently published by Matthew Brown that again is pushing the line that inhibiting IL A and F with bimekizumab reduced the rates of uveitis.

They're not going to do a separate uveitis study at this stage, but it's intriguing that blocking F can reduce the incidence of uveitis in these patient populations and they claim it's not selection bias being the third 17 to market, people not putting patients in who had a history of uveitis. They claim the background rates were normal but the rates on treatment compared to placebo were reduced with a seventeen inhibition if you block F. Is F important in the uveal tract? That I'm not so sure about but there needs to be some more work done in this area. There's another paper from the Accura group who have a IL-seventeen inhibitor that only needs to be given every six months and showed very good efficacy.

The question is if you do run into candidiasis issues, say esophageal rather than just nuisance mouth, or you run into the rare incidents of inflammatory bowel disease, new onset, if the drug hangs around for six months, is that going to be a problem? They also have an IL-twenty three inhibitor that lasts six months. That needs to be given once a year, sorry, twice a year. There are even talk of extending it to once a year by changing some of the amino acids. And the twenty threes have such a nice safety profile.

I think twice yearly or yearly injections really looks very exciting with, twenty three inhibition. Finally, there's an intriguing paper looking at axial PSA and the IL-twenty three inhibitor, risankizumab. Because up till now, the only flaw in the twenty three landscape is that it hasn't been able to show improvement in axial disease either axSpA or the axial element of PSA has never been studied. In this study, again it was a retrospective study, but they looked at patients, sorry it wasn't retrospective, was a study done in The US and Europe, that a couple of 100 people, two thirds of them had one third derm, two thirds rheumatologists, and the patients on risankizumab had less spinal pain, less morning stiffness, less night pain, less persistent low back pain, less sleep disturbance, but they had no validated ASAT ASAS outcome measures. However, these patients were aged about 45 as a mean, and they had very marked reduction in spinal type symptoms acknowledging that only ten to twenty percent, sorry, twenty to thirty percent of them had radiographically proven sacroiliitis but they got significant improvement numerically at least in their symptoms related to axial involvement.

Very intriguing because up till now the 20 three's haven't been able to show efficacy in the axial domain. The large guselkumab axial study is underway given they had a post hoc analysis of radiologically proved sacroiliitis and they showed benefit in that particular post hoc analysis. So another watch this space. Will the 20 three's work for axial? We're gonna wait and see.

So signing off. Thank you very much.