ACR24 - Day2d Save
Assessment of axSpA:Dr. Antoni Chan
Defining Difficult to Manage axSpA:Dr. Lihi
DISH in SpA:Dr. Sheila Reyes
Generative AI in Rheumatology: The Good, The Bad, The Ugly:Dr. Akhil Sood
Native Americans with RA Die Young:Dr. Eric Dein
Precision Immunotherapy in Axial SpA:Dr. Marina Magrey
When, What and How Long to Treat GCA & PMR:Dr. Janet Pope
Transcription
I'm Anthony Chan reporting here for RheumNow here in ACR twenty twenty four in Washington. And there have been some very interesting abstracts today, looking at the assessment of axial spondyloarthritis. Firstly, in the whole area of using the scores that we use to measure outcomes. We traditionally have been using something called the BEST DISE score, which is the Banff Ankylosing Spondylitis Disease Activity Index. And for a long time there had been an arbitrary cut off of two or more than four in terms of assessing whether the patient is in remission or whether the disease is active.
But that actually hasn't been validated. Here in ACR twenty twenty four, abstract number eight eighteen looks at the assessment of the best eye score in comparison to other outcomes such as the S test, the ankylosing spondylitis disease activity score, axial spondyloarthritis disease activity score, and they have developed some new cutoffs. And the new cutoffs of remission is the best die of less than 1.4, low disease activity is best die of less than 2.8, and very high disease activity is best die of 5.9. Now one of the things about coming to these meetings is to kind of think what we would do when we get back to our clinics and how we could be using some of the new information. So this is one abstract that I think will will help us to kind of use the new data in terms of assessing our patients if this using these new cutoffs which has some validation.
The second, abstract in the field of XBAW is in, abstract number eight nineteen and this is about the definition of difficult to manage access spondyloarthritis. All of us will have these patients in our clinic where sometimes they can be difficult to manage for a few reasons. And they have defined situation for patients who have difficult treatment response, they have high disease activity scores, they have, raised inflammatory markers such as CRP or positive MRI, and also that they can be clinically assessed as difficult to manage that despite, having good objective measures, the patient still has a poor quality of life. So here are some of the things that we can be using in terms of trying to define this population a bit better. And this is, work that has come from the ASAS group with eighty nine percent concordance among the people who voted for this new definition of difficult to manage excess spondyloarthritis.
So here we are in ACR 24 with these two abstracts from today, eight eighteen and eight nineteen, which I think will help us inform how we manage our patients with Axis Pondyloarthritis going forward. I'm Antony Chan reporting for RheumNow here in Washington at ACR twenty twenty four.
Hello, everyone. Lihi Eddard here from the University of Toronto reporting from the ACR here in DC. I'll be talking about a presentation, a new definition for difficult to manage axSpA that was presented. It's abstract number zero eight nineteen. This is the new definition, ASAS definition for difficult to manage axSpA.
So this new definition refers to the patients that we all see in our practice. These are patients who failed multiple modes of action and are more difficult to manage and in order to understand better how we can better take care of these patients, we need a new definition. So ASAS proposed that these patients include those that failed two separate modes of action, but also have some additional definition which include high burden of symptoms as measured by ASAS or a high level of CRP or evidence of active inflammation by MRI as well as patients who showed progression in radiographic damage. Importantly, they also emphasized the patient perspective here. So if the symptoms are perceived to be difficult or important by the patients, that is also important and counts not just a rheumatologist perspective.
They also include in this new definition a subgroup of refractory to treatment patients and this means that these patients in addition to having symptoms, they also need to have objective evidence of inflammation either by blood tests, CRP, or by MRI, the evidence of inflammation in their spine. And this is to separate them from those who have other confounders that might affect symptoms like depression, fibromyalgia, so on. And this subgroup of maybe truly immunologically resistant patient might be a more focused target group for research or combination therapy or other approaches. So overall, I think this new ASUS definition is important. It's a step forward that is similar to other projects of difficult to treat patients in PSA and RA and hopefully will move this field forward and address this major issue that we all face in clinic a source or as tool to help us do better research and better manage our patients.
Thank you.
Hi. I'm Doctor. Sheila Reyes from The Philippines reporting live for RheumNow at the ACR Convergence twenty twenty four here in Washington DC. I would like to talk about abstract fourteen forty seven from the group of doctor Giselle and colleagues. It struck me a little bit interesting because they compared the frequency of cervical dish in patients with SPA versus age and sex matched controls.
So their findings showed that the frequency of DSH is the same for both populations and that SPA patients with DSH were significantly younger. Now interestingly, DSH was seen more in axSpA patients who were HLA b twenty seven positive while dish was reported more among psoriatic arthritis patients who were HLA b twenty seven negative. Now how can these results help us in clinical practice? Probably not as much, but at least knowing that dish is not just a mimic of axSpA, but that it can co occur or it can occur simultaneously with AXPA helps us to understand disease the disease of our patients, especially when we're already giving our biologic DMARDs or traditional DMARDs, and patients do not respond to treatment probably because it's not the inflammatory type of back pain that's causing the symptoms, but it's more of the mechanical type. So knowing these can also guide treatment decisions for clinicians.
Follow me on x at RheumNow, and tune in to RheumNow for more updates and news on the ACR convergence twenty twenty four.
Hi, my name is Akhil Sood. I'm reporting for RheumNow here at Washington DC. Today I want to talk about generative AI in rheumatology, the good, the bad, and the ugly. At ACR, of the biggest highlights has been artificial intelligence. It's exciting to think how AI can make our lives easier especially since so much of our work is tied to computers.
But this raises two questions, should AI handle all our tasks or just a select few and what are the risks? I had the opportunity to explore these questions firsthand. At ACR I presented abstract ten seventy six where we tested the ability of chat GBT to respond to questions about recombinant zoster vaccine in patients with thrombotic diseases. Here's what we did. We fed prompts into CHATGPT based on ACR and ACIP guidelines and we also had frequently asked questions available from the CDC.
And the results were interesting. CHATGPT responded to most prompts with high accuracy and completeness. But there was one instance were scored very poorly. And this brings me to the bad. While ChatGPT and other large language models can respond well to most questions, it carries the risk of misinformation and this risk comes down to two main factors.
First, the data these models are trained on. Second, the structure and the style of the prompts we input. And if we don't address these issues this brings me to the ugly. Misinformation in AI can have a ripple effect. It can increase bias and this can worsen inequities especially in our vulnerable populations.
So how do we fix this? For starters we need better and more prompts available and we need more representative data. And finally validation is key. AI models need to be tested in different settings before we can trust them in clinical practice. In conclusion generative AI has incredible potential but should we ask it to do everything?
Probably not. Some tasks are probably better left to us. And I'll close with a quote that I came across recently. I want AI to do my laundry dishes so I can focus on my art and writing. And maybe that's the point.
Let AI take care of the routine so we can focus on the more meaningful. Thank you.
This is Eric Dine from RheumNow. I'm a rheumatologist from New Jersey here in DC for day two of ACR convergence. I'm joined with, Parmita Das, a college student at UCLA who just, gave an oral abstract in the rheumatoid arthritis session. Tell me about your your research.
Yeah. So our my research is on RA mortality, and we looked at it by racial and ethnic groups to kinda see if RA mortality differs with these different groups. So we kinda use the data from CDC's wonder database, which has over ninety nine percent of all the deaths across The US. So it's a strong database, and we compiled this data. We did logistic regression analysis, and we did looked at ASMR.
And through that, we found that for native Americans, they had a significantly higher ASMR relative to all other racial and ethnic groups for RA.
I I think, unfortunately, that wasn't information that surprised me. What what really surprised me was the magnitude and that it seemed like there was a difference. It wasn't just at all ages. It was particularly in in younger younger patients with RA who are of that background. Tell me about that.
Yeah. So first are, like, we noticed that it was so the significance of, like, the increase in RA was so high. So then we're, let's look at it also by different age groups. So we looked at that. We looked specifically into three different age groups.
So 44 and below was our lowest. And in that, we found it was over tenfold higher difference in ASMR for Native Americans compared to all other racial and ethnic groups. And so that was very striking to us. We also looked at we further looked at that RA young RA RA mortality, and we looked at YPLL, which is years of potential life lost. And we found that it was almost 9.4 times higher in Native Americans compared to the lowest, ethnic group that we found, which is high.
And then also for younger females and younger males, they had the highest odds of death of RA mortality for Native Americans relative to the reference group of the white population.
Yeah. I thought that was just very dramatic and worth highlighting the fact that, you know, those younger individuals 44 that over a 10 times risk of death compared to patients with RA that were not from Native American background. So, unfortunately, it seems like your your data can't tell exactly why that is, but we know that there's socioeconomic factors. There's disease specific factors. And so sounds like it's something that we need to look into more and learn more about.
But I think it's definitely a huge need. It is. Yeah. So thank you so much for for doing that study, and and best of luck with medical school and Thank you. And for the journey into hopefully rheumatology.
Yeah. Thank you so much. It was great speaking with you.
Yep. Thank you very much. That's, day two of ACR Convergence. More on RheumNow.
Hello. This is Marina McGray again, reporting for RheumNow at ACR Convergence twenty twenty four in Washington DC. I'm going to report this very interesting abstract, is talking about precision immunotherapy in ankylosing spondylitis. This abstract was presented this afternoon. As we all know, ankylosing spondylitis is a T cell mediated disease.
However, you know, trying to deplete T cells is not possible because that would input the patients at a very high risk of infections. A subset of T cells have been, incrinated in pathogenesis of ankylosing spondylitis. The this subset carries this unique receptor t receptor b v nine. And this is this these cells are thought to, know, bind with the antigen presented by HLA b 27 positive cells and has been implicated in pathogenesis. In this abstract, a bispecific antibody was developed against this subset of T cells carrying this receptor, TRBV nine receptor.
They neutralized these cells showing to be with using this antibody, the risk of infections was low. Cytokine release was low with this binding. So the concern for cytokine release syndrome was minimum. And the recommendation was that by binding and, you know, or depleting this subset of T cells, one could reset these autoreactive T cells and produce long term remission in axial spondyloarthritis in AES. So it was very exciting, and, you know, I will have to wait till actual human studies are done with this bispecific antibody.
There there has been a case, report from Russia last year, which was published showing that these antibodies are work. So something very exciting for the future of axial spondyloarthritis. There was another abstract keeping up with the same theme presented today, which was which took patients with the you know, which had uveitis, acute anterior uveitis, HLA b twenty seven positive. So they took their ocular cells and blood cells, and they found that blocking this TR this T receptor, b v nine T cells may not be enough. They also found another receptor that may be implicated in patients with uveitis, t r b v five.
So they were there and what can the gist from that abstract was that blocking one one receptor may not be enough and maybe need to block both receptors. Well, this is, you know, very early data. Ultimately, it needs to be vetted in real human studies and see what works for our patients. Thank you so much.
Hi. I'm doctor Janet Pope. I'm here at RheumNow, ACR 2024 in lovely Washington DC with pretty good weather. Okay. I wanna talk about when, what to use, and for how long to treat GCA and PMR.
And I'll be covering a lot in a lot of my personal opinions in this, but there was a whole bunch of abstracts of RCTs, sixteen ninety five, sixteen ninety eight, sixteen ninety seven, and 1,700. So here's the take homes. Number one, cirulimumab is approved in The US and is a prednisone sparing drug. And doctor Jeff Curtis actually looked beyond that and found that cirulimumab was superior to methotrexate, looking at effectiveness from a very large database. And another group looked at a trial of methotrexate versus placebo and PMR.
And guess what? Methotrexate didn't do any sparing. So cicerolimumab is in for PMR and does steroid spare. And it's for PMR that has failed steroids, or it's recurred or you can't get the dose down. Okay, what do we do in GCA?
Number one, in GCA, the standard of care in many places now is starting at the beginning of a person with proven or highly suspected GCA, glucocorticoids, and an IL-six inhibitor, tocilizumab, which has approval in many countries. What if tocilizumab doesn't work? What if it's stopped and the patient rebounds? What if they're partial responders? Because there's never a 100% response.
We do know in PMR, if you withdraw tocilizumab at six months, even in PMR, the disease wakes up. So we know you have to go longer in PMR. We know that a lot of trial, the approval was based on the initial trial of Tocilizumab in GCA. So here's what we know. We know that upadacitinib fifteen mg a day is as superior to, placebo and a more rapid taper of glucocorticoids better benefit.
We don't know how long to use upadacitinib. We know there's an IL 17 trial underway, and we also know that there was an attempt using, IL-one inhibition with anakinra for four months that was not successful. It was underpowered but didn't show any benefit. So I think the take home is number one, GCA, use a steroid sparing drug from the beginning. Number two, PMR.
If it's difficult to treat, you can't get the steroids down or it relapses, consider a steroid sparing drug. We already have a menu with a couple options on it for each of those diseases and more will come. Follow us at RheumNow. Thank you.
But that actually hasn't been validated. Here in ACR twenty twenty four, abstract number eight eighteen looks at the assessment of the best eye score in comparison to other outcomes such as the S test, the ankylosing spondylitis disease activity score, axial spondyloarthritis disease activity score, and they have developed some new cutoffs. And the new cutoffs of remission is the best die of less than 1.4, low disease activity is best die of less than 2.8, and very high disease activity is best die of 5.9. Now one of the things about coming to these meetings is to kind of think what we would do when we get back to our clinics and how we could be using some of the new information. So this is one abstract that I think will will help us to kind of use the new data in terms of assessing our patients if this using these new cutoffs which has some validation.
The second, abstract in the field of XBAW is in, abstract number eight nineteen and this is about the definition of difficult to manage access spondyloarthritis. All of us will have these patients in our clinic where sometimes they can be difficult to manage for a few reasons. And they have defined situation for patients who have difficult treatment response, they have high disease activity scores, they have, raised inflammatory markers such as CRP or positive MRI, and also that they can be clinically assessed as difficult to manage that despite, having good objective measures, the patient still has a poor quality of life. So here are some of the things that we can be using in terms of trying to define this population a bit better. And this is, work that has come from the ASAS group with eighty nine percent concordance among the people who voted for this new definition of difficult to manage excess spondyloarthritis.
So here we are in ACR 24 with these two abstracts from today, eight eighteen and eight nineteen, which I think will help us inform how we manage our patients with Axis Pondyloarthritis going forward. I'm Antony Chan reporting for RheumNow here in Washington at ACR twenty twenty four.
Hello, everyone. Lihi Eddard here from the University of Toronto reporting from the ACR here in DC. I'll be talking about a presentation, a new definition for difficult to manage axSpA that was presented. It's abstract number zero eight nineteen. This is the new definition, ASAS definition for difficult to manage axSpA.
So this new definition refers to the patients that we all see in our practice. These are patients who failed multiple modes of action and are more difficult to manage and in order to understand better how we can better take care of these patients, we need a new definition. So ASAS proposed that these patients include those that failed two separate modes of action, but also have some additional definition which include high burden of symptoms as measured by ASAS or a high level of CRP or evidence of active inflammation by MRI as well as patients who showed progression in radiographic damage. Importantly, they also emphasized the patient perspective here. So if the symptoms are perceived to be difficult or important by the patients, that is also important and counts not just a rheumatologist perspective.
They also include in this new definition a subgroup of refractory to treatment patients and this means that these patients in addition to having symptoms, they also need to have objective evidence of inflammation either by blood tests, CRP, or by MRI, the evidence of inflammation in their spine. And this is to separate them from those who have other confounders that might affect symptoms like depression, fibromyalgia, so on. And this subgroup of maybe truly immunologically resistant patient might be a more focused target group for research or combination therapy or other approaches. So overall, I think this new ASUS definition is important. It's a step forward that is similar to other projects of difficult to treat patients in PSA and RA and hopefully will move this field forward and address this major issue that we all face in clinic a source or as tool to help us do better research and better manage our patients.
Thank you.
Hi. I'm Doctor. Sheila Reyes from The Philippines reporting live for RheumNow at the ACR Convergence twenty twenty four here in Washington DC. I would like to talk about abstract fourteen forty seven from the group of doctor Giselle and colleagues. It struck me a little bit interesting because they compared the frequency of cervical dish in patients with SPA versus age and sex matched controls.
So their findings showed that the frequency of DSH is the same for both populations and that SPA patients with DSH were significantly younger. Now interestingly, DSH was seen more in axSpA patients who were HLA b twenty seven positive while dish was reported more among psoriatic arthritis patients who were HLA b twenty seven negative. Now how can these results help us in clinical practice? Probably not as much, but at least knowing that dish is not just a mimic of axSpA, but that it can co occur or it can occur simultaneously with AXPA helps us to understand disease the disease of our patients, especially when we're already giving our biologic DMARDs or traditional DMARDs, and patients do not respond to treatment probably because it's not the inflammatory type of back pain that's causing the symptoms, but it's more of the mechanical type. So knowing these can also guide treatment decisions for clinicians.
Follow me on x at RheumNow, and tune in to RheumNow for more updates and news on the ACR convergence twenty twenty four.
Hi, my name is Akhil Sood. I'm reporting for RheumNow here at Washington DC. Today I want to talk about generative AI in rheumatology, the good, the bad, and the ugly. At ACR, of the biggest highlights has been artificial intelligence. It's exciting to think how AI can make our lives easier especially since so much of our work is tied to computers.
But this raises two questions, should AI handle all our tasks or just a select few and what are the risks? I had the opportunity to explore these questions firsthand. At ACR I presented abstract ten seventy six where we tested the ability of chat GBT to respond to questions about recombinant zoster vaccine in patients with thrombotic diseases. Here's what we did. We fed prompts into CHATGPT based on ACR and ACIP guidelines and we also had frequently asked questions available from the CDC.
And the results were interesting. CHATGPT responded to most prompts with high accuracy and completeness. But there was one instance were scored very poorly. And this brings me to the bad. While ChatGPT and other large language models can respond well to most questions, it carries the risk of misinformation and this risk comes down to two main factors.
First, the data these models are trained on. Second, the structure and the style of the prompts we input. And if we don't address these issues this brings me to the ugly. Misinformation in AI can have a ripple effect. It can increase bias and this can worsen inequities especially in our vulnerable populations.
So how do we fix this? For starters we need better and more prompts available and we need more representative data. And finally validation is key. AI models need to be tested in different settings before we can trust them in clinical practice. In conclusion generative AI has incredible potential but should we ask it to do everything?
Probably not. Some tasks are probably better left to us. And I'll close with a quote that I came across recently. I want AI to do my laundry dishes so I can focus on my art and writing. And maybe that's the point.
Let AI take care of the routine so we can focus on the more meaningful. Thank you.
This is Eric Dine from RheumNow. I'm a rheumatologist from New Jersey here in DC for day two of ACR convergence. I'm joined with, Parmita Das, a college student at UCLA who just, gave an oral abstract in the rheumatoid arthritis session. Tell me about your your research.
Yeah. So our my research is on RA mortality, and we looked at it by racial and ethnic groups to kinda see if RA mortality differs with these different groups. So we kinda use the data from CDC's wonder database, which has over ninety nine percent of all the deaths across The US. So it's a strong database, and we compiled this data. We did logistic regression analysis, and we did looked at ASMR.
And through that, we found that for native Americans, they had a significantly higher ASMR relative to all other racial and ethnic groups for RA.
I I think, unfortunately, that wasn't information that surprised me. What what really surprised me was the magnitude and that it seemed like there was a difference. It wasn't just at all ages. It was particularly in in younger younger patients with RA who are of that background. Tell me about that.
Yeah. So first are, like, we noticed that it was so the significance of, like, the increase in RA was so high. So then we're, let's look at it also by different age groups. So we looked at that. We looked specifically into three different age groups.
So 44 and below was our lowest. And in that, we found it was over tenfold higher difference in ASMR for Native Americans compared to all other racial and ethnic groups. And so that was very striking to us. We also looked at we further looked at that RA young RA RA mortality, and we looked at YPLL, which is years of potential life lost. And we found that it was almost 9.4 times higher in Native Americans compared to the lowest, ethnic group that we found, which is high.
And then also for younger females and younger males, they had the highest odds of death of RA mortality for Native Americans relative to the reference group of the white population.
Yeah. I thought that was just very dramatic and worth highlighting the fact that, you know, those younger individuals 44 that over a 10 times risk of death compared to patients with RA that were not from Native American background. So, unfortunately, it seems like your your data can't tell exactly why that is, but we know that there's socioeconomic factors. There's disease specific factors. And so sounds like it's something that we need to look into more and learn more about.
But I think it's definitely a huge need. It is. Yeah. So thank you so much for for doing that study, and and best of luck with medical school and Thank you. And for the journey into hopefully rheumatology.
Yeah. Thank you so much. It was great speaking with you.
Yep. Thank you very much. That's, day two of ACR Convergence. More on RheumNow.
Hello. This is Marina McGray again, reporting for RheumNow at ACR Convergence twenty twenty four in Washington DC. I'm going to report this very interesting abstract, is talking about precision immunotherapy in ankylosing spondylitis. This abstract was presented this afternoon. As we all know, ankylosing spondylitis is a T cell mediated disease.
However, you know, trying to deplete T cells is not possible because that would input the patients at a very high risk of infections. A subset of T cells have been, incrinated in pathogenesis of ankylosing spondylitis. The this subset carries this unique receptor t receptor b v nine. And this is this these cells are thought to, know, bind with the antigen presented by HLA b 27 positive cells and has been implicated in pathogenesis. In this abstract, a bispecific antibody was developed against this subset of T cells carrying this receptor, TRBV nine receptor.
They neutralized these cells showing to be with using this antibody, the risk of infections was low. Cytokine release was low with this binding. So the concern for cytokine release syndrome was minimum. And the recommendation was that by binding and, you know, or depleting this subset of T cells, one could reset these autoreactive T cells and produce long term remission in axial spondyloarthritis in AES. So it was very exciting, and, you know, I will have to wait till actual human studies are done with this bispecific antibody.
There there has been a case, report from Russia last year, which was published showing that these antibodies are work. So something very exciting for the future of axial spondyloarthritis. There was another abstract keeping up with the same theme presented today, which was which took patients with the you know, which had uveitis, acute anterior uveitis, HLA b twenty seven positive. So they took their ocular cells and blood cells, and they found that blocking this TR this T receptor, b v nine T cells may not be enough. They also found another receptor that may be implicated in patients with uveitis, t r b v five.
So they were there and what can the gist from that abstract was that blocking one one receptor may not be enough and maybe need to block both receptors. Well, this is, you know, very early data. Ultimately, it needs to be vetted in real human studies and see what works for our patients. Thank you so much.
Hi. I'm doctor Janet Pope. I'm here at RheumNow, ACR 2024 in lovely Washington DC with pretty good weather. Okay. I wanna talk about when, what to use, and for how long to treat GCA and PMR.
And I'll be covering a lot in a lot of my personal opinions in this, but there was a whole bunch of abstracts of RCTs, sixteen ninety five, sixteen ninety eight, sixteen ninety seven, and 1,700. So here's the take homes. Number one, cirulimumab is approved in The US and is a prednisone sparing drug. And doctor Jeff Curtis actually looked beyond that and found that cirulimumab was superior to methotrexate, looking at effectiveness from a very large database. And another group looked at a trial of methotrexate versus placebo and PMR.
And guess what? Methotrexate didn't do any sparing. So cicerolimumab is in for PMR and does steroid spare. And it's for PMR that has failed steroids, or it's recurred or you can't get the dose down. Okay, what do we do in GCA?
Number one, in GCA, the standard of care in many places now is starting at the beginning of a person with proven or highly suspected GCA, glucocorticoids, and an IL-six inhibitor, tocilizumab, which has approval in many countries. What if tocilizumab doesn't work? What if it's stopped and the patient rebounds? What if they're partial responders? Because there's never a 100% response.
We do know in PMR, if you withdraw tocilizumab at six months, even in PMR, the disease wakes up. So we know you have to go longer in PMR. We know that a lot of trial, the approval was based on the initial trial of Tocilizumab in GCA. So here's what we know. We know that upadacitinib fifteen mg a day is as superior to, placebo and a more rapid taper of glucocorticoids better benefit.
We don't know how long to use upadacitinib. We know there's an IL 17 trial underway, and we also know that there was an attempt using, IL-one inhibition with anakinra for four months that was not successful. It was underpowered but didn't show any benefit. So I think the take home is number one, GCA, use a steroid sparing drug from the beginning. Number two, PMR.
If it's difficult to treat, you can't get the steroids down or it relapses, consider a steroid sparing drug. We already have a menu with a couple options on it for each of those diseases and more will come. Follow us at RheumNow. Thank you.



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