ACR 2025 Daily Podcasts Day2c Save

This is an ACR twenty twenty five podcast coming to you from Chicago. Hope you enjoy it.

Hello, everyone. I'm Richard Conway from Dublin, Ireland reporting for RheumNow from ACR twenty twenty five. I wanna talk to you today about abstract number two three five nine, which was a poster presentation. It's by Consta et al. It was a study in radiographic axial spondyloarthritis or ankylosing spondylitis.

And this looked at the question of do NSAIDs, non steroidal anti inflammatory drugs, add anything extra in terms of inhibiting radiographic progression? So they had two sixty two patients, all of them were on TNF inhibitors, and then they had one hundred of that two sixty two who were also on NSAIDs, and the other one hundred and sixty two who were just on the TNF inhibitor. And what they found was that there were new syndesmophytes in thirty six percent of those who are on the nonsteroidals compared to fifty eight percent of those who weren't. And the change in the modified stoke and closing spondylitis spinal score was 0.1 compared to 0.7. So, again, favoring the group who are on the nonsteroidal anti inflammatory drugs.

And then the other nice thing they did is kind of had an internal control almost for this, where they looked at hip changes, and they found no difference in the hip changes between the two groups. So this suggests that potentially non steroidal anti inflammatories have a specific effect on the spinal radiographic changes, probably because these are more osteoporotic in nature. So this is an interesting study. It adds to kind of the ongoing debate in this area. They've kind of gone back and forth about what effect nonsteroidals have, and is there any such effects potentially beneficial?

I think it's still very much an open question, but I thought this was an intriguing study. So I'm Richard Conway. Follow me on Twitter at Richard p a Conway, and do tune in to RheumNow for all the updates from ACR twenty twenty five in Chicago.

Hi, my name is Marina Magre. I'm professor of medicine at Case Western Reserve University, University Hospitals Cleveland. I'm here at ACR Convergence Meeting twenty twenty five in Chicago and reporting for RheumNow. Last year we had gotten approval by FDA for bemecizumab, which is a dual inhibitor of IL-17A and IL-17F for the treatment of axial spondyloarthritis. In this year's meeting, lot of data has been presented about long term efficacy and safety of bimekizumab.

There are two abstracts that were presented about three year efficacy and safety of bimekizumab showing that has sustained durability and safety. The efficacy abstract, the data was pulled from both non radiographic and radiographic patients from B Mobile one and B Mobile two studies And these patients had achieved, you know, about forty more than forty percent of these patients had achieved an ASAS 40 response at week sixteen and also achieved a low disease activity, at week 16. About eighty percent of these patients continued to maintain this ASAS 40 response up till third year. And similarly, about more than seventy five percent of these patients maintained a low disease activity up to three years. And, fifty percent of these patients actually did not lose low disease activity, is pretty impressive.

Again, reiterating that, you know, vemikizumab is both sustained efficacious and is also durable. Then similar study that looked at, long term safety of bimekizumab, it looked across, two, you know, disease groups, axial spondyloarthritis and psoriatic arthritis included all, patients from phase two, phase three trials, open label studies. And, what this study showed was that bimekizumab was safe, over a period of three years. The most common side effects that weren't seen were, upper respiratory tract infections, nasopharyngitis, COVID-nineteen infections. Keep in mind some of these studies were actually done during the COVID period, and, there was some increased, incidence of, fungal infections.

Most of these infections were mild to moderate oral candidiasis, and, very infrequently did patients discontinue treatment because of these infections. There was no increased risk of other opportunistic infections or MACE events. The patients do not have an increased risk of uveitis flares in the Axial SpA group or IBD group, suggesting that the safety profile was similar to what was previously published and the drug remains safe over a period of three years. This is very important to us as clinicians because a lot of our patients, they lose response after being on a medication for some time. These data looked very promising that some of these patients stayed on bimekizumab for three years with sustained efficacy and it remains safe.

Hello everyone. My name is Youssef. I'm a consultant rheumatologist from Leeds. I'm reporting for RheumNow Live at Chicago for ACR twenty twenty five conference. As we all know, that achieving complete and deep peripheral B cell depletion is key, and this is also associated with a good therapeutic response.

Accordingly, there have been so many abstract and also clinical trials currently in progress to evaluate the efficacy and safety of CAR based therapies and also T cell engagers. What I would like to highlight today is one of the T cell engagers what we call it bispecific T cell engagers, BITE. As we all know, last year there was a BITE drug called blinatumomab has been showing some efficacy in a case series in systemic lupus. Now there's more companies investing on BiTE, so one thing that I want to highlight today is the abstract title six forty six. This is a study in China of 12 patients with refractory lupus.

Just trying to jog on the memory a bit. Mechanism of action of BITE is they do have two. One is binding to the CD3 and another one binding to CD19. So what happens when this cross links together, it will then bring this T cell closely to B cell to kill it. So in this study, what they've shown is a dose ranging escalation.

So patient had a low dose initially in week one, and after that they were then followed by week two to four within dose escalation. What they've reported was in the lowest dose there was incomplete B cell depletion but complete depletion in the moderate and higher dose. And in in term of efficacy, all in a patient in the three groups showed remarkable efficacy in terms of SRI four, and about half of them reached LLDAS. One patient withdrew the study due to renal complication, and also there was a one grade two cytokine release syndrome in the median dose. So although it is still early days, and I would like to see in a longer duration before we can then determine the efficacy compared to blinatumomab, this compound seems to be quite promising currently, but like I say, with all these early trials, we have to take into context that we need a larger sample number and also for longer term safety data as well.

So I hope you found my summary interesting. Follow me u six yusuf for more, and also my colleague at RheumNow for more content coverage. Bye everyone.

Hi, I'm Doctor. Sheila Reyes from The Philippines and I'm here in Chicago reporting live for RheumNow for the ACR Convergence twenty twenty five. It's day two of the conference and lots and lots of information have been coming in since the start of the day. And for my video, I would like to talk about abstract number fifteen twenty four which was presented in the poster sessions earlier by the group of Doctor. Karp and colleagues entitled Hydroxychloroquine Reduces Auto Antibody Levels in Persons at Risk for SLE.

So just a brief background before I continue. The SMILE trial was an RCT that set out to determine whether hydroxychloroquine could prevent the development of SLE in patients at risk and results showed that hydroxychloroquine did not prevent the progression of SLE and within that trial, some of the other outcomes were to collect biospecimens for mechanistic studies. And so this study, which is what I'm talking about now, abstract fifteen twenty four, assessed the effect of hydroxychloroquine on antibody levels to a panel of 120 potential autoantigens. And again, as I mentioned, biospecimens were previously collected from the SMILE trial. They underwent analysis and where levels of the antibodies were compared from their baseline levels and those levels at the end of the trial or the last study visit.

And also the participants were grouped into either the progressors and those who developed SLE and the non progressors and of course the antibody levels were compared. Now results showed that the participants who received hydroxychloroquine had significantly lower autoantibody levels. That's about 93 out of the 120 autoantibodies that were studied at the end of the study compared to those who received placebo. And individuals who progressed or developed SLE had greater decreases in autoantibody levels than non progressors. Interestingly enough, the study also showed that the autoantibodies that were associated with progression or SLE were different from the autoantibodies that were affected by hydroxychloroquine.

Now, there are some limitations of course in the study and we have to really understand this based on context. Specifically, taking into consideration that the patients that were enrolled in the trial were or those who had milder disease and probably where only hydroxychloroquine can be given. So results of this study can give some insights into the other possible mechanisms of how hydroxychloroquine affects disease activity or how it can better inform us for making better clinical trials. But until then, we'll have to wait for further data. I'm Sheila Reyes.

Follow me on X at RheumOrampA and tune into RheumNow for more updates of the ACR twenty twenty five.

Hi, I'm Doctor. Elaine Husney. I'm here at the RheumNow booth and excited to welcome you again to day two of ACR twenty twenty five I am leading with a group of people on interesting psoriatic arthritis topics at the meeting. I'm going to go over specifically abstract number fourteen twenty six and I find this really interesting. It's called understanding the drivers of VASDY back pain scores in psoriatic arthritis patients.

So as you know, PASDAI very commonly used, very easy to use. Many of us use this in clinic and it's one of the most common tools, for assessing, back pain. What's interesting is that, five out of the six questions are pretty focused on general health measures over specific axial measures. And so this raises some concerns about what this tool is actually measuring. And in psoriatic arthritis, where we are trying to pick up patients early with axial involvement because it does have implications for treatment, BasDy is commonly used.

So in this particular study, they aim to evaluate the utility of BasDy in a observational cohort of psoriatic arthritis patients. So there was quite a big number, about ten fifty nine patients that got PASDAI every six months was used in this cohort. And the items in their conclusion that influenced PASDAI scores included age, sex, peripheral joints, and skin disease regardless of their axial symptoms. So it makes you wonder how accurately does FASDi reflect the axial component of psoriatic arthritis. So I think this abstract to me was interesting to note to kind of remind us about the components of BasDy and maybe there is some room to improve in thinking about a more precise or accurate scoring system that can be used to pick up axial disease earlier in psoriatic arthritis.

Hi, everyone. This is Aurelie Naj from Glasgow reporting live from ACR twenty twenty five in Chicago. We are day two. It's been an absolute joy to move around through the poster hole and go from session to session. And there's one poster that caught my attention today, and it's about handedness, dominant hand, and PSA.

Why is it that interesting for me? Because usually we know very well that biomechanic stress can be involved in disease activity, joint damage in psoriatic arthritis in particular, And we often ask patients, at least I do often in my clinics, I say, hey, you know, what is your dominant hand? And usually you find more disease activity there, but is this also associated with more joint damage? So, this poster was number 1415, 1415 and it was looking at a cohort of patients. So, it was a prospective PSA cohort from international cohorts, three fifty nine patients, and they were able to look at what their dominant hand was and it was self reported.

And as you expect, it was roughly ninety percent of right hand dominant people and about ten percent of left hand. Those who were left handed interestingly were older, had a longer PSA duration and a higher BMI. I'm not so sure why and they were not really able to explain that either but certainly what they did when they did their linear mixed model analysis, they did account for these differences in the two groups in the first place. The other thing that I found quite interesting is that they looked at x rays and decided to score for damage but they didn't use the modified Sharpe score. They used the modified Steine Broker score which is easier but it might be less sensitive.

So anyway, what they found is that left handedness is associated overall with the worst prognosis after having adjusted on the variables that were described earlier which I found quite interesting but also that left handed people had worse erosion scores on both hands, which also was quite interesting, but in particular in the left hand and the association between being left handed or handedness and damage was higher, was stronger in the people with left handed situation, which was the explanation they gave was you know interesting. So, it could be more mechanical stress due to less things in life being made for left handed people, in particular tools, and so it could be that, or it could be also a different thing. It could be a confounder that we've missed, or it could be the fact that also they did not use the Sharpe score and so maybe they missed some damage or association using this score. And finally, the last thing that I wanted to say is that this has not been reproduced in any other cohort. So, this is something definitely to look into.

That's quite interesting. And also, how can we prevent this as a consequence is something I'd be quite keen to look more into. Anyways, I'm gonna let you go now and invite you to join RheumNow. Have a look at the website and follow me on Twitter orilyromo. See you around.

Hi, everyone. My name is Brian Jaros. I'm here at ACR twenty twenty five. And with me, I'm joined by doctor Brendan Denver. He is a third year rheumatology fellow at Johns Hopkins, and he'll be telling us about his research today in airway disease and GPA.

Thanks for being here, Brendan.

Thank you

for having me, yeah.

So tell me to kind

of kick this off, how

did you think to look into airway disease and GPA?

Yeah, so airway disease and GPA can be a particularly nagging disease manifestation. We have good medications to treat GPA now that show good results in clinical trials, but we find that, airway disease is often refractory to these treatments, and it's a small subset of GPA patients, but a particularly challenging subset. I think that will probably resonate with

a lot of people, who listen to this and certainly with me. You know, I see a lot of vasculitis patients. And even it seems like when other manifestations of the GPA get bigger, the airway disease, the subglottic stenosis, etcetera, can just really nag on despite that other treatment. Totally. Totally.

So tell me what your group did to kind of help answer the question of what should we be doing in the situation of these patients?

So we looked retrospectively over the last fifteen years at airway GPA patients that have been seen at our center. And we looked at immunosuppressant use and the incidence of relapse. And we defined relapse as the need for a dilation of the airway. And we were interested in knowing if there are some immunosuppressants that are particularly effective for preventing relapse. And

in your group are you finding that you're treating most of these patients in general with immunosuppressive agents?

Yes, so all of these patients had diagnosed GPA. We excluded idiopathic subglottic stenosis patients, which we also see in our center and will sometimes offer immunosuppressants. But for the purposes of this study it was true GPA patients.

Awesome. And tell us what you found. So there were

four immunosuppressants that we looked at comparing patient time on them to patient time off them. For Rituximab and Azathioprine and Methotrexate we found no association between the use of those medications and dilation incidents. But for the conventional synthetic DMARR leflunomide we found a reduced incidence of tracheal dilation for time on leflunomide. So

I thought that was a really interesting finding, you know, when I think about my approach to limited GPA, for example, I often may try a DMARD before rituximab. And I'm often reaching for methotrexate as opposed to leflunomide. So walk me through kind of your interpretation of the finding, and does that change your Are you, you know, searing more towards leflunomide compared to methotrexate when you're thinking about DMARDs?

Sure. Yes. So there were 16 patients in our cohort of 56 that, received leflunomide at some point. That's higher than most cohorts. I would think most people's practice in line with what you're saying methotrexate first before something like leflunomide or azathioprine.

The reason that we have a lot of leflunomide patients is because Filcio, one of my mentors was treating patients and had a preference to a practice pattern for trying leflunomide often based on a 2014 network meta analysis that showed there was a trend for better outcomes in leflunomide compared to methotrexate and azathioprine. So I think that this paper, this study that we're talking about of mine corroborates some of that idea that leflunomide might be more effective for ENT manifestations of GPA, particularly in the airway. Awesome. Whether I'm actually doing that more, yes and no. There are certain patients that are the right patient for leflunomide and certain patients that aren't, but at least it is a consideration.

Yeah, think it definitely brings up an interesting point for those of us, again, treating these patients as another option and certainly something that I'd be interested to hear more about and think about trying. Tell me from your perspective, obviously there's a ton to learn about GPA in general, but of course these airway patients. What do you think are kind of the next steps that will help guide us in our treatment and management approach of this manifestation?

Totally. So this is a single center study. So I think expanding the cohorts to be multicenter is a first good next step. We can continue to do retrospective data, but I think it would be important to start collecting data prospectively. And that could include other outcome measures besides dilation incidents.

Can start using peak expiratory flow, for example, which would be helpful for delineating medication effects in a shorter time frame than dilation incidents. And then I think there's also a translational component to future research. Why is this disease manifestation more refractory than other disease manifestations? Is something different on a tissue level? That's something that we're also exploring as kind of a future next step.

Yeah.

Yeah. Last question for you. What, are your thoughts on Avacopan and airway use? Was that something you thought about looking at? Did you examine it in this study?

Or would that be a future direction as well?

Yeah, we did not examine that in our study. Most of these patients were being treated before Avacopan was on the market or being used. But that's interesting area. There was a sub analysis of the ADVOCATE study that showed Avacopan's efficacy for ENT manifestations. Whether it's particularly effective for subglottic stenosis, especially Avacopan in isolation, a super interesting question that I think we just need more data for.

Awesome.

Well, we really appreciate you being here. Yeah. Again, this is doctor Brendan Denver. Thanks everyone for listening, and we'll be back with more coverage.

Hi, everyone. This is Oily Naj reporting live from Chicago ACR twenty twenty five. I'm from Scotland, Glasgow, by the way. So today is an important day. Today is the day where finally, after many, many, many negative studies, we had a positive vagal nerve simulation trial that was positive.

So what does it take to make a positive trial in vagal nerve stimulation? It takes to implant it inside of the patient. So a lot of the studies we've seen that were negative were studies with external stimulation and in this specific case, so that was presented in the RA session, abstract sixteen seventy five. So in this specific study, it was an implantable device and so it was quite interesting. So the study is called RESETRA.

They had randomized patients. So everyone had the implantable device placed through surgery, but half of the population, so it was two forty patients in total, half of them had the device turned off for three months. And then after three months, everyone had the device on and it was this open label studies that continued for another sixty six weeks. So, it was really interesting to see that the inclusion criteria was a bit surprising to me because usually you want a DAS calculation that is above 3.2 to define active disease. In this case, it had to be what they call moderate to severe RA, but then it was minimum four tender and swollen joints.

There was no other criteria, which was fairly surprising to me. But the good thing is the population was already resistant to one biologic at least. And very importantly in this population, fifty percent of the people or actually thirty had not responded inadequately to two or more and thirty five percent had responded inadequately to at least three biologic. So we're looking at a resistance population which is good because these patients are not usually included in trials that much. So primary outcome, three months ACR20, so quite soft primary, but even then it seemed to be very efficient, or at least more efficient than the placebo, the control, the sham control group, which wasn't placebo.

42 versus ninety percent, and then at twelve months, once people had kind of all gotten to the active group, it was sixteen percent of ACR seventy, which you know is not that high, but equally these are people that are mainly resistant to multiple biologics anyways. The good thing as well is that at twelve months, there was no need for rescue therapy or change of biologics in eighty two percent of the people, which again, I think it's a good result. Persistence was good. There was one severe adverse event though that was admitted to be related to the implant and it took that they had to remove it from the patient, but aside from that, there was a question I think in the audience about whether or not the sham was an actual sham because does the patient know if their device is on or off? But aside from that, I think it is promising, but it is invasive.

So I think it's definitely a conversation to have with the patient. If we were to develop that, would you want to have this device implanted considering, you know, the improvement is moderate? But it's still better than nothing. So that's something definitely to keep an eye on. And then there's a poster that's presenting the structural data, 2614, showing that apparently at three months, the active group had less erosions or had less radiographic progression using the MRI RamRay score, and it was forty percent versus nineteen.

So, I found that surprising that so quickly in three months you can see such an important difference in the imaging, so I would be quite careful with that one, but definitely something to keep an eye on. The authors explain it by saying that vagal nesting relation can reduce RANK ligand, which is a protoaclastic cytokine and therefore reduce bone damage. That's, I think that's seductive, but we need to definitely keep an eye on that and see if that's confirmed in larger studies. That was me for today. Tune on rheumnow.com for more content and follow me on Twitter at oriliRheumNow.

Hi. This is Bella Mehta reporting for RheumNow from the ACR conference in 2025. One of the very interesting talks here is about GLP one, which I think is in all medical conferences across a lot of disease states. As you know, a lot of patients the indications for GLP one currently are diabetes and probably obesity, but they there are trials for knee osteoarthritis too, which are ongoing. And, for example, the data from the STEP nine trial is out there.

It's the NEJM publication looking at how these have changed outcomes. Seems like GLP-one do help knee osteoarthritis outcomes in pain. The question still remains is that is this because of just weight loss because we know that weight loss helps knee OA, or is it because of another effect mechanism? So there are a few abstracts at at ACR this year talking about two things that it may modulate. One is inflammation and one is fibrosis, and they've tested this in different animal models, also looking at how injecting these drugs in mice over a period of time does change the synovitis as well as the fibrosis in knee joints, and these are sort of the two big markers which help in pain as well as structure, which is fibrosis in knee OA.

So I think over the next year, there's more data gonna come out on GLP one. The title of the talk was interesting. It said, should we give it to everyone? I I don't think we should be giving it to everyone. One is I mean, these are relatively safe drugs, at least out there, but, you know, there's a cost involved.

There's still a lot of other things that need to be happening, but we know that weight loss works, so in any shape or form for knee osteoarthritis along with strength training, exercise. Those are things that you can tell your patients. At this point, it's not an indication for some of these drugs, but I think in the next year or so, we'll see more of this data and indications for NEOA for GLP one drugs. So with that, signing off, this is Bella Mehta for RheumNow.

Hello. My name is Rinalini Day. I'm a fellow in rheumatology and internal medicine in London in The UK, and I'm reporting for RheumNow here from ACR Convergence twenty twenty five in Chicago. I'm very delighted to be joined by doctor Laura Plantinger, who is an associate professor at UCSF, University of California San Francisco here in The US, and we're gonna be discussing the topic of physical function in individuals living with, systemic lupus erythematosus SLE. And this pertains to abstracts sixteen thirty nine and sixteen forty that were presented here this morning.

Thank you for joining me Doctor Plantinga. Thank you for having Thank you. So just to start with it would be useful for our audience to know could you give an overview of the work that was presented here today?

Yeah So we actually use two population based cohorts in The United States. So one was the Georgians Organized Against Lupus at Emory University and CLUSE, which is California Lupus Epidemiology Study in the Bay Area. And we wanted to look at how they compared between the cohorts. And then also because we had measures of both self reported physical functioning and objective physical from a short physical performance battery from both of the studies. We wanted to look at the coherence between those two measurements in people with lupus.

Perfect. And how did you go about doing this and what did you find?

Yeah. So, Clues had already done this assessment, so I didn't have to do much there. For a goal, we actually did a ancillary study to goal, called appeal, where we brought everybody in for an in person visit and measured multiple geriatric measurements including the short physical performance battery and the self reported physical functioning. And then we looked at distributions of scores. We looked at associations of scores with each other.

So kind of the difference between them by cohort. And then we also looked at concordance of the measures of self reported and objective physical functioning kind of over both cohorts.

Perfect. And what did you find?

Yeah. So in terms of physical functioning, we found quite a big difference in physical functioning between the two cohorts. So in the CLUSE cohort, both the short physical performance battery and the self reported physical functioning scores were higher in than they were in appeal slash goal. So, they were not explained by individual characteristics including age, sex, race, but they were somewhat attenuated by clinical characteristics. So kind of the higher disease activity that we saw in goal seemed to explain some of that difference.

In terms of the concordance, so I believe, don't quote me on the numbers, maybe about half of them were concordant in terms of, you know, where they fell in a quartile of those scores. But there were a lot of discordant people. So some people were kind of what we called overestimating their physical functioning. So they were, you know, reporting really good functioning and then not doing very well on the short for physical performance battery. And then we had kind of underestimation of people who did pretty well on the short physical performance battery but reported low physical And then we looked at predictors of that.

And so some of the things that predicted it were disease activity. We found that people who had high BMI tended to underestimate, which may be due to kind of stigma and ideas about kind of having a high BMI and what you're physically capable of doing. Yeah. And then we also found that males were more likely to overestimate their function than females. And it was actually quite interesting because the order in which we did it in the study visit, they actually had already done their objective physical performance Fine.

Measurement. So, they already knew how well they did on that. Yeah. They were a little bit worried that they would, you know, kind of use that. Yeah.

But a lot of people were still fairly discordant in Yeah.

Their assessment. So, what's the clinical implications

of this?

Yeah. So I mean, think in terms of just the differences between the cohorts, thinking about, you know, your patient populations are very different, that you can't, you know, use Yeah. Individual characteristics to think about, like, what their physical functioning is going to be. Thankfully, there's some kind of new quality measures coming down the line where we're gonna be measuring physical functioning in lupus patients, so it's something that you can discuss with your patients and what the factors are individually for them. In terms of their concordance, I think kind of the main thing is that seeing their self reported physical functioning, is what's gonna be the easiest thing to measure in a clinic, You're not gonna be able to do a short physical performance battery every time they come in.

Yeah. Just knowing that that doesn't necessarily represent what they can actually do. More a combination of what they can do and how they're feeling about it. So keeping in mind kind of the both the mental and physical that's going into that score.

Absolutely. And I feel that, you know, physical function that we've been talking about, it's been an under sort of studied and underappreciated Mhmm. Aspect of living with lupus, which obviously comes with a lot of comorbidities, a lot of morbidity. And so I think, yeah, this work will really drive into people's minds, hopefully, to pay attention to someone's physical function regardless of how we actually, of course, measure it in clinic when they go back to their clinical practice next week. Right.

Right. And what's next for this piece of work?

So we've actually we've measured many geriatric syndromes. So we have some papers coming out. And some papers already out on cognitive performance in people with lupus, activities of daily living Yeah. Falls, and some papers soon to come out on polypharmacy and urinary incontinence. Now that some time has passed, we're trying to start starting to look at outcomes in people who, you know, had impairments or restrictions or limitations in some of our measures, and what happened to them, several years down the road.

So that's kind of our next step. And then hopefully, pulling more cohorts together because this was kind of our first foray into Yeah. Putting cohorts together.

So

Perfect. And obviously, like, you know, activities of daily living, physical function, polypharmacy, these are the real things on the ground that really matter to people. Yeah. And so it's really good that, you know, there's this new body of work coming out now that really addresses this. So that's really great.

Well, thank you for discussing your work with me today, doctor Plantinga. If you'd like to find out more about doctor Plantinga's work, then it is 1639 and 1640 here at congress. And if you'd like to know more about what's going on here at ACR twenty twenty five, do follow along the RheumNow coverage. Thank you.