RheumNow Day 1 Recap ACR Convergence 2024 Highlights Save

Hi, Welcome to the RheumNow daily recap from ACR Convergence twenty twenty four. We're all here in Washington DC, and we're going to this evening on this recap, give you our views of what was the most notable of abstracts today. I'm joined by the RheumNow faculty who are here. I gonna ask everyone to introduce themselves and then we'll get into what the highlights of the day one here in Washington DC was. I'm Jack Cush from Dallas, Texas.

I'm joined by Mike.

Hi everybody. Thanks so much for having me.

That's Mike Putman in

Medical College Wisconsin. Mike from Medical College Wisconsin. Thanks for having me, Jack.

Adela. Hi, I'm Adela Castro from University of Tennessee Memphis. Thank you for having me.

And Sheila.

Hi, I'm Sheila Reyes from The Philippines and my first time joining RheumNow face to face.

Yeah. So I love this group. I know all of you. What And you need to know about this group is they were all over the place today and they had fun. And learning should be fun.

And if you do it right at ACR, it's really the only way to go. So why don't we begin with Sheila and then we'll do Adela and then Michael. Sheila, go ahead.

Okay. My first would be the abstract eight nineteen. So it's from the group of Doctor. Dennis Padapny, where they defined, they gave the ASAS definition of difficult to manage axial spondyloarthritis. And so I was able to also interview doctor Fodami earlier, and this criteria took a while.

It took them around three years to come up with a consensus definition because there were a lot of stakeholders. So basically they came up with a criteria for a difficult to manage AQSA that included like three main elements. The first of which included treatment failure of at least two DMARDs with different mechanisms of action. And then another included signs and symptoms showing inadequate response or high disease activity in terms of high CRP. There are persistent symptoms of inflammatory back pain, and other symptoms that are connected with ACFA.

And also there was a third element, which was also interesting because they also included signs and symptoms, which the physician or the patient think is still problematic that is making the axSpA worse. And also within that subgroup of the difficult to manage axSpA definition, they also came out with refractory axSpA, where they define it as failure of two biologic DMARDs, and then an ASDAS activity score of more than 2.1 plus either a positive CRP or a positive MRI finding, and other causes or other signs and symptoms that did not really, or was it not really included in the difficult to manage ACTBA. So I think there is still future directions and that we would eventually know if these will be included in the new guidelines and how it would fare with how to manage patients with ACPA, including who will be using or like which group will be using this definition of difficult to manage ACPA?

So Adele, I'm sorry. Sheila, let me get this right, that the refractory definition is different than D2T, a difficult to treat, and it sounds like it's supposed to be even more evidence of activity, is that right?

Yes, it sounds like that. So it's a subcomponent of the difficult to manage axSpA in that, so it's a smaller population of patients that are difficult to manage, so they become refractory to treatment.

Let me ask our other panelists, what do you think of this? Is this an advance or is this just nomenclature and nosology that means nothing to the practitioner? Adela, what do you think?

Think it's more like nomenclature, but I also think it's important to have that consensus definition so we know particularly which patient population we should be targeting more like, Hey, this patient's going to get more difficult to treat, because the reality is that there's still unmet needs for treatments, particularly patients with axSpA. And we know that the difficult to treat patients are the ones that have other comorbidities like uveitis, they have inflammatory bowel disease, they have other conditions going on. So there's definitely a need for treatment of these patients. So identifying these risk factors and identifying and having a consensus on the definition in particular, which patients are these difficult to treat patients, then we can approach a more multidisciplinary and we have to discuss with the patients and get this risk on earlier when we start seeing the patients.

Bring what you're saying. I'll say that it's nomenclature, but that it also may be useful. I think that often with our diseases, we try to think of them as a monolith, some sort of homogenous entity called the axSpA, but more likely there's multiple underlying immunophenotypes that are driving these outcomes that are so different from each other. And so anytime you can find a meaningful way to separate subgroups of patients within a rheumatic disease, I think that winds up being progress because you can understand better and then study better these populations that are more refractory. Cave guys, you always need to separate non autoimmune things out and it's hard in diseases like XBA because there's a lot of benign, not benign, there's a lot of musculoskeletal disorders that wind up mimicking or if not mimicking, at least exacerbating some of the things that positive outcomes in these diseases.

So nomenclature that could be useful as long as you're careful would be my take home.

Yeah. I think it's also important because inflammation may not be the only driver that's causing problems. So there can be like psychological factors or depression, fatigue, musculoskeletal.

But this is where it gets muddy, right? I mean, has all been done by RA. We have a UR definition for RA. And that one was applied to populations, generally shows ten percent, twelve percent of all RA patients are D2TRAs. But then now you get into how many of those are inflammatory or non inflammatory pain because pain is the largest driver of these D2T populations.

What I like about what Dennis was doing is that he's trying to put in activity requirements that are more objective, maybe more inflammatory get you towards, because if you have a definition of D2T axSpA, maybe with that definition now you can study interventions. The problem is if the intervention is functional, biologic is going to do you no good and whatnot. So I think they need to work. I was almost liking the sound of these, that it might be trying to avoid the fibromyalgia, depression, anxiety, my dog ran away kind of personality things that can factor into this. Failing drugs, because there's a lot of reasons why people fail drugs, that might be the entry in, but trying to homogenize that population with these definitions might be a step ahead of what they're doing in PSA and in RA, my opinion.

Yeah, on evaluation on the research studies, they were more strict that you have to meet these three criteria, were like, one of them was very objective, which was the elevation of the CRP and then Hw27, as well as the failure of at least two biologic or targeted with different mechanism of action. I think that that was a little bit more stringent as far as a little bit less broad.

Right, okay. Let's get on to our next one. Doctor. Kastra, what do you got?

So I find it very interesting. There's Abstract five zero five about cycling to TNF inhibitors versus switching to IL-17A after a first TNF discontinuation among patients with psoriatic arthritis and axSpA patients. And this was very interesting because guidelines sometimes say the guidelines actually say, hey, you can use either TNF or IL-seventeen, but it doesn't say what to actually do after stopping the TNF in particular. So could you continue? Should you switch?

So what I like about this abstract in particular, they evaluated the effectiveness of cycling on a second TNF versus switching to IL-seventeen inhibitor in patients with psoriatic arthritis and asthma from the core evidence registry, and the primary outcome for psoriatic arthritis was the change from baseline on CDAPSA, and the primary outcome for AHPPA patient was the change from baseline on Basti. Interestingly, so in general, the cohort was mostly TNF users compared to the IL-seventeen inhibitors, but interestingly, there was no difference between cycling the TNF or switching to IL-seventeen in terms of the primary outcomes, which was the change from baseline in these metrics, but it was interesting that particularly for psoriatic arthritis patients, there was some significant evidence in the physician global assessment of arthritis and psoriasis in switching to IL-seventeen inhibitors as opposed to continuation or cycling the TNFs. As far as the axSpA, there was no major difference, but it did make a difference on IL-seventeen inhibitors switching in terms of fatigue, which I thought it was kind of interesting. So in general, in clinical practice, depending on these patients, we tend to it seems that definitely the TNF inhibitors are widely used for psoriatic arthritis patients and asthma patients.

But then it is important to consider, should this patient most likely will benefit from switching mechanism of action? Predominantly in psoriatic arthritis patients, I would think about more like the domain involvement, particularly the ones that are having disease activity, like arthritis or psoriasis involvement, as opposed to the asthma patients. So I think this was a very interesting and still creating some controversy, something that I found that it missed in this abstract was the reason of TNF discontinuation. So was it because of a primary failure or was the patient going to continue because of a side effect or something like that? So that definitely changes things a little bit.

Were these people who only failed one TNF, or could they have failed multiple TNFs to get in the study?

One. One.

Okay. So maybe that makes why the second TNF didn't do so badly. The more further you get down the line, lose that efficacy. Mike, Sheila, what do you think of this data?

Go I

It's up to you.

Okay, well, I think what it means for me as a clinician and in a resource limited air setting would be, well, at least you get options. Although as Adela said, there was really no statistically significant difference from cycling for switching among the psoriatic arthritis patients in asthma, but it gives you confidence or it reassures you that whether you give another TNF or you switch to an IL-seventeen inhibitor, the chance of the patient improving will still be there.

Okay, Mike, what do you think?

Yeah, I have a couple of thoughts. I mean, I am generally a fan of switching for people who are primary non responders. And I mean, the thing about IL-17s is that they're marginally more user friendly, and I think that they do a better job on skin. And so my general clinical preference has been to shift towards cycling. This was a small ish study.

Wasn't, it was large enough. If there was a big difference, you'd think you would have found it. There was a little trend toward there being a small benefit towards switching. And so I don't think it changed my priors too much other than saying that I'd be more comfortable trying another TNF. Going back to what was saying about immunophenotypes, mean, I think the people who don't respond to the first TNF upfront are less likely to respond to the second one.

Later on, late failure, especially if that's due to the of anti drug antibodies, then yeah, you probably still have some juice and a squeeze for TNFs at that point. But my general preference is to switch people who don't respond well to a specific class upfront.

Yeah, I think that that makes some sort of sense. I think we're all aware of the fact that a primary non responder needs to change to another class of drugs. But in these situations where you don't know it or they are a secondary or even a side effect issue, it seems reasonable to try to cycle within the class as opposed to switching to another MOA class. So this seems reasonable and whether it becomes a guideline or whatnot, studies have to be done really well to show up in guidelines. And they're not always done well.

That's the problem. A lot of these are retrospective observational cohorts and whatnot That sometimes limits their interpretability or extrapolatability, I guess, if you will, especially when it comes to making guideline rules. Right, Doctor. Putnam, what do you have?

Yeah, so these recaps, I just want to give you the hardest hitting abstract that I saw or experienced during the day. The thing I'm going to bring home from the meeting and that was definitely abstract seven seventy, which was the plenary session that started at the third of the morning today that investigated the use of upadacitinib, a Janus kinase inhibitor for patients with giant cell arteritis. This study is called Select GCA. And this is certainly a study that I'm gonna remember. Full disclosure, I was a participant in this trial.

We didn't enroll any patients, but I have been interested in this for some time. I think we're all well aware for the past five or six years now, we've been using Tocilizumab and Erleukin six inhibition in giant cell arteritis. But if you look at the GIACTIV trial, there's a large number of people who did not respond. We still see people flaring through it. We have not yet found the perfect cocktail for patients with rheumatoid or with giant spondylitis.

And so we've all been excited about a lot of the activity in this space. There's IL-17s, there's JAKs, there's a number of different agents being investigated. And so this was a big deal to get to see this presented. It was a big study that was conducted with no preliminary data. There hadn't been a big case series or anything.

They just went straight to a phase three, which is my bias and my preference is to, if you have an agent you already have a rough sense for the safety profile let's just test them and test them properly move things forward. There's a big four twenty eight people were enrolled double blind randomized placebo controlled trial. There are three groups. The one group got fifteen milligrams of upadacitinib. There's a seven point five milligram group that didn't do very well.

We want to be on par with placebo and a longer taper. And then there's a placebo group. And the thing is they gave you the investigation agency got upadacitinib in a twenty six week steroid taper or you got placebo in a fifty two week steroid taper. So even if this had been equivalent, that would have been considered maybe a little bit successful. But what they saw was that patients who got upadacitinib, forty six percent of them were in remission at week fifty two compared to twenty nine percent.

So more likely to be in sustained remission. Looking at people who had complete remission, thirty seven percent in the upadacitinib versus sixteen percent in the placebo group. So pretty good differences favoring the new drug or padacitinib that's where statistically significant and that's in the context of these people doing a steroid taper that was half as long. There's a bunch of subgroup things that they tested. It looked good for facet fatigue and all of the smaller things that they looked into.

Safety is a big question with JAKs. This is an ongoing debate since the oral surveillance trial. I think that in general, we should look at this as a class effect with the caveat that thus far we haven't seen any clear safety signals for this particular Janus kinase inhibitor. But I'll tell you that when talking to patients about this, I still mention it as a problem with the JAKs writ large. And it's hard to sell people who are 50 on a drug that might cause cardiovascular disease and cancer.

They don't like those. But all that said, I think that this trial was definitely successful and will be approved. I think this will be an option for patients with giant arthritis going forward.

So the question is, will the attractiveness of an oral JAK in these patients be enough of an attraction to overshadow the small safety concerns of JAKs in elderly people who may be at risk. I'll just tell you guys what happened at At ULAR, I chaired a session where David Liu and Janet Pope, two of our faculty, did a debate. And the debate was, should rheumatologists be worrying about oral surveillance data? And the interesting thing about those two people is that they both said that they could have argued either side of the argument because the data is so versatile in that way. But in the end, it's clear as to who may be at highest risk from oral surveillance, elderly, cardiovascular history, smoking, those are the ones you worry about.

And that could be this GCA population. Otherwise, it doesn't make sense to worry about JAK use in 23 year olds with alopecia areata or something else you might be treating. In the end, when we ask the audience, how many of you are still using JAKs in spite of this warning? The vast majority of the audience raised their hand. We asked the converse and only a minority said that they significantly altered their JAK use.

I think most people put the caveat into play. So Mike, with that information in mind, how do you think rheumatologists are gonna respond to this?

Yeah, it's funny. I mean, I think that you're kind of striking the balance correctly there where, you know, I think that there are some rheumatologists who will just be uncomfortable with this and I understand where they're coming from. I think the safety risk is real. I think it's small though. And I think for many patients, it does make sense to use one of these agents.

So if it gets approved, which I expect it will be, it's certainly something that I'll be offering. It's hard to know whether this goes ahead or behind tocilizumab. It's kind of interesting if you look at the different curves, it looks pretty similar to the tocilizumab data as far as efficacy. And then if you consider a small risk and maybe it's more user friendly because there's no injecting that you have to do diverticulitis, but maybe that's just safety issue. It gets really complicated.

At the end of the day, I think you just need to explain to patients, make sure they understand that these are small risks, but real risks. And I think that a lot of it will come down to patient preference for me.

I agree with you. In particular, when was there in that session, and the first thing that crossed in my mind was, of course, they had to do the placebo one, but we do have an approved agent for GCA. So I was like, why are they then just comparing it to tocilizumab because it leaves us as to where do we put it in, we do it for tocilizumab non responders, or should we go ahead and just know, Hey, you have an oral medication that might help with this? It's, of course, very nice to have more options, especially to discuss with these patients. But I also was like, Oh, no, I'm not sure where exactly am I going to put it in my order of starting these patients.

Yeah, I think that's the big question. Sheila, how do you feel about this data? Will it change what you do if it were to become available in The Philippines?

Yeah, well I think it might, it might. For me, what's important is as long as there's a drug that can really avoid giving too much steroids on these patients, because you know, all boils down also to the, just like what Mike said, patient preference. And also I think it's important that they know what they're getting into and the monitoring that they should be monitored. And, you know, we'll see. We'll see in the future what this will bring.

And hopefully it comes to The Philippines. And then maybe I'll give more data I'll give more feedback.

All right, that's very fair because these questions often take years to figure out and we learn by our experience. I want to give you an abstract and I'll do kind of quickly. I was going to do the TAPER study, but I watched Mike Putman do a video on the TAPER study today. It's a steroid withdrawal study in GPA. He did a fabulous video.

You should look at that on RheumNow, or maybe Mike, you can do that as your next one. So taper study and steroids and GPA, whether you should wean or not, that's kind of I'm going to talk about the fate of seronegative RA, a poster four fifty eight from the Mayo Clinic today. It's on their 20 experience and one hundred and seventy six seronegative, meaning ACPA and RF negative RA patients followed for over fifteen years. And the interesting thing, the bottom line is in this study, you can't beat Mayo Clinic data, you can argue with it, but I used to say all the time, really hate Jim Model and Ted Pincus because I have really strong opinions, but they have really strong data. And as much as I might yell, data trumps your sound opinion or loud opinion either which way and Mayo's always got good data.

And, what they came up with is a 15% conversion rate, in following people at least for the 10 cumulative incidents was fifteen percent. The majority of those by the way were spondyloarthropathy. So it was like thirty something people changed, diagnosis. About a third of them changed to either PSA or AS, six of them. So that's about, twenty percent turned seropositive RA.

And now we go five with OA, three with Crystal, three with the non diagnosis of CTD, one infection, one paraneoplastic, one RS3 PE, and one sarcoid. That's been seen in other studies, but I always quote, I think it's four fifty three, four thirty five patients a finished study by Taliki Soka followed ten years. They had a sixty five percent conversion rate on seronegatives. So there's quite a bit of variability. I always use this as one to remind the audience that seronegative is not seronegative until you keep asking yourself the question, is this still seronegative?

And you remain inquisitive at least for a few years. It really is your opportunity to ask that question and to consider it. Then what they did find was of their patients, I want to say twenty seven percent went into drug free remission. So, five percent had seronegative RA didn't become something else, twenty seven percent went into drug free remission and nineteen percent had refractory disease enough to require either a biologic or a JAK inhibitor. So that seems reasonable.

The data on seronegative is that to be seronegative, you almost have to have pretty severe disease. It's not easy. Not all seronegative is aches and pains and something that you think meets criteria, but a lot of them actually have severe disease and erosive disease. Meaning they have to make up for not having the serology to actually have the diagnosis. I do think it's instructive if only to remind us how we should be considering these patients.

Anyone have a different view of this?

I wonder if like, you know, the ones that went into remission, I'm thinking when they go into remission, it makes me wonder more about an alternative diagnosis, you know, because we know that remission definitely needs medication in rheumatoid arthritis. We know when patients are in their treatment and then we try to taper or stop the medication during remission, they have chances of flaring again. So when they have sustained remission drug free, I'm still thinking, and seronegative, I'm thinking, is this an alternative disease? So that's what I always think about in these type of patients.

Yeah, would echo that. I always have two thoughts on seronegative RA. The first is I always tell my fellows, well, we're going to treat this just like seropositive rheumatoid arthritis for now. And that for now is really important. And then the second thought is that the OR really matters in seronegative RA.

So if you have a patient who think it's seronegative rheumatoid arthritis or polymyalodramatica, I'm actually gonna reach for an IL-six agent for that patient. Had a patient recently who I thought was a seronegative RA or dual onset Still's disease and we tried IL-six. She actually benefited when we put her on IL-one, did great. And so I think that seronegative RA, you should always ask yourself, given this patient's demographics, given their constellation of findings, that funky rash they had, they had paragrais, figure out what the ore would be. And then we have a lot of options in RA.

You can kind of bend your or towards what, or your treatment toward what their or would be.

Yeah, I mean, I agree with you because there, I get to see a lot of steroid negative RA and I think what's important is giving it time over time. Sometimes there are new symptoms that will come up. There are new signs. So if you think that your initial treatment is not working, then yeah, consider the OR and that they're a negative RA patient.

I like that. It's definitely a good policy to have. All right, so we're gonna do one more go round with our three faculty and get shorter presentations to wrap this up. Sheila, what's your next one?

Okay, so my quick hit is from the year interview earlier. It's the research by Sepoletta et al, I hope I pronounce it correctly, about gout flares that are followed by an acute CV risk. So they found that within the thirty to one hundred twenty days following acute gout clearance patients were at risk of developing cardiovascular problems. And so I think what what the message then to us rheumatologists is that all patients with gout, regardless of the duration, especially at the first onset or first diagnosis, seen for CV risk and managed.

Really important. Did anybody else go to the year interview?

Yes, I was there as well. Think that's-

Do you have a favorite from there?

Yes, my favorite over there was definitely the CAR T cells because of course, we can see that in different, like initially, they were kind of very small just cases, but now we're getting more and more cases of patients, severe autoimmune diseases that are responding to CAR T cells. Interestingly, it works, but it's extremely expensive, like $1,000,000 per patient. So I was like, oh my god, is the cost worth the benefit? But at the same time, was thinking patients with these severe autoimmune diseases, seeing them, treating them, actually, they're very costly as well, also in the terms of disability as well. So I was like, maybe down the line, maybe the cost will be worth it.

And something that also caught my attention there was they presented another one on the CAR T cells about the allogeneic CAR T cells that they can actually be preserved for like a year. So that was pretty interesting too.

Yeah, the other thing that Mike Pillinger did in his 10 abstracts, he had three of them on knee OA, a treatment we really don't have much for, all making big splashes in New England Journal. Krill oil in NEOA, methotrexate in NEOA, and what's the other one?

The maglotide. Yeah,

weight loss drug, the GLP-one in NEOA. Anyway, all right, what's your quick hit, Adela?

My quick hit is hang in there, I have the number here of the abstract. It is abstract five ninety nine, and it was about sex related differences in efficacy of biologics in axSpA patients, and this was a systematic review on meta analysis. Over 11 studies were included. Over 11,000 patients with axSpA were included here, and they evaluated responses for VASD50, VASDAS low disease activity response, and ASAS40. Interestingly, most of the patients included in this trial were male, and most of the male patients also were age limit 27 positive.

And what was interesting about this abstract was that males were more likely to achieve bus die 50 and as does low disease activity compared to female patients, while ASAS forty was kind of gender neutral. So of course, it made me wonder, are female patients having more complicated disease? Is the delayed diagnosis more in female patients that leads us to difficulty in achieving these responses? Or should we just pick like a gender neutral measurement like ASAS forty to evaluate these patients?

Kind of a hot area. Gender differences in drug responses. It's one thing to say to heighten the awareness of this. It's another thing to have an approach to it. And I'm not sure what the approach is to be honest with you.

Mike, what's your Quick Hit?

Quick Hit, another hot area with, I'm not sure what to do about this. So there's a debate right now in the vasculitis world about what to do with imaging. How much to image, when to image, and when we find abnormal things, where do you go? So abstract seven forty two was the use of PET scanning to monitor activity among patients with GCA who were on Tocilizumab. What an interesting idea.

They followed 36 patients at the NIH. They have a big cohort there and they followed them to see what would happen with the PET scanning. And what did they find? Half of patients had persistent activity and not like little some of these were pretty active patients. They have some beautiful pictures in their poster that you know are the kind of thing that you would treat and so this is a real conflict that I have where I say, you know, if I see inflammation, I want to try to treat that.

But what do they see? And this is from their poster they said, ongoing FDG pet activity was not associated with longitudinal outcomes, including angiographic progression of disease or relapse risk. And this is where I just get so nervous. We have all these amazing ways to find inflammation, diagnose inflammation that we didn't have before. And all of a sudden we're treating things that we may not have treated before.

And if there's inflammation that you can only find on a PET scan, but it isn't causing long term complications, does that patient really need another six to twelve months of 60 of prednisone or another DMARD or should you be stopping tocilizumab to put them into remission because you saw some inflammation on the pet? And so this opens up this Pandora's box of questions but these are questions that I really think we have to be answering. If we're going to be searching for inflammation in GCA and PMR, we really need to define whether or not that is going to benefit our patients. And so I thought this was a great abstract. They ultimately concluded, they said routine or serial monitoring not advisable in GCA, which is a tough pill to swallow for a lot of us who think that we need to have something to track.

But I'm hoping in the next coming years we'll figure this out more. It's a tough spot right now and people have very strong views about it.

So these people that had the scans, were they like theoretically in clinical remission on tocilizumab?

Five had active clinical symptoms, but thirty one were in clinical remission. So they were in remission, but half of them had inflammation. And so that's challenging, As a rheumatologist, I treat the patient, I treat the symptoms. And for people who aren't having symptoms and aren't doing well and aren't progressing, oh boy, that's tough.

So Mike, you're a vasculitis guy. Can you help me in the audience? I think of FDG PET as the great test for extent of inflammation but not damage, and that other CTA or MRA are better at damage. Is that true? And then how do you reconcile that with this data?

Yeah, there's certainly some truth to that in the sense that if I wanna really characterize a stenotic lesion, then I want some angiography. If I really wanna characterize activity, low light inflammation, I do prefer PET. Although truthfully you can get a lot out of a good CT angiogram. So you know for differentiating damage I usually if I think someone has damage in an area I will track it with something else. If I'm just trying to answer the question is there inflammation here or I hope there's no inflammation here.

Then I do reach for PET. In this case, it's interesting, you know, had we been imaging these people with something that was maybe less sensitive to activity. And so say we're doing MR angiograms instead, I wonder maybe fewer of these people would have lit up, fewer of them would have been categorized as active and maybe that was actually would have been a better balance between finding disease that matters or finding disease that doesn't. But it's tough, it's a small cohort. You don't have infinite follow-up here.

And so it's tough. I don't want to over conclude it, but I'll say that it did confirm my underlying biases in this area.

Is lot of people. Sometimes, you know, it will be ideal to have like a baseline, you know, a diagnosis, baseline imaging, and then monitor that down the line. Okay, are they responding? So is this inflammation less than compared to baseline versus it's just inflammation that is new? Then that will make me think about alternative treatment or something else.

But if it's actually improving, then I'll be like, and the patient is clinically improving, then I'll be like, maybe our medication is actually working.

The problem is this finding has been shown before in the vasculitis world. Patient's doing well, but they still have evidence of ongoing disease. The question is, what do you do about it? In the case of RA, think about it there. You do have patients who have ongoing synovitis even though the patient's in remission.

And there doesn't seem to be good evidence that going for the imaging outcome or the finer outcome gives you a measure of better protection. But it really does make you worry and you're the guy that ordered or the gal that ordered the test that you have to ignore. Oh my goodness.

All

right. Well, let's wrap up there. This was really fun and I'm glad you guys took the time to share with the audience your best stuff from today. We're going to do this every day, day two, day three, day four of ACR. Enjoy the rest of the meeting, guys.

We'll talk soon. Bye.