EULAR 2025 - Day 2 podcast Save

You're listening to a RheumNow podcast coming to you from Barcelona, Spain, and EULAR twenty twenty five. Hope you enjoy it.

This coverage is sponsored by Johnson and Johnson, the organization that believes health is everything.

Hello. It's doctor Janet Pope reporting at EULAR twenty twenty five in beautiful Barcelona, Spain. I tweet for RheumNow, and my handle is at JanetBurdope, so I hope you'll be following the meeting. It was off to a great start, Euler was, and I'm going to talk about some seronegative arthritis breakthroughs. So there were three areas that I thought were kind of novel.

The first one was using bite cells for the treatment of axial spondyloarthritis. So to remind you, bite cells are bispecific T cell engaging antibodies. And they've been looked at at least theoretically and with a little bit of data, particularly in lupus, little bit and difficult to treat other more seropositive autoimmune diseases and connective tissue diseases. So I looked at this poster, it was on the poster discussion and I was really intrigued. Why?

This was a BiTE or a bispecific T cell engager targeting this area called TRBV9 positive autoreactive T cells. So why would they ever pick this? Well this was an off the shelf bite cell or T cell engager that was actually in an area where HLA B27, particularly HLA B2705 binds. So it would stop this autoantigen problem from happening. Now this came out of Hopkins.

It was in poster board B33. And it's too early to know if something like this will work, but I thought it was really interesting and something I hadn't thought about. Okay. What's the next cool technology? So I looked at an oral TYK2.

Now we already have one for psoriasis and PSA to be approved in some jurisdictions already approved, do cravasidenib. So this was called Zazosidenib, and their claim to fame as needing another tick to was that they might be able to fully spare Jack, which Duker does, but also they're in late stage development in psoriasis. And what they looked at was that the clinical doses of this molecule, the oral TYK2, Zazo, I'll call it, that they found high inhibition of TYK2 and it didn't affect the other JAK pathway. So it was a pure TYK2. There was no one, two, or three JAK changes.

And they compared it to ducravacitinib, and what they found was a far higher maintenance of inhibition. So is this going to be better, same, or worse? First of all, no head to head trials. This is an early pharmacokinetics, pharmacodynamics of how this mechanism of action might be different than DUCRA, but time will tell if it pans out clinically to see if it has a different benefit and or a different safety effect than ducravisindib. So this is poster 15.

The last sort of cool thing was another novel antibody. And this is novel because this thing called ORKA slash zero zero two. So I'm going to call it Orca but it's not a whale. It's ORKA. This is a novel platform technology that when we think of the monoclonal antibodies, the ends of the monoclonal antibodies have been changed to change the signaling.

So what there is is technology of homo and heterodimer signaling, and this monoclonal change at the tips of the antibodies will make it stay in the system longer. And you could say, well, what's the advantage of that? Well, what they've done is they've put in an IL-17AF inhibitor. So as you know, we have bimekizumab as one of the inhibitors that's already on the market. So they used an IL-17AF inhibitor and they found that they could probably or possibly dose this monoclonal antibody with the neat technology, the ORCA-two technology in the platform.

They could dose it once every, listen to this, six to twelve months. And this is poster 16. So again, would this be able to really help adherence, would have a long term effect? Well, all of us in rheumatology, we know another mechanism that will prolong an antibody and that's pegylation. And pegylation would be an idea like circlizumab pegol or as we know it as Cynzia that prolongs it in the circulation and you get less anti drug antibodies.

We know another PEG, PEG uricase, that's highly antigenic, prolongs in the circulation, but you get a lot of antibodies to the PEG. So I think this pathway and platform is really cool. All of these things I've talked about today might not be ready for prime time, but I think will help my patients with seronegative diseases. See you at the next blog and RheumNow presentation. Thank you.

Hi guys, this is Oily Naj from Glasgow reporting live from Barcelona on day one of EULAR twenty twenty five. I saw a lot of really exciting science today, and there's one poster in particular that really caught my attention because it was about a topic that we just really never talk about with our patients, at least I don't, but I will after this. And it also comes together really well with this old saying that a laughter day keeps the doctor away. So in Poster six eighty five, Suzuki and colleagues looked into laughter in rheumatoid arthritis. So they're not new to the topic because in 2024, they did publish a paper that was looking at the association between laughter, frailty ty and depression in rheumatoid arthritis.

And they found out that people that had more frailty, higher frailty scores and higher depression scores had less frequency of laughter. And it was a cohort of about 200 people and they wanted to increase the number and correlate laughter frequency with a lot more patient reported outcomes. So that's what they did in this study. So they interrogated over six seventy patients and they classified them in four different groups. So the first group was people who laugh almost every day, people who laugh one to five days a week, people who laugh more than one to three days a week and people who never or almost never laugh.

And it also made me wonder what category do I belong to? But I'm gonna let you guys guess that. So when they looked into correlating patient reported outcomes, in particular, HACTI, social fraternity scores and this is activity, they found out that the people, there was definitely an association between social fraternity and physical function. And in particular, people who had less frequent laughter had higher HACDI and higher social fratty scores, but there was no association with this activity. And in their conclusion, the authors suggest that future research should assess the impact of laughter focused interventions.

And I'm not sure what these would be, but it also is something that I wish I could have asked the authors, but I didn't find them at their poster. But certainly it would be really interesting to know if that could improve health outcomes in RA. With this, I am going to invite you to follow RheumNow on eggs for more content and follow me orliromo, and I see you guys around. Hi, everyone. This is Aureli Najme reporting for RheumNow in sunny Barcelona, day one of the conference.

A lot of very exciting content and science. And there's one abstract that particularly caught my attention today amongst many really, that looked into a different way to assess methotrexate adherence and what it means for people living with rheumatoid arthritis who maybe stopped their methotrexate when they started biologics. So it was posted from a team from Manchester, poster five sixty three. And we know very well from the points to consider for treatment in rheumatoid that were updated in 2023, that it's recommended by EULA for people starting biologic to remain on a conventional synthetic tumor, in particular methotrexate, pretty much regardless of the biologic, and we could discuss that, but that's not the point. They also recommend for the methotrexate dose to be reduced to ten milligrams a week because we know it improves the outcome and potentially immunogenicity.

But in a lot of studies, we look for methotrexate adherence, this is self reported adherence, which is prone to measurement bias. So they came up with this alternative way to measure extrinsic adherence. And I'm gonna have to read my notes here because this is very complex. This is high sensitivity liquid chromatography tandem mass spectrometry, LC MSMS. And that's a very objective way of measuring.

It looks for composites from the drug after it's metabolized. And so in their cohort of two fifty patients, they looked into whether the adherence measured by this objective method was dropping after starting in biologic. And it does drop from ninety one percent to eighty one percent when people start biologic drug. So that's six months after starting the biologic. The two things here I wanted to say is that first of all, ninety one percent is really good.

And so it's telling you that it's definitely a selected population that is willing to participate to research. And so it's kind of biased there because I'm pretty sure if we were to do that same measurement objectively into the standard of care, secondary care population would probably have lower rates. The other thing they looked into was whether this drop in adherence was associated with a less likelihood of reaching EULA response, at least if it was associated with EULA response or reaching EULA remission. And no there particular association. However, there was a trend towards an improved change in DAS 28, but the numbers probably made it mean, at least it wasn't significant statistically.

There was no information as to whether this was associated with specific drugs in particular as opposed to other, But I think it's quite interesting. Obviously this is not something I'm gonna use in clinical practice. I don't think it's ready yet. And we wouldn't use mass spec in clinical practice every day anyways, but I think it just brings a different perspective on endurance and this is certainly something to reflect on. So that was it for me today.

I invite you to follow RheumNow for more content and to follow me also on X AureliRomo. See you later.

Hi, everyone. My name is Jieha Li, and it's my pleasure to highlight an abstract from EULAR twenty twenty five, which kicked off today here in beautiful Spain, Barcelona. Today's abstract is one I found personally meaningful, but I think it's both inspiring and important for the rheumatology community as well, because we're caring for an increasingly aging population. The abstract I'm going to discuss is POS0627. It is titled Examination of Clinical Outcomes by Treatment Duration of Biologics and JAK Inhibitors in Non Agenarian Rheumatoid Arthritis.

It is by authors Koukatayama and Hiroshi Ito from Japan. So the study examines RA outcomes in non Asian areas. And I have to admit, even as someone who specializes in geriatric rheumatology, I had to double check and look up what this word meant. And it actually refers to people aged 90 years and older. Now, this is a different concept than how we think about older adults in The US.

Typically, would categorize them as younger old between 65 and 74, middle olds between 75 and 84, or oldest old being more than 85. So the patients in this study, they're at the very top of the aging spectrum and they're the oldest of the oldest. And that's one of the things that makes this study very powerful and rare, because a systematic review by Palmosky and all showed that the average age of participants in RA studies is actually in the mid-50s. And actually about 30% of the studies exclude older adults just purely based on this age. And this pattern is seen also in observation and population based study.

What that means is there's a real gap in our knowledge of how best to treat for older adults with RA, even though this population are growing and older adults continue to be newly diagnosed with elderly onset or now better known as late onset RA. So a study like this that looks at real world outcomes in people over the age of 90, it's not only rare, it's essential. So let's take a closer look. So this was a single center study out of Japan, and it included sixty six patients who were all currently in their 90s and were receiving treatment for the past two years. And this center took care of more than 3,000 patients and out of sixty six were over the age of 90.

They were divided into two groups. Group A, it included twenty five patients who developed RA after on or after the age of 84. So on average, they're about 88 at the time of diagnosis. And at the time of study enrollment, they had an average age of 92 and were on treatment for about four years. In comparison, Group B, it included forty one patients who developed RA earlier than 84.

So their average age at diagnosis was 76, at time of enrollment, similarly 92, and obviously they've been on treatment for a longer period of time for about sixteen years. And here's where it gets really interesting. The rate of use of biologic and JAK inhibitor was remarkably high. In group A, the older group, about just over half, so fifty six percent received advanced therapies with biologic or JAK inhibitors within six months of diagnosis. And in group B, just under fifty, forty six percent received biologics or JAK inhibitors.

But there was a little bit of a delay from the time of diagnosis, on average about seventy years, understandably because they were in their mid-70s when they were diagnosed and had probably less comorbidities and could tolerate step up therapy or had time for it. But just to put this in perspective, in The US on a Medicare based study, less than thirty percent of older adults diagnosed with late onset RA after the age of 65 are put on any treatment within the first year. And the rate of biologic use is less than ten percent. So the fact that the Japanese are more experienced and prescribing these treatment, I think is really remarkable. Moving on to the outcome.

So, importantly, clinical disease activity measures improved in both groups. But what this study adds is they absolutely also looked at functional outcomes, which is really important for older adults. So Group A, the older group, the walking independence improved by about twenty percent from sixty four to seventy three percent. And that rate was similar regardless whether it was treated with biologics or non biologics. Now, what was a little bit perplexing to me when I was looking at this study in Group B, the younger old, the walking function actually declined.

But it's important to note that they had a higher functional independence at the beginning of baseline. So for group A, the older older baseline was about 55 to 64. For the older old, it was 64 to 95. So there was very little room for improvement. And it may have been having had disease for a longer period of time, more tolerant, they were more active.

And therefore, if anything, we were seeing declines. The decline actually was coming from higher rates of fracture in this group. And I think we'll see this in the manuscript, but likely more related to their social structures or their activity levels. But again, importantly, they looked at functional outcomes in addition to clinical outcomes and both improved. So yes, adverse events occurred, also including infections and malignancy and age can be an independent predictor.

But the overall takeaway is clear that with careful monitoring treatment is both feasible and beneficial, even at an advanced age into the patient's 90s. So, my message and the conclusion that I took away from this is that this study makes a compelling case for why older adults should and need to be included in clinical studies. We need data to inform our guidelines and that when we have guidelines to assure that we actually implement them in this growing population of older adults with RA. So non agentarians is a new word I picked up today. They not only tolerated biologics and JAK inhibitors, but they benefited from this.

So let's move beyond age based assumptions and commit to treating older adults with the same rigor and respect we give every patient. Thoughtful, effective RA care should be guided by need and not age. Thank you for watching. This is Jeehali reporting for RheumNow from Barcelona, San Diego, Spain, and there will be more highlights from EULAR twenty twenty five. Thank you.

Hi, everyone. This is Adela Castro from Memphis, Tennessee reporting from Barcelona, and I am going to present the abstract OP0096, which is sonilocumab in psoriatic arthritis. What is very interesting about this medication is that it's a novel IL-17A and IL-17F blocker but it's actually a nanobody which makes it different to the previous one already we are using. And this was studied in patients with psoriatic arthritis. This is a phase two study, so the population that's been studied is a little bit smaller, so only like forty two patients.

In this study, it shows that the patients with both doses, sixty milligrams and one hundred and twenty milligrams with induction, achieved its primary endpoint at week twelve. And they also achieved significantly higher rates of ACR 50 compared to placebo. And it was also noticed that this effect was sustained all the way through week twenty four. It was also very interesting that the proportion of patients achieving important outcomes like minimal disease activity as well as other important outcomes that we like to see in patients with psoriatic arthritis. Something that is interesting about this molecule is nanobody technology seems to enhance efficacy given the smaller molecular weight, and it can also seems to be better kind of like penetrating tissues.

So for more information, please stay tuned at RheumNow.

Hi, this is Eric Ruterman from Northwestern University in Chicago, and I'm coming to you from the EULAR meeting in Barcelona for RheumNow. I've been looking at, a lot of the abstracts on psoriatic arthritis at this meeting. And one interesting thing that I've seen have been some abstracts really looking in detail at using combinations of DMARDs to treat psoriatic arthritis. The abstracts in particular are, OP0093, OP0106, a poster, poster 106. What these are looking at is the idea of using combinations of a conventional DMARDs rather than going to a biologic in order to get control of disease.

It's not something we do a lot in The US, but I think in other parts of the world, either because of availability of drugs, or because of, their healthcare system that requires, use of conventional DMARDs before going to a biologic. It's an issue that's come up a lot. A couple of papers have come out of, The UK looking at, an early inception cohort of psoriatic arthritis, and looking at their treatment. They pulled out in one of those patients who were treated on two different DMARDs before going to biologic. And while on the one hand, it suggested that those patients did not always respond to DMARDs and many ended up on a biologic, it really is sort of a glass half full glass half empty proposition, because about fifty percent of the patients on a combination of methotrexate and sulfasalazine, or methotrexate and leflunomide did well enough that they needed didn't need to take a biologic.

I don't know that it's something we routinely do in The US, but it's certainly something that's a possibility and it certainly raises the question about whether we really need to move straight to a biologic. The dermatologists often do that, because of the control of skin disease. But for joint disease, we may do okay with combination therapy. One of the abstracts here actually came from a Dutch study that looked at combining methotrexate and leflunomide. And they had presented that study previously, but at this meeting they talked about some of the longer term data.

And again, many of the patients did well, but about fifty percent of them had to go on to a biologic. And interestingly, it was the glass half full glass half empty proposition, because their conclusion was that that wasn't all that successful. So I think it depends on how you look at it. But in my mind, people switch off of biologics all the time. So patients who, do well 50% of the time, that's not a bad track record.

And, I think in many cases, it may be worth at least thinking about combining DMARC and not going straight to a biologic, certainly for cost reasons that makes sense. You know, it's challenging these days, certainly in The US, when biologics are more available and patients want to go straight to the target. So that may be a difficult proposition to persuade them as we talk to them about it, but certainly worth thinking about. Anyhow, that's one of the issues I'm seeing here at the meeting at EULAR in Barcelona. And again, this is Eric Ruderman coming to you from RheumNow.

This coverage was brought to you by our ULAAR sponsor, Johnson and Johnson. Check out their new data this week on the first and only IL-twenty three inhibitor proven to significantly inhibit progression of joint structural damage in active psoriatic arthritis by visiting RheumNow's virtual poster hall at rheumnow.com.