EULAR 2025 - Day 8 podcast Save

You're listening to a RheumNow podcast coming to you from Barcelona, Spain and ULAr twenty twenty five. Hope you enjoy it. Hello, everyone. Welcome to RheumNow's review of ankylosing spondylitis, the spondyloarthritis from EUR twenty twenty five in Barcelona. I'm here with the faculty that covered SPA and all its great presentations and posters.

Last week, we were all in Barcelona. We're all home, rested, and we've had time to reconsider what we heard and we're gonna present that to you today, our favorites from ULAr twenty twenty five. I'm Jack Cush in Dallas. I'm joined by Adela.

Hi, I'm Adela Castro from University of Tennessee, Memphis.

Youse? Hello, my name is Doctor. Youse Yousef. I'm a rheumatologist from Leeds, United Kingdom.

Professor Nash.

Hi, Peter Nash, professor of rheumatology, Griffith University, beautiful downtown Brisbane in Australia.

And Anthony.

Hello, I'm Anthony Chen. I'm a consultant rheumatologist, from United Kingdom.

So we are globally represented. The rules here, we're going to each present two of our favorite abstracts and discuss its impact and import for you. Let's start with Doctor. Castro.

All righty, so the first abstract is the OP0307, and this abstract was a South Korean study that aimed to improve the clinical diagnosis of axial spondyloarthritis, And in this study, they used a deep learning model that integrated structural and inflammatory changes on sacrum MRI. They took data from two ninety one patients with chronic back pain who underwent MRI, and these were analyzed. In general, one hundred and sixty three patients were classified as having axSpA with a sensitivity of over eighty five percent and specificity of also over eighty percent. And this was also with an accuracy of eighty five percent. So this was very interesting to see.

Something that also caught the attention because it was a little bit in the session, it also caused a little bit of emotions, was that there was a small amount of patients that did not meet MRI criteria, but were actually classified with actual spondyloarthritis.

So what was the gold standard when they were comparing the AI results? Was it the locally read or was essentially read images?

So in general, were doing the combination of the model with the structural images. So they kind of like the radiology with the bone marrow edema, with the STIRR and T1 weighted images, with the deep learning model analyzing it. They were not in-depth as far as what was the gold standard comparing it, but they were saying is that that's what it caused a lot of controversy over there, was that they felt that the combination of the deep learning model with the previous imaging was very useful of the trial.

Anthony, what do you think of this kind of report?

I think that it's useful. Increasingly, are seeing more of these type of AI type models, but I think it's also important for a few things. One is that there's a human in the loop in the model so that there is some verification at the end. I think these things at the moment are stratifying, whether this is high risk or low risk of a particular condition and rather than being definitive.

So Peter, one of the problems with imaging being read, there's a big difference between locally read and centrally read. Do you think that AI being applied can supplant essentially read image reading?

I think it's very important, Jack, because if you're misdiagnosed, as we all know, can happen with MRI by itself, especially read by radiologists who's not specifically interested in musculoskeletal medicine, people carry a label and they just cycle endlessly through biologics. So I think any attempt to increase the specificity is very important. And these kinds of things will only help.

Yuz, I'm sure you have a comment on this because you're at Leeds, and Leeds is like a world leader in imaging and advanced imaging. What's your impression of this, and what are you hearing about what's going on at Leeds?

Yeah, so I think pertaining to the abstract as well, I think they mentioned the area under the curve, I think it's a little about 0.9 after using the AI. I that's pretty high compared to the standard rating. But certainly, think more validation needs to be done. But also sometimes we also can't treat things like machine, isn't it? So I think it has to be correlated with patient's symptoms.

That's where the clinician input also really matters this way. But certainly around The UK as well, certainly there's a move now where not just for XBA, but also other diseases are using more AI generated in the new reporting. I think that is coming to your door, but certainly we just have to be careful on that as well.

Nadella, you get final comment on this.

So I agree with all of what you said. I think we're going to see more of these. I think this is helpful, I think it combines the clinical with the findings on imaging. I think that with the more universal that it stays at, more validation that it gets, it's more going to be applicable for our patients.

Excellent. Let's move on to Doctor. Youssef. Youssef.

Yeah, okay. So, to the abstract I want to present, the, number is OP0099. So essentially, we know that a patient with ankylosing spondylitis can have various comorbidities, and one of them is psychiatric comorbidities, such as depression and anxieties. What we don't really know, and a limited study about it, is what hap you know, what happened in terms of the incidence of these, you know, following a diagnosis of axSpA. Basically, this is a study that was done using a combination of Denmark and Sweden.

It is an inception cohort whenever the first patient is diagnosed, and then they followed up. It's very large in the population, I think over nine thousand seven hundred in total in combination. They will also then compare it to a matched population, like general population, so basically a ratio of 10 general population to one patient, and this is a match with age and sex. In terms of the incident itself, they record about the anxiety and depression, so using the ICD code, and also they try to compare the incidence of a patient who receives outpatient and inpatient psychiatric care for anxiety and depression, or patient just inpatient psychiatric care, and also whether there is any suicide. What they found out of these three variables that they were looking for, Patients who's been diagnosed with AXPA have increased incidence of outpatient or inpatient care for anxiety and depression.

The hazard ratio was around one point three four. There was no difference for a patient who required inpatient care or suicide in between general population. So what this study showed that we are very good in managing patient inflammatory symptoms, and also we are getting better at improving patient's quality of life and symptom control. But also we need to also emphasise on communities, particularly people with asthma, and depression and anxiety is one of them. So I think we really need to look into our services so that we can have this provision of access of this psychological therapy potentially, And also as clinician in clinic, also need to know how to signpost if the patient has some depression problems, need to signpost to the appropriate services.

Did they link this finding at all to spondylitis stage or disease activity?

No, they didn't search for that.

Peter, what do you think?

I think it's important, Jack, because this whole complex to manage story is very much driven by anxiety, depression, as well as chronic widespread pain. Some of the drugs have been accused of causing aggravation of depression, but I think rheumatologists are very poor at managing this whole area of our care. I say the word depression and the patient says, You think this pain's in my head, doctor? I say the word psychiatrist. They say the same.

So I just think we manage it poorly, and it's an important part of the patient profile.

Yeah, Anthony, how do you handle these issues?

Yeah, I think these are important topics and we increasingly are measuring PROs in our patients routinely, because even if we find that the disease activity score improves, the PROs don't improve at the same rate. And if you go back to the some of the original papers, if you look, scores like HAC or BASFI, the functional index actually poor predictors of future biologic response. And now we are starting to understand that there is this non inflammatory pain, that is also working in conjunction with, some of the treatments that we are giving our patients.

Yeah, Adela, what do think this data does or finding depression, anxiety does to clinical responses?

We already know that, you know, has been associated in patients with difficult to treat as well. So I think this is important to screen. We do have the rapid questionnaire to screen for depression, and then we definitely have to take action because that's when we see the patients not responding in cycle in different therapies, and the problem that they had initially was depression and anxiety.

Yeah, so you don't need to do a Beck depression inventory to find this. You can do a simple nine question PHQ-nine, but a two question PHQ-two, and add that to your documentation. I have one question on my survey form that all my patients see and it's bold. Do you have depression and anxiety? And then after that, it's up to you to address it in a manner that you think the patient is going to be receptive to.

And I think that Peter's point is, how do discuss these sensitive issues and bring it up when they may be resistant to discussing it or bringing it up? But I think that it starts with us and identifying the problem. Yuz, any last comments on this?

I think I do agree with, you know, all the discussions that we talk about. I think we just need to be a bit more better now to screen for these comorbidities.

Okay. Let's move on to Doctor. Nash and what he enjoyed.

Well, this is a little bit obscure, but I think it's still pretty exciting, Jack. They found b twenty seven patients with AS and those without. In their blood, the synovial fluid, the synovium, they had these particular c d a t cells that express this motif called t r b v nine plus. And about 4% of your T cells do that. And in twenty nineteen, they found a patient who was positive for this.

They found this in their peripheral blood. So they gave this monoclonal antibody to t r b v nine, and he went into remission. He fled six nine months later. They gave it to him again, and he went into remission again. And he's been in remission for four years.

And it turns out that b 27, presents cell from bacterial antigens to T cells, and some of them become autoreactive T cells. So how could they make this monoclonal last longer? They used the BiTE therapy, and they took a bispecific antibody made a bispecific piece c d three plus t r b v nine is expressed, makes a T cell die. They use CRISPR technology to really specifically target that one motif on the T cell. So it only kills the four percent that express this motif, leaves all the ninety six percent alone.

So it's non immunosuppressing. They showed it's potent and specific. Now they've got to get out into human trials. But I think it's an exciting avenue because this particular motif is expressed in the whole axSpA spectrum: AS, PSA, uveitis. It's even expressed in Crohn's, in celiac disease, and a series of other autoimmune diseases and might represent a nice, completely alternate way of treating these patients.

So this was a proof of concept with a patient experience and then now the idea of rolling it out the clinical trials. Correct?

Exactly. So this particular paper just talked about the manufacture of the bite and how potent and specific it is with no clinical details. They really made something that might be more profound in getting rid of the T cells that are autoreactive alone and last much, much longer.

What's the expectation on B27 positive patients with AS? How many will be TRBV9 positive?

A high percentage of them will. And it's quite specific, the immune suppression. It's not broad knocking out all those T cells. It only knocks out the T cells that express and react in this motor.

Anthony, do you think that this is going to do for spondylitis what CD 19 CAR T cells did for lupus?

I think it's going in that direction whether this is the only cell clone that we might discover more. But at least it's a start and I think I was also I did attend this post as well and I was quite interesting to see how much it developed since it first was discovered. This is going to be a first of its kind really for this pub because we haven't had this type of a more specific targeted therapies.

What do you think, Jules?

Yes, I think this certainly opened my eyes as well actually. You thought all these BiTEs and CAR T cell will be more for B cell driven disease and not so much in NASPA, but you do found there's some molecule that express it. It'd be interesting, you do have the proof of concept for many more studies, but we just need to see what happens translate to human studies. I think if it has a role that potentially maybe we can consider this in patients who are in in a treatment refractory, which we are going to be discussing later on in our panel, maybe there is some subgroup of small, small patient that can benefit from this potentially.

Doctor. Castro, what do you think?

I agree with you at this point. I really want to see the studies actually, because a lot of times we see a lot of things in basic science, and when we translate, it doesn't translate equally. But if it actually works in the studies in human, I think it will be a very good way to do more precision medicine in this type of patients.

Peter, I'm glad you presented this because our friends who we run around with at the meetings, the ones who are those spondylitis mavens, which you guys are all part of, they're really excited about this TRBV9. And to target it makes a lot of sense.

Yep, I think it's got legs and other diseases as well.

Yeah, excellent. Alright, let's move on to Doctor Chan.

So I've got a OP 98. This is the concept of difficult to manage XBA and this is study from the rabbit register, the German registered at over 1,800 patients, forty eight percent were biologic naive and then they found in this group that eight point five percent of them were classified as difficult to manage based on the ASUS classification which is two or more biologic DMARDs and the physician and the patient feeling that their disease remains active. But in that group, there was two point five percent which they class as treatment resistant and that is difficult to manage, plus one of a few things high CRP, high S test, positive MRI and sacroiliitis. So there were many other similar studies at this conference which kind of dealt with this concept of a D2M and a treatment resistant. So I thought this is going to be a start of this classification and how we would think of the different treatments for these patients.

So we heard about D2M and C2M yesterday and talking with spondylitis faculty. They seem to be excited by this. Peter, what do you think?

Well, I think it's only going to be relevant, Jack, if we can have predictors and then change the way we start our treatment and do some strategy trials. I think the key difference is one group has to have objective evidence of inflammation, either on imaging or on acute phase reactants, etc, Eye disease activity scores. And the other, we treat differently. Duloxetine, physical therapies, injection surgery, and not cycle endlessly through expensive biologics. So if you can hive off that small group, we should start in combination.

We should then bring down the maintenance. We've got to do all those strategy trials, think.

Adela, you follow this literature?

Yes.

You saw happened in PSA and now here there's a little difference between GRAPA and the UR people who are looking at this. Are you pretty clear on where this is going? Are you confused by the nomenclature and nasology differences?

No, I'm not confused, but something that I remember I like about from Elena Marz Ortega that she said that this is not a different disease. This is a state of the disease that can vary over time. This is something that is important to recognize, and it's important to address and find not only the biologic factors, but also the comorbidities, the inflammatory factors, the reaction, the medication that we're using. So, it's going to be important to take more than one consideration, not just the disease activity itself.

Jooz, do you think this will help clarify treatment choices in the future?

Yeah, so potentially. I think the implication is what, as per Doctor. Nash mentioned earlier, example, people with D2M, potentially we may need to start combo therapy. So it's not just cycling through the immunosuppressive therapy, the other aspects like comorbidities or in an aspect with fatigue, fibromyalgia, that we need to tackle together. And certainly just looking at this report from this registry, the rates of the D2M is quite similar to other diseases as well.

So I think other diseases in rheumatoid arthritis and psoriatic arthritis, the reported prevalence around five to twenty, and they found around eight point five percent. So I think it fits in, it matches. The only thing I just want to slightly comment is I heard a few patients were talking during the conference actually. I think because when they see the topic and title, we discuss about difficult to treat. So I think we understand what it means, but I think from a patient perspective, they really sometimes take it to heart.

They say, well, are we being difficult? And sometimes they went to children in the conference, they burden, like they felt like they were burdening us. Think maybe some, you know, language is thinking that, you know, we need to

It's changed the treatment refractory now.

All right. So that was presented by Doctor. Chan, correct? Yep. Now we're going to begin our second round with Doctor.

Castro. These are shorter, go.

The next one is the abstract OP0310, and it was also very interesting. These actually evaluated structural lesions on the spine of patients with early axSpA compared to patients with non axSpA and chronic back pain, and this used the data from the SPACE cohort. They combined the findings at baseline on conventional radiography and MRI, and then compared it with the findings two years later. They did not see any difference between the axSpA and the non axSpA in terms of conventional radiology. However, on MRI, they did find that patients that had early asthma had more fat lesions, and these fat lesions could be a potential markers of disease activity in patients with asthma because they did not see these on patients with non asthma with chronic back pain.

Question is how significant are fatty lesions or even bone marrow edema when the most specific are erosions, right? I don't know who's our axSpA MRI expert here that wants to comment?

I'm not sure. I think that the real problem is you need a clinician to interpret this stuff or you make tremendous overdiagnosis. And who does x rays anymore other than when you have to for the government MRIs are the kind of the key diagnostic criteria now with clinical features in a CRP so it's we've practically stopped x raying these patients.

Really? Anthony?

Yeah, we only use x rays for classification because there was a time when we had to differentiate between non radiographic and radiographic for access to treatment but that's all changing so we are losing less of X rays. I just wanted to check with Della, did they look into the group with OCI, osteitis condensans ili in the non radiograph in the non expa group because that group often can cause a lot of misdiagnosis and follow-up is that group is probably more important.

No, they didn't. They just had like the cohort from the from the spa patient from the space cohort and they just compared it to the non asthma with chronic back pain who went both imaging, but they didn't say you know what other conditions that non asthma patients with chronic back pain had.

Okay, revealing. Let's go on to use.

Yep, so a quick round one, the abstract OP0097. So in terms of the treatment to target in ASPA, so the Asthat Society has defined criteria in order to aim target of inactive disease, defined by Asthat's less than 1.3, or at least low dysactivity, which is defined by 2.1 or below. So although these patients can meet the targets, some people still have some symptoms, not perfectly, completely in remission as we say. So as we know that when we do have targets, one of the important objectives is trying to prevent from flare and also improve long term outcomes. So what this study did it's actually a Dutch study, so using a SPANET cohort.

So what they found is they're trying to evaluate whether these people who met the criteria of at least low disease activity, whether do they have any flare over the next twelve months, and if there is, what other things could be predictive. So what they found over the twelve months, they found a rate of flare of twenty six percent flare. So when they look into variables, with variables predicting the flare, they did separate into two variables. One is the objective residuals. Basically there's some component if you have, for example, one swollen joint count or if have a little bit of psoriasis or raised inflammatory markers.

Those are the objective one, also there were some residuals, like patient residuals. So this, for example, if you have a little bit higher fatigue score in a back pain and also in a bus fee. So what they found in the multi variable analysis, so patients who have experienced residual despite being on low dose activity were associated with risk of flare for about a ratio of 3.4 and also time to flare as well. Looking at a bit more detail in terms of these patient symptoms, the one that predictive is more like fatigue and bushy, not the back pain. So I think what really this study shows is although patients are categorised in meeting our target, we still have to focus on other symptoms such as fatigue management and also other things like limitation in physical function, may need some input from occupational therapists and so forth, because all this holistic approach will hopefully will then prevent from risk of flare over the next twelve months.

So, don't think it's surprising that people who are in low disease activity state more so than remission are at higher risk for a little flare, more flares going forward. But what this study showed was that the ones with objective inflammation were half the flares and the other ones with the subjective things were the other half. We're getting back into C2M and refractory disease, non inflammatory disease versus inflammatory disease. Doctor. Chan, do you view it differently than I?

No, I think it's the same concept. This is why having these definitions are going to help us in terms of choosing our treatments. And also what we are seeing is that across all these studies we are finding common, factors being female, having peripheral arthritis, obesity, depression. These are the factors that are going to have patients still complaining that they're not well despite us achieving a low disease activity or remission state.

These are all important points as relates to whether you're going to, as Doctor. Nash says, write a prescription for therapy or duloxetine or for a new $60,000 biologic. Any final comments?

I'm not even sure half of them are flares, Jack. If you get a bit of extra back pain and a bit more fatigue, that sounds like me on a after a game of golf. So I just think without objective evidence either on imaging or, in bloods, I I think a lot of this can be overdiagnosed.

Okay, Peter, what's your second, favorite?

This is a very quick one. It's really this question of Axial PSA is very different to AS with a rash. I think it's a nonsense argument, I'll try and give you some background. This is POS two ninety seven. They looked at the Eurospar, five countries data, five eighty patients, three seventy three PSA, two zero eight what they call axSpA plus psoriasis.

They looked at imaging to see MRI and radiographic sacroiliac joint involvement in these patients to see if they could separate them. Lo and behold, one in three of them had evidence on imaging of XBA, and about the same number met the New York criteria. You're younger, you're more likely to have inflammation erosions. If you're older, you're more likely to have ankylosis. And guess what?

If you've got PSA, you're more likely to have dactylitis and nail disease. If you're an axSpA, you're more likely to have uveitis, enthesitis, inflammatory back pain, a positive B27. I simply think this is two ends of the same disease, two different phenotypes, NASH type one and NASH type two. All it means is that the genes you're dealt decide what kind of expression you have. If you're B27 positive, you'll have axial involvement.

If you've got a different set of genes, you'll end up with peripheral arthritis, nail involvement and a rash. Otherwise, we're going to have to have axial dactylitis and axial enthesitis and axial uveitis. I think this argument is a false argument. They're two ends of the same spectrum.

Did I hear you right calling this NASH type one and NASH type two?

Was gonna call it Cush Talk, man, Cush Talk too.

I'm thinking the NASH is gonna stick. But I think that these are sage comments and good ways to consider this. Of course, the big issue is why does IL-twenty three inhibition not work in spondylitis and will it work in PSA spondylitis? I mean, those issues are being studied in a clinical trial, are they not?

They certainly are, yeah.

Any other comments on this?

Just now, Peter, do they compare about prevalence of bowel symptoms in between the two?

They looked at, I'm not sure exactly if they labeled it or not, but I think they would have in fact looked for that as well. But I think the the just think of leprosy. The same antigen. One end you got tuberculoid. The other end you got lepromatous.

They're the same disease.

Mhmm. Let's be clear. Spondylitis has nothing to do with leprosy. Let's just be, you know, for lawyers that may be listening to this.

Yeah. So I think this is the whole discussion of whether you are a lumper or splitter. And I think the discussion tonight is probably we are lumping everything together as one disease.

Very good. Alright, Doctor Chan, give us your your final presentation.

So the, my final one was the Axia app. This is the late breaking abstract two. This is the Axia app presented at 200 patients. They were randomised in RCT one to one between doing the app or doing standard of care, twelve week RCT and the app one, with a reduction in Best Buy, Best Fee, quality of life, ASUS twentyforty better in the app group compared to the standard of care. The app was demonstrated it has, interventions such as exercise, education and some gamification as well so kind of keeping people interested in this.

So I thought it was interesting the first digital therapeutic that I've seen with a positive outcome. Why would we need it? Well, I think there are issues with, shortage of workforce and ability to see people in clinic. This could be an option in that situation.

So for clarity, it's AXIA.

This is

a phone based app. It teaches people a number of different algorithms on exercise, and they either were engaged with that half the group and the other group didn't have an app. So they had nothing. The first person to ask a question at this session was Doctor. Castro.

Adele, why don't you restate your question and your concern about, again, very obvious differences. The treatment group had clinical trial like results as far as ASAS40, ASAS20, FASD eye change, etcetera. And very little change in placebo or control group, big changes in the axial group. Go ahead Adele, what was your comment?

Yeah, so my question, because of these differences in the results, even the placebo effect was very minimal. So my question was if there was any specific bias, particularly the Hawthorne effect, the patients that are being evaluated, of course, do better because they know they're being evaluated. But then that was something that was a question because other patients were on nothing. So that's something that they were like, you know, it's possible, but again, they circled around. But it is a valid bias on these type of interventions when we don't have any other competitors.

Is this Austrian or German? German or Austrian? I think it's very cultural. German. Who will pay attention to do as they're told?

It was German. Right?

Yeah. It was German.

I'd like them to try it in Australia. I'll tell you there'd be a difference.

Well, other there was a few first off, I see an app working really well in a non pharmacologic I'm like so excited about this, so into this. But if you follow the details, the results are kind of believable, if you're a skeptic, maybe not. And then if you looked at the details, seventy four percent of the intervention group were female. Fifty two percent of the placebo group were female. I thought ankylosing spondylitis was a male disorder.

Then You asked that question.

Yeah, and he paid no attention to me telling me that spondylitis is a one to one disease. I said, yeah, if you wanna be politically correct, then you got a microscope out on everyone, sure, but not in the real world. And then the other problem was that, and I like his point was that women are really good at filling out apps. Women are really good at following instructions. Women are really good at doing exercise.

And that may be underlying some of their results. But if you look at the profiling, thirty two percent, thirty three percent of both groups were active in athletics. Peter, how many of your spondylitis patients are playing cricket and rugby on the weekends?

Man, they're too busy working, trying to earn a crust to be doing anything like that. Think

it's exciting. Yuz, what's your comment on this?

Yeah, so yeah, I've heard both of your questions on the day. You had quite a lot of grilling in the Q and A session. I think also just to think about in terms of dissemination and scalability and also languages. I know they said they've started rolling out in Austria, but obviously there's quite a lot of things. You need to translate in English and other languages as well to be wider applicability, so I think that's probably a different challenge as well after this.

Peter, Austria compared to Germany, isn't Austria Germany with better beer?

Be careful there Jack, it's got to be politically correct.

I'm getting calls. Any closing comments on this exciting abstract?

I did find it very exciting because it's a non pharmacologic therapy, whether the result that they presented, I found them that they're too great to believe. I think ideally on a controlled study with the same app for everybody would be ideal, especially because even all the measures were even better than the biologic therapies, which you see really high placebo responses as well. I was like, I need more data on these.

They need to share that to compare it to. Anthony, you get final Yeah,

we need longer term data for this to see whether this is sustainable. But if it is, I think this comes back to a whole discussion about complex to manage. And with all these kind of patients, have a lot of these other non inflammatory could be that we could send them this app.

Okay, I wanna thank our spondylitis mavens for their hard work last week at the meeting and covering, spondyloarthropathies, and educating our audience with all the good stuff from UR twenty twenty five in Barcelona. That's it for this review. There's plenty of more content that you can consume either by video or by podcast. Thanks to our faculty. Good night.

Thanks, Jack.

Hi, everyone. This is Jieha Li reporting for RheumNow from UR twenty twenty five with a study that raises an important question. When older adults report better mental health in the setting of chronic pain, is that a sign of resilience, or could it be something more complicated? The asterisk I'm going to be discussing is POS 0402. It is titled the role of aging in the relationship between chronic musculoskeletal pain and health related quality of life.

It is a study from Maastricht, Netherlands. So this is a population based analysis of over 8,600 adults aged 40 to 75 years. Nearly thirty percent had chronic musculoskeletal pain lasting at least three months. The researchers looked at how that pain affected both physical and mental health as well as work participation across different age groups. So as expected, chronic pain was associated with worse physical health and also more days missed from daily activities, also used discussed terms using presentism or absentism.

But they also found that older adults, especially those in the 65 to 75 age group, reported better mental health and fewer missed workdays than younger adults with similar levels of pain. Now, they describe this as a possible protective effect of aging on mental health, potentially due to resilience, which they suggest may reflect stronger coping skills, more stable life roles, or emotional adaptation developed over time. And that's certainly possible. I mean resilience after all is the capacity to maintain or regain mental well-being despite adversity, especially even in the health context or chronic comorbidities. It's a powerful framework and many older adults embody it in remarkable ways, but there's another lens that we really need to consider, one of resignation.

What if these mental health scores aren't signs of thriving, but signs of adjusted expectations or even ageism? Is the quiet acceptance possibly rooted in decades of being told that pain is just part of aging. If older adults underreport distress because they've normalized discomfort, we may be mistaking emotional suppression for emotional stability. We see echoes of this in RA. Like, a recent comment on one of myRoomNow piece about polyrefractory RA pointed how often persistent pain and fatigue in the absence of inflammation are misclassified sometimes as treatment resistant RA.

And in fact, this may actually reflect central sensitization of fibromyalgia like pain, goes unmeasured and undressed in most trials. So when we see a protective effect of aging, we really need to ask, is this truly resilience or is it resignation, so silence we've taught people to adopt? So if we don't make space to explore this difference, we risk potentially missing meaningful pain, especially in older adults. And that can lead to misdiagnosis, inappropriate escalation of treatment, or neglect of noninflammatory contributors to poor quality of life. So yes, part of what we see in this study may be resilience, but part may be resignation.

And our responsibility as rheumatologists is to recognize pain even when it's quiet and to treat not just the inflammation, but the experience. This is Chiha Lee reporting for EULAR twenty twenty five for RheumNow. Thank you for watching.