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Hi. It's Janet Pope at Janet Burdope, and I'm AtRoomNow, ACR twenty twenty four. I wanna talk about a few things of stuff I learned at ACR twenty twenty four. So first of all, I think there's hope for Sjogren's syndrome. So Nipocalimab, abstract two five two seven was a plenary phase two RCT in Sjogren's showing that this molecule decreased fatigue, improved symptoms and signs in Sjogren's.

Now interestingly this molecule has also been approved for myasthenia gravis, a couple other indications, so I think more will come in the phase three. I also learned there's a lot of CAR T studies and a lot of talk about bispecifics. I think we are borrowing from oncology and maybe some of these studies or molecules will be transformative for our patients, in particular those with connective tissue disease are being looked at. Now the final little niche thing that I learned was abstract number sixteen ninety six and that was a randomized controlled trial properly designed, properly executed of a 150 patients with active Takayasu's otteritis. It was investigator initiated and took a long time to enroll.

What did they do? They wanted to compare mycophenolate mofetil about two grams a day plus methotrexate usually about fifteen milligrams once a week added together at the beginning of treatment and active disease added to glucocorticoids randomized to that arm or cyclophosphamide and then going on to azathioprine for maintenance therapy. In the groups, it was a two to one randomization and I'm telling you right now it's changing my practice because methotrexate plus MMF seemed to be well tolerated and it was better on steroid sparing and overall effectiveness in Takayasu's Arteritis. We don't see a lot of it, but when I do, I know what I'm going to use next in treatment. Please follow us at RheumNow.

Thanks.

Hi, this is Eric Dine from ACR Convergence Day three. Here's what I'm looking forward to today on our last full day in Washington, D. C. I'm looking at the IL-seventeen data. There's a lot of information about some of the new medicines like bimekizumab and also some data about some of the older medicines like secukinumab.

We know that one of the benefits of IL-seventeen is its efficacy on enthesitis. One of the abstracts being presented today is 2586 looking at the tissue effects on an inthesial tissue. The EBO study is looking at minimally invasive ultrasound guided biopsies of enthesitis, particularly looking at the lateral epicondyles of patients with active enthesitis. What they do is they established a baseline ultrasound guided biopsy and then they repeated it after at least three months of being on fecacitamab therapy. They had 10 patients enrolled in the study.

They had nine of them that they got the secondary biopsy to complete a before and after. Found what was they found that there was definite improvement in that tissue inflammation in the enthesis after initiation of the IL-seventeen inhibitor. They found that neutrophils, CD4 plus T cells, and IL-seven was decreased with a particular benefit of the IL-17A fractions of cell types being decreased in patients on an IL-17A inhibitor. So this is very useful information. They showed major effects on the transcriptional states of the resident endothelial cells.

So it's good to see in practice, in actual data in the tissue, to see that when we give an IL-seventeen inhibitor that we see that inflammatory response actually decreasing in the target in those entheses. So definitely great data to show that our agents for IL-seventeen are helpful for addressing our active enthesitis. Lots of great coverage here at RheumNow. Stay tuned for more information.

Hey everyone, it's Brian Jaros here. I'm reporting live from ACR Convergence twenty four here in Washington DC. Today I'll be telling you about abstract number seventeen fifty six. Now this is an abstract, that's being presented with the ankylosing spondylitis therapy group. It's out of, a group from Europe.

Their question is really interesting. They're looking to see whether patients who were previously exposed to TNF therapy had longer times to remission when they used another TNF inhibitor or an IL-seventeen inhibitor compared to those that had never been on TNF treatment before. And in order to do this they had a very clever design where they used a bunch of registries from across Europe in order to really gather a strong pool of patients to help answer this question. And I think this is a really important question to ask because our most recent guidelines out of ULAAR and ASAS suggest that after failing NSAIDs, either TNF inhibitors or IL-seventeen inhibitors in addition to JAK inhibitors may be used for refractory symptoms, not providing specific guidance whether TNFs are preferred first or IL-seventeen agents are preferred first owing to a lack of head to head data about these agents. And so this study might be interesting to tell us a little bit more about patients who fail TNF inhibitors first line, whether it's beneficial to class switch and go to a different agent like IL-seventeen or to stick with the TNFs.

So let's get into the data of the study. And so as I mentioned, they used about 13 registries. They excluded patients who had been on other biologics besides TNF inhibitors or IL-seventeen inhibitors and their primary outcomes were the time it took for the patient to achieve low disease activity or I'll refer to it as LDA and they defined this as an egg spot disease activity score of less than 2.1. The other primary outcome was looking at durability and so once people achieved low disease activity, how long did they stay in low disease activity until a subsequent visit where they became active? So in total they had over fifteen thousand patients who initiated initiated TNF inhibitors and over two thousand patients who initiated IL-seventeen agents, largely with similar baseline characteristics between the groups, although with more biologically naive patients in the TNF group.

And the results are really interesting. So they showed that the mean time to achieving LDA or low disease activity increased based on the number of exposures patients had had to TNF inhibitors previously. It was shortest if they'd never been exposed before and that was around an average of thirty three weeks for the TNF agents and thirty seven weeks for the IL-seventeen agents and increased all the way up to fifty one and forty six weeks respectively if they'd used two or more agents. In some ways this is not surprising, it might suggest that people who have failed a previous treatment have more refractory disease or a more severe phenotype in general, but it was interesting that both TNF inhibitors and IL-seventeen inhibitors suffered from this delayed LDA in those that had tried just a TNF before. Now, the other outcome that I mentioned was the duration of the low disease activity.

So how long it actually lasted once they achieved and this finding was even more interesting. It showed that the patients who were switched to IL-seventeen therapy actually had a shorter durability of low disease activity in the patients who had previously trialed TNF inhibitors. And this was different than the patients who were prescribed a new TNF inhibitor and actually maintained durability. And I thought this was quite surprising. Know, oftentimes we think about patients failing agents and the idea of class switching, which is, you know, switching to an agent that has a different mechanism with the idea of trying to target inflammation, trying to target different disease from a different way but this study actually suggested people who stayed in the same class, who stayed in TNF inhibitors performed better in terms of staying in that low disease activity.

So in some ways this gives us a little of insight into maybe using additional TNF inhibitors before switching to IL-17s but I think it also is one of those studies that actually raises more questions than maybe it gives answers. It'd be really interesting to see if the group went back and sorted these people from primary failures, which is, you know, no response to the TNF upfront versus secondary failures where they responded to the TNF and then had a, you know, wearing out effect over time to see whether the class switching to IL-seventeen had a more profound effect in those with secondary failures since this is something that we often think about when we're making our clinical decisions in practice. That's all I have for you today. Tune into RheumNow for more.

Hi, I'm on access at Janet Burdope. I'm here at RheumNow at ACR twenty twenty four in Washington. I want to talk about a session and, at full disclosure, I was part of this session. So it was can we make clinical trials better? This was AB's session number 18 ms.

2.5. So here's what I learned because there were three presenters, there was audience questions, I actually thought it was quite a nice session to move forward to improve our clinical trials in rheumatic diseases. So I learned that up to eighty percent worldwide of randomized controlled trials are under recruited. I also learned that listening to the patient and having a patient preference might inform risk and benefit. And there was a nice illustration, would you take a drug that maybe gave ten percent of people nausea but gave slowing of joint damage in RA in sixty percent of people and most would prefer yes and the drug was methotrexate.

Just looking at what the patients have preference is for. Then also there was a nice discussion on how can we embed research into our clinical care. So this would mostly be at sites that are investigative sites or research sites. So not always academic but academic or community sites. And if you approach a person, every patient in your clinic as they come through with a chronic rheumatic disease and say you know research is important if we don't do any research we won't be better than we are today.

I'd like you to learn about it. That means that you're not systematically excluding people and it means that when the time comes that someone has active disease, they already have a bit of knowledge. And this has actually been a randomized trial and it has helped by peers, patients, talking to other patients and teaching them about clinical trials. Then barriers to the protocols. If we eliminated unnecessary exclusion criteria and made inclusion criteria that were more like patients that we would treat, so more pragmatic designs, we could lessen barriers.

So an audience did come from, sorry, the audience participation was, well what about our patients that live remote or our minority population? How do we get them involved? So I think it takes a long time and I think you have to develop trust with, special groups of patients where, for many reasons there has been mistrust of the medical, community. The final thing is if we had a letter of information that wasn't 22 pages, but just was one sheet with the major things that are important to the patients, I think we would have better informed consent. So please follow us for the ACR coverage at RheumNow.

Thank you.

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

It's obviously one of the most common drugs that we do use. And we know that the side effects of steroids can include metabolic syndrome and increased risk of cardiovascular events. So this was a study that was done in the veteran affairs cohort and it was looking at cumulative glucocorticoid exposure and how that relates to future MACE risk. And, actually, this study found that in this it was a retrospective matched nested case control study, and this found that that greater cumulative steroid exposure was associated with greater risk of MACE regardless of baseline MACE risk. So why is this important?

So we've known for a very long time that rheumatoid arthritis is associated with an increased risk of cardiovascular disease, but clearly more needs to be done in order to manage the risk factors much more. And we've heard quite a lot about that during the congress. In this case, really, there is evidence that we should be doing more to try and reduce the cumulative MACE exposure and try to get people onto disease modifying agents much quicker where possible. In relation to this, I know that in the aging session, there were some data presented particularly with in people with late onset rheumatoid arthritis that quite a large proportion of those patients are not getting onto DMARDs, at all, and many of them do remain on steroids. These are the people who do have the greatest risk of cardiovascular disease in any case.

So this was, a really good, piece of work that just adds to this growing body of evidence, with steroids, with comorbidities, including cardiovascular comorbidities, and that was abstract one seven one nine. If you'd like to know more about everything going on here at ACR twenty twenty four, do head over to the RheumNow website for more information. Thank you.

Hi, everyone. My name is doctor Trish Harkins reporting for RheumNow from ACR twenty twenty four. Today I have the absolute pleasure of being joined by Doctor Sebastian Sattu, a professor and rheumatologist from the University of Pittsburgh. He's also an author on the recent Lancet series of Rheumatology on Ageing, which if you guys haven't checked out, I'd highly recommend that you do. However, today we're going to talk about both our passions, so polymyalgia, rheumatica, frailty and aging and it's his abstract number seven forty eight which is entitled The Effectiveness of the IL-six Receptor Inhibitors versus Conventional Synthetic Immunomodulatory Therapy for the treatment frail patients with PMR.

So first off, thank you so much Sebastian for joining us today. My first question is what led you to performing this study?

Great, so thank you so much for the question and the invitation to talk as you say on a topic that we're both very passionate of it, even if I don't have a voice. This work was done also in collaboration with colleagues from Sanofi who have also recognized the importance that both of our work has actually shed light on. So we understand that patients with BMR, and this is a condition that primarily affects older adults, frailty is actually quite an important topic. Why? Because both my preliminary work and your preliminary work has shown that patients with PMR have worse outcomes, whereas there's having actually worse patient reported outcomes, pain, physical function, and fatigue, which are crucial symptoms in the management of this condition that affect patients' quality of life.

So we know that, and what again our work is leading to, is that we are potentially identifying with frailty a subset of patients with PMR who have worse disease and are at their high risk for worse outcomes. And at the same time, we know that frail older adults are also at higher risk for other adverse outcomes, including what we get concerned the most is steroid adverse events. So, in our previous work, again in collaboration with colleagues from Sanofi, we actually shown, we know that the role of IL-six, IL-six is actually inhibitors have shown to actually have a good outcome and minimize glucocorticoid steroid duration in patients with polymyalgia rheumatica. But we know that certainly the trials that have been done have not done compared to what other communities I'm sorry. The conventional immunotherapy such as methotrexate, which are still what I think in the real world and some of my data and some of the other kind of investigators in Europe or other parts of the world have shown that are commonly used.

So, comparative effectiveness is certainly important. Think it's something that we're more and more getting into our world in rheumatology, that was the interesting thing. We had previously shown in other work that L6 inhibitors, and this was again prior to authorization of serelumab vusin in The US, shown a better effect with regards to glucocorticoid steroid duration compared to methotrexate. And then in this analysis, we looked specifically in a cohort of frail PMR patients using a community frailty index using CMS data and matched controls, match initiators of other kind of frailty patients with PMR. And she looked at the comparative effectiveness of the discontinuation of glucocorticoids on those who went on IL-six inhibitors either as a second or third line agent, so these were patients who were already on steroids and were not able to discontinue steroids compared to those in methotrexate.

And surprisingly, we found not only that, yes, IL-six inhibition had a bigger effect with regards to showing discontinuation of glucocorticoids, but actually in this subgroup of frail patients compared to the overall population had an even higher effect. So over two times, frail PMR patients, frail patients with PMR who were started on an AL6 inhibitor as a second or third line, were actually over two times more likely to discontinue glucocorticoids compared to those of methotrexate. And the interesting thing as well for this is that we know that IL-six is a crucial cytokine, inflammatory cytokine in the pathophysiology of PMR, and it's also for frailty and other adverse events, outcomes of aging. It marries personalising treatment in these patients who are certainly at a higher risk for adverse outcomes.

It's just amazing and it actually has tangible benefits for our patients which is great as well. Even just to conclude, what do you think this will mean for our clinical practice of our PMR patients moving forward?

I think we're recognizing more and more one is that frailty is prevalent in patients with PMR, again, which makes sense given the population that is affected by this condition. Rightfully so, think, besides us, certain societies, including the French Society of Rheumatology, have actually mentioned the importance of including frailty as well as we consider comorbidities in the assessment of PMR patients as well. I think it is potentially showing light in how to personalize the care, improve outcomes of patients with BMR outside of the usual concepts or constructs of rheumatology, with fail to be one that is particularly relevant not only for the disease but the age group that is affected by this condition.

Absolutely. Well, thank you so much. It's a really exciting time for PMR. Thanks for listening today and follow RheumNow for more updates on ACR twenty twenty four. Thank you so much.

Hi. I'm Quailin Connolly reporting for RheumNow at ACR twenty twenty four. I'm accompanied now by doctor Asim Mohammad who presented abstract one one six four evaluating the role of IVIG in the treatment of immune mediated necrotizing myopathy. So Doctor. Muhammad, thank you so much for joining me today.

Do you want to tell me a bit about why you did this research study?

Hi, well thank you so much for having me today. This was great and a good opportunity to put our work out there. I mean, immune mediated necrotizing myopathy or IMM as we refer to it, is kind of a rare disease. And I believe that the disease chose me and it didn't choose it. So, when I was first starting my fellowship, in the first month I've seen four cases of this.

And my mentor at that point was like, Hey, I saw four cases in the last four years and you've seen four cases in the first month of your fellowship. So I was like, This is meant to be. Beside that it's kind of a rare disease, but it's a very it's one of those fascinating diseases that you can see it. And down patient being down and once you put them in remission, they're back up. They're debilitated.

They can't get off their chair and you treat them, you you get that success and next day they're they're skiing. So I think it was just a fascinating disease to look at.

And what did you look at in particular about IVIG in these patients?

So IVIG, we mostly know, showed great success in treatment of dermatomyositis, in the prodrome study. And then after that it was used to treat immune mediated necrotizing myopathy as a variant of muscle disorders. But we don't have any studies out there that shows how much of IVIG should we do, how long should we do the IVIG for. The question just popped up as we were in clinic. We were sitting there and we were about to start one of our patients on IVIG to treat the neck myopathy.

I was asking my mentor, how long shall we tell them? Six months, one year? The answer was like, we don't know that yet. So I said, well, why don't we try to find out? And that's why we started gathering the data and looking at all our patients to try to find how long at least shall we treat people for necrotizing myopathy for beginning to prevent relapses.

Okay, so what did you find?

What we were aiming for and we were looking for, hoping for was to get a duration that says, okay, you give them this duration and now they're in deep remission and they're not going to flare back again. What we found is unfortunately because of the study design, people who required longer terms of IVIG are actually the ones who were flaring longer. It was a positive proportion. So we didn't get that magic duration that we were looking for, but at least now we know the duration that we treat most of our patients with. We know that most of our patients are getting IVIG for at least over a year.

So the the mean that we found was, the mean was a fifteen ish month. So I think what we could use out of that study is we can say when we're starting the conversation with our patients is like, let's set some expectations about at least for the next year we're gonna be doing this therapy.

Right, you know, I think that's really helpful because necrotizing myopathy, as you said, can profound impact on quality of life and it's very scary diagnosis for patients given the ability associated with it and at least being able to give them a framework as to duration of therapy is very helpful. So thank you very much for your time today congratulations on your research. So that's that's it for now. If you want more information, go to rheumnow.

Thanks. Hi. I'm doctor Sheila Reyes from The Philippines, and I'm here at Washington DC reporting live for RheumNow at the ACR Convergence twenty twenty four. This time, I'll be talking about abstract number five five nine by doctor Diego Benefant and his group on the use of machine learning in predicting future flares for patients with XPof. The study aimed to develop and validate a predictive model for XPof flares in patients who were treated with biologic and synthetic DMARDs using machine learning.

And their results showed that among the predictive models, they selected the reduced logistic regression because it had high performance, interpretability, and simplicity. And this model identified the following factors that are predictive of a flare within six months. So this included low ASDAS, history of enthesitis among the patients, a number the number of previous flares, as well as a longer disease duration. More data might still be needed to establish its utility in in practice or maybe its future use in clinical trials. But knowing these risk factors from a clinical standpoint can help us profile our patients and monitor them closely so that we would give the proper treatment and we can also educate them in knowing what to look for, when they do develop flares.

Follow me on x at RheumNow, and tune in to RheumNow for more updates and use of the ACR coverage of the ACR Convergence, rather, 2024.

Hi. I'm doctor Janet Pope here at ACR twenty twenty four in Washington, and I'm an at RheumNow reporter. So I wanna talk about as the meeting is soon drawing to a close. So, really, are JAK inhibitors safe? So first of all, there was a big absence of anything much about oral surveillance at this meeting.

So not that the safety issues of tofacitinib that we know about have gone away. I think it's kind of died down, and I believe in a good way. So what did we learn from oral surveillance? There were slightly more cardiovascular events numerically than, TNF inhibitors. Maybe they both reduced MIs.

That's what I would wonder about. We also learned there's more malignancy and more studies are probably needed to know why. However, I think JAK safety is helpful because there's a lot of populations. So atopic dermatitis has approval for some JAKs in very high doses. IBD has approval for two JAKs, one in U two in UC and one in Crohn's often at higher doses than we use.

JIA has approval for JAK inhibitors. Lupus has the ongoing trials of both a TYK2 and a JAK inhibitor. The JAK inhibitor trial is upadacitinib thirty milligrams a day, so higher doses than we use in RA. And GCA had the upadacitinib fifteen milligrams a day looked safe in the population of older people on glucocorticoids. So the bulk of the data of what I've seen over this last meeting is that I think the safety will continue to be monitored.

I think it looks acceptable, at least in my eyes, and I think there will be an expansion of new indications for the JAK inhibitors. So are JAKs really safe? Yeah. And I think they're here to stay. Thanks and keep following us at RheumNow.

Hello. My name is Rinalini Day. I'm a clinical research fellow, in London in The UK, and I'm here in Washington DC at ACR twenty twenty four reporting for RheumNow. Now today, we have a very special video, which will be discussing the workforce crisis, which is a shared dilemma between the country which I work in, is The UK, and ace and The USA, where we are now for ACR. I'm delighted to be joined by two very special guests.

Firstly, doctor Louise Pollard. Thank you for joining me. And she is a consultant rheumatologist at Lewisham and Greenwich hospitals in London in The UK as well as being the training program director for the South London region for rheumatology. I'm also joined by doctor Burak Kumar. Thank you for joining me.

Who is the rheumatology fellowship director at the University of Iowa. So the rheumatology workforce crisis is a shared dilemma between The UK and The US. A few years ago, ACR put out a report saying that there is difficulty recruiting to rheumatology across the country, and this is being an ongoing campaign for them to try and increase recruitment levels. Similarly, in The UK, our society, the British Society for Rheumatology, also produced a similar report in the last couple of years saying that there is a workforce crisis, at consultant or attending level. So why is this?

And are there any similarities and differences between the two countries? So I'm gonna start with you, doctor Pollard, if that's okay. So the first thing I think I'd like to discuss is, from your perspective as a training program director, have you seen the landscape change and how have

you seen the landscape change in terms

of recruitment at the consultant level to rheumatology?

Thank you. I think over the last few years what we have seen is actually an expansion in consultant numbers in The UK, but what we haven't seen is an expansion in the training numbers. So the residents or trainees who are coming into rheumatology, we haven't seen an expansion in those numbers to then be able to recruit into the consultant. Work workforce, which is an issue, of course, because we are expanding our numbers, which is great, and it's great to have more rheumatologists. We do need more rheumatologists in The UK, but if we're not got the trainees there to be able to fill a post, what we're left with, which is what the BSR is saying, are empty posts sitting within The UK, and that is an issue.

Thank you. And I think I'd put the same question to you, doctor Kumar, if I may. Have have you seen it personally as well where you are?

Yes. I have. But it's actually very interesting because it's the opposite problem we have on the side of the Atlantic. That is we haven't had a meaningful expansion in our training spots, but we've had extensive increase in the number of applicants that are actually applying for dermatology and a lot of interest. And now actually we're one of the most competitive specialties, subspecialties along with cardiology, GI and hem onc.

But without an increase in training spots, we're just not able to get these people into practice. So very different situations, but the endpoint is the same. There needs to be support for for these training programs and these trainees. So

Thank you. Yeah. So I mean, Polar, you might have something to say maybe about the the trained spots as well in the in The UK, but why do you think this is happening at the consultant level, sort of a

a lack of people going into rheumatology at that at that point? As I said, I'm not sure that it's

a lack of people going in at consultant level. I think that quite rightly, they have increased the number of rheumatologists. And I think actually as consultant rheumatologists now in The UK there are more people just doing rheumatology. Whereas I think there used to be a lot of jobs that included internal medicine. Because of the perceived need for more rheumatology they started to take the two apart.

And so there are an awful lot more jobs now that are just pure Rheumatology to try and get those Rheumatologists in. But if we don't have the people coming through training programs to fill those extra posts, we're left with empty posts. And so it's difficulty to the difficulty is getting in from the bottom end and getting the people in. We do recruit from other places in the world, of course. But there are still significant numbers of posts sitting throughout the country that have been unfilled for years now.

So this is not a new problem. It's just getting worse.

And if I may just expand on that a little bit, do you think that's to do with sort of socioeconomic disparities or just, you know, where people why why do you think that there is that sort of lingering posts as it were, which which may remain unfilled for a while?

It people do vote with their feet. So the of course, popular or perceived popular good posts will fill. So the people who are there and the people who are finishing their training will go for certain posts when they have them. And those centers are very lucky. They attract people and they will fill.

What are perceived to be less popular posts would be empty. They did have this this plan in The UK called redistribution, which they changed to distribution, where they were moving some training posts to what were felt to be less popular areas with with higher rates of unfilled consultant posts. Because when you train in a certain area, as I'm sure Bharat will tell us if the same is true here, is that where you train, you're more likely to go for a job when you finish your training in that area. So there was the idea of moving more training post to areas that weren't so popular that had empty posts. Seems to have changed a little bit, and I think that residents and trainees are, again, voting with their feet and not wanting to go to those areas.

So another rethink, I think, has to be had.

So great. I think we can already see some similarities and differences emerging. And from your point of view, why why do you think that there's a there's a crisis at your side?

Yeah. So I that is absolutely true as well that, wherever people train, they tend to stay at. In The United States, it's very different in terms of way how they fund and allocate these spots. And a lot of it is dependent on Medicare. A lot of it is done by local institutions and graduate medical education programs.

And so it's not that easy to move around to fit this allocation problem. So that creates an issue, especially in very rural areas in which there just aren't that many resources to support as many rheumatology programs, although there is an acute shortage in rural areas, more so than even in other areas. The other issues as well is that there's been a lot of retirements in our field. Our field is generally aging. There's been a sudden surge actually of, folks who have autoimmune disease, or at least have concerns for autoimmune diseases.

And so there's been this sudden expansion in the demand and yet the supply has been about the same and probably decreasing quite a bit. Of course, there are a lot of other differences now. I don't know about in The UK so much, our non physician providers, NPPs or APPs, advanced providers, they've been very, very helpful in filling that kind of gap. But it can't happen by itself. We have to have increased training programs, we have to have better allocation of those training programs, and that requires a lot of legislation and a lot of regulation that happens here in Washington, D.

C. And that cannot be very easy. Right? Yes. So

Thank you. So I guess my final question would probably be, what can we do to improve this situation?

That's a very question without an easy answer, I think. I mean, what we would really be looking for is expansion of training numbers and so, you know, more places. And as I said, this idea of the redistribution, we actually lost some posts in London because of the the idea they had they brought in the idea of more general medicine, more internal medicine, wanting to make more doctors generalists, which I get there's the idea of generalists, we are specialists for a reason and it's slightly detracting from that. And I think as I'm sure we'll hear in The US as well, it's all about money. It's all about having the money to fund those extra posts.

And currently, there isn't that money. And how all we can do is advocate. All we can do is discuss the British Society of Rheumatology. Obviously, it brought up the poor, does has ACR, and that's the that's the correct thing to do. And all we can do is advocate for people and advocate for our patients.

At the end

of the

day, it's about the patients and just want and you know, having enough doctors to look after the patients. But how to fix it? Not an easy answer.

So

absolutely. How do you feel about the future?

Well, how do I feel about the future? We may we may go a little over time because of that, but you say the right word, right? Which is advocacy. And it means that we unite together patients, physicians, all these different groups in order to advocate for more physicians, more funding from Medicare, more funding from the Veterans Administration and other payers in order to get to that spot where we can have enough. The other thing, of course, is that it's the quality of the workforce, too.

About one third of academic rheumatologists are actually considering leaving their job because there's an unprecedented crisis in terms of burnout. So making sure that our workplaces are safe for physicians and other clinicians actually working is another major part of the solution. Unfortunately, there are no easy answers to that apart from reform that happens on much larger layers of our society and our politics, and that starts with advocacy. So contact your senators, contact your house representatives, contribute to the RheumPAC, which is the political action committee, work through the Rheumatology Research Foundation and through the American College of Rheumatology's Government Affairs Committee in order to, you know, bring this to the forefront so that we can get more rheumatologists and consult this crisis.

Thank you. Yeah. Lots of great ideas there even though we can't solve it all in twenty minutes. Any final thoughts?

No. I think the important thing is we're talking about this, and that we continue to talk about this because it is an important issue. And we do in the gay again, in The UK, we are losing senior consultants. We had a whole issue in The UK over pensions, which has driven a lot of people. We won't even go there, but it drove a lot of people into retirement early and, again, lost a lot of senior good people.

But we need to keep talking. We need to keep advocating, and maybe together we can get there.

Any final thoughts, doctor Kumar?

Yes. Of course. So I I think it's advocacy, advocacy, advocacy. And many of the times, the way how these regulators and legislators, how they come up with their agenda is just whoever complains the most gets what they want. That is the democracy.

That is how our systems, both in The UK, I'm I'm sure, and The US work. So please don't be afraid to complain because you are complaining for a good cause. And if you don't complain to this cause, nobody else will, and other people will complain for the causes they want, which may not necessarily be your causes. So please, as we mentioned earlier, contact your representatives. Unite with forces that are for expansion, such as the Rheumatology Research Foundation, and the American College of Rheumatology, and RheumPack, etc.

And make sure that your workspaces are great so that we don't feel like leaving the workforce, right, to begin with. So those are my final thoughts.

Thank you so much. Thank you, Doctor. Pollard and Doctor. Kumar for joining me on RheumNow. I think we've heard a lot of great we are more similar than we think, I think, in terms of the issues that arise around the workforce crisis and plenty of food for thought there.

If you'd like to know more about this topic, you can go to the ACR and BSR websites for both of those reports and further information about how to advocate. It is ultimately about the patients as we have heard. If you'd like to know more about everything going on here at ACR twenty twenty four, you can follow the RheumNow website or you can follow me on Twitter at x, sorry, at doctor mini day. Thank you.

Hi. I'm doctor Sheila Reyes from The Philippines, and I'm reporting live for RheumNow here at Washington DC for ACR Convergence twenty twenty four. Earlier today, there was a session that was highly attended, and I think it was really looked forward looked forward to. It was about the session on the latest updates of the 2024 ACR lupus nephritis treatment guidelines. And what I wanted to do this morning is to give some of my take home points from the session.

So the guidelines so they came out with recommendations, about 28 graded recommendations where it included strong recommendations and it included conditional recommendations. And I think one of the most important strong recommendations that still does exist in the current management of lupus nephritis is the strong recommendation to screen all patients without a history of lupus nephritis or newly diagnosed patients with lupus with lupus to screen them for lupus nephritis. And a strong recommendation continues with the use of hydroxychloroquine for all the patients as well as the use of RAAS RAAS drugs in the management of proteinuria. Of note, for suspected lupus nephritis, doing a kidney biopsy was a conditional recommendation and they did recommend to do the biopsy promptly or to do a repeat biopsy in case that a new flare of the lupus nephritis would occur. Now, the guidelines also are they also showed that conditional recommendations came for the use of glucocorticoids and that for patients with newly diagnosed lupus nephritis, high dose corticosteroids, high dose false corticosteroids, we're still conditionally recommended and to taper it slowly and eventually in the next six months and if if probable would be to taper it as low as less than five milligrams per day.

We all know that steroids have a lot of side effects, have a lot of complications, and so keeping our patients down to the bare minimum or the least effective dose would really help our patients to avoid side effects as well and long term complications. And so the treatment overview for lupus nephritis included recommendations for class three and four with five or the purely class V alone. And what's new with this guideline is the use of triple therapy over dual therapy. So when we talk about triple therapies, this would include or triple continuous therapy. So this would include, false steroids or oral steroids to taper plus, mycophenolate mofetil and a choice between belimumab or AC and I.

And so alternatives for triple therapy would include low dose cyclophosphamide plus belimumab and glucocorticoid pulse or steroid taper less than five milligrams. Now, the reason why the they chose triple therapy over just the dual therapy is because of the evidence from RCT specifically BLISS LN and AURORA in that triple therapies showed improved outcomes in patients with lupus nephritis and also to save the kidneys because ongoing, continuous ongoing lupus nephritis loses nephrons and time is kidney. So I think that were the important points that really struck my mind and also the guiding principles. You should not forget that we have to collaborate with our nephrologist colleagues in the treatment of lupus nephritis and that we have to remember that treatment of lupus nephritis, treatment of lupus in general, should be a shared decision between the patients and the physicians. Follow me on X at RheumNow for more updates of the ATR convergence twenty twenty four.

Hi, David Lou from Melbourne Australia reporting on ACI twenty twenty four and really just to talk to you about JAK inhibitors and where the future lies. And my premise to you today is that actually, while JAK inhibitors were first developed in rheumatoid arthritis, and that's where the majority of the use is, and the majority of the use apart from rheumatoid arthritis is inflammatory arthritis, the real value is going to be in other diseases. In diseases where there's great need at the moment, because we've got lots of options in rheumatoid arthritis, we've got lots of options in PSA, we've got lots of options in AXPA, it's a crowded market. And as much as the JAK inhibitors have advantages there, and they're good drugs there, a lot of the benefits are going to come in places where we're really struggling for options. And so, I'm picking out a case series today to talk about.

And I think it just really gives an example of the kind of benefit and what we might need to do to get to the point where we see true benefit in the clinic. So, this is a case series from Beijing in China of eight patients who have had upadacitinib for Behcet's disease. And the long and the short of it is they get had Behcet's as open label for twelve weeks, it works really well. The Behcet's disease activity score dropped down, steroids are able to be weaned. It's all open label.

So, there's all the caveats around that. But it was really well tolerated. And it worked really well. And there are good reasons why it might work in specialist disease. A lot of the same pathways are pathways that are relevant to JAK1.

Now, you might say this is a case series, since when do we talk about case series on RheumNow? I think gives us a bit of an illustration as to where things might go. Behcet's disease is a classic example of a disease which we've really underserved in terms of therapies before and in terms of clinical trials. We haven't had good options. We've tried to co op therapies from other diseases like rheumatoid arthritis, taking methotrexate, say, from rheumatoid arthritis, and trying to fit a square peg in a round hole when it comes to Behcet's disease.

And it works, it works okay. TNF inhibitors, you know, there's clearly some role for benefit there. But we're really lacking a lot of good options in Behcet's disease and patients do suffer as a consequence. Something like Behcet's disease is a classic candidate for JAK inhibitors. And, we've seen that.

We've seen previously there have been some reports about once again K series, but tofacitinib in Behcet's disease, baricitinib in Behcet's disease. We need to do a bit better to be able to get structured investigation of JAK inhibitors in diseases where JAK inhibitors are needed, less common diseases perhaps, or perhaps just generally historically underserved diseases, so that we've got good options there. And that's going to become easier once we look at things like tofacitinib coming off patent. Because when we're able to churn out generic tofacitinib at low cost and the cost starts to plummet, then we can start doing investigator initiated studies, or thinking about clever ways in which we can look at the impact of these therapies and these diseases, trying to document that better, and then really giving these patients options. And the fact is as well, is that all the questions that come about because of oral surveillance, comparing TNF inhibitors versus JAK inhibitors and rheumatoid arthritis, all become much more distant questions when you're making a different comparison, like higher dose steroids versus upadacitinib in Behcet's disease, which is a very different story.

So, hope that we can do better for that. I hope that in iterations of ACR to come that we will look at JAK inhibitors for diseases that need it. So, for plenty more on JAK inhibitors and everything else ACR, you know where to go. Rheumnow.com. David Liu from Melbourne here as part of RheumNow's ACR twenty twenty four coverage.

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

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

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

But overall, most people got a response. What about other mechanisms which might be relevant to developing a vaccine response? Well, we've seen at this meeting that patients with upadacitinib seem to do reasonably well with developing a zoster response, a zoster vaccine response, particularly important knowing that they've got an increased zoster risk. What about nipocalimab? So, nipocalimab is an FcRn inhibitor that's just had a breakthrough designation for Sjogren's by the FDA.

And by nature of what it does, it reduces IgG, clears IgG, but potentially, well, you know, maybe it might not necessarily affect the vaccine response quite as dramatically. And so what we saw in abstract number nineteen eighty eight was actually data on nipocalimab and vaccine response. We've seen that actually, naturally it reduces dyneinitis as it should as part of its mechanism of action. But eventually patients get there. Patients eventually get that response.

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

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

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