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Hi, this is Bella Mehta reporting for RheumNow. I came across a very interesting abstract looking at lab testing in rheumatology patients and when should we be doing this. So this is abstract number 2,619. And in this retrospective cohort study, they used a large national health organization database, and they had around five thousand or six thousand adult patients with rheumatoid arthritis, spondyloarthritis, psoriatic arthritis, as well as IBD. And these patients were either treated with biologics or synthetic DMARDs as monotherapy, and they were followed for at least twelve months.

So they looked at these patients and saw how many times did they get routine blood monitoring that we usually recommend for every three months or so. It was interesting that this study found only nineteen percent of patients who were either on biologics or synthetic DMARDs were adherent to the three month recommendation. And even looking at those labs, most of the lab abnormalities that they found were not clinically significant. The sort of at least they found some signals saying patients who were older had comorbidities or were using either IL six inhibitors or rituximab, the likelihood of having some lab abnormalities were higher. But those with just ENFs with RA, they have fewer issues.

So maybe we recommending every three months of lab monitoring may not be necessary for all groups. And, again, this comes to the fact that everybody's talking about, which is personalized medicine. You know? Plus, there's a lot of cost burden to the system as well as the patient coming in, going to do labs. So personalized testing intervals can also be something that we should be looking at in the future based on the medication type, patient risk factors, and whatnot.

So with that, I'm signing off here, and follow me for more updates on Twitter at bella underscore meta and RheumNow. Thank you.

Hi. Dave Lou here again. Talking to you a little bit today about PMR and JAK inhibitors. I hear a lot said about, well, there's potential for JAK inhibitors to help in PMR, but what about the data from oral surveillance and the concerns there, and really let's wipe that off the table? And it's been a really interesting conversation because I think there's an increasing realisation, especially now that we've got a registered medicine for polymyalgia rheumatic in the form of cirilimab, There's been a really interesting conversation about glucocorticoid side effects in polymyalgia rheumatica, the burden of persistent disease in polymyalgia rheumatica, the fact that we have over half of patients having over a year of disease, over a third of patients having over two years of disease, we've got this massive burden of polymyalgia rheumatica that's really been unaddressed.

And it is one of the diseases, and especially as far as common disease is concerned, it really stands out as something which we've left unsolved. So, what we saw at this meeting was some data on polymyalodramatica and JAK inhibitors, but I just want to give you a bit of a schema first in terms of where polymyalodramatica therapy sits. Because we often think about refractory disease and I guess that's what we think about in rheumatoid arthritis, think about moderate to severe disease. That's similar to refractory PMR. We've also got newly diagnosed PMR as well.

So, thinking about starting a steroid sparing agent or DMARD at the very beginning of therapy when we're first starting steroids. So, they're two different paradigms and there's different challenges with both. I guess if we think a lot about the refractory paradigm, which is where cirulimab is registered in, and JAK inhibitors make a bit of sense there because they're hitting all the relevant cytokines, and in particular, they're hitting the cytokines relevant to interferon, well, the Th1 pathway in GCA, and that potentially we might be stopping the risk of future GCA there in those refractory patients. And we know that JAK inhibitors have had success in GCA in the SELECT's GCA study, which was presented at this meeting as well. So, that is certainly something to think about, but that also probably does involve more persistent use of JAK inhibitors, whereas actually in newly diagnosed PMR, are some certain advantages to JAK inhibitors which might be of real relevance.

That's where the Bachelor study came in. So the Bachelor study was presented at this meeting, Abstract eight fifty eight, from French colleagues, from Valerie de Chevelle Pensek and her colleagues in breast, looking at baricitinib in newly diagnosed PMR. So starting at the same time as glucocorticoids, starting baricitinib then, first at a slightly higher dose and then gradually tapering down. And what they found, in fact, was that in that first twelve weeks versus placebo, they found that actually baricitinib was able to deliver a seventy seven percent response rate versus a thirteen percent response rate for placebo. In fact, it's surprising that placebo was even that high.

And, really, I think there's a lot of encouragement there, because this is a new therapy in an area where we don't actually have any proven therapies newly diagnosed polymyo dramatica. This is obviously not phase three level data, but it gives us a lot of encouragement. I think there's a lot of reasons why we could get excited about JAK inhibitors in newly diagnosed PMR. Firstly, they've got a relatively rapid onset. They're able to be titrated as well.

The daily dosing or twice daily dosing in case of tofasidenib means that we can titrate up and down. And so, in fact, in the Bachelor study, they looked at titrating down from four milligrammes up to twelve weeks down to two milligrammes after that. And that's certainly a very valid strategy that you could imagine rolling out with upadacitinib or tofacitinib. And really the key as well is that we're talking about an early short, sharp burst at the beginning of PMR to try and prevent future damage. So, really the safety risk is limited because we know that with JAK inhibitors, cardiovascular and cancer risk does appear to be related to exposure when we're looking at versus TNF inhibitors in rheumatoid arthritis.

So, when we're talking about this context, we're talking about maybe twelve weeks, maybe twenty four weeks of JAK inhibitor at the beginning of a polymyo dramatic patient's therapeutic course. That's really quite limited risk. And, of course, then the final kicker is that tofacitinib is coming off patent or has come off patent in most of the world. And that really means that generic tofacitinib, to be cheap to produce, could really open this up and get down to a cost which may be, while not competitive with prednisone, is certainly in the rough ballpark. And that's a key factor here for a common disease that affects a lot of people.

So for plenty more on JAK inhibitors and actually putting more on polymyalgia rheumatica, you know where to go, rheumnow.com.

Hi everyone, I'm Victoria Concept, covering from the ACL convergence in Washington 2024. I selected an abstract that I found very interesting. It's from Gregory McDermott and colleagues from the Brighamen Women's Hospital in Boston. They're actually doing or covering treatment strategies in rheumatoid arthritis. And what they did is they selected two cohorts of patients with RA from the BA Million Veterans Program and the Brigham Young General Program.

And what they did is did genotyping and electronic health record analysis in these patients. So they looked into prescription patterns of these patients with Markov mixture models and also into genetic risk scores and they actually found three groups or clusters of patients when starting TNF inhibitors. So for once patients staying on TNF inhibitors, TNF resistors as they call them, patients switching from TNF inhibitors to Abartocept and patients really cycling around after failure to TNF inhibitors. Then they did genetic risk scores in these patients and found that the genetic risk is really different, patients who stayed on TNF inhibitors had more of a SPA, predominant risk genotype, and RA patients were more prone to switch to a lot of cells, for example, or RA genetic risk patients. So I found that interesting because it was about treatment strategies in RA and we are still lacking those.

It will be interesting to see where this will go with this data.

Hi. This is Bella Mehta from New York reporting from ACR twenty four, and wanted to talk to you about what's new in relapsing polychondritis. This is abstract two six four nine, and this is a study which aim to improve the diagnosis or the speed of diagnosis for relapsing polychondritis, which is often delayed and patients go from one physician to the other sometimes because there are different phenotypes and how patients present may be very different. So Marcella Ferreira used this latent class analysis on a a very large cohort of relapsing polychondritis patient. Again, relapsing polychondritis is a rare disease, and considering that, she has around one sixty patients that she's doing this analysis with.

And they found three classes. One is where there's ear and nose damage with subglottic stenosis. Type two is tracheomalacia and bronchomalacia, and type three is no tracheomalacia. So using a decision tree based method based on tracheomalacia and your damage, this accurately predicted subgroups assignments in this type one, type two, or type three with around 98 to 100% accuracy. Basically, this may support quicker, more accurate diagnosis and not only guide treatment, but also research, which is much needed in in sort of rare disease groups because those are the patients which suffer the most sometimes.

And with that, which is signing off, follow me more on Twitter at bella underscore meta. Thank you.

David Lu here from Melbourne Australia reporting on ACR convergence twenty twenty four. I wanted to talk a little bit about cardiovascular risk and JAK inhibitors, just in case we haven't heard enough about it. Actually, there was surprisingly little overt mention of oral surveillance at this meeting. There's a lot of data about JAK inhibitors and cardiovascular risk, and actually other therapies in cardiovascular risk, and that's what I want to talk about today. So one poster that I saw from the Monday session of posters was looking at self reported international data from the Fares database.

So that's spontaneous pharmacovigilance reports looking at side effects and therapies. And so you can look at how reports come in from Verusly and how they relate to the proportions of other reports they have for any given medicine, and then see whether there's a disproportionate amount for a certain adverse event for a certain medicine. So that's commonly done with FAERS data. And so what we can do is look at our rheumatic disease drugs and then look and see what the risk, whether there's a disproportionate reporting of myocardial infarction, stroke, angina, cardiac failure. And so investigators from Louisiana did just that, looked at FERS data and looked at our medicines.

And yes, for tofacitinib we saw some increased reporting odds ratios for myocardial infarction of about one point five straight from one point six, not so much for angina or cardiac failure. But do you know what else was up there? And in fact, as far as myocardial infarction was concerned, certainly exceeded that? Prednisolone. And I think that's always a missing part of the discussion.

So as much as we talk about oral surveillance as controlled trial environment versus TNF inhibitors where both therapies had good effect, similar effect, and so therefore really had similar steroid exposure in that controlled trial environment, The reality is that the reason why we have DMARDs is to try and reduce down steroids, and steroids are actually a big part of what conveys cardiovascular risk. So we actually saw another abstract from the last day oral sessions, abstract 2,673, which came from colleagues in British Columbia, looking at reported data there about steroid exposure, what happens when you stop steroid exposure, and then cardiovascular risk after So they looked at twenty eight thousand steroid exposures in rheumatoid arthritis patients. And what they saw was that actually there's a substantial increased risk still in patients after they'd stopped steroids. So if you'd only been on steroids for six months and then stopped after that, you still had one and a half years of cardiovascular risk that, for cardiovascular death. If you were on steroids for twelve months, three and a half years of risk.

Twenty four months, ten years of risk. Now, you know, are some caveats on these data and there's a risk of residual confounding there and it may not all be entirely the steroids. But certainly it's a good reminder that as much as we're worried about the relative cardiovascular risks in different DMARDs versus other DMARDs, the real cardiovascular risk we should be concerned about is prednisolone. For plenty more on JAK inhibitors, you know where to go, rheumnow.com.