ACR20 - Day 2.2 Save

This is the RheumNow podcast, and you're listening to highlights from the ACR twenty twenty virtual meeting. Our faculty reporters have been doing videos and recordings so that you could stay up to date. Hope you enjoy these and our panel discussions.

Hi. I'm David Lu, rheumatologist from Melbourne, Australia, reporting for RheumNow from this virtual ACI twenty twenty, here online. It's been a great meeting. Lots of great content across the board today. I wanted to tell you about one particular abstract that made one of the plenaries and also was mentioned in the press conference.

And that's covers a very topical area from investigators from Columbia University looking at particularly about hydroxychloroquine and QTc prolongation. And this has really been in the media as of late and in the general consciousness. Before this, obviously as rheumatologists love hydroxychloroquine for there are indications with the proven benefit that we know associates with that, the life saving benefit that occurs in lupus with hydroxychloroquine, and then the really beneficial effect we can see with hydroxychloroquine in addition to things like methotrexate and rheumatoid arthritis. But that's all been thrown in recent times. I remember first when I heard about hydroxychloroquine and COVID, the discussion that came up from our pharmacists about, well, what have you been doing about the QTc interval?

And all the discussion that surrounded that. And of course, part of the concern about using hydroxychloroquine in COVID has not just been about cannibalising the supply for rheumatic disease patients, but more importantly for the patients who do receive it for COVID, are they potentially at risk of prolonged QTc on their EKGs? And are they potentially therefore at risk of tussade de pointes and sudden cardiac death, which is not ideal clearly. So the question from that, the risk in COVID comes about, well, are patients at risk? Are rheumatoid arthritis and lupus patients, are they at risk as well?

So investigators looked at this, looking at some existing cohorts where EKGs had already been taken. So three zero seven rheumatoid arthritis patients and three seventy four lupus patients. And they looked to see what the drivers of that QTC prolongational QTC length in general were. Now they excluded patients with existing cardiovascular disease. And I think that's fair because we don't want other things that are going to influence the QTC length.

But when they looked at it and they adjusted the QTc for known risk factors of QTc prolongation, they saw that the length of the QTc length between patients treated with hydroxychloroquine versus patients not treated with hydroxychloroquine in that group of patients, there was no difference. There was no association with hydroxychloroquine and QTc prolongation in general. Really the things that drove it were age, corticosteroid use, smoking things that we know are linked to QTc prolongation. Now, where do we how can we resolve this with COVID-nineteen? And I think this really speaks to the fact that adverse drug reactions, in general are contextual.

It really depends on what drug and which disease you're using, what dose you're looking at, and what combinations of medication are in play. And of course, this is exactly what differentiates the COVID use of hydroxychloroquine to its use that we know and love in rheumatoid arthritis and lupus. Fundamentally, in COVID, we're looking at underlying disease which may well be affecting the heart. We're looking at potentially quite different doses, but more importantly, the combination with other things like azithromycin, which can also lead to QC prolongation and you have that combined effect as well. So some reassurance from the data, and when we're in doubt, we should always go to the data, that our use of hydroxychloroquine in rheumatoid arthritis and lupus really isn't something that we need to be worried about or necessarily monitoring EKGs for.

It's interesting, I ran a poll today. Got exactly in the first couple of hours, we've got exactly 100 votes asking you and your colleagues, when we're prescribing hydroxychloroquine for rheumatoid arthritis, lupus, or other rheumatic diseases, do we routinely order an EKG either before or during? And so the choices were eleven percent said yes, 81% said no, and 8% said why would I? And I think I can understand how that reflects in practice. So interesting provoking stuff about QTc hydroxychloroquine, and plenty more about all the topical things that are happening at ACI twenty twenty on our website, roomnow.com.

Come and join us there. Thanks for joining once again, and I'll catch up with you very soon.

Hi, I'm Doctor. Janet Pope at RheumNow reporting at the ACR Virtual Meeting twenty twenty. I'd like to talk about abstract number seven ninety nine. My question to you is can we get our patients to take our drugs more often? So in other words, can we improve adherence?

And it's a big deal because a lot of attenuation of drug benefit in my opinion over time is that they're not taking it. If you don't take their drugs, then the drugs don't work. So this was a very laudable randomized controlled trial. And what they did was they looked at patients with RA initiating a biological DMARD and they had electronic monitoring and they decided that adherence was anything less than 80% and patients randomized to usual care had usual care, Patients randomizing to the electronic monitoring had basically ways that they would see they weren't taking their medication. They would get alerts.

They would have behavioral modification and all sorts of important interventions. Bottom line, it didn't work. Now, does it really not work? What they said was the patients overall were quite adherent. And in general, in my opinion, patients with active RA are more apt to take their new drug because it really bothers them unless they're afraid to take it.

Their RA bothers them, they have active disease. So would this work if you had a population of patients who were losing benefit on current therapy or a population of patients that you know weren't taking medications regularly and you were afraid about loss of benefit over time. I think Abstract seven ninety nine raises more questions than it answers. I think it's a great idea but the wrong population studied. So please go to RheumNow and follow us on Twitter.

Thank you.

Hello ACR Convergence twenty twenty. This is Doctor. Robert Chow coming to you virtually from Fairfax, Virginia. I'm joined today by Doctor. Stephanie Wade who just had a very interesting discussion on medical education.

Doctor. Wade, would you care to tell us more about your project?

Sure, thank you so much for having me, Doctor. Chow. So my talk today was on, using an intervention to see if we could increase active learning within our introductory rheumatology curriculums in my training program. And so the main intervention that we performed was transitioning, to a flipped classroom. And so, the reason this is important is because, active learning has been proven in multiple studies in medical education to be better for helping learners sort of retain knowledge over time and apply it better over time.

And so we used a flipped classroom approach. And so what a flipped classroom is, is essentially just taking a traditional classroom model, such as when we all went to, you know, high school, and we went to class, and then we had a homework assignment, and flipping it around so that instead of doing the homework assignment after the class, you do some reading or learning or some sort of activity prior to coming in. And then you use your class time for inquiry, application, and assessment. So in this model, faculty would act more as a guide to trainees during interactive class cases, rather than just simply lecturing for fifty minutes straight. And so what we did was we initially performed a needs assessment in the 2019 on our introductory rheumatology curriculum.

And we had initially found that these active learning was low in our introductory lectures. And so then we held a faculty development workshop, teaching faculty how to implement this flipped classroom and how to create assignments for fellows to complete prior to their talks. And then for our post intervention period, this was the following year in the 2022, and we reassessed active learning scores in the flipped classroom. And so the neat thing about this, and sort of the surprising thing about this, was that our post intervention period actually occurred in a virtual classroom due to the COVID-nineteen pandemic and pressures on needing to be social distancing and not being able to meet as a group in person as we historically did in the past. And despite this sort of inherently less interactive nature of the virtual learning environment, we were able to show that active learning scores increase post intervention compared to pre intervention.

And this was very statistically significant. And we did this for 16 lectures in our introductory rheumatology curriculum, And we use pairwise comparisons to compare each lecture pre versus post intervention and found these scores go up in seven out of eight active learning domains, essentially. And so we're quite excited about our results. And it'll be interesting to potentially see how this holds up in the long run. And if at some point, we're able to get back into the real life classroom, whether we really would see even more increases in active learning using the flipped classroom model for fellowship training.

That's really fantastic. Do you think that's something that will likely continue in your fellowship curriculum where you are currently?

I hope so. I'm a third year fellow, so I'll be out going in June and moving sort of across the continent. But I certainly think that it's a sustainable model that we've created. And I'm very much hoping that this is something that will be continued. Sort of supplementary to our primary outcome, which was these active learning scores, we also surveyed faculty and fellows.

And we found that fellows quite enjoyed this and did the vast majority of the pre lecture assignments. And we also found that faculty seemed to enjoy it as well. Satisfaction scores didn't change pre versus post intervention. And they've sort of already adapted their talks to be more interactive and to sort of work with this model. And so I think it'd be very easy to continue this and may just need some ongoing faculty development in order to continue this and expand.

Right. And that leads me to my last question, most important question. Do you think that faculty are willing to continue this in the long term?

Yeah, I mean, I think it's tough to say, but certainly with faculty satisfaction scores being high, I think it's something that once you start, it's certainly easy to continue. But this is something that we've only implemented for introductory rheumatology fellowship curriculum, which is in the summer months each year. And so, you know, the potential would be that this could be used to create a more longitudinal curriculum for rheumatology fellowship programs, and potentially have the pre reading assignments and the lectures targeting the material that is board testable and available to us through the rheumatology blueprints and the in training exam material.

Well, thank you so much for your time. Appreciate the discussion on this very interesting topic. Thank you everyone for joining for tuning in. Please follow roomnow.com for coverage of ACR twenty twenty. And please follow me on Twitter at Doctor RBC.

Thanks.

Thanks, Rob. Have a good day.

Hello, I'm Anthony Chen. I'm consultant rheumatologist from Reading in The United Kingdom. And today I'm reporting from ACR20 at the psoriatic arthritis abstract session. There has been a lot of interesting abstracts today at the ACR20, but I wanted to highlight to you some very important abstracts, which I think will be of great clinical relevance to us, because one of the things that we hope to take back from the ACR is how we can practice this in our clinic. So one of the issues that we have in our clinic as we assess patients with psoriatic arthritis is to try to understand where the pain might be coming from.

And sometimes we see a lot of patients who have joint pains, but it appears that they don't have a lot of tender or swollen joints. And one of the theories that we think about in psoriatic arthritis is where the actual disease starts. And so there is a concept of the synovial antisis interface, where this complex between the synovium and the antisis is thought to be the origin of where the inflammation starts in psoriatic arthritis. If that is the case, then we should think about how we assess in the early parts of psoriasis and psoriatic arthritis, the enthesis or the organ that where the tendon joins onto the bone. And we need to find ways to try to assess this.

Now, clinically, have ways to do that by assessing the enthesis such as around the elbows, the knees or the Achilles tendon. But what a study has shown today is abstract number three eleven, and I think this is of importance to us because they have used ultrasound to assess the antesis synovial junction, and they found a very strong correlation with the power Doppler signal and the ultrasound signal at the junction between the joint, the synovium and the antisis. And this correlates well with the clinical features and clinical examination found on these patients as well. So adding in ultrasound could be one additional way, especially in the early parts of psoriatic arthritis to assess the antisis where we also believe it could be the site of where the inflammation starts. Another challenge that we have in our clinic is assessing patients with fibromyalgia or coexistent fibromyalgia when they also have psoriatic arthritis.

And many of our clinical scores that we use such as the DAPSA score, or the PSARC score can often be affected by the presence of fibromyalgia. And so when we assess this, there are very important things that we need to be thinking about. And in abstract number three fifteen today, there is a very interesting study that showed that if you had used ultrasound in addition to your clinical examination, that it can be helpful to try to differentiate what is inflammation at the sites of joint pain or tendon pain, as opposed to what is from fibromyalgia. So they studied two groups, one group with people with fibromyalgia and one without fibromyalgia in the context of psoriatic arthritis, and found that ultrasound was quite a sensitive way in detecting the difference between the two groups. And another study in abstract three thirteen also showed that ultrasound was very sensitive in picking up swollen joints, but less useful in terms of picking up tender joints.

And in a way that helps, it kind of helps us to understand what is inflammatory and what is non inflammatory sites of pain. And again, ultrasound in both these two abstracts could be useful for us in our clinical practice. And finally, abstract three fourteen again, shows us that the ultrasound can be very useful, especially when we assess patients with psoriatic arthritis, as they have a mixture of joint disease, tendon disease and also antisis pain. And using the ultrasound helps us to determine where's the source of pain in these patients. Is it the joint?

Is it in the tendons or is it in the antisis? And that again can be quite helpful for us. So in addition to our clinical examination, our clinical use of our skills, ultrasound could be another useful way, especially in the early phases of psoriatic arthritis, or in the patients who may have coexistent fibromyalgia to try to tease apart this very complex condition where there's a mixture of not only tendon, but also joint and antiso pain in the context of fibromyalgia, it can be quite challenging for us. So I think today's session and today's abstracts really has helped us to kind of tease apart some of these challenges that we have and how we can use other imaging modalities such as ultrasound in our clinical practice. So that is my kind of takeaway from the psoriatic arthritis session today.

I'm Anthony Chan, and you can follow me on Synovial Joints on Twitter, and I look forward to reporting further as the ACR conference progresses. Thank you very much.

Hi, good evening. I'm Leanne Gensler, a rheumatologist from UCSF in San Francisco, and this is day one of ACR twenty twenty. I'm here to report on spondyloarthritis for the meeting today. There were some fantastic abstracts that were presented that I'm going to review for you today. They all came from oral abstract sessions.

Several of them really dealt with treatments in psoriasis and psoriatic arthritis in particular. So the first study that I'm gonna talk about is the MACEMIZE trial, and this was abstract number five zero five presented this morning by Xenophon Baraleakos on patients with psoriatic arthritis who have axial involvement and really thinking about the efficacy of secukinumab on those axial manifestations. Now, these patients were defined as having axial involvement by their investigator, and really thinking about how much disease activity they had by the Baz dye, including patients having a lot of inflammatory back pain. This study really showed that patients had efficacy from an axial standpoint in patients with Casper criteria psoriatic arthritis. And in fact, they had some MRI data that showed a decrease in the bone marrow edema in the sacroiliac joints and spine compared to placebo, though the confidence intervals were wide, and this was a smaller group of patients.

They did not report on peripheral joints, whether they had swelling or tenderness or enthesitis or dactylitis. So it would be fantastic to see those data so that we can prove that this response is really the axial manifestations responding and not just the general psoriatic arthritis getting better, because we know that PASDAI improves in peripheral disease activity too. So but a very important study and really thinking about this group of patients who have psoriatic arthritis with axial involvement, psoriatic spondylitis, axial PSA, there are lots of ways to think about this, and seeing that there may be real efficacy in this particular manifestation of psoriatic arthritis. The next abstract that I'm going to talk about is abstract number five zero seven, and this was a post hoc analysis of the EXCEED trial presented by Grace Wright. And this was a trial that was one of the first head to head trials of a TNF inhibitor adalimumab compared to secukinumab.

And what they looked at in this trial is whether there were gender differences in response to treatment. And so they stratified the trial by men and women, and what they noted was that there was a higher treatment response and retention in men compared to women. And interestingly, secukinumab compared to adalimumab had greater efficacy in skin endpoints, but only in men. And so really what this trial is showing us, and I think this is something we've talked about for a while, is that as we think about clinical trials, we should really be stratifying by gender in that men and women are really different, they respond differently to treatment, and so we should really be thinking about them differently as we approach clinical trials. The third study I'm going to talk about is abstract number five zero six, and this was presented by Ian McGinnis.

It was the fifty two week extension trial of the DISCOVER trial with guselkumab in psoriatic arthritis. And what this showed was that there was sustained improvement and maintenance benefits in particular with radiographic progression, an important endpoint, and also reassuring longer term safety data. This is always important as we see those long term extension studies. The last treatment trial I'll mention is abstract five zero four, and this was the upadacitinib in psoriatic arthritis trial presented by Philip Meiss. And this was done in patients that were refractory to biologic DMARDs, really showing good efficacy in the twenty four week period, including all core domains.

And so that's also important as we think about psoriatic arthritis and really hoping that we don't just improve joints, but also enthesitis and dactylitis and other co domains in psoriatic disease. The final abstract that I'm going to mention was from the second oral presentation session. This was a study looking at the phenotype and genotype predictors of patients that go on to develop psoriatic arthritis. It was presented by Jesse Walsh from the University of Utah. And what she showed, and I'm just gonna talk about the phenotypic predictor was that in patients that had psoriasis, a predictor of going on to develop psoriatic arthritis was really those patients that had nail disease, that's not a new finding, but also really showing that the induration of the plaque, the psoriatic lesion was a predictor and in fact, in a dose related effect, and those patients that have more induration developed psoriatic arthritis earlier.

So really thinking about those patients with more severe psoriasis having a much higher risk for going on to develop psoriatic arthritis. This is Leanne Gensler reporting for spondyloarthritis at ACR twenty twenty. For more information, please go back to room now.

Hi, this is Vela Mehta reporting from New York for ACR twenty twenty. The abstract number that I want to talk about is four forty. And what we want to talk about is the representation of women as authors in the rheumatology research articles. So as you know, globally there's increased representation of women over the past few decades as physicians. In rheumatology about forty one percent of rheumatologists in The US are women.

The ACR estimates that by 2030 about fifty seven percent of US rheumatology workforce would be women. As we all know in academic medicine, journal article authorship is central to career advancement and promotion. And thus it's important to look into the gender bias in authorship of scientific articles. This gender bias is well known over the years across multiple scientific disciplines. And this study aimed to look into what are the disparities or what are the gaps in this particular research field.

So all original articles published over a five year period between January 2015 and 2019 were included in the analysis. And all rheumatology articles with an impact factor of greater than three and all general medical journals with an impact factor greater than 15 but publishing rheumatic diseases were included in this study. And the gender of the first author and the last author were determined. They scanned about 7,000 articles from rheumatology journals and about 100 articles from general medicine journals, again with an impact factor which is pretty high, greater than 15. What they found is that 51.5% articles with women had first authors but only thirty five percent of women were senior authors in these studies.

So there was definitely a gap in senior authorship. And when they looked into categories of which diseases has senior authorships with women, mostly they were pain syndromes or pediatric rheumatology. Whereas most articles with rheumatoid arthritis, lupus, systemic sclerosis, or vasculitis had more male senior authors. Also articles which were industry funded or investigator initiated but industry funded had much more representation from men as compared to women. And one of the key points that they make is women were much likely to be first authors but not as much as senior authors in randomized controlled trials.

And as you know randomized controlled trials have the highest impact in rheumatology and even medicine. So underrepresentation of women was particularly apparent in articles reported in randomized controlled trials especially those funded by industry. Again, the findings may represent just low number of women in academia as compared to men, which is reflected in other studies. But it also highlights the importance of institutional and industry leaders to take steps to ensure women are in leadership positions and also are adequately represented in academia. Thank you so much for listening to the video.

Follow me on Twitter belameta for more of these.

Hello, I'm Jeff Curtis, and I wanted to share something quite practical that was presented at the American College of Rheumatology's Virtual Convergence meeting. It's Plenary Abstract nine thirty nine. It's the results from the SEEM RA trial. So this is a trial that tested the very practical question for somebody with rheumatoid arthritis who's been doing great, like at remission or very close to it for a long time, six months, a year, or perhaps years, who's on etanercept and methotrexate and perhaps a little bit of glucocorticoids, you know, prednisone up to five milligrams a day. But those people have to stay on all those therapies for the rest of their lives.

As we know, there's a whole lot of people who frankly just don't wanna be on methotrexate, and they might grudgingly agree to stay on it for the most part, but they don't really wanna be on it. And yet, if they have to remain on it for what might be years stretching into decades to maintain remission, they might be willing to do it, but they're not going be very happy about it. And of course, if you have to keep giving yourself injections indefinitely with some of the safety concerns and the insurance and hassle factor associated with doing that, then so be it. But if you didn't have to do that, certainly there's a lot of our patients that might like to get off. So the purpose of this trial was to compare whether stopping methotrexate, leaving you only on etanercept monotherapy, or stopping etanercept and leaving you only on methotrexate monotherapy might be superior, and there's a comparison.

Just leave people on both and let them stay that way. You might think to yourself, wait, haven't I seen this trial before once or twice? Actually, you haven't, and the way in which it's different, these people had to be in remission, not DAS28 remission, but real remission. SDI less or equal to 3.3. And even if you don't measure the SDI, you basically have to have zero or at most one tender and swollen joints, pretty normal CRP, and a global score of one.

Like, this is real remission. This is not DAS remission. So these people had to be, in the investigator's opinion, doing great for at least six months. And then they had a 24 lead in period with three visits where they pretty much had to be in STI remission. You were allowed to bounce around just a little bit.

You could have an STI up to 11, that's up to low disease activity, but not higher than that and still qualify. So if you made it through that three visit, twenty four week lead in period and you more or less stayed in remission, then you could be randomized. And the randomization was two to two to one to etanercept monotherapy, methotrexate monotherapy, or just stay on the both as a comparison group. The main results of the study showed that etanercept was superior by itself to methotrexate by itself with respect to the maintenance of remission. So in other words, if you're going to peel something back, take away the methotrexate rather than taking away the etanercept.

Now overall, roughly fifty percent of the etanercept monotherapy patients stayed in remission. It was only about twenty nine percent of the methotrexate monotherapy patients. That was a very statistically significant result that delta is approaching double. Interestingly enough, though, in the combo therapy arm, the proportion who remained in remission at week forty eight was roughly the same as etanercept monotherapy. It was fifty three percent.

That was also significantly different than methotrexate monotherapy. So the two etanercept arms were more or less comparable. So what that teaches us is that if you're going to peel something off, probably better to peel off the methotrexate. But that even if you leave them exactly as is and you change nothing, you just put them in a blinded randomized study, you know, there are people that are going to bounce in and out of remission and, you know, may have some near misses. The second important feature of the trial is that if they needed rescue therapy, and they needed rescue therapy if they still had persistent disease activity or FLAIR beyond two weeks and tried some short dose glucocorticoids and some pain meds, the likelihood that you could recapture them either back to remission was about seventy five percent or to low disease activity was almost one hundred percent.

So as a practical matter, what it means is that if you're going to try to take one of those two meds away, metho or etanercept, if that doesn't work out, the chances that you're going to get them back where they started in remission or close to it are exceedingly high and approaching one hundred percent. So this is nearly a risk free thing to explore with patients and see how it goes. For those that did flare or had disease worsening, by and large that occurred into about a six or so month timeframe. Some people a little bit early, as early as three months say, but it's really three to six months that's the sweet spot, where the people that were going to do badly did badly in that timeframe by and large. So I think as a practical matter to communicate to patients, for those that might say, Sure, I'm interested in stopping one or the other, most of my patients at least have a preference about which they'd rather to stop, the trial showed that you're probably going to do better if you stop the methotrexate, continue the etanercept, but there's not that much downside if you have to put the one that you quit taking back again.

You're going to recover the vast majority of those people and they're going to be able to do well again. So I think it is a very practically designed study with regard to who's in it. You know, these actually are really the people that I personally would be taking off therapy or at least having that discussion. I think this provides some useful guidance with some real outcome data that stopping one or the other is reasonable, gives the nod to stopping the methotrexate rather than etanercept, but then makes it in a fairly risk free way to do so, to just put it back if you have to. What's not yet known is what are the predictors of people continuing to do well?

There's a lot of ongoing work to try to sort that out at a patient or a patient phenotype level. But at least on average, I think this is very encouraging. For those that are interested in stopping or tapering therapy to OFF, that the chances of success are pretty high.

Hi, I'm Jack Cush with RheumNow. It's the first day of the meeting. I hope you're enjoying it. I am this is my report called best thing I saw today. You know what?

It's not the best thing I saw today, but it certainly made me think a lot. And that's why I'm gonna present it to you because it's about practice. Specifically, it's about the issue of preclinical RA and should you use a DMARD or not. Preclinical RA is defined as patients who are at risk because they're first degree relatives. They're ACPA positive, and they have arthralgias, but they don't have swollen joints.

Should you treat them? Should you watch them? Should you worry about them? Well, abstract o four eight one titled subclinical synovitis in arthralgia, how often does it result in clinical arthritis was presented by Cleo Roger from, Erasmus, and she had a very interesting report. Actually, what they did was they looked at patients who had subclinical synovitis based on ultrasound in two large cohorts and MRI in another cohort.

So these three cohorts, 166, four seventy three, you know, looks like they had almost a thousand patients between them, and they follow them out over time to see what would happen to them. Their characteristics are about 40 years of age, mostly female as you would expect. They had one to five tender joints but no swollen joints. They were roughly fourteen or twenty percent ACPA positive, one cohort was fifty six percent ACPA positive. I've talked before and said ACPA positivity significantly increases your risk of progression to, inflammatory arthritis and then RA.

And they all had some kind of subclinical arthritis. But the number of patients who progressed to inflammatory arthritis within one year was really only about twenty percent. The question is, why and what are you going to do about it? Well, it turns out that the most influential factor here, and they looked at the rate of patients not progressing to inflammatory arthritis, I think they should most studies have actually looked at the rate of progression to inflammatory arthritis or RA, but they looked at it from the other standpoint. The bottom line is that, ACPA positivity doubles your risk over ACPA negativity.

So the patients who are ACPA positive in all three cohorts had roughly a forty five to fifty five percent chance of progression to inflammatory arthritis within one year. And I think that's the issue here. And since it seems like it's a toss-up, even in ACMA positive individuals, the point is, should you treat them or not? In this cohort, they were not treated. That wasn't the point of this particular study.

But the authors came out and said that just because you're aqua positive and because we've proven that you have subclinical synovitis on MR or ultrasound, you don't have clinical inflammatory arthritis until you get clinical inflammatory arthritis because it's still a toss-up. So, again, I think this goes to do you treat a lab? No. And do you treat an ultrasound or an MRI? I would say no.

They have to have swollen joints that you are convinced of. Progression rates are about fifty percent, maybe as high as sixty percent in people who are gonna be aqua positive. You watch them closer. You worry about them a little bit more. You know, the more worried you get, the more you make indecisive decisions like using hydroxychloroquine.

Hopefully, methotrexate or biologics. Again, they made the point that DMARD initiation in this cohort would constitute overtreatment. I'm a big fan of overtreating, but I think when you're in still in the preclinical phase, and that preclinical group of patients who might could get RA, I think you don't need to treat them until they you need to treat them, which is when they have swollen joints. That's it, and tune in for more videos on RheumNow.