ACR 2025 RA Topic Podcasts Compilation 6 Save
ILD in Patients with Connective Tissue Disease
Fiber and Methotrexate
RA ILD Prediction: simple as a dipstick?
"Leftover Pain in Inflammatory Arthritis"
Transcription
This is an ACR 2025 podcast coming to you from Chicago. Hope you enjoy it.
This coverage is sponsored by BMS. At Bristol Myers Squibb, we're deeply committed to advancing rheumatology. With ongoing studies in psoriatic arthritis, SLE, and Sjogren's disease, we're driving innovation to support patients with these conditions. You can learn more at bmsclinicaltrials.com. To watch and listen to educational insights from key thought leaders on emerging topics and disease state education in psoriatic arthritis, visit www.insidethescience.com/understandingpsa.
Hi. Welcome. I'm doctor Janet Pope here at RheumNow, ACR twenty twenty five in Chicago. I wanted to talk about the connective tissue diseases and, and rheumatoid arthritis and interstitial lung disease. And, hopefully, with this, we'll be breathing more easily and so will our patients.
So the first abstract was number 0154. And what it did was they combined data from market scan and Optum looking at people with either a label of CTD and specific ones in particular or rheumatoid arthritis. And they had between the two datasets nearly thirty thousand patients. Patients. So the mean age, depending on the dataset, was anywhere from, 56 65.
And as expected in, these autoimmune connective tissue diseases, three quarters were women. They looked at the frequency of interstitial lung disease by a diagnostic, algorithm from these databases, and what they found was as a for instance, systemic sclerosis, ILD, that seemed clinically relevant was about fifteen percent. Now we have found that in an old study that we published as an Ontario, incident study over about ten years. Obviously, ILD is even higher if you're gonna look, more thoroughly. That leads me to talking about scleroderma, and ILD.
So there was a whole session devoted to systemic sclerosis of which a lot was talking about ILD. So the first question was, can we predict who will progress? And the answer is not so well, but SCL 70 is a risk. Men, certain racial characteristics such as in The US, people who identify as black. But we don't really have a good prediction model.
So two different studies looked at k l six, which is used in Asia as a prediction, and they also looked at other, factors. K l six and in the other studies, some other factors, MIG, etcetera, were predictive, but they're not strongly predictive. So the answer there is you have to keep following and screening your patients. The next thing was how common is ILD in our patients with the limited subset? So we you might have think of it before as being called CREST, but it's limited cutaneous systemic sclerosis.
And in that group, up to a third had interstitial lung disease. And if you followed for the time of the study, in the database that they had, a good one in six patients will progress. So the take home from all these studies are we have to be vigilant. There is ILD in our patients with connective tissue disease. Within scleroderma, we don't have a good biomarker that says who will progress.
So in scleroderma, because the incidence and prevalence is so high of CTD as a complication that you have to screen regularly. The other good news is you can breathe more easily because there are treatments. Nirandelomast will be approved at some point as a PDE four inhibitor in the treatment of progressive pulmonary fibrosis, and it was well tolerated. That's the FibroNir ILD study, and there are other treatments on the horizon. There's immune suppressive treatments in early diffuse scleroderma and in limited as well where ILD is relevant.
So please follow us at RheumNow. Thank you very much.
Hi. I'm Jack Cush at ACR twenty twenty five Chicago. Today, a presentation, a great poster, abstract l b late breaking 15. The title of this had something to do with fiber and methotrexate. Did you take your fiber today?
This is an interesting story. The idea, behind fiber is that it's good for you and maybe one of the ways it's good for you is it could change your microbiome. And maybe you follow the microbiome literature, maybe you don't, but there's some literature in there about the microbiome changing disease sometimes by changing how drugs work. Either the metabolism of the drugs or their absorption or their effectiveness, and this applies to a lot of chemotherapies. It's been linked to methotrexate.
So in this, small pilot, multinational study of forty nine patients with mild to moderate rheumatoid arthritis, they looked at what happens when you give fiber to RA patients. Who are these forty nine RA patients? Mild disease. Generally about five to seven tender joints. About two swollen joints.
CRP, medium was seven milligrams per liter. So again, mild to moderate disease. It's a one month study. Half the group got twelve grams of inulin, which is a source of complex dietary fiber or a sugar pill, and they looked at the outcomes one month later. It turns out that at thirty days, the ones who got fiber had, and again, had mild disease to begin with, had greater achievement of EULAR good status fifty seven percent versus the placebo twenty two percent.
They had a reduction in both Th 17 cells in the periphery as measured by flow cytometry and the ratio of Th 17 to Treg cells, and this was significant. And then lastly, for those who are on methotrexate, they had a a significant drop in DAS score minus one versus those that were on placebo where the DAS didn't change very very much, it was minus 0.38. Now and again, the numbers here are too small to be significant. But the but when you look at the the graphics on this, it looks like dietary fiber can augment methotrexate responses. They had a a a small control group of patients, but there are only six that were on other DMARDs, and it didn't look like fiber did anything for them.
But they need to repeat this. It's a good pilot study. Dietary fiber could make methotrexate more effective. More from ACR.
Hi, everyone. This is Oily Naj reporting for RheumNow. I'm from Glasgow, Scotland, but I'm currently in Chicago. Day three of the conference, ACR twenty twenty five. Absolute joy.
I went to this session this morning, and it was an RA ILD session, which obviously, for me, is is is the most amazing thing because that's most of my research. So I was quite excited about that, and it was so interesting. So the same way we've been seeing so many abstracts about how do we predict who's gonna develop RA in the people at risk. There was a lot of prediction studies looking at what is what is the biomarker of ILD? How can we identify people with RA that will go into developing ILD?
And so that was quite interesting actually. And there's one in particular that caught my attention because I found the ID quite exciting. So it was a new a urine study, basically. So they did urine proteomics. They linked it with blood proteomics, but the result of the blood proteomics wasn't presented.
So it was abstract seventeen fifty. There's a few caveats here that we're gonna discuss at the end, but generally a small cohort, 14 patients with RA, LD, so that's not huge. 64 controls, RA, no ILD. It wasn't clear whether the people with that ILD had had a chest CT to verify they didn't have any form of ILD and also the cohort was too small to get granularity in the pulmonary fibrosis patterns between UIP and NSIP and so and so on. But but what they found overall is a couple of proteins.
I could give you the name, but you will forget them the same way I did. So it's SPOCK one and PGRMC one. But these seem to be associated with fibrosis response in terms of the biology as well as cell stress response. So interestingly, these two proteins, they were elevated in people with ILD in their urine. And there was a correlation as well between the levels of the proteins, in particular one of them, and the severity of the lung disease but also when they did their multivariate analysis, they showed that it was independently associated with the risk of predicting of of developing ILD.
It was another ratio of about six, which is quite high. And so they developed a prediction model with these two proteins, and then with and without clinical parameters as well, such as age, sex, duration of the disease or seropositivity. And they were able to predict development with a round of the curve of 0.94 with the whole model, but with proteins only it was 0.9. So it was actually pretty good. It's obviously not validated in the second cohort.
So that's something we're gonna have to be looking out for because there are so many studies that show one market elevated and then, you know, you never hear about it again. But certainly, small numbers not yet validated. The other caveats there could be the issue with urine, you know, when it didn't seem to be particularly standardized the way they collected it. You know, depending on time of the day, there might be variations and stuff, and that was brought up during the questions. And also the function of these proteins in the ILD development pathogenesis are not really clear yet, but certainly if we're able to predict who's going to develop ILD in our patients using a dipstick, that would be quite cool.
So that's what I wanted to share with you today. Go online and check RheumNow for more content and follow me on Twitter AurelieRaimo.
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 axial spondyloarthritis and psoriatic arthritis. And today, I'm joined here by doctor Mohammad Biktar, who is also an assistant professor at Oregon Health and Science University.
Doctor. Biktar'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?
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 and 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 at 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 ACTFL 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 axSpA, actually default mode network got activated, which is abnormal that means patients are focusing on the brain is focusing on pain and that's why they go into a chronic pain state.
Also the salience network it got exaggerated responses in Salience Okay. In 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 in rheumatoid arthritis and psoriatic arthritis. Do you want to tell us about that?
Definitely. And there was a very interesting oral abstract that was presented 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 insula 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 we will hopefully one day find the differences of how the brain works with nociceptive and nociclastic and neuropathic. Those are the three different 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.
This coverage is sponsored by BMS. At Bristol Myers Squibb, we're deeply committed to advancing rheumatology. With ongoing studies in psoriatic arthritis, SLE, and Sjogren's disease, we're driving innovation to support patients with these conditions. You can learn more at bmsclinicaltrials.com. To watch and listen to educational insights from key thought leaders on emerging topics and disease state education in psoriatic arthritis, visit www.insidethescience.com/understandingpsa.
Hi. Welcome. I'm doctor Janet Pope here at RheumNow, ACR twenty twenty five in Chicago. I wanted to talk about the connective tissue diseases and, and rheumatoid arthritis and interstitial lung disease. And, hopefully, with this, we'll be breathing more easily and so will our patients.
So the first abstract was number 0154. And what it did was they combined data from market scan and Optum looking at people with either a label of CTD and specific ones in particular or rheumatoid arthritis. And they had between the two datasets nearly thirty thousand patients. Patients. So the mean age, depending on the dataset, was anywhere from, 56 65.
And as expected in, these autoimmune connective tissue diseases, three quarters were women. They looked at the frequency of interstitial lung disease by a diagnostic, algorithm from these databases, and what they found was as a for instance, systemic sclerosis, ILD, that seemed clinically relevant was about fifteen percent. Now we have found that in an old study that we published as an Ontario, incident study over about ten years. Obviously, ILD is even higher if you're gonna look, more thoroughly. That leads me to talking about scleroderma, and ILD.
So there was a whole session devoted to systemic sclerosis of which a lot was talking about ILD. So the first question was, can we predict who will progress? And the answer is not so well, but SCL 70 is a risk. Men, certain racial characteristics such as in The US, people who identify as black. But we don't really have a good prediction model.
So two different studies looked at k l six, which is used in Asia as a prediction, and they also looked at other, factors. K l six and in the other studies, some other factors, MIG, etcetera, were predictive, but they're not strongly predictive. So the answer there is you have to keep following and screening your patients. The next thing was how common is ILD in our patients with the limited subset? So we you might have think of it before as being called CREST, but it's limited cutaneous systemic sclerosis.
And in that group, up to a third had interstitial lung disease. And if you followed for the time of the study, in the database that they had, a good one in six patients will progress. So the take home from all these studies are we have to be vigilant. There is ILD in our patients with connective tissue disease. Within scleroderma, we don't have a good biomarker that says who will progress.
So in scleroderma, because the incidence and prevalence is so high of CTD as a complication that you have to screen regularly. The other good news is you can breathe more easily because there are treatments. Nirandelomast will be approved at some point as a PDE four inhibitor in the treatment of progressive pulmonary fibrosis, and it was well tolerated. That's the FibroNir ILD study, and there are other treatments on the horizon. There's immune suppressive treatments in early diffuse scleroderma and in limited as well where ILD is relevant.
So please follow us at RheumNow. Thank you very much.
Hi. I'm Jack Cush at ACR twenty twenty five Chicago. Today, a presentation, a great poster, abstract l b late breaking 15. The title of this had something to do with fiber and methotrexate. Did you take your fiber today?
This is an interesting story. The idea, behind fiber is that it's good for you and maybe one of the ways it's good for you is it could change your microbiome. And maybe you follow the microbiome literature, maybe you don't, but there's some literature in there about the microbiome changing disease sometimes by changing how drugs work. Either the metabolism of the drugs or their absorption or their effectiveness, and this applies to a lot of chemotherapies. It's been linked to methotrexate.
So in this, small pilot, multinational study of forty nine patients with mild to moderate rheumatoid arthritis, they looked at what happens when you give fiber to RA patients. Who are these forty nine RA patients? Mild disease. Generally about five to seven tender joints. About two swollen joints.
CRP, medium was seven milligrams per liter. So again, mild to moderate disease. It's a one month study. Half the group got twelve grams of inulin, which is a source of complex dietary fiber or a sugar pill, and they looked at the outcomes one month later. It turns out that at thirty days, the ones who got fiber had, and again, had mild disease to begin with, had greater achievement of EULAR good status fifty seven percent versus the placebo twenty two percent.
They had a reduction in both Th 17 cells in the periphery as measured by flow cytometry and the ratio of Th 17 to Treg cells, and this was significant. And then lastly, for those who are on methotrexate, they had a a significant drop in DAS score minus one versus those that were on placebo where the DAS didn't change very very much, it was minus 0.38. Now and again, the numbers here are too small to be significant. But the but when you look at the the graphics on this, it looks like dietary fiber can augment methotrexate responses. They had a a a small control group of patients, but there are only six that were on other DMARDs, and it didn't look like fiber did anything for them.
But they need to repeat this. It's a good pilot study. Dietary fiber could make methotrexate more effective. More from ACR.
Hi, everyone. This is Oily Naj reporting for RheumNow. I'm from Glasgow, Scotland, but I'm currently in Chicago. Day three of the conference, ACR twenty twenty five. Absolute joy.
I went to this session this morning, and it was an RA ILD session, which obviously, for me, is is is the most amazing thing because that's most of my research. So I was quite excited about that, and it was so interesting. So the same way we've been seeing so many abstracts about how do we predict who's gonna develop RA in the people at risk. There was a lot of prediction studies looking at what is what is the biomarker of ILD? How can we identify people with RA that will go into developing ILD?
And so that was quite interesting actually. And there's one in particular that caught my attention because I found the ID quite exciting. So it was a new a urine study, basically. So they did urine proteomics. They linked it with blood proteomics, but the result of the blood proteomics wasn't presented.
So it was abstract seventeen fifty. There's a few caveats here that we're gonna discuss at the end, but generally a small cohort, 14 patients with RA, LD, so that's not huge. 64 controls, RA, no ILD. It wasn't clear whether the people with that ILD had had a chest CT to verify they didn't have any form of ILD and also the cohort was too small to get granularity in the pulmonary fibrosis patterns between UIP and NSIP and so and so on. But but what they found overall is a couple of proteins.
I could give you the name, but you will forget them the same way I did. So it's SPOCK one and PGRMC one. But these seem to be associated with fibrosis response in terms of the biology as well as cell stress response. So interestingly, these two proteins, they were elevated in people with ILD in their urine. And there was a correlation as well between the levels of the proteins, in particular one of them, and the severity of the lung disease but also when they did their multivariate analysis, they showed that it was independently associated with the risk of predicting of of developing ILD.
It was another ratio of about six, which is quite high. And so they developed a prediction model with these two proteins, and then with and without clinical parameters as well, such as age, sex, duration of the disease or seropositivity. And they were able to predict development with a round of the curve of 0.94 with the whole model, but with proteins only it was 0.9. So it was actually pretty good. It's obviously not validated in the second cohort.
So that's something we're gonna have to be looking out for because there are so many studies that show one market elevated and then, you know, you never hear about it again. But certainly, small numbers not yet validated. The other caveats there could be the issue with urine, you know, when it didn't seem to be particularly standardized the way they collected it. You know, depending on time of the day, there might be variations and stuff, and that was brought up during the questions. And also the function of these proteins in the ILD development pathogenesis are not really clear yet, but certainly if we're able to predict who's going to develop ILD in our patients using a dipstick, that would be quite cool.
So that's what I wanted to share with you today. Go online and check RheumNow for more content and follow me on Twitter AurelieRaimo.
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 axial spondyloarthritis and psoriatic arthritis. And today, I'm joined here by doctor Mohammad Biktar, who is also an assistant professor at Oregon Health and Science University.
Doctor. Biktar'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?
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 and 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 at 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 ACTFL 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 axSpA, actually default mode network got activated, which is abnormal that means patients are focusing on the brain is focusing on pain and that's why they go into a chronic pain state.
Also the salience network it got exaggerated responses in Salience Okay. In 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 in rheumatoid arthritis and psoriatic arthritis. Do you want to tell us about that?
Definitely. And there was a very interesting oral abstract that was presented 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 insula 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 we will hopefully one day find the differences of how the brain works with nociceptive and nociclastic and neuropathic. Those are the three different 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.
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