ACR 2025 PsA Topic Podcasts Compilation 2 Save

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

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Hey everyone, I'm Brian Jaros and I'm coming to you live from ACR 2025. Today I'll be talking to you about Abstract seventeen-thirteen. This was a group that looked at delayed diagnosis in psoriatic arthritis and how that affected patients' imaging outcomes. As we all know as rheumatologists, it's never easy to diagnose our patients. They present in a lot of different ways and it's always keeping us on our toes with a high level of suspicion, in order to make the correct diagnosis and get our patients started on treatments.

Psoriatic arthritis is no stranger to this compared to something like rheumatoid arthritis which has biomarkers that can aid in our diagnostic armamentarium, psoriatic arthritis may require a higher level of clinical suspicion in order to make that diagnosis. And of course there's concerns that if we're not making the correct diagnosis efficiently enough patients of course are suffering from a clinical standpoint and there's also been concern from a radiographic standpoint that patients may accrue damage over time that we'll have trouble reversing. This has been shown in other disease states like spondyloarthritis and this group wanted to explore this question in psoriatic arthritis specifically. So they searched, the PubMed and other research databases for any observational study of psoriatic arthritis that included the terms diagnostic delay and performed a meta analysis ultimately capturing 15 studies, that were included in this analysis. Patients had to be diagnosed with psoriatic arthritis based on either Caspar criteria or a physician determined diagnosis and ultimately throughout these 15 studies that were included they captured a population of over twenty two thousand psoriatic arthritis patients.

Now when we get to the actual results this is pretty interesting the pooled mean diagnostic delay of these patients was nearly thirty one months So that's patients taking over two and a half years on average to get a diagnosis when all of these studies were looked at. And we can imagine just from a patient perspective how challenging that must be to be searching for a diagnosis for all of that time. They actually stratified by country of study, and so we saw actually quite a big range geographically where rates varied from being lowest reported in India with a mean of about six and a half months, then increasing for The US, The Netherlands, Singapore to around one year, and then highest reported rates, of diagnostic delay from Spain at forty eight months, China at fifty months, and Italy at sixty two months. Of course, this may partially owe to the timing of the studies, the different ways diagnosis was determined in each study, and the specific methodology, but I think the takeaway here is that we're seeing a vastly different range of diagnostic time when looking at different studies around the globe. They also didn't just look at diagnostic delay, but also referral delays finding that it took a long time for patients to even get to rheumatology.

The mean being either fifteen or twenty one months depending on the specific statistical analysis used. So it's taking these patients a long time to see rheumatology to get a diagnosis. How does that affect their outcomes? When they looked at radiographic changes or damage they saw that delays were associated with an odds ratio of either two point eight or two point five depending on which effect model was used but the takeaway being that these diagnostic delays were associated with increased odds of a patient presenting with radiographic damage by the time they got their diagnosis. So overall, I think this is a really important takeaway for us as a rheumatology community to keep our eyes vigilant for these patients, to keep educating, other specialties, dermatology, primary care physicians, get them into our clinics more quickly, to decrease that referral delay, and then increase our clinical suspicion to decrease that diagnostic delay.

Certainly we also need better biomarkers, better tools to diagnose psoriatic arthritis, if the diagnostic time is taking this long as well. So that's what I have for today. I'll be signing off, and I'll see you tomorrow. Bye.

Hi. Welcome, everyone. It's, doctor Janet Pope. I'm tweeting for AtRoomNow at ACR twenty twenty five in Chicago. I want to talk about head to head or for us joint to joint or even toe to toe.

I wanted to talk about two comparative, head to head RCTs that are late breaking abstracts. The first is l b zero nine. This is the question that is always on our mind. A patient has axial SpA, so what we think of as ankylosing spondylitis, and they are TNF inadequate responders. Most in general are a secondary loss of effect.

Now what's going what are we going to use next? It's a great clinical question. So this was an RCT randomizing patients to the next TNF inhibitor or an IL seventeen inhibitor. So the bottom line is it doesn't really matter. There was no superiority.

They could both do well. So I think the take home on this head to head is if your patient isn't doing well enough on a TNF inhibitor, an Axiospot, you can try another TNF inhibitor, a second line advanced therapy, or you could go to an I o seventeen. No superiority. What about the next one? I've got a patient with psoriatic arthritis, and they've been TNF, inhibitor exposed.

This was a randomized controlled trial of moving on out of class. Psoriatic arthritis, TNF exposed. Now they are randomized to secukinumab, so an IL seventeen a inhibitor, or eusukinumab, an IL twelve twenty three inhibitor. So it's a big question to know because the derms in general seem to like, IL, 20 threes, but also IL twelve twenty threes on skin and IL seventeens do very well on skin as well. The winner is, drum roll please, Cosentyx.

Why? It was both an ACR 50 and a PASI score superiority. I think the other questions would be, what if I tried a different IL seventeen? What if I tried just an IL twenty three inhibitor as opposed to a twelve twenty three? However, superiority with clinically relevant differences in tender and swollen joint counts as well as I as I mentioned the ACR 50 and the PASI score.

So bottom line is head to head trials in real world situations really do help me to choose the next treatment for my patients with seronegative, various types of, seronegative arthritis. Thank you. Please follow me at Janet Bourdeaux. Thank you.

Hi. It's doctor Artie Cavanagh, University of California, San Diego here at the ACR twenty twenty five convergence in Chicago. So a lot of things happening across fields, lot of things happening in psoriatic arthritis, and that's what I wanted to talk about a little bit this morning. One of the really exciting aspects is novel approaches to therapy. Now we have many mechanisms of action.

We've had the biologic agents, the TNF inhibitors are fantastic, then we have the twelve twenty three inhibitor. Now we have IL-seventeen inhibitors, and we have several of them and more to come. We've had the IL-twenty three inhibitors, and then the JAK inhibitors, and a lot of things that are in development, and the PDE4 inhibitors. Now, we also have some conventional synthetic DMARDs, which I mentioned partly because the older medicines, methotrexate, the sulfasalazine, leflunomide, the cyclosporine, they're oral, and the route of administration is something that affects patient choice of therapy. Some of the newer medications, the eupremelasto PD-four inhibitor, the jackanips, the tofacitinib and the upadacitinib, they're oral as well, But I think an exciting new approach is that we're starting to see some development in oral versions of the same mechanisms of action that we're used to seeing in parenteral, in subcutaneous or intravenous medications.

So there are a number of those that are in development. Now, sometimes happens in psoriatic arthritis or colleagues in psoriasis are ahead of us. They get to see these new therapies first, and there have been several that have been tried in psoriasis and show promise. There's an inhibitor of tumor necrosis factor, and it blocks binding through receptor. We know that the TNF inhibitors really change the whole approach to psoriatic arthritis and psoriasis, so is it possible to get that in a pill?

Most recently, IL-twenty three inhibitor, iCotrokinra, has been looked at. Interesting data in skin psoriasis. Mechanistically, it looks as if it may well be IL-twenty three inhibitor. One of the things we see when we have newer versions of medicines for which we already know the mechanism of action for the TNF inhibitor, when the fourth and fifth TNF inhibitors came along, we kind of treated them as, well, we know what to expect from this class of therapy. With these oral agents, that's going to be a question.

Are they really just oral versions of the parenteral medications? I think we would think that, and we would hope that, but of course we have to see. It's just absolutely fascinating. We had thought for many years as fantastic as the parenteral medications were. They were proteins, and protein's not really susceptible to oral therapy because their body treats them like food and digests them, but with progress in the pharmaceutical technology, now able to have inhibitors that are oral.

It's interesting. It raises some issues for discussion. If something is oral and you have to, say, wait a while when you first get up in the morning, if you take a pill then you can't have any food, Things we've been used to, if you think of it, with the bisphosphonates for osteoporosis. You absorb very, very little of each individual pill, so you really can't take it with things that have calcium because you'll go right through. You won't absorb any of it.

These medicines might have some of those same considerations. What time of day do you have to take it? What are the rules as far as what else you can take? And with oral medicines, we know the other condition or the other factor that we consider is the frequency. If something once a day, that gives much better compliance.

If it's twice a day, you lose a little bit. The kind of issues that we've thought about when thinking about oral medications for the conventional synthetic DMARDs, for the JAK inhibitors and the PDE4 inhibitor, now we may be on the verge of having oral versions of our other biologic agents. Of course, another aspect of this is, does that lend itself better, perhaps, to combination therapy, to induction, and then consolidation approaches to therapy? So, a lot of interesting things that will be coming. So, a lot of new information here, a lot of excitement, a lot of buzz at the ACR twenty twenty five convergence, and the best place to keep up with that is RheumNow.

This is doctor Arty Kavanaugh. Thanks for watching.