RheumNow Day 3 Recap ACR Convergence 2024 Highlights Save

Everyone, welcome to the RheumNow ACR Day three Recap. This is where we as a faculty get together and share our thoughts on what we thought were the highlights of today. Hi, I'm Jack Cush from Dallas, Texas. I'll ask my other faculty members to introduce themselves. Bella?

Hi, I'm Bella Mehta from New York.

And Brian.

Hey everyone, I'm Brian Jaros. I'm from Chicago. Thanks for having me.

And Queeland.

Hi, I'm Quelyn Bonnelly. I'm a rheumatologist in Galway, Ireland.

Nice. Okay, so we're going to go around the horn and get our best impressions of today. The little preamble here is that one of the big highlights of today was the ACR new recommendations on the diagnosis and treatment of lupus nephritis, the Class III, IV, and V disease. It was a long session, a great session. We could spend an hour on this and we're not going to.

We're going to recommend you look at other things. We have other videos and articles on this on the RheumNow website. There's a lot to consume there, but it's a hot topic and it was featured today. That being said, let's start with, Doctor Mehta.

Hi. So I think there was a bunch of great sessions today. The plenary especially, this morning, abstract number two five three two. So this is an a study which was looking at immune checkpoint inhibitors. They they looked at a large data set, the Trinexx Diamond Network.

This is a large multi central network of US medical health records. So this is information pooled from a lot of places. And they wanted to see if patients who had pre existing autoimmune diseases and then they get checkpoint inhibitors. Is there a difference in mortality? Because that's the clinical question, right?

Should we give immune checkpoint inhibitors to patients who already have say RA or psoriatic arthritis or something and have a cancer then because the worry is that maybe there's a change in mortality. So again, they did like survival analysis and they found that around twenty five thousand patients with autoimmune diseases were also on immune checkpoint inhibitors, and they compared it with those who did not have autoimmune disease, around seventy eight thousand patients. And this when they looked at mortality, the mortality was slightly higher in the autoimmune patients, like seven percent. But when they did a propensity control matching because rheumatology patients or patients with autoimmune diseases already had higher diabetes, hypertension, cardiovascular risk factors which led to higher mortality. So when they adjusted or did propensity score matching, the mortality was not very different between the two groups.

Thus, saying that, hey, we can use these medications even in preexisting autoimmune patients without much risk to the mortality. Well, when it comes to symptoms, we'll have to manage it. But at least this sort of a big dataset picture of this gives us a good overview.

So, Bella, did they address the issue that, is there more morbidity? Meaning, are patients with psoriatic arthritis more likely to get other autoimmune and other IRAEs, compared to people who don't have those conditions?

They didn't go into it too much, but I think the point they were trying to make is mortality. So, if you get into those trouble with any patient, have to manage it. But yeah, yeah. I see your question. Yes.

Yeah. I've been on the impression from some literature that our patients are at higher risk for our complications as far as IRAEs. Anybody else have that impression?

Yeah, I had that impression. And another thing that I found out during this conference and I've been interested in is actually whether certain immunotherapies themselves, like the actual agent proposes a higher risk compared to other agents. I saw an abstract related to that in the vasculitis world that pembrolizumab seemed to be less provocative for whatever reason for GCA and PMR related adverse events. I don't know. Did this abstract subgroup mortality by different specific agents?

I don't think so.

Okay. Mm-mm. It's okay. What do you think?

Yeah. I I think this is a really important study, particularly given that, you know, checkpoint inhibitors are now standard of care really for for a vast number of cancers now. And also, it's being used more and more earlier in disease. So, it's great to have this kind of backup data to discuss with patients, you know.

I'm encouraged by this data and really what's happened in this area and IRAEs in the last two years. Many rheumatologists have gotten very comfortable with this, and I think they're working well with the oncologists on this. So this is certainly good information to hear. Let's go on to Brian. What's your next one, Brian?

Yes, so my, abstract I'll talk about is Abstract 2,650. It is extent of vascular inflammation on cranial vessel wall MRI and ophthalmic complications in GCA. It's by Yang et al. A little bit of a mouthful of a title, but it's really interesting. So basically the question they're trying to answer here is can we make a predictive model or a predictive score to help stratify which GCA patients are at high risk for which is what is, of course, the most feared complication, you know, vision loss or ophthalmic complications?

Because right now, you know, our strategy is upfront. We kind of treat everyone this very similarly, at least according to the ACRVF guidelines with the exception of pulse, you know, high dose steroids for people who have already developed ophthalmic complications. But, you know, what what can we do to help, like, predict that? So essentially they used a certain type of MRI with which is vessel wall protocol. It pays more attention and resolution to the wall of the vessel itself to help look for inflammation or uptake.

And they cranial MRI to everyone who had suspected GCA and basically used like an additive score of how many vessels were involved, branches of the superficial temporal artery, the occipital artery, maxillary artery, and used it in an additive fashion to come up with a score for each patient. And then they followed them clinically to see which ones actually ended up having GCA, which ones ended up having frank visual complications. And they also screened people with orbital MRI to see if people had like optic nerve enhancement or other features that have been shown in previous literature to be suggestive of possible impending vision loss. And they did find that essentially of the patients who went on to develop GCA, ocular GCA had a higher overall kind of composite score. They called it the CAMRAS score, which is cranial artery MRI score.

But patients had a higher CAMRAS score were more likely to go on to develop ocular GCA. Patients with an intermediate camera score fell more into the non ocular GCA group and patients without GCA, you know, had a very low overall score. Similarly, the additive score seemed to correlate with positive orbital MRIs. So it was predictive of that optic nerve sheath enhancement, even in people without frank visual GCA. So I think the question, you know, to go from here is like, does this help then predict, you know, response or relapse or tell us, you know, long term, like what the clinical trajectory of the cases, they did reimage a subset of the groups at one month, six month and twelve months, and did see that that additive score in general declined in patients with treatment over time.

But again, didn't really stratify that according to specific treatment or relapse or things like that. So I think it's a really good launching point for like this discussion of, again, how we risk stratify these patients. You know, does everybody need this high dose upfront, you know, to protect from visual loss or can we get away with lower dose steroids and people at low risk, you know, who might just have headache, you know, jaw claudication, things like that.

So Brian, let me just clarify, by ocular GCA, do you mean findings in the eye or that they actually had blindness and visual loss?

Yeah, they determined it. It was a composite, either an ophthalmologist or rheumatologist said based on typical visual symptoms and ophthalmologic findings or the imaging definition, which was the presence of this optic sheath enhancement on orbital MRI.

But that's a little scary, right? Because that point they don't have it. But what if they have it in like a day from the MRI done and they have like worse symptoms? It's tough not to, you know, the the implications of not treating can be scary. So I I don't know what they're trying to sort of tell us to do.

Yeah, I kind of echo that sentiment because you don't want to be very brave to be using like lower intensity immunosuppression just because they have this lower composite score, know, given the risks associated with not treating appropriately, but maybe they're brave enough to do it. I guess if you have very close monitoring, possibly.

Did they show a real predictive value to what their findings were? That how you get a sense you could be more, it sounded like you're saying higher scores, higher risk.

Yeah, I mean, they showed that the higher score was associated with like things that, you know, qualify as disease severity. So again, like the ocular findings and even things like positive temporal artery biopsy, you know, higher score correlated with a higher chance of having a positive biopsy. So I think it's predictive but I think similar to what others have said, the question is like, what do we do with this information clinically going forward?

Does the extent of imaging here cover the need for, you still have to do other extracranial imaging in a newly diagnosed patient, correct?

Yep, exactly. Yeah, you would still, and in fact, think for a lot of us, we would probably would not do this extent of full cranial imaging, you know, even at baseline. So it would be in terms of like thinking of like additive cost of tests and realisticness of incorporating this, you know, this would be like an added thing. Think most people are not doing, you know, vessel wall cranial imaging routinely in these patients.

I guess I do it when I can't get a biopsy and things are iffy. So the vessel or protocol comes handy for, you know, for whatever reason. Patient refuses or comorbidities or whatever it may be.

Mhmm. Alright. Let's go on to doctor Khan.

Great, yeah, I wanted to highlight Abstract two thousand two fifty nine, which is looking at anti obesity medications in rheumatoid arthritis. It was a retrospective study, one hundred and fifty two patients with RA who are either on semaglutide or tirzepatide, and looked at the impact of that on several parameters, including weight, BMI, inflammatory markers, and then also pain on the visual analog scale. Also looked at the impact on lipids and the results were quite interesting. It had very positive impact on weight, on BMI as you'd expect, but also had quite a positive impact on inflammatory markers and overall level of pain reported by patients. Notably, up to a quarter of patients did discontinue therapy owing to GI side effects or difficulty accessing the medication.

But I think it's a very important study because it's something that we're going to have to consider integrating into our care. I think it's something that this time next year, there's going to be an absolute avalanche of studies looking at the impact of these therapies in our inflammatory diseases, as well as the non inflammatory diseases like OA. But I thought it was a very neat little study and very thought provoking and will open up the doors to lots of other studies, I think.

Let me clarify something. You said that many You of them their mean their rheumatoid therapy or the GLP-one therapy?

GLP-one, yeah. And mostly it was because of either GI side effects or insurance access issues. So, they're the two main causes of discontinuation.

Think a lot of my patients are on GLP-one. You know, you meet them after like three months and suddenly it's like they look different. They're definitely losing a lot of weight and it is helping things like disease activity. I don't know how long, you know, as long as you're on drug, I guess you're gonna be okay. There was another abstract that even showed some retrospective work on lupus nephritis and that it's not only just the weight loss, there is some anti inflammatory effect that it does have.

I mean, again, this was just data sets. I mean, we need much more data sort of looking at it on a histological or molecular level to see if it's actually affecting inflammation, not from just weight loss, but that's interesting.

Yeah. Yeah. Like, think, you know, the, you know, our understanding of what fat tissue does and how active it actually is, you know, is evolving as well. But I think, you know, it's reservoir of pro inflammatory mediators. So I think addressing that should really become something that we always consider in our treatment algorithms, as well as obviously treating with disease modifying agents.

But I do think it's going to be a game changer in terms of the management of a lot of our inflammatory diseases and will be a very important adjunct and hopefully will will help a lot of people.

Brian, what do you think?

Yeah. I think they're promising. I think my question for the group is is if these develop an anti inflammatory effect, I mean, I've already had patients ask me as a rheumatologist, can I prescribe them? And I actually know of a few, you know, practices that have incorporated GLP agonists in their prescribing practice. What do you what are your take on that in terms of taking that on as a community?

Well, you know, I think we already take on a lot already in terms of managing cardiovascular disease, you know, or cardiovascular risk should be part of the standard of care that we provide. I know it's just, another round of prior auths and everything that would have to be done in The US. Europe, it might be slightly different, but addressing cardiovascular risk, particularly in our rheumatoid arthritis or psoriatic arthritis or lupus patients is very important. It is something that would add to the burden of admin particularly, I think, but I think if you're going to be waiting for an endocrinologist or somebody else to do it, it may never happen. That would be my take on it.

But the logistics of it, it might be too.

I agree. But I think we need to make sure to prove very, very solid data to know that it has anti inflammatory effects. If it is just helping because of weight loss, I would not take it on. It depends on where we draw the line in a way. Plus not everybody needs to be, I mean, I feel like it's in some ways, at least I don't know if it's all prescribed, but a lot of patients he's like, want to lose five pounds weight.

Can you prescribe this to me? And those are the kinds of requests that I'm having right now. I don't know if I want to get into that at least right now.

Well, I can tell you there are a number of rheumatology clinics who are taking on obesity clinics as part of their practice, and these become a part of that. Lily, who makes these drugs and arthritis and osteoporosis drugs, is looking to do research I believe and others will do research in this area that will answer Bella's question. So this remains a hot area for the future as Cleveland points out. So, all right, our next round we're going to call sort of a quick hit round, a little shorter presentations, a little bit more commentary. Doctor.

Mehta, what do you think?

So I just wanted to look at some of the auto inflammatory abstracts today. 2651 was one looking at vexus and vasculitis. Again, vexus syndrome is something that in the past two or three years we've, you know, sort of newly discovered vacuoles, E1 enzymes, X linked, auto inflammatory, somatic UBA1 mutation. So these are the, these investigators looked at eighty one males with vexus. I mean, and these are older, like 65, 66 year old.

And they found that vasculitis was present in twenty seven percent of these patients and mostly cutaneous small vessel vasculitis. Less common medium and large vessel vasculitis, which is sort of severity wise much much more. And symptoms resembled conditions like cranial headaches, you know, things that we were just talking about, like GCA sort of symptoms. At least twenty percent had GCA sort of symptoms. So again, you know, what I wanted to highlight is there's a lot of cutaneous vasculitis that you will see in these Vexis syndrome patients and to catch them and sort of screen for them or think about it is very important clinical practice.

So on our panel, how many of you have seen AveXis since this was just described? Okay. Brian?

Haven't seen one.

Are you good? I haven't seen one yet. So I'm looking.

I you know, I like vascularis. Maybe it's

Yeah. Yeah. Okay.

Brian, what you what do have?

Yeah. So my I was gonna talk about so I I went to the Takayasu arteritis. It was pearls, pitfalls. It was a fantastic session. One of the presenters, Doctor.

Jason Springer, talked about management. And of course, when we think about vasculitis and talk, you know, I'm mostly thinking about pharmacologic management, but he talked about data from a study that was fairly recent that I'd never heard of where a Chinese cohort actually randomized Takayashi patients to resistance exercises for an hour a day for like twelve weeks and compared it to just, you know, resting non exercise. And the results that they reported were actually quite profound and very surprising way. They measured disease activity, which I think, you know, I'm a little critical of because they used BVAS, which is sort of a less specific marker of vasculitis activity for Takayasus, but significant decreases in the resistance exercise group at about four weeks and continuing all the way through the twelve weeks of exercise compared to the non group. They didn't specifically talk about like kind of like breaking it down, like what manifestations in particular, but overall, the vasculitis activity score seemed to improve drastically.

The other kind of interesting thing and these patients were all on background treatment. The other interesting thing is they measured serum biomarkers. So they looked at CRP, ESR, and actually levels of TNF cytokine and found decreases that were also significant in the biomarkers in the resistance exercise group compared to the resting group. So I thought this was fascinating. Resistance exercise is frankly not something I ever thought about or have counseled patients with Takayasu specifically on.

Doctor. Springer mentioned he has incorporated that into his practice with things like just telling a patient with like a stress ball, if they have, you know, subclavian or axillary artery involvement on that side an hour a day, but I wanted to bring it up. I thought it was of interesting. And if you all had ever heard of this or is that part of your practice?

No. I wanna ask a question. My biggest problem is in the serial assessment of patients with tachyassos and identification of new disease. Is there a new standard other than a detailed pulse exam?

In terms of, like, assessing disease over time?

Yes. And whether they're developing knocking off new vessels, have subclinical inflammation I'm not picking up on, that I need to step up on therapy about this is my I can't keep I can't keep doing CTAs or MRAs. The insurance will not approve it.

Yeah, so that was part of, that was the first part of the talk also. And frankly, imaging seems to be the continued standard of care. It really was, I think more so based on older data that a significant portion of patients were silently progressing, so not having new exam and clinical abnormalities. And then when they would serially scan them developing new abnormalities, though Caitlin Quinn from NIH presented more recent data as well from, I think, NIH cohort and others that at least in more recent studies, this rate that was previously reported, you know, in the double digits now may be actually much less than we thought, like around four percent. I think one cohort actually had zero percent of patients with silent progression.

So to your point, that actually, I think calls into question if silent progression really is a lot less than we thought it was before, do we need to be doing fixed interval, you know, imaging screening or you're right. Can we, you know, in the absence of having adequate, you know, novel biomarkers, can we go based on clinical assessment and, you know, inflammatory markers? Okay.

Anybody have an wanna weigh in further on this? Okay. All right. Cleveland, what's your last and best abstract?

Last but not least. Yeah, so I'm going to talk about 2,639 staying on a theme. So weight trends in PSA. And essentially in this study, they looked at about seventeen hundred patients with psoriatic arthritis and the impact, you know, different therapies had on weight. And they found that, you know, IL-seventeen, IL-twenty three, and other DMARDs were linked to weight loss, which, you know, makes sense in terms of achieving disease control and things improving.

But TNF inhibitors and IL-twelve twenty three therapies were associated with weight gain. So again, I thought it was interesting just the impact of the different therapies appeared to have on weight. Also, found that the people treated with a primalast, there was a trend towards weight loss as well, but not significant. So again, just highlighting that we should probably be considering you know, the impact on weight of these therapies in these patients given cardiovascular risk and a lot of them have those cardiometabolic kind of disease as well.

So weight loss was with the 17s and Jack's? 23, Doctor. And then weight gain was with TNF? Doctor. The TNF IL-1223s.

Doctor. Just makes no sense to me at all. Weight gain, well known to be associated with TNF inhibitors because when you have lots and lots of TNF, you're anorectic, right? You actually lose weight and so they're removing you from the anorectic effect of TNF excess. And so you gain back you know, five, six, eight pounds.

Know, no one gains 40 pounds from a TNF inhibitor. But, you know, how you lose weight with 17, did they explain how that could happen or were they 23?

No, they didn't really explain it, but I guess thinking about it was that they achieved better disease control and start moving a bit more is how I would think about it.

Makes sense.

Which you'd kind of expect with the twelve-23s as well, but it's just in considering therapies for patients. Now we have so many great biologics and options, just something to factor in the overweight or obese patients, I think.

Well, now you've created a conundrum for those rheumatologists who love psoriatic arthritis and are thinking of starting weight clinics, or getting into weight loss as a comorbidity management to manage psoriatic arthritis better. Maybe they don't need to do all that. Just use the right drug and get control of the disease. Bella, what do you think of this data?

I don't know. I mean, I want to actually see the study myself, even with, I mean, maybe I don't know what was the concomitant steroid use with this, right? Like maybe these patients were getting steroids to like one group versus the other or like did they match on steroid use? I don't know.

No, they didn't match on steroid use.

Psoriatic arthritis, presumably not a lot of steroid use, right? All right, folks. I think this is a great discussion. Thanks so much for your contributions and hard work at ACR. I want to remind the audience to tune in tomorrow for the final day, the day four recap, same time, same channel.

We'll see you then. Take care.

Bye.