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Hi, everyone. Jack Cush. I'm on the floor of the ACR Exhibit Hall. It's ACR convergence twenty twenty four. We're in Washington DC.

This is day one, morning one. We're excited to be here. Looks like a lively meeting. Lots of folks, lots of buzz. The exhibit floor and our booth is really happening.

If you're here at the meeting, come by, visit us. We'd love to meet you. Say hello. Give you one of the new RheumNow pens. Hope you like that.

I want to talk to you about what I think you should be doing and what's new at this meeting. You know, the meeting is is really the same meeting. Right? It's face to face and that's what people want. Some things are new.

And we have the same old sessions, the great debate. This morning they had the year in review. We're going to have knowledge bowl and other highlights including the wrap up at the end. But plenary sessions are have flipped. They're in the morning at 09:00 and the posters are beginning right about now at 10:30.

So that's something that's new. I think for you watching this video, how am I gonna learn the ACR? I'm gonna give you a few pointers that I think you should pay attention to. Number one, come to the meeting. See us at the booth.

Go to your favorite sessions. Number two, if you're at home, I'd recommend that you follow us on Twitter. On Twitter, you're going to get this constant stream of information and what's happening really right to the minute. And it's almost like watching a ticker tape of what's going on at the meeting. I think that's kind of exciting, but maybe you're not a Twitter person.

And maybe you wanna get a feel for what happened at the meeting. I'm gonna give you three ways that you can do that. Number one, that is at the end of every day at 6PM eastern time. We're gonna live stream the daily recap where it's gonna be me and three or four of the faculty, and we're gonna review the happenings of that day and what was notable, exciting, and something you wanna take home. Number two, starting next week when you get home, you can view the video that's gonna be called the lupus topic panel or the RA topic panel or the PSA.

We have topic panels with me and four experts in lupus, RA, etcetera. And we're gonna do RA, PSA, SPA, lupus, JAK inhibitors, tick inhibitors, and IL seventeen drugs. And so that's like six different videos that you'll be able to look at. And the third way that makes the most amount of sense is this go to the RheumNow website and you might already subscribe and get a daily email or a weekly email. But if you're an RA person or a lupus person, we have an email list and you could sign up, check the box.

I want the topic email list that'll come out once a week. And if you check the box on whatever topic you like, you're gonna get an email after ACR and all the lupus stuff that we produce. So you'll have that in your inbox to review. By the way, everything I just said that's in video form will also be in podcast form. You can listen to the daily recap podcast.

You can listen to the topic panels in a in a podcast. And you can also listen to podcast accumulated podcast reports from all our faculty who are here covering the meeting for you. Hope you enjoy this meeting. I'm going to. We'll talk more.

Hi. This is Eric Dine at RheumNow, Convergence day one from from New Jersey here on-site in DC, and I'm joined with Joshua Shay. So Joshua is a sophomore in

high school who did a fantastic job and and contributed, posted our presentation,

abstract four seventy four. So I wanted to hear a little bit about, tell me about your study.

Thanks Eric. Yeah, so what we did in our study was we conducted a systematic literature review looking at the association between rheumatoid arthritis and cancer patients survival. So to start this process we conducted a search within three databases and collected a total of about 2,000 studies. And between myself and two of my colleagues, we narrowed this down to 10 relevant studies to our question. And from there, from those 10 studies, we abstracted data from them.

And then my mentor, Doctor. Singh, she helped us line up our abstractions. And from this data we saw, we found that due to the heterogeneity and small number of studies, we couldn't do a meta analysis on these studies. That being said, we did find a hazard ratio for lung cancer patients in a subgroup of lung cancer patients and we found that there was no significant difference in mortality in lung cancer patients at RA or at RA. Yes,

I saw that the hazard ratio was one point zero four, so essentially no difference in survival. So I guess that means that if we were talking to patients about what their survival risk would be for lung cancer, we'd say, based on the studies, that there really wasn't a significant difference, but it sounds like the biggest problem was just that there wasn't enough studies to do too much analysis for.

Yes, that's correct. I think one of our main takeaways from the study was that since there weren't very many studies out there and they were very conflicting, it shows the necessity for future large scale studies that look at this association between rheumatoid arthritis and cancer. So I think it really stretches that importance for the future.

We know that rheumatoid arthritis is a

risk factor for development of some cancers, it's really helpful that if we could get that data and see what can we say to our patient that has a new diagnosis of cancer and their survival.

I'm encouraged that with lung cancer that there was no clear signal and hopefully use this research and use it as an impetus to do more studies and get more information. Thank you very much. It's wonderful to have a high school student here with us

and really phenomenal that you're on it. So hopefully, and hopefully medicine that

we can get you in the fold into the rheumatology field really. Best of luck with your training. Hello,

my name is Manalini Day. I'm a fellow in The UK and I'm here at ACR twenty twenty four in Washington DC reporting for RheumNow. And I would like to highlight abstract one six seven six, which is being presented today on Sunday of the press, which is on changing the mindset of people taking methotrexate with with regards to the side effects. Now, this really caught my eye because as a clinician, we prescribe methotrexate quite a lot. I see a lot of patients with rheumatoid arthritis in my practice, and it's often quite a significant part of the conversation about what the side effects would be, and also many patients do come back after a while and do say they're reporting side effects such as nausea and various other side effects as well.

And so, this abstract really looked at whether we can use an intervention in order to just reframe those side effects to positive signals and see if that actually changes patients perceptions off whether to continue with their drug and how they see those side effects. So this was an abstract that came out of work done in Switzerland and it involved forty seven patients with inflammatory arthritis and twenty six of these patients did experience a side effect. But with the intervention, most of them were able to reframe the side effects of positive signals. So what was this intervention? So the intervention was approximately a seven minute video, which was sort of basically reframing the non severe symptoms of methexate as positive signs that the medication is actually working.

And so, in the end, the group found that the mindset intervention in the form of this video reframes the role of these non severe side effects. And this looks to be a good approach in which to improve the symptom experience and also crucially just keeping the patients on this drug which we know works for conditions such as rheumatoid arthritis. This is something really to think about because actually creating a video, while it does take a little bit of work, it clearly is a good investment in ensuring that our patients are able to understand the side effects of their medications more. Provided it's framed in the correct way, it can actually improve aspects of just medication adherence, for example. So if you'd like to know more about that particular abstract it was sixteen seventy six and if you'd like to know more about everything going on here at ACR twenty twenty four do head over to the RheumNow website or you can follow me on x doctor.

Vk. Thank you.

Hi this is Doctor. Jiha Lee, a rheumatologist from Michigan at ACR Convergence in Washington DC. I'm here with Doctor. Elam from Augusta University to talk about her abstract number seventeen forty six looking at incidence osteoporotic fracture in RA population and its relationship to disease activity. As we all know patients with rheumatoid arthritis are at an increased risk of osteoporosis and it affects their mobility and function especially in older adults and it's an important comorbidity that we need to address.

And so Doctor. Ellen, what are the traditional risk factors that we consider about and what tools and approaches do we have and what made you think that we need to look at disease activity as a measure when we think about this population? Sure.

Great questions. So traditional risk factors that we usually think about when we're risk stratifying for fracture are participants age or people's age. The older you get, the more at risk of fracture you are. There's also race and ethnicity factors as well as your sex, but those are things that aren't modifiable. So the more important things to look at to me are modifiable risk factors.

Things like smoking, alcohol use, glucocorticoid use and then having RA is a risk factor. At this point we haven't got to the scientific level where we can prevent RA from happening, but there is some data that if you have higher rheumatoid arthritis disease activity, so more active RA, that leads to less bone density or a weaker quality of bone and then also leads to fracture. So that's what made me interested in wanting to use RA disease activity to maybe help us predict or at least know the incidence rates of fracture by how active the RA disease is.

And we do know that the goal is to go for remission or lose disease activity because not only does it occur ARIA related outcomes but other comorbidities. And the FRACS score only asked for the yes and no, but you're trying to get at the more granular level. And when you looked at this, what kind of trends did you find?

Right. So what we saw was that the two different fracture outcomes we looked at in our study were the two fracture outcomes that we use in the FRACS model which are hip fracture and major osteoporotic fracture which is a composite of distal forearm, upper arm, spine or hip fracture. And so we looked at these two outcomes and we saw that for hip fracture if you have high disease activity level compared to someone in RA remission you had higher rates of hip fracture. And then for major osteoporotic fracture, we found that whatever level of disease activity you were above remission. So low, moderate, or high disease activity level compared to RA remission had greater rates of major osteoporotic fracture.

And how do you bring this into the conversation with the patient when you're trying to talk to them about how to mitigate the risk, whether it be in terms of lifestyle or thinking about how you approach RA treatment?

Yeah, so I think that it's usually not hard to convince an RA patient that they want to be on treatment usually because a lot of them are having joint pain and symptoms that make them want to get treated but there are some patients who maybe don't see the benefit of doing a biologic therapy over the medicine that they're already on and this can add to the data that we have to suggest that really reaching that remission target has benefits even outside of what they're perceiving on the day to day in their joints. And then also something that this study didn't look at but something we're planning to look at in the future is the issue of glucocorticoids which we know to be a strong risk factor for fracture and something that is still used to control RA. And so this just gives us kind of makes the thinking more complex here. Is it that if we control RA, but we're controlling it with glucocorticoids, those are bad for bone health. Maybe we need to make sure we're controlling it with something other than glucocorticoids.

And that's sort of the next steps in what I wanna look at with this project.

Wonderful, so as you said we know that RA patients have a higher risk of osteoporosis for two to three folds so as Doctor. Alamo was saying it's not just about the unmodifiable risk factors but what we can play a role in is in modifiable risk factors particularly when it comes to disease activity because that is where our skill set lies. Aim for remission and treat the patient especially when it comes to older adults.

Hello. My name is Rinalini Day. I'm a clinical research fellow in London in The UK, and I'm delighted to be reporting for RheumNow here in Washington DC at ACR twenty twenty four. I'd love to highlight an abstract that was presented at the congress one seven one nine on cumulative glucocorticoid exposure major adverse cardiovascular events or MACE. So up to seventy five percent of patients take steroids at any given time for rheumatoid arthritis.

It's obviously one of the most common drugs that we do use and we know that the side effects of steroids can include metabolic syndrome and increased risk of cardiovascular events. So this was study that was done in the veteran affairs cohort, and it was looking at cumulative glucocorticoid exposure and how that relates to future MACE risk. And actually, this study found that in this it was a retrospective matched nested case control study, and this found that that greater cumulative steroid exposure was associated with greater risk of MACE regardless of baseline MACE risk. So why is this important? So we've known for a very long time that rheumatoid arthritis is associated with an increased risk of cardiovascular disease, but clearly more needs to be done in order to manage the risk factors much more.

And we've heard quite a lot about that during the congress. In this case, really, there is evidence that we should be doing more to try and reduce the cumulative MACE exposure and try to get people onto disease modifying agents much quicker where possible. In relation to this, I know that in the aging session, there were some data presented, particularly with in people with late onset rheumatoid arthritis that, quite a large proportion of those patients are not getting onto DMARDs, at all, and many of them do remain on steroids. These are the people who do have the greatest risk of cardiovascular disease in any case. So this was a really good piece of work that just adds to this growing body of evidence with steroids, with comorbidities, including cardiovascular comorbidities, and that was abstract one seven one nine.

If you'd like to know more about everything going on here at ACR twenty twenty four, do head over to the RheumNow website for more information. Thank you.

Hello, everyone. I'm Richard Conway reporting for RheumNow from ACR twenty twenty four. I'm here to talk to you today about a study presented in the RA ILD abstract session on Saturday. This was study abstract eight zero two from Gregory McDermott and Geoff Sparks Group. And this was the SAIL RA study, so multicenter prospective study of patients with early rheumatoid arthritis.

So less than two years of disease on recruitment to the study. There are one hundred and seventy two patients in the present analysis. And the interest of this particular presentation was looking lung disease. And first things, the numbers with lung disease were quite interesting. So sixteen percent of these patients with early rheumatoid arthritis had RA lung disease.

Now, that's just kind of a broad term and included interstitial lung disease, emphysema, and bronchiectasis. And perhaps one could argue that the second two of those would be rheumatoid related, but could also be related to other things. But it's still a relatively high number. And when they looked at just interstitial lung disease, eleven percent of patients had interstitial lung disease. Now, that is a high number compared to certainly some of the more revisionist estimates of how many patients with rheumatoid arthritis get interstitial lung disease.

And do remember, again, this is patients with early rheumatoid. This is early on in the disease course. Potentially later on, even more of these patients will have interstitial lung disease. So they went and looked and analyzed with a multi variable analysis about what predictors there might be of patients who do get lung disease. And for rheumatoid lung disease, so the three things, interstitial lung disease, emphysema, bronchiectasis, two things we know about, so age and being male.

So about twice the risk and with increasing age, four times the risk if you are male. And then the one which I find really interesting, moderate to high disease activity, four point eight nine was the risk with us. It got even more interesting when they looked at interstitial lung disease and in that alone, so interstitial lung is alone, the moderate to high disease activity, the number was six point one seven for having moderate to high disease activity. So this suggests a couple of things to me. It does seem that disease activity is really important in the development of interstitial lung disease and rheumatoid arthritis.

It suggests that maybe there is an amplification of this window of opportunity concept that we have in rheumatoid for these patients. And it's even more important to really aggressively treat patients who might be falling into these risk groups at the start to prevent the development of interstitial lung disease. And then the thing that I know everybody is waiting for me to say, the ACR guidelines, our recent ACR ILD guidelines. For rheumatoid arthritis ILD, they recommend as their first line treatment options agents that have either very limited effect on disease activity or not as good as other agents we have on disease activity, so especially mycophenolate mofetil, azathioprine. And this is another piece of evidence and something in support of what I have said from the start.

And that really the first thing we should be doing when we're trying to treat people who have rheumatoid interstitial lung disease is controlling their disease activity with whatever agent we need to do that. And then we can worry about what may or may not be better from the limited evidence we have for the interstitial lung disease itself. So I've been Richard P. A. Conway on Twitter and follow RheumNow for all the updates from ACR twenty twenty four.

I'm Richard Conway reporting for RheumNow from ACR twenty twenty four. And today, I'm going to talk to you about an abstract presented in Sunday's poster session. This was by Mark Gibson and colleagues from King's College London. It's abstract number nine eighty nine. So this was a Bayesian network meta analysis.

And I know a few people have already glazed over that combination of words, but I'm going to try and keep it real simple for everyone. And we'll try not to get too bogged down in the details. But I think it's an important and provocative study that's been presented. So this was looking at malignancy. And it was looking at JAK inhibitors, TNF inhibitors, and patients on placebo, and trying to compare those different groups.

It was across inflammatory diseases. So there's patients with rheumatoid arthritis, with psoriatic arthritis, with psoriasis, and with inflammatory bowel disease, and axial spondyloarthritis. They included one hundred and ninety six studies. So this is a large meta analysis. They had over one hundred and twenty thousand patients and one hundred and thirty thousand patient years of exposure.

There were sixty eight thousand patient years of exposure to JAK inhibitors, fifty six thousand to TNF inhibitors, and ten thousand to placebo. During this, they saw just over one thousand malignancies when they excluded non melanoma skin cancer. So this is other malignancies. Now, it said it's a Bayesian network meta analysis sort of figures they report as a log ratio, which is we're not used to looking at that. It's confusing to us.

So I'm not going to get too bogged down in it. If you want to go check out the poster, please do for those finer details. But I'll just stick to the bottom line of what they found, because I think it's very interesting. So they found that TNF inhibitors had a significantly lower risk of malignancy than JAK inhibitors. So we expect this given oral surveillance.

So this kind of fits with our priors. But then it got really interesting. So TNF inhibitors compared to placebo have a significantly lower risk of malignancy. JAK inhibitors compared to placebo seem similar for any type of cancer. And JAK inhibitors seem to have a lower risk than placebo for hematological malignancies.

So this is a very provocative study, I would say. It's kind of jiving with what some of us have been saying about oral surveillance, that maybe it's not that the JAKs are bad, it's that the TNFs are good at preventing malignancy. It's one meta analysis. We can't place too much weight in it, but I think it's a very, very interesting one. So I'm Richard Conway.

You can follow me on Twitter at RichardPAConway. Remember to tune into RheumNow for all the best coverage from ACR twenty twenty four.

Hi, everyone. Jack Cush here on the Convention floor at ACR twenty twenty four. Great meeting, even better when I run into great friend, great colleague, great mentor, doctor Ted Pincus. Ted, how long have we known each other?

Oh, close to forty years,

I think. Yeah.

Yeah. He's still trying to teach me. Yeah. So we met on the on the

And you're teaching me, sir.

Well, that's the great thing about education, right? It's it's always the give and take. Yep. So we met on the poster floor yesterday. We were talking about a poster that Ted did today that was about estimating using a scale that you can use at practical use for patients that'll address a lot of things that we often don't address.

Tell me kind of what you did.

Okay. So the impetus for all of this is that, as you know, even before Jack was a fellow, we were taught that we should do a formal joint count on all patients with rheumatoid arthritis. Most doctors don't do that. And there's a simple reason for that, I think, which is that a joint exam can be performed in fifteen seconds that tells us whether we have two, twelve, or 22 swollen joints, and we can make a clinical decision. But in order to recognize whether we have one or two or 11 or 12 or 21 or 22, we have spend an extra sixty to ninety seconds to write down 54 clicks or notations of a joint count.

So we developed a zero to 10 scale for inflammation, which we have found actually explains variation in the swollen joint count at our poster with a correlation of point seven versus a physician global of point three seven, so it's twice as likely to be, found there. In addition though, we've added a zero to 10 global scale for the physician for damage and for patient distress. And it turns out today, and this has been found now in New York, Chicago, Nashville, and Sydney, Australia, that the scores for damage and patient distress are actually higher than inflammation. So and, unfortunately, the original 28 joint count included a score for deformity or limited motion, which has been dropped from the 28 joint count that's done in clinical care because in clinical trials, you don't include that. And so we only measure tenderness and swelling, but we should be aware of damage because we have now data of several, RA cohorts where the median swollen joint count is zero, meaning that half the patients have no swollen joints, but the median pain score remains four to five, and that's because of damaged joints and patient distress.

And that shows up on the scale, on

these scales. Right? Yes. Absolutely.

That's wonderful.

That's where the data come from, Jack.

Okay. So when you are taking these scales and putting them into practice, give me a practical application as to how it works. The good one was that one right there. The SJC swallow is zero. Right.

And then but these are abnormal. How does that going to affect what you do next?

Well, for example, I have seen a number of patients who've been tried on five or six biologicals who have a damage score of five and a patient distress score of five. And these patients,

have

to think about because all I'm really doing by giving them another medication is exposing them to side effects that isn't gonna necessarily help them.

Right.

So I think we should recognize that because that's true in all rheumatic diseases, as you know. Damage, once it occurs, and we published, only around 1979 that seventy percent of patients with rheumatoid arthritis have erosions within the first two years of disease, And it's still the case that from first symptom to biological is one point four years in our clinic. Right. All the patients have damage, which proceeds on a biomechanical basis. So it's the real issue now is early treatment if we're going to meet the best capacities of our biological agents.

So I wanna tell the audience that this man is responsible for the hack, the modified hack, the MD hack. Rapid three, and at his center, when he was in Vanderbilt, his center developed the 28 joint count. So when Ted Pinkus comes with scales that you should be using to estimate what's going on, where can people start to use this? Or where is this gonna go?

I I use it in all patient. I've been doing that for twenty years. And there's a very important point that I'd like to make to anybody who's listening to, watching this, video, which is that it actually saves you time to have an MD hack. It saved me three minutes. I used to see 30 patients a day when I was very active, and most of the doctors could see 20 or 25 because I saved three minutes on average per patient.

And the Rheumatrix takes, which is the scales with the 10 clicks, takes about twenty seconds, whereas a 28 joint count takes ninety to a hundred and twenty seconds, which we published in the past. So you're actually saving time by using these tools and having quantitative data about damage and patient distress really helps you a lot.

Do you know the poster number?

Poster number, I have it in my pocket if Okay.

I'll I'll I'll you look it up and I'll I'll I'll close. So make sure you tune in for more videos and more content. Again, we everything on video is gonna show up in daily podcasts and in podcasts and whatnot. So, hopefully, you'll follow this poster and this report. Here we are.

Poster 1077. Check it out. Thanks very much.

Hello. I'm Jonathan Kaye reporting from ACR Convergence twenty twenty four in Washington DC on day one of this meeting. I'm here with professor Ernest Choi of Cardiff, Wales who presented poster number five six zero about a transcriptomic analysis of blood from patients with a variety of inflammatory rheumatologic diseases treated with a variety of combinations. And the question is, can you identify a subpopulation that is most responsive to specific combinations of therapy or specific therapies that could be used in combination to better treat our patients? So Ernest, tell us a little bit about your poster.

Okay, so as you know, rheumatologists are spoiled for choice. We have lots of lots of different classes of advanced therapy, but as you know, most patients actually don't

solely do remission, which is

the goal of treat to target. So there's a desire to use treat to target, to find the right combination is not that easy. So we developed this program trying to see whether we can find a logical way to find the best combination quicker before we test any patients. So the program is to take on advantage of the bile that are available in Spain. This patient has a range of different polyinflammatory diseases treated by viral therapy.

So the first step is to identify the genes that may be driving the active disease in the non responder. And then the hypothesis is that to find the right combination means we must find a drug that will suppress this actively expressed genes in the nonresponse. So we pull the result of all the responders to the biologic agent, and we have reasoned that the genes that are suppressed by this treatment if it mapped to the actively activated genome of the responder, then we should find the best combination. And what was surprising in this analysis that we find actually many of the biologic agents have fairly overlapping effects. The benefit from combining them will not be great.

But we did find one combination which is TNF plus an IL-six inhibitor. Together they seem to have complementary effect in patients with rheumatoid. So the next step was to do in this experimental study is to do a clinical trial to see whether we can prove that this is the case.

So this is a different approach from Kospitallis' approach in the R4R trial where he found that there were three different subtypes of rheumatoid arthritis, which lymphocytic form or myeloid form and a fibroblast driven form, each of which probably respond to different therapies that are directed toward that cell type which is most active in that disease subtype. So you're looking at a relatively heterogeneous mix of non responders. Are there any signals that you pick up in terms of transcriptomes which might indicate what cell type is not responding to the current therapy?

Yeah. That was a great question because we when we did single cell sequences, most of the response was mapped to the myeloid population. So it is possible that it's myeloid.

Would you be able to look at a different population or a different way of analyzing this biobank to come up with perhaps an emphysetic driven disease or fibroblast driven disease, looking at scleroderma patients or interstitial lung disease, to try to come up with a combination that would work better in a fibrotic disease?

So that's part of cost collaboration with you. I think for myeloid disease it's possible to find similar fibrones. Very hard for fibrones. In general fibrotic disease you need to go to the tissue to find the right symmetry. So yeah, so it's something that we're gonna move forward to.

I think the results are complementary. I completely sign up to the fact that RheumNow, Francis has had the genes. But the but, you know, it's not abstinence.

So this work suggests that the next era of biologic therapy will be looking at combinations of biologic therapy. Gastroenterologists are already ahead of us in that they're looking at Vedalizumab in combination with TNF inhibitors, finding that the combination is superior to either alone. So this is very interesting work. As always, you're doing great work at the cutting edge. Thank you so much for talking with us about this.

For more about ACR Convergence 2024, I'm Jonathan Kaye for RheumNow. Go to rheumnow.com.

Hello. I'm doctor Guillermo Valenzuela. I am reporting from ACR twenty twenty four from Washington DC. Today, I will be quickly the concepts related to the poster L10, which relates to the neuro immune modulation in adult patients with rheumatoid arthritis with bio DMARDs targeted synthetic DMARDs, inadequate responses at 12 and 24 using a sham controlled double blind. So you'll be surprised to know that this is not a therapeutic intervention with a traditional oral medication or a biologic medication, but this is using implantable device that stimulates the vagus nerve.

Of concern to many and interesting aspect of the science as I will show you further. So the purpose was to evaluate essentially the safety and efficacy of an implantable device in the cervical vagus region. And patients would be subject to constant daily stimulation. The total cohort in this study was two forty two patients that were randomized in a one to one ratio to a sham, which was essentially the device being turned off for the first twelve weeks and then every patient coming onto the active arm after twelve weeks of treatment. So this double blind assessment allowed to obtain information during the first twelve weeks which were critical to understanding perhaps the signal that therapeutic intervention could show.

So the patients had to have a previous failure to at least one Bio DMAR or one targeted synthetic DMARC. There were secondary endpoints that were also as important as the primary, which was the ACR20. And the secondary endpoints included DAS28, MCID, HAC, and one important one that perhaps gave this study a value of objective assessment was the erosion progression score using a Rambris score. So that would work essentially as control of the activity. And also the DAS remission was part of the secondary endpoints.

After week twelve, as I mentioned before, there was an active crossover. So every patient at week twelve received the neuromodulation by this device, was surgically implanted in left, in the vagus nerve of these patients. Just a word about the demographics, patients were an average of 56 years of age and eighty six percent of these were females and the average duration of disease was close to twelve years. In terms of the breakdown of previous exposure to therapies, it's interesting to know that the patients who received bio DMARDs, thirty nine percent of them had failed one previous DMARDs, about twenty two percent two DMARDs, and three DMARDs about thirty nine percent of them. Fifty three percent of these patients were seropositive and the high sensitivity C reactive protein was 8.2 milligrams per liter.

So important now is the results. At week 12, we saw a statistically significant difference in the groups, in the active groups versus the sham groups. There was a thirty five percent of the patients who achieved a ACR twenty versus a twenty four percent in the sham group, which gave a P value of 0.02. Now, it's even important to see that week 24, fifty one percent of the patients on the active group continued to show ACR 20s, of which fifty three percent of them were the ones who were previously in the sham group. So all the secondary exploratory endpoints also show a tendency that correlated with the ACR scores.

In other words, there an accomplishment of the goals of the secondary endpoints, such as one of the most important ones perhaps is week 12, the CRP Low Disease Activity DAT score. There's also the progression of the erosion through MRI was demonstrated. And the most important one which you can all think about is safety. Regardless of the surgical nature of the procedure, it was a rather safe procedure. Serious adverse events were only one point seven percent.

And as we can imagine the most common adverse event was a post surgical transient hoarseness and related symptoms to the surgical procedure itself. There were no reported deaths and as a conclusion, I think this is a very interesting and absolutely novel way to modulate rheumatoid arthritis by a non traditional mechanism, which is not an oral agent or injectable agent or infusible agent as we are accustomed to seeing our armamentarium is rather an implantable device with all the implications that it brings up. So perhaps the final word would be, we are interested in knowing the long term effects of these outcomes, and I hope to be able to report those findings in the next presentation. Thank you very much.

Hi, this is Bella Mehta reporting for RheumNow. I came across a very interesting abstract looking at lab testing in rheumatology patients and when should we be doing this. So this is abstract number 2,619. And in this retrospective cohort study, they used a large national health organization database. And they had around five or six thousand adult patients with rheumatoid arthritis, spondyloarthritis, psoriatic arthritis, as well as IBD.

And these patients were either treated with biologics or synthetic DMARDs as monotherapy, and they were followed for at least twelve months. So they looked at these patients and saw how many times did they get routine blood monitoring that we usually recommend for every three months or so. It was interesting that this study found only nineteen percent of patients who were either on biologics or synthetic DMARDs were adherent

to

the three month recommendation. And even looking at those labs, most of the lab abnormalities that they found were not clinically significant. The sort of at least they found some signals saying patients who were older had comorbidities or were using either IL six inhibitors or rituximab, the likelihood of having some lab abnormalities were higher. But those with just ENFs with RA, they had fewer issues. So maybe we recommending every three months of lab monitoring may not be necessary for all groups.

And again, this comes to the fact that everybody's talking about, which is personalized medicine. You know? Plus, there's a lot of cost burden to the system as well as the patient coming in going to do labs. So personalized testing intervals can also be something that we should be looking at in the future based on the medication type, patient risk factors, and whatnot. So, with that, I'm signing off here, and follow me for more updates on Twitter at Bella underscore Mehta and RheumNow.

Thank you.

Hi. I'm Anthony Chan reporting here for RheumNow in Washington and ACR twenty '24. And today, I have with me professor Andrew Cope from London who is the author of the Epipra study who presented the data last year. But here at ACR twenty twenty four, there is a follow-up information on the Epipara study. So Andrew, welcome.

Tony, it's good to be back.

So tell me tell us about the trial design for the Epipara study.

Yes. So Epipara was a randomized controlled trial of 213 at risk individuals. So positive anti CCP or ACPA or together with arthralgia. And these were randomized to receive one year of abatacept or placebo and then they were followed up for a year after that. And what we found and what we discussed with you guys last year was that on drug there were very few events, few people progressing to RA compared to placebo where there were a substantial number particularly over the first six months and then when the drug was stopped we saw a subset of people receiving abadacept progressing to RA but by twenty four months there was still separation of the survival curves, really suggesting to us that there may be something else going on long term and that prompted the follow-up.

So you followed up these patients and what's the outcome?

Yes, so we enrolled and we invited all of the study subjects to come back in for follow-up and we managed to enroll a 143 of those. And because there was a gap between a and Alto, we actually there was a delay and so some of the individuals who were recruited at the beginning of a pipra were followed up for almost eight years and then those who were the last enrolled in the pipra we got at least four years of follow-up. All of the 143 were followed up for at least four years in total. That's one year treatment and three years of observation.

So some of these patients were high risk of developing rheumatoid arthritis how did they do in the follow-up phase?

So the big surprise was that was that the the separation of the survival curves persisted to just beyond four years and we saw a statistical difference there. And what was interesting is when we looked particularly at the individuals who either had developed RA or three swollen joints or had started DMARD, the survival curves sort of didn't converge for almost almost five years.

So looking at those with positive autoantibodies, what were their sort of clinical features?

Yes. So the really striking thing was that those individuals with high t to anti CCP or a sort of a more complex extended autoantibody profile were at much higher risk of progressing that was true in Epipipra and also in the Alto follow-up but the striking thing was that these individuals were also more sensitive to the abadacept treatment so we have a high risk progressive group but who appear more responsive to drug and we saw that extending out to four to five years.

And in terms of clinical features either clinical exam or ultrasound did you see any differences?

Yeah we had a good look at that. So one of the things that identifies risk is we do it in the clinic the MCP joint squeeze and it turns out that if you identify those who had tender MCP joints and had these high teto autoantibodies, their risk of progression was even higher so that was one group and then we did ultrasound at baseline and every six months during the Epipra study not during ALTO. And those who had a PD score of one or more at baseline were much more likely to progress together with the extended serotype whereas those who had no PD signal and there were quite a lot of those in Epipra, their progression rates were were much less. So it's we we've we've sort of the high risk phenotype is the joint pain, the auto antibodies, the distribution of joint pain, and the ultrasound scores.

That's very positive. So there you have have it. That's the kind of longer term follow-up from the EpiprA results which was presented last year and nice to see these patients continuing to respond long term. So, Endy, thank you very much for your time today. This is Anthony Chan reporting from RheumNow in ACR twenty twenty four.

Hello. My name is Rinalini Day. I am a clinical fellow and trainee in London in The UK, and I'm delighted to be reporting for ACR twenty four here in Washington for RheumNow. There was a fantastic session earlier today on RAILD, and I'd just like to highlight one particular abstract, zero eight zero three, which was on serum adipokines and the risks associated with RAILD. So as we know, adipokines have been associated, of course, with metabolic syndrome, but also they have been seen to be associated with the incidence of idiopathic pulmonary fibrosis, which is obviously closely related to ILD, but the evidence within RA ILD specifically is still lacking.

So in this particular study, this was conducted in the Veterans Affairs Rheumatoid Arthritis cohort. There was just under three thousand patients who had prevalent ILD. And they found that while there was no association between adipok ines and prevalent, or incident ILD, there was an association with prognosis. So specifically, fibroblast fibroblast growth factor 21 was associated with a poorer prognosis in people with RAILD. So why is this important?

So we know that metabolic dysregulation in our patients with rheumatoid arthritis is an important topic. Extra articular manifestations in general and comorbidities, We know that they should be managed better in order to improve outcomes in our patients with rheumatoid arthritis. So this just adds to that growing database of evidence that we have, on this topic. And the fact that adipokines are so closely associated with the prognosis in RAILD tells us that we should be doing more to manage aspects such as healthy living, obesity, and weight management in our patients in order to improve outcomes not just for their disease activity and their quality of life but also aspects such as their extra articular manifestations such as RAILD. If you'd like to know more that was abstract eight zero three And you can also check out the RheumNow website for further updates, or you can follow me at doctor mini day on x as well during the conference.

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 is a a college student at UCLA who just gave an oral abstract in the 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 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 like, 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, 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 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. I'm Jonathan Kay reporting from the first day of ACR convergence twenty twenty four in Washington DC. Today at abstract four six four poster, there was a presentation about paraoxonase one as a predictive biomarker for progression from anti CCP positive patients at risk for developing rheumatoid arthritis to developing inflammatory arthritis. Paraoxonase one is an HDL associated enzyme which is involved in metabolizing oxidized lipids, and elevated levels of paroxonase one are associated with a reduced risk of cardiovascular events. In this study, the investigators looked at the sera cohort of anti CCP positive patients at risk for developing rheumatoid arthritis, collected at University of Colorado by Kevin Dean and colleagues, and looked at paraoxonase one levels and found that paraoxonase one, when elevated, actually predicted a decreased risk of progression to inflammatory arthritis.

So this is very interesting. This is an enzyme on HDL cholesterol which metabolizes oxidized lipids and seems to both decrease the risk of developing cardiovascular disease as well as decrease the risk of progression to rheumatoid arthritis. Future studies should be directed at looking at the genes and coding for this protein, and look for association between genetic polymorphisms and progression to inflammatory arthritis. This will be a very interesting area to study because there are large cohorts of patients with rheumatoid arthritis who've had increased risk of cardiovascular events. For example, those in the oral surveillance study treated with tofacitinib, and to see what the correlation might be, between paroxinase one and cardiovascular events on a JAK inhibitor.

Very interesting topic, much to come in the future. I'm Jonathan Kaye from ACR Convergence twenty twenty four in Washington. For more on this and other abstracts, please go to roomnow.com.

Hi. I'm doctor Jeehao Li reporting for RheumNow at ACR Convergence twenty twenty four in Washington DC. And this morning, have I doctor Beth Wallace, an assistant professor from University of Michigan Ann Arbor and the Ann Arbor VA. And we're gonna talk about some of her work that pertains to steroid tapering. She has abstract number 02031719, and she was also part of a scientific session 17 s 19 with discussing on this topic.

So the discovery of steroid in 1950 was a pivotal moment in medicine and it was awarded the Nobel Prize but increasingly there's scrutiny regarding its long term use and we're going to

delve into what that means for rheumatology. So, Wallace, how risky is steroid use? Well, when steroids initially came out they were touted as a miracle cure for rheumatoid arthritis but within a few years of that seminal paper that won the Nobel Prize, we started to realize that steroids had fairly significant toxicity. And that toxicity has really been a problem for over seventy years. We've learned a lot about the risk of high dose steroids over that time, but really only over the past ten to twenty years have we learned that even low doses of steroids and even short durations of steroids can be very toxic.

Even fourteen to thirty days of steroids can be associated with increased risks of serious infections, gastrointestinal bleeds, broken bones, blood clots and these risks really should be discussed with patients when we're prescribing steroids for them.

That duration is shorter than what we would expect because with bridge therapy it's very common we have to use it for a couple of months. So how low is a low dose steroid and how bad or how much long term and low dose steroid are we seeing in rheumatology patients?

So the definition of low dose is really variable depending on who you ask. In the guidelines it's been cited anywhere from five to ten milligrams but the consensus now is really anything below about seven point five milligrams is considered low dose. That being said, even doses as low as two and a half milligrams have been shown to have toxicity so we can't assume that five, below five, is safe.

How much are we seeing in terms of this low dose long term steroid use and are physicians aware of it?

Yeah, anywhere from onethree to onetwo of RA patients use steroids long term and the definition used in the literature typically for long term is more than about ninety days or three months. About onethree to onetwo of patients who start steroids when they're diagnosed with RA are still on steroids twelve months later. And a lot of this is because we have trouble tapering people off steroids once they start, not because people mean to remain on steroids for that long.

The tapering is an interesting question. I don't think it's definitely in our guidelines to recommend to do so, but it's not routinely taught or do we know actually how to do that. What are some challenges with tapering?

Yeah, tapering is definitely an art and not a science. Part of the reason for that is the studies that have been done around steroids, particularly in rheumatoid arthritis, which I study, focus on their effectiveness at various doses and not really their safety or the ability to get people off of them. We're realizing that now, especially since the guidelines, the American College of Rheumatology guidelines, are now recommending against steroid use when possible in RA, but we really need more data to help us learn how to effectively get people off steroids once they start. One major problem is when people have symptoms, when they taper, we don't always know why. We don't know if it's because it's their disease coming back, their rheumatoid arthritis coming back.

We don't know if it's because they have problems, endocrinology problems related to high dose steroid use or even low dose steroid use having to do with their adrenal glands. We don't know if it's because of something called the steroid withdrawal syndrome which is a very common complex of symptoms that happens when people reduce their steroid dose and don't have physiologic issues. We need more studies looking at that question. Steroid withdrawal syndrome, what kind

of symptoms would that be and how do you differentiate that from chronic pain or fatigue syndrome that our

patients already commonly have? It's extremely difficult to differentiate it. Way that steroid withdrawal syndrome is defined in the literature is any symptoms that happen when you taper steroids that aren't because of your disease coming back and aren't because of an endocrinology problem. So it's very very difficult to distinguish those things. The symptoms are very non They're things like fatigue, muscle and joint pain, can be nausea or GI upset, can be mood disturbances and these things very commonly happen with active rheumatoid arthritis.

They also very commonly happen with adrenal insufficiency or endocrine issues related to steroid take rate. So again, we need more data, need more research to learn how to differentiate these things from each other.

Absolutely. And I think one of the key themes that I'm hearing throughout this conference is that we need to aim for remission, but also that remission should be steroid free because as you said, there's a lot of documented steroid use, but I think I saw in one of your work is that there's also stockpiling of steroids and patients may be taking annoyingly. So we need to actually make a concerted effort to ask about their active use. So until we have some approaches, what should rheumatologists do? Does the amount of steroid that they're started on at the beginning have any correlation with how much steroids that are on at the end and how do you approach taper now when we actually don't

have evidence but need to inform and engage patients now? Yeah, the factors that influence how much steroids people remain on are not clearly known yet. Some that have been suggested are if you have more chronic pain, you tend to remain on steroids for longer. If your RA is more active or more severe at the beginning and if you don't get enough what we call steroids bearing treatment. So the disease modifying drugs we have for rheumatoid arthritis that do not include steroids.

We should really be trying to get people on adequate treatment quickly which we've known for many years to target in rheumatology, especially rheumatoid arthritis. When we do taper, we should make sure patients have their disease in remission or at least low disease activity before we start. We should start relatively quickly above a dose of about ten mg, so reduce by ten or twenty mg every one to two weeks down to ten, but below ten or really seven point five to five mg we need to go a lot slower. When people have symptoms, it would be helpful. It's helpful if we can try to figure out what those symptoms are from, so try to differentiate whether someone's disease is active versus they're having symptoms from another reason.

But if you can't do that and you end up going back up on the steroid dose or the patient themselves goes up on the steroid dose because about a quarter to a third of patients, as you said, have a stockpile of steroids at home, resume a slower taper and that can mean reducing the dose by one milligram with a larger interval. So maybe instead of one milligram a month, one milligram every six weeks. Or it could mean alternating. So instead of going from five to four milligrams, going from five every day to five for alternating or even from five every day to five every day except one day before and a lot of people will tolerate a slower taper like that with less symptoms.

What I see from you from that is that it's not a one size fits all and that if you fail tapering one time doesn't mean this person is not going to be able to taper down. Just have to be more cognizant of the time duration and have patience with these patients. So as we're learning more and more about the increased risk of steroid use even at low dose, It's very important as rheumatologists for us to really embrace treat a target aiming for remission as studies have shown even that incremental difference between low disease activity and remission give better functional outcomes. As though there are more studies to be done, we need to be, as the prescribers, very aware of the impact we have in terms of steroid use and make a concerted effort to try to get our patients off for better outcomes.

Hello. I'm Jonathan Kaye reporting from ACR Convergence twenty twenty four in Washington DC. Here on the second day of the meeting, I'm with professor John Isaacs of Newcastle in The United Kingdom who presented poster number 1349 about withdrawal of therapy from patients with rheumatoid arthritis taking conventional synthetic DMARDs. And you developed a molecular signature that predicts flare among patients in whom therapy is withdrawn.

Yeah. That's the case. Well, was a circulating biomarker signature. And we increasingly achieve remission in patients with early RA on simple drugs like methotrexate, maybe with some hydroxychloroquine, and patients are starting to ask us whether they need to take these drugs for the rest of their lives. Traditionally, we've always said yes, but because we're being asked more and more, we've started to set up studies to find out what happens when we stop drugs.

And actually in that population, if we do stop, then fifty percent of patients flare and fifty percent of patients stay in remission. The ones who flare, we can readily re achieve remission with a shot of steroid and putting them back on the original drug in most cases. But what would be really cool is if we could develop a signature which tells us when it's safe, in inverted commas, to to stop that treatment.

And the biomarker signature that you derived was what?

It's it's three circulating mediators. One of them is an acute phase reactant s 100. I'm gonna say three a. I forget I forget the exact name. There's an IL six receptor.

And the third one I'm struggling

MMP nine.

MMP nine. That was what it was. That was right. So so so that yeah. So an interesting three biomarkers.

You wouldn't necessarily associate them with with prolonged remission, but they seem to predict.

And this was a prospective trial, and it's difficult to enroll patients in trials. But if you're telling patients that you're gonna find out whether you can predict flare if they stop their drug, they must be excited about enrolling in a trial like that.

I've never found it so easy to recruit to a trial. In my in my entire career, patients were knocking on our door to to to take part because they don't wanna take their drugs. And and so we we were way ahead of our recruitment target. So it was a a nice study to run.

So with this molecular biomarker signature of MMP nine, s 103 a, and the IL six receptor, if you find this signature, you could predict which patients might flare upon withdrawal of therapy, and you might not withdraw therapy from them. But if they don't have this a negative predictive value of lack of FLAIR would be very helpful.

Yeah. That's right. And we validated it actually on a separate cohort. So we've done we've done this twice now, and it and it validates area under op curves about 70%. So it's, you know, it's good enough, think.

And you're right. So so if if we then would prospectively apply that signature, we would avoid flares in about fifty percent of patients.

And this is the type of biomarker panel that is useful in patients with rheumatoid arthritis. A panel that predicts which patients do not need to continue therapy, whether patients might not respond to a TNF inhibitor with a genetic signature or in this case with a biomarker signature, patients who might flare if they were withdrawn from their therapy. So this is very exciting. And for more information about this and other presentations at ACR Convergence twenty twenty four, go to roomnow.com. I'm Jonathan Kaye.

Hi. This is Eric Dine from New Jersey here at ACR Convergence day two. We just wrapped up a a great day, and I'm here to talk about some of the oral rheumatoid arthritis abstracts that were just presented. So, we had a wonderful afternoon session where one of the things that we talked about the first abstract was seventeen forty three which looked at the difference between low disease activity and remission. The the goal is we love having patients in remission, but, you know, from the guidelines, we often say that that low disease activity is good enough that we got them pretty close so we don't need to up titrate their medicines to the highest degree.

But is there a difference between LDA and remission? The the study looked at LDA, which is, again, that C. Diffeile less than 10, remission less than 2.8, and they also had another group of very low disease, which is between the two point eight and six, kind of the lower part of the very low disease. What they found is that, particularly when you look at that higher level of the lower disease activity between six and ten, the patients did not do as well as those patients in remission or very low disease activity. They were not feeling as well.

Their patient reported outcomes, their fatigue, their pain were notably higher. It's not a surprise, of course, that they're not quite as good, but it did have significant impacts and it showed that they were utilizing healthcare more. They were using ambulatory devices like canes more. And so this is a suggestion that says maybe we should have a little bit of a higher target. Maybe we should be going for a little bit better disease control.

If not remission, maybe a C. I. Under six for a very low disease control. So, I I think that is something that that we can change our practice with and and take into account when we see someone who's kind of has a c die of eight or nine doing kind of okay, but, you know, maybe not well enough for for what we want. The next oral abstract that came just afterwards was seventeen forty five which was taking a look at the oral surveillance study again.

So, we've talked about the oral surveillance a lot over time. Did another post hoc analysis, but I think this one really adds a little bit more color to what we've heard. Of course, with the oral surveillance, we know that the main takeaway was tofacitinib was not non inferior to TNF inhibitor, that the JAK inhibitor showed that there was the higher MACE events. One question they had though is what if we specifically look at statin usage? Does that make a difference?

And what was interesting was first of all, at baseline, there was not enough statin statin usage in the group. Only, you know, less than a quarter of patients were using a statin. And of patients that had the known risk factor of MACE events, it was fifty percent of them. Half of them were not on appropriate treatment for someone who has had a history of a MACE event. In the patients that were on a Saturn, they did as well as the patients on TNF regardless of if they were in the TNF or TOFA category.

So, that provides some reassurance to me that if you have a patient that has been doing well on tofacitinib and they're worried about their MACE risk, then maybe you can still do it as long as you're doing the other preventative things well or secondary prevention by having them on a statin, you know, for appropriate care. And this is something that I think is helpful, gives some more information as to why patients may not do as well on the TOFA. Again, know, they weren't on the appropriate background therapy with the statin. And so, you know, there's always more information we can glean when we go into those numbers from the oral surveillance. So, I thought those were two of the highlights from that oral session and a lot more, that me and my colleagues will be having on RheumNow.

Hello. I'm Jonathan Kaye reporting from ACR Convergence twenty twenty four in Washington DC. I'm here with Doctor. Cecile Georgeau Villalat from Nimes in France, who has presented poster number three sixty about shared decision making in patients who have been prescribed targeted therapy. Most of the guidelines for rheumatic diseases, rheumatoid arthritis, axial spondyloarthritis and others, talk about shared decision making.

The question is, do the patients agree with the physicians that they've shared in that decision process? So, Ojumu Viella, you studied patients who were prescribed target therapy and interviewed or provided a questionnaire to both the physicians and the patients, and what did you find among responders compared to non responders?

Thank you so much.

It's a very important point to consider. We have asked the patients, do you participate as much as we want in the decision, in the choice of the therapeutics and of the treatment? And the answer was on the five point scale. We consider the patients completely agree with this point as a good shared decision making. And you have asked the nearly same question to the physician.

Have you practiced shared decision making and completely what's the best point to consider a very shared decision making? It's very interesting to note that in patients with good adherence to the treatment, the answer is the confidences between the physician and the patient perception on the chair decision making are very close. But in the patients who never adherent to the treatment, there were a disconnection in the perception, a discordance between the the physician who thinks that the patient is happy and the decision is shared, and the patients only 20% think that was great shared decision making. So I think that's really a point to consider to improve adherence of the treatment.

Did you find any specific differences between the non adherent patients who felt that they had not participated in shared decision making compared to those that did feel that they had participated?

No, but I think the most interesting and maybe something I think I'm not happy with this result because the physician have not this perception. They think that the patient is happy with the decision and they think, yes, we have made a great shared decision making. And it was not the perception of the patient at all, and they don't precise these these facts.

So what would you suggest that physicians do to change this perception?

Maybe ask a more open question. What do you think? Not just you are agree? Okay. That's fine.

Just what do you think? What's your expectation? What's your what's the goal of your treatment for you? Maybe something more open, more cooler, maybe. It could be great point to avoid this perception, this disconnection in the perception.

Shared decision making is not I explain you, it's that, it's that, that's a good way. You are me, you're okay, okay. I have made a great decision, shared decision making. No. It's not like that.

So this is very important because although we think that we're sharing the decision making process with the patient, patients don't necessarily perceive the same. Shared decision making is an important approach to the physician patient relationship, And this abstract number 360 highlights that there's still room to go in improving this. So is shared decision making really shared? Not necessarily, but let's improve that. This is Jonathan Kaye reporting from ACR Convergence twenty twenty four in Washington.

For more on the ACR Convergence twenty twenty four meeting, tune in to rheumnow.com. Thanks.

Hey, everyone. My name is Brian Jaros, and I'm reporting to you live from ACR Convergence twenty twenty four in Washington, D. C. I'll be telling you about abstract number thirteen sixty two. So as we all know, as rheumatologists, rheumatoid arthritis is one of our bread and butter conditions that we treat, and one of the most common diseases that we see in rheumatology.

We're lucky enough now that we've developed really an arsenal of treatments that we have to offer patients with rheumatoid arthritis. That leaves us with the question of always which medications will be the most effective. Several groups have sought out to answer this question, and one group in particular is trying to see is there a particular type of JAK inhibitor that's more effective for rheumatoid arthritis compared to the others? And of course, this is really relevant to our patients. If we can pick a JAK inhibitor that we know upfront has better data, has better success for putting people into remission, it'll hopefully decrease the amount of time we spend cycling through meds and getting patients to an area where the disease is quiet.

This abstract is from Peter Taylor, et al, they used real world data to complement trial data that's been shown in the past regarding this question. They had a really clever design to try to increase the power of the study where they sent out surveys to rheumatology practices internationally throughout North America, Europe, Japan, many countries being involved, and they included patients who had rheumatoid arthritis and had been treated with any kind of JAK inhibitor for at least six months. Now, when they sent out these surveys, they were asking physicians to report on outcomes of these patients, specifically DAS28 scores, outcomes of pain and fatigue, and outcomes of compliance to the JAK inhibitor that the patient was prescribed. They then took all of this data back and tried to look for statistically significant differences between the different types of JAK inhibitors. Ultimately, they accrued a pretty good sized population of 1,400 patients, a majority of whom were taking upadacitinib fifteen milligrams, and some other patients taking mostly tofacitinib or baricitinib.

Analyzing this data, they found that patients on upadacitinib fifteen mg compared to the other JAK inhibitors were actually more likely to achieve DAS28 remission in comparison, and this was on the order of about fifty four percent of patients on upadacitinib achieving DAS28 remission compared to an average of forty four percent on the other JAK inhibitors. So An absolute difference of ten percent between medications is significant, both statistically and clinically, for when we're treating our patients. There are other outcomes in terms of patient reported fatigue and pain mirrored this DAS28 response. They saw that patients on upadacitinib had less fatigue, higher rates of decreased pain, and actually higher rates of compliance, which is of course multifactorial. It might suggest that the patients had less side effects or maybe just also suggests that the patients had more success with the medication, were feeling better, and were more likely to stay on it.

The study is really important because we've had meta analyses of phase three trial data which have suggested that numerically upadacitinib might be more effective compared to other JAK inhibitors in RA, but this is one of the first studies to look at real world practice data, and again internationally representing a huge body of patients, and further demonstrate this finding. So for me, I might now reach for upadacitinib a little earlier compared to other JAK inhibitors given the choice in treating patients with rheumatoid arthritis based on this data, complementing the trial data, again, these post hoc analyses showing that upadacitinib might be more effective in putting our patients into remission. That's all I have for now. Thanks for listening and keep tuning into RheumNow.

Hello. I'm doctor Philip Meats. I'm director of rheumatology research at Providence Swedish Medical Center, in Seattle. It's been a busy and interesting ACR meeting for me. One of the highlights, was the data on the phase two trial of Sonalocomab.

Sonalocomab is a novel IL-17A and inhibitors, so a dual mechanism, which is a nanobody construct, so just 40 kilodaltons. It binds to IL17A and F as well as to albumin. The albumin binding, as well as its small size, allows it theoretically to penetrate difficult to reach areas, and be highly effective in covering the IL-seventeen family. So, we saw phase two twelve week data for the psoriatic arthritis program previously. In that twelve week data, we saw ACR 50 response in approximately forty six percent of patients treated with the sixty milligram or one twenty milligram monthly dose of this medication.

We also saw MDA or minimal disease activity criteria achievement in approximately forty four percent of patients. Now we're looking at twenty four week data. There were some changes in the groups that patients were in. For example, if they weren't responding to placebo or to a sixty milligram dose, they might shift upwards. But we saw some really exciting outcomes.

For example, the ACR fifty response in the sixty and one hundred twenty milligram groups went up to about sixty two percent of patients achieving an ACR fifty, and the minimal disease activity criteria we saw arise from forty four percent up to about sixty percent of patients achieving this composite holistic way of evaluating psoriatic arthritis in all of its domains. So very effective. In terms of safety and the one item to mention is that because we know that IL-seventeen protects against surface candida, we did see a couple of cases in the sixty and one hundred twenty milligram arms each in the twenty four week program. These were generally mild and easily treatable. Otherwise, there were no unexpected findings relative to the IL-seventeen mechanism.

So this is a neat new molecule, a new approach by having a nanobody and more complete coverage with IL-17A and F inhibition. Thank you so much.

Hello, everyone. I'm Richard Conway reporting for RheumNow from ACR twenty twenty four. I'm going to talk to you today about a study presented at Sunday's plenary session. This was from Cornelia Quack and colleagues from The Netherlands. It's abstract number sixteen forty seven.

So this was a study looking at rheumatoid arthritis and looking at treat to target. I was particularly interested in the pregnancy space. So to do this, they had a new study, which was called Pre Cara, and they were comparing this to their previous study of these patients around pregnancy, which is called Para. There were two fifteen patients in the new study, two forty five in the old study. And the difference between them was that the old study was kind of a standard of care study and the new one was this treat to target implementation in this group who were intending on becoming pregnant.

So to do that, they had this escalating regime of drugs, starting with sulfasalazine and hydroxychloroquine, and if necessary, adding in a TNF inhibitor. And they also based on previous knowledge of how medications affect pregnancy, had a real focus on trying to limit non steroidal anti inflammatories and glucocorticoids in these patients. So the first thing, did the treat to target achieve what it set out to do? Did it reduce disease activity? And it did.

So DAS CRP was 2.33 in the new study compared to 3.84 in the old study. And then looking at fertility. So they did this by looking at the time to pregnancy. And that was eighty four days in pre Cara in the new study compared to the historical one hundred and ninety six days. And then when they looked at kind of problems conceiving or bigger problems conceiving, so looking at twelve month cut off, who got beyond twelve months, it was twenty three percent of patients in the new group compared to forty two percent of patients in the older cohort.

So this study, I think, really very much says that fully controlling disease activity and using the agents we need to do that improves fertility. And so now we know that it improves fertility. We already have other data showing that it improves pregnancy outcomes, reduces stillbirths, preterms, births, miscarriages, those sorts of things we really want to avoid. I think this increasing evidence that we need to be better and need to be optimized the treatment of patients who are planning pregnancy and becoming pregnant. We need to overcome the fears that many patients have regarding these medications through education and spending the necessary time with them.

I think we definitely also need to overcome a bit of an inertia among both physicians and patients regarding these agents and not putting things off until after pregnancy, that everything will be better. And we can confidently say that based on the data that we now have, if we treat these patients with certain of the medications we have available to us. So I'm Richard Conway. You can see me, I am on Twitter at Richard P A Conway, and do check out RheumNow for all the up to date coverage from ACR twenty twenty four.

Hi, my name is Jeff Sparks. Welcome to ACR twenty four and I am really glad to be joined by Doctor. Scott Matson from the University of Kansas, a pulmonologist here who gave an invited talk on abstract 17 S 14. This was about treatment considerations for RA ILD. This was an incredible talk.

It was standing room only and actually the overflow room was also completely filled. So a lot of interest in this topic. So first I wanted to see what are the most recent advances in the treatment for RA ILD?

Yeah, thanks Jeff. It's a great question. You know what our group's been focused on is how we can best understand the kind of individual patient factors for patients who have RA in terms of what about their ILD can help us understand how they may respond to available treatments. And I think there's been a paradigm in the pulmonary field certainly where we think about these patients as either having a fibrosis predominant ILD or a more inflammatory patterned ILD. And so what we presented today was from data from our group where we've looked at treatment outcomes for patients with RA ILD who were started on immunosuppression and we looked at a few different things about those patients.

So we looked first of all at the overall outcomes and what we see is that these patients generally do worse before they get this directed ILD, immunotherapy and then at the time of immunomodulation initiation for these patients they have stabilization of lung function. And what we talked about today was some secondary analyses from that outcome where we looked at patients who had RA that had a UIP pattern, the more fibrotic pattern ILD compared to those without. And what was interesting in this data set is that these patients with UIP who had the more fibrotic pattern ILD actually had a numerically greater improvement in their FVC trajectory when compared to the non UIP group. And we followed that up with some quant CT analysis of the same cohort and what we see in that analysis too is that the degree of fibrosis and the degree of ground glass, even though the paradigm is sort of that it's only those patients with more ground glass and less fibrosis that we think we should potentially only treat those patients with immunomodulation, immunomodulation. In our analysis, it's essentially all negative data.

And so I think what this means is that there's a lot of questions still about which patients with RAILD will respond to immune suppression best, but at least as of now it seems like radiographic pattern and the way we define fibrosis on these CT scans is probably not the full story there and those patients may still have a positive response to immune suppression.

So you had given some data that many different immune suppressants seem to stabilize the disease course. Could you tell us about what if patients continue to progress and when would you consider getting anti fibrotic in the mix?

Yeah, it's a good question. So the data that we looked at was a real world observational outcomes of patients who had been on Rituximab, Azathioprine or Mycophenolate and that was immunotherapy that was started to target the ILD. And I think in the real world what we see is that a lot of times even when you start that kind of therapy patients continue to progress. And I think what we know from the trail one investigators and anti fibroidics and RA ILD is that it's safe to add anti fibroidics to these patients and that it does have meaningful improvements in FVC change when compared to placebo. So I really don't hesitate in the real world to trial patients who are progressing who have fibrosis on anti fibrotic because you can continue to alter immune suppression in the background and if a patient can tolerate it, it does seem to probably have meaningful outcomes especially if you imagine that carried forward beyond one year.

So you're a pulmonologist here at a group of, many rheumatologists. I'm curious from your perspective, do you have any advice about practicing rheumatologists when they find RAILD how would they best co manage the patient with a pulmonologist?

Yeah, it's a great question. I think that bringing together these two fields of expertise in terms of how frequently we should monitor it, in what ways we assess disease progression, and then I think it's just really about this kind of collaborative care. A lot of times there's so many variables we have to adjust that if you can be on the same team and time some of those adjustments so that if you're adding an anti fibrotic it's not at the same time as you're altering immune suppression, in those scenarios you can maybe better tease out in that individual patient which patient's responding and which patient's not. Yeah.

And I'd say in closing the it's incredible how little data we know. There's only been one dedicated RAILD trial and in fact there's probably less than 300 patients who've ever participated in a randomized trial for RAILD. So there's really a lot of opportunity despite it being our most common disease. There's already been other abstract sessions. There's another session about lung disease, tomorrow.

So this is definitely a topic that, there's a lot a lot more room for growth. So thank you very much for your interest in our field, and I look forward to continue collaborating. So thank you again for your attention, and we'll look forward to next videos at RheumNow. Thank you.

Hi, everyone. I'm Victoria Consett covering from the ACA convergence in Washington two twenty twenty four. I selected an abstract that I found very interesting. It's from Gregory McDermott and colleagues from the Brighamen Women's Hospital in Boston. They're actually covering treatment strategies in rheumatoid arthritis.

And what they did is they selected two cohorts of patients with RA from the BA Million Veterans Programme and the Brighamen General Programme. And what they did is did genotyping and electronic health record analysis in these patients. So they looked into prescription patterns of these patients with Markov mixture models and also into genetic risk scores and they actually found three groups or clusters of patients when starting TNF inhibitors. So for once patients staying on TNF inhibitors, TNF resistors as they call them, patients switching from TNF inhibitors to Abatacet, and patients really cycling around after failure to TNF inhibitors. Then they did genetic risk scores in these patients and found that the genetic risk is really different, patients who stayed on TNF inhibitors had more of a SPA, predominant genotype, risk genotype,

and RA

patients were more prone to switch to aldosterone,

for example,

or RA genetic risk patients. So I found that interesting because it was about treatment strategies in RA and we are still lacking those. It will be interesting to see where this group will go with this data.

Hi. This is Bella Mehta reporting for RheumNow from the ACI convention. I'm from New York, and I wanted to discuss two very interesting abstracts looking at AI and ultrasound in rheumatology hand images. So the first one is late breaking abstract number four, which is basically looking at an AI model which compared the synovitis scoring, synovial hypertrophy, Doppler signals that you get on an ultrasound, when it is done by a human compared to an AI model, which was trained to detect these things. So for patients with hand pain, they scanned twenty two joints, MCP's, PIP's, DIP's, and DIP.

And they looked at a synovial hypertrophy Doppler as well as osteophyte severity. They graded it according to the standard EULAR, OMRAT classification criteria or the GLOIS score. And they had a lot of images. Right? They had 7,300 images to do this study.

And what they found is that the AI model actually performed pretty similar to what rheumatologists who are trained in musculoskeletal ultrasound performed. So these sort of tools might be a valid way to score sinusitis because that's the best way to get to know if the patients actually have swelling or not. The next abstract, sort of on the same lines, is the late breaking abstract number 20, which is now not only automating the read the reading of the ultrasound once we have the images, but also there's a machine that they call Arthur, which which scans the patient's hand images by itself. So it is a fully automatic machine, which is standardized and takes images from patient's hands, ultrasound images, and then they have another fully automated system which can read these ultrasounds as if it's a radio first thing is radiograph or a technician doing it, and then the second thing is a radiologist actually reading it. And they had an automated system who could do it.

So for and they first looked at images that the computer or the AI system took, compared it with the rheumatologist, and also had a third totally blinded rheumatologist evaluate both this AI generated as well as human generated images. The third rheumatologist whose experience with these ultrasound images is established as the ground as the ground truth. So interestingly, between the AI and the rheumatologist, which is the ground truth rheumatologist, there was around 8686% similarities in their readings. Whereas, between the two rheumatologists, there was just 53 50 to 60% similarities in how they are reading these ultrasounds. So, basically, what I'm seeing more and more, and more and more interest in ACR, is things that we can automate machines to do for us.

Given that rheumatologists are gonna be lesser and lesser and there's more requirement, automating some tasks like this might be a great thing in the field of rheumatology. We'll see if this is open access, how expensive it is, if this actually can be deployed to clinics. But these two abstracts show a lot of promise, and I see I I wanna say that we'll start using these in the future. So with that, follow me on RheumNow and on Twitter at bella underscore meta, and thank you.

David Liu from Melbourne here as part of RheumNow's ACR twenty twenty four coverage, getting right across the meeting. And I want to talk to you today a little bit about vaccine responses and what DMARDs mean for that. We've started to be conscious about the DMARDs that we use as levers on developing a vaccine response, it makes perfect sense that the therapies we use to try and change an immune response might actually, as part of autoimmunity, may well change an immune response to a vaccination. We became very conscious of that during COVID. We saw especially with rituximab patients getting very poor immunogenic responses to COVID vaccination, and the consequences at a time when they really needed protection against COVID.

At the moment, I think we've become particularly conscious about the recombinant zoster vaccination and responses to that. We are very conscious about what our patients experience as far as shingles is concerned, and about the consequences of that postherpetic neuralgia and beyond. Is a good example for thinking about vaccinations and DMARDs going forward. And we've seen a number of different abstracts at this meeting looking at this. One of a pair that is really interesting are 24048.

They're from a Brazilian randomized controlled trial looking at zoster vaccination in rheumatic disease patients. And what they saw is that actually, they're once again, rituximab patients do quite badly as far as developing a response or concern. They actually saw as well, they looked at mycophenolate patients. And so, they got a decent response, but they got a better response when you were withheld for two weeks after the mycophenolate dosing.

So, there

were things that you could do there. But overall, most people got a response. What about other mechanisms which might be relevant to developing a vaccine response? Well, we've seen at this meeting that patients with upadacitinib seem to do reasonably well with developing a zoster response, a zoster vaccine response, particularly important knowing that they've got an increased zoster risk. What about nipocalimab?

So, Nipocalimab is an FcRn inhibitor that's just had a breakthrough designation for Sjogren's by the FDA. And by nature of what it does, it reduces IgG, clears IgG, but potentially, well, you know, maybe it might not necessarily affect the vaccine response quite as dramatically. And so what we saw in abstract number nineteen eighty eight was actually data on nipocalimab and vaccine response. And we've seen that actually, naturally it reduces dyneinitis as it should as part of its mechanism of action. But eventually patients get there.

Patients eventually get that response. And I think that gives us enormous reassurance as we start to use that. What I think was particularly depressing was data looking at a And I guess it makes sense once again, abatacept co stimulation might be important in terms of the way that we develop an immunogenic response. So, abstract number 1,009 looked at patients with recombinant zoster vaccine and abatacept. And unfortunately, that's really depressing.

It's a bit of a swing and a miss. I think we've got to think about strategies in those type of patients when we're vaccinating them. We can't just go with a normal two dose strategy. We've got to think about how we can improve the immunogenicity, either by withholding a Baticept like we've done with microfelade and methotrexate before then, or potentially extra doses. Somehow trying to get these people some response, otherwise we're probably wasting our time to some extent.

We've got a bit more to figure out in this space, but it gives us pause for thought, especially as we start to think about other vaccinations that will come in the near future. No doubt the same is going to apply for RSV, and it's still worthwhile thinking about influenza, COVID vaccination, and other vaccinations, vaccinations, really to try and reduce that the infective burden that our patients face. For plenty more on the whole meeting, you know where to go. Rheumnow.com.

Hi, this is Bella Mehta from New York reporting from ACR24. And wanted to talk to you about what's new in relapsing polychondritis. This is abstract 2,649, and this is a study which aimed to improve the diagnosis or the speed of diagnosis for relapsing polychondritis, is often delayed and patients go from one physician to the other sometimes because there are different phenotypes and how patients present may be very different. So Marcella Ferreira used this latent class analysis on a very large cohort of relapsing polychondritis patient. Again, relapsing polychondritis is a rare disease, and considering that she has around one sixty patients that she's doing this analysis with.

And they found three classes. One is where there's ear and nose damage with subglottic stenosis. Type two is tracheomalacia and bronchomalacia, and type three is no tracheomalacia. So using a decision tree based method based on tracheomalacia and your damage, this accurately predicted subgroups assignments in these type one, type two, or type three with around 98 to 100% accuracy. Basically, this may support quicker, more accurate diagnosis and not only guide treatment, but also research, which is much needed in in sort of rare disease groups because those are the patients which suffer the most sometimes.

And with that, which is signing off, follow me more on Twitter at Bella underscore Mehta. Thank you.

Hi. From day three of ACR convergence, I'm Eric Dine from New Jersey. I'm joined with doctor Jonathan Kay from University of Massachusetts, and we're here in Washington DC. And doctor Kay just finished a great chat about biosimilars and the experience across the world from hearing about Canada, UK and from you about The United States. Tell me first of all, if we switch from an originator to a biosimilar, what would we expect in terms of outcome differences?

So a biosimilar that's been reviewed and approved by the FDA has been shown to be equivalent in both efficacy and pharmacokinetics and comparable in analytical studies and safety and efficacy without clinically meaningful differences. So it's essentially like another batch of the reference product. Switching from a patient who's on the reference product to its FDA approved biosimilar should be no different than going from one lot of the reference product to another. Someone came up to me after my presentation and said that he was used to switching patients who were inadequately responsive to adalimumab to etanercept because he was unsure about whether a biosimilar would be effective. But there's much more risk of lack of response if you switch from adalimumab to etanercept than if you were to switch from adalimumab reference product to an adolinmab biosimilar.

And tell me, you had discussed in this talk about this concept of interchangeability. It's something we hear a lot about in terms of it. Can you can you shed some light on what that what that means?

Sure. Interchangeability was a term that was coined by the United States Congress as part of the Affordable Care Act, which was passed in March 2010. And this is a term to imply that if a health care provider writes a prescription for an interchangeable biosimilar, someone other than the healthcare provider can substitute the interchangeable biosimilar for the reference product, not for another biosimilar but for the reference product without the informing or consent of the prescribing provider. So interchangeability is a designation and the FDA came up with guidance in 2019 with a switching study where patients were randomized to either a switching arm or a non switching arm. They were all treated with the reference product, then they were randomized.

And the switching arm underwent three switches from the reference product to the biosimilar back to the reference product and back to the biosimilar ending up on the biosimilar with primary endpoints being pharmacokinetic parameters. And so far there have been 14 biosimilars that have been approved as being interchangeable. Three of the adalimumab biosimilars have that interchangeability designation. But the FDA has issued draft guidance this year in 2024 that an interchangeability study may not be necessary if the manufacturer can provide data from the analytical and clinical studies that would demonstrate no expected difference in efficacy if a patient were re switched to that biosimilar.

And to have 61 approved biosimilars in The United States, 14 with the interchangeability, not all of the 61 are on the market currently. Certainly we know that they're cheaper medications. I think the the biggest question that a lot of us have is cheaper for whom? So they're

not really cheaper because they're high quality. They're less expensive in theory, but because the reimbursement system is so opaque, pharmacy benefit managers put them on formulary and the pharmacy benefit manager gets a two to 4% administrative fee based upon the list price of the drug so medication to be put on a PBM formulary is the one with the highest list price, which also allows the most room for discounts and rebates, not all of which are given back to the plan sponsors. The PBM makes its profits on the basis of retained rebates and discounts as well as the administrative fee. So there's a rather odd incentive for the PBM that's disaligned with that for the patient. So in most cases biosimilar is less expensive but not always.

But it's important that the savings be passed on to the patient in some way or else there's no benefit to the patient of switching from the reference product on which they've been doing well to a biosimilar.

I think that's the most important point is that the patients see these benefits and it's hard and confusing for the patients but I think the other speakers who have had longer term experience in other countries really talked about the transparency that's needed. We explain what these medicines are and why there's the benefits to them and to the system.

Absolutely. So two things. One, in The United Kingdom and in Canada, there are single payer systems. In The United Kingdom, it's the National Health Service, which is national. In Canada, each province has separate regulations, but the provincial government is the single payer.

In The United States, we have these vertically integrated systems where CVS has its own PBM, CVS Caremark, it has its own specialty pharmacy, CVS specialty pharmacy, and its own insurance, Aetna, and Cigna the same. Cigna has its own insurance. It has its own PBM Express Scripts and its own specialty pharmacy Accredo. So there are benefits to the integrated, vertically integrated business, which are not necessarily aligned with those for the provider or the patient. So that has been delaying the widespread acceptance and benefit of biosimilars in The United States.

You you definitely had the an enviable task of explaining the much the much more complicated system than the other than the other speakers with covering The US perspective because it it's definitely opaque is the right word for that.

It's it's complicated, but ultimately, for example, Blue Shield of California, which covers about, 40,000 Humira prescriptions each year and spends over a $100,000,000 on Humira each year, has now contracted with Fresenius Cavi for their biosimilar alemumab and is going to be providing that at a low cost to the Blue Cross I'm sorry, Blue Shield of California, and they're going to allow patients to receive this oftentimes with no co payment required of the patient. So that's the beginning of a system where patients, where the insurers bypassing PBMs and is going to effectively deliver biosimilars, effective biosimilars to patients at a lower cost.

That's fantastic. Last question, we know that the nocebo effect is real, that people, the opposite of the placebo, that when they're expecting something bad to happen and often will be perceived that it does, if not actually does. How do you counter that or how do you communicate with patients to help make sure that these transitions go smoothly?

Well first of all I share with the patient my comfort that with the fact that FDA approved biosimilars have been carefully studied, reviewed and approved by regulators in a highly regulated area so there should be no concern about problems that are unanticipated. There's been extensive experience in Europe and elsewhere with these molecules so that there's post marketing experience elsewhere. And education plays a major role in decreasing the nocebo effect. There was a study called the BioSwitch Study in Nijmegen in The Netherlands where patients were informed that they were going to switch from Enbrel to an etanercept biosimilar with a lower incidence of injection site reactions and a lower cost and so it was going to benefit society. And what they found was that when they notified patients that they were going to be switched and provided them with an educational presentation made by either a nurse or a pharmacist in the rheumatology clinic, there was an excellent survival rate of drug therapy in this patient population.

So education and the physician or healthcare provider expressing confidence that this is a very appropriate therapeutic approach helps to reduce the nocebo effect and ensure the success both economically for society and therapeutically for the patient of using a biosimilar.

Well, it's definitely coming so I think it's something we all need to be knowledgeable and prepared for. So thank you very much for your time.

My pleasure. Thanks, Eric.

Stay tuned to RheumNow for lots more coverage of ACR Convergence.