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Hello, everyone. Welcome to RheumNow's daily recap from UR twenty twenty six here in London. This is the day three recap. It's Friday, one more day to go. It's been a busy week.

We're all here live face to face in London with about 14,000 of our best friends looking over the many posters and abstracts. One of the new things or really shouldn't be new, but it is new is that abstracts and posters, mainly posters have gone back to being real posters pinned to a board. You know, sometimes they're about the size of a postage stamp and that's kinda interesting, like what were you thinking? Sometimes they're big like they're supposed to be where you can point at them and look at them and touch them and, you know, and and take pictures of them. In the last few years in the COVID aftermath, we were doing electronic and distancing, and it was kinda messy.

Anyway, we're back to doing real posters, which was a substantial part of today's activity. Anyway, let's begin with, panel introductions. I'm Jack Cush from Dallas, Texas. Sheila?

Hi, I'm Sheila Riaz from The Philippines.

Nelly.

Hi, I'm Nelly Ziade from Beirut, Lebanon.

Jeeha.

Hi, I'm Jeeha Lee from Michigan, United States.

Excellent. All right, so this is like all of our other recaps. We're gonna do two rounds of what we saw today, that was our favorite. Now, of us actually comes to the meeting sort of a list of things that we're gonna cover so that we kinda cover all the things that are important in rheumatology. But in these recaps, you know, anybody can talk about anything.

You know, I might be a lupus person, but today I was really impressed by, you know, crystal disease or whatever. So, let's begin with, Doctor. Lee.

Yes, thanks for letting me start. I'm going to discuss, abstract numbers OP0348. So this is a Mayo study that they were using existing CT scan to look at muscle composition in persons with RA. And I liked it for a couple of reasons. Like, it comes from a broader abstract session looking at innovations in imaging for RA.

And a lot of the theme was leveraging existing data and also using AI or computerized modalities to analyze this. So what they were set out to do, and they did a really nice job of it, they had close to 900 individuals with RA. And they were cross matched to about 500 patients without RA. And we tried to match them up across different covariates like age and also kind of set an RA index date. In terms of the CT scan, these were all existing ones that were collected from usual care around 2020.

And internally, they had already developed and validated a means of looking at CT scans again to look at body composition. And what's different from what they usually do using DEXA is that they can actually differentiate between visceral fat versus adipose fat or muscle overlay fat. And this is important because we know our RA patients, they really prioritize function independence, and the term is sarcopenia, like the loss of good muscle mass quality leads to poor outcomes, falls, and things like that. So what they found is that unsurprisingly, with RA had lower quality muscle, more fat infiltration intramuscularly more than anything else, and that there was no actually difference in terms of the distribution of which parts of the body of the muscle was really affected. And like I said, I like this for a couple of reasons.

One is leveraging existing data, and they have a really good robust means of looking at what it is. And what that means, I think, for us is that you can get a better understanding of different outcomes, and not just disease activity scores, but for, there's a lot of talk right now with PSA about body composition, obesity, GLP-one affecting it. So as we look at lifestyle interventions, treatment, things like that, could this be another endpoint or a measurement and not just joint based measurements as well? I think though one of the limitations is, according to the European definition of sarcopenia, it's not just about muscle mass, but there needs to be function. So there's the imaging component of it, but missing of the functional aspects of it.

But again, I think this just lays the groundwork for those who are entering trial, who happens to be have it, now that we're using machine learning for target trial emulation. So maybe not just using obesity, but there can be protocols developed whereby you look at body composition as an outcome measure and then add on some functional measures of promise or even perspective collection. So I just thought it was really interesting overall, like I said, for introducing a component of ARI that we may overlook but that patients prioritize, utilize existing imaging. There's some computerized aspects of analyzing data, and some implications in terms of how we think about treatment and designing studies.

So this is a quantitative and qualitative tool for sarcopenia in these patients, correct? And then has sarcopenia, which is getting a lot of play, it's an important factor, has it been shown to be an independent predictor of subsequent outcomes?

Yeah, it has been. So I think as rheumatology, we've been talking about this in different terms. I like the fact that we're unifying the language, was studying aureka cachexia was an older term, but sarcopenia and NAATs were broadly, not just in rheumatology, but every field, especially with aging population, kind of taken into as a geriatric syndrome and a functional outcome. So in terms of, I think it was John Giles' group, and there was a session at last year's ACR where they actually looked at sarcopenia having association with functional decline, as well as patient reported poor outcomes in patients with rheumatic diseases.

And how much of this sarcopenia, these measures was related? You said twenty twenty, which is a number of the six in everyone's head with COVID and hospitalizations. Were these CT scans related to that and patients being sicker?

So the way we did it, so the study was between like 2013 and 2019, and some imaging going after. So we tried to get imaging within that time period, but preferably try to get something closer to 2020. So trying to just select more contemporary CT scan if patients had multiple available. So that's an interesting question whether they had illness or not. It's not there.

I will say along with that, one of the limitation or what I would have loved to have seen is some correlation with treatment. Like, was there a difference between RA patients who were exposed to steroids versus certain type of treatment? I'm sure this group or others may be thinking ahead of that, or hopefully they Okay.

Let's go on to our next one. Doctor. Zayed.

Nelly. Yeah, so I was just thinking about the treatment question that was just presented because of the fat and the lack of response with TNF, so just thinking about that. So I will talk about posture two ten. It's an interesting design. It's the effectiveness and safety of sequential therapy of infliximab and tofacitinib in axial SpA.

So one might ask why would I want to give a sequential therapy? If you look at the authors, the authors are from India, and they justify this for economic reasons, because in India, small molecules are very very cheap and the TNF inhibitors are much more expensive. So what they wanted to do is to study effectiveness and efficacy of one arm with infliximab followed with tofacitinib and the second arm was tofacitinib just from the beginning. So this was a prospective spot study, a small sample size 46 patients with active axSpA refractory to NSAIDs. So, the primary outcome was the time to achieve ASDAS inactive disease.

So, twenty patients received TOFA monotherapy and twenty six received emphyxma for zero to six weeks, then followed by tofacitinib. Now, when they looked at week four, there was a significant reduction in ASDAS from baseline and the sequential therapy group compared to the TOFA from the beginning. So the mean change was 3.19 versus 1.65 in ASDAS. At week twelve also the difference was significant but when we look at week twenty four the curves are just joining and it's the same. And also for the primary outcomes, the achievement of ASDAS inactive disease more frequently in the sequential therapy at week four and week twelve, and at week twenty four also the curves are joined.

So they also studied other outcomes and it followed also the same pattern. So their conclusion is that the sequential strategy of infliximab followed by TOFA allow more rapid attainment of remission and functional improvement compared with TOFA. So at twenty four weeks, it's the same, but they gain twenty four weeks is a long time for a patient who is in pain, so it allows them to gain some time. I know there are a lot of questions that may arise from this design. This is the first time I have seen it, but I think that in low resource settings, it could be justified in patients who are in pain.

So this patient has a high ASTHAS at the beginning, it was 4.2.

So did they start with infliximab and then tofo? If so, why? Because infliximab, know, tofa's onset of effect is faster than infliximab. Yes,

but the Asthat's response was quicker when you start with emfliximab than follow with TOFA compared to Do when you start with TOFA

you think that could have been due to like the pre med protocol that would include steroids potentially rather than the infliximab itself?

I don't think this is an issue in axSpA because usually steroids are not recommended, so I don't think so. It could be the placebo effect as well because we know that the placebo effect is higher in injectable compared to oral treatment. I don't know, I think that it was interesting, their approach was interesting.

I was curious because like, oh sorry, our institution is just part of the protocol whenever regardless of disease when you put in an infusion order, there's a ready set pre med that they just get regardless.

I was

thinking Even in asthma?

Regardless of disease. So it's just based protocol based on the drug.

Okay. Yeah.

I was wondering Nelly with the results of this study, was there any mention of like the safety events, the incidence of infections?

Yes. I mentioned this, and they said that there was no safety signal.

Interesting. You know, I've always thought that if you look at results of all trials, the experience that we all have, that patients always seem to do pretty well in a lot of things and they do well for six months, eight months, nine months, and then they you know, why not have as a goal that you're going to you choose in Michigan and The Philippines and Beirut what your top three drugs are and give them six months at a time and just change them no matter what, you know? And the point being that, you don't have a chance to develop a secondary failure, you don't have a chance to develop autoantibodies, you don't have a chance to develop a bias and immunologically you're keeping a very complex deranged immune system confused. Because RA amazingly seems to be able to escape whatever perturbations you put in its way. I think there's something really interesting about this, but how you protocolize this in a way that it becomes totally believable that we all sit here and go, Oh yeah, that makes sense.

As opposed to shooting holes in it.

I don't

agree that in axSpA, it's not really justified to change. We've seen patients who've been doing so well on the same drug It's for 10 not the same as

I must say, on RheumNow, I publish a lot of sort of outcomes reports, and there are tons of reports about the durability of RA, DMARDs and biologics. It's not that good. You know, the best drug that we have is methotrexate as far as durability. And biologics don't look all out great. You know, it's even worse than psoriasis and psoriatic arthritis.

My goodness, drug survival is really poor. But I agree with you, Nelly. I think that AS patients, once they get on something, it could be that because they're all men and men don't complain and men are the imbeciles of healthcare. And they'll just keep taking a drug and telling you they're doing fine. Now, I'm trying to be snarky here, but it is interesting that I think that they have a better durability.

But I've never seen good reports on that. I'm sure there's some, but I don't remember them, but I agree with you.

Most studies are from the the big registries and the real world data, and you see that, like, some people will stay on one drug for for several years.

Yes. I think yeah. And I think that's what the original, the CRESPA study showed, but this was in patients with early peripheral Yeah, a number of them over a ten year follow-up period, they stayed on galinolumab with really no safety signals.

Yeah, exactly.

Cool. All right, Doctor. Reyes.

Okay, so my first abstract is OP0342. So this is the interim analysis of the ASTER study, which is a multinational observational post launch study showing real evidence on the effectiveness of anifrolumab in patients with SLE. Data collection is still ongoing because the study period is up to five years, but this interim analysis is from one year after pretreatment. So the investigators evaluated the effect of anifrolumab on disease activity and multiple organ systems in patients who received at least more than one dose of anifrolimab over a one year follow-up period. And a total of five thirty patients were included in the analysis.

So what they saw was that there was improvement of the CDAI 2K scores from pre treatment up to twelve months post visit and compared to pre treatment visits, eighty five point six percent of patients had a total decrease in total SLEDAI two ks scores at twelve months. And the proportion of patients with SLEDAI two ks organ involvement also decreased during the twelve month visit. It's also interesting to see that mucocutaneous musculoskeletal and hematologic system involvement showed the greatest decrease in the SLED I2K activity compared to pretreatment scores, meaning that anifrolumab led to improvement in SLE disease activity even across multiple organ systems. So I think it's reassuring data on the use of anifrolumab in SLE, particularly in patients who have organ involvement. And I think it's still interesting to find out what the long term study data on this real world evidence will tell us.

Sheila, do you wanna just repeat the organ systems that responded best for skin and joint?

Yeah, it was the skin, the joint, and the hematologic systems. So they had the greatest decrease in slight A2P activity.

Does this goes to positioning, does it not? Where is enafrolimab going to fall in our arsenal of lupus drugs? And I think that needs to be better defined. I mean, I think there's very, very strong evidence about its effects on skin and joint. But then when we get into other organ systems, but you said these people had organ damage and most of them did well.

So I do think that that is the power of a long term follow-up like this to define, you know, maybe trajectories of organ system change. They have to find ways to use this data. Because when you get a drug approved for lupus based on, you know, Doris and Sleedi and general lupus outcome measures, you're now leaving it up to prescribers to figure out how to use the drug. Was the problem when belimumab got approved. You know, I didn't know exactly who to use it in.

Now, it got used in difficult patients, refractory patients, ultimately nephritis patients with their indication. But, you know, lupus is a nine headed serpent and, you know, you want to know what to do next. But, did you come away from this thinking that it gives you with more confidence about one aspect of how you treat lupus?

Yes, actually. So that's why I think I chose this to share because you would think of, again, where would what patients or what population of what profile of my patients would I give anifrolumab to? Yeah.

Think one conversation I've heard regarding this is its potential use for alopecia, especially with the injectable form becoming available, with it being driven by skin inflammation. So I think for our patients, that is something that really affects their daily life and something they really want to address. So I think that may be one area with this finding could support its use for alopecia.

Yeah. And that's why it's it's it's interesting to see that apart from the mucocutaneous and the musculoskeletal system, this real world data shows, like, its effect also on hematologic system. And I think there's other one other poster, but I for I couldn't really expounded it enough, but there was another poster that also expounded or looked into the effects of anifrolumab on the hematologic system, but from a different cohort, I think.

Well, again, I agree that skin data is very encouraging on anifrolumab. So my report is sort of like annually I'm supposed to come here and sing about the same tune. And this is POS0337 emapalumab, the gamma interferon monoclonal antibody, targeting therapy, and its use in treating macrophage activation syndrome associated with stills. I've done this now, I think four years in a row. The interesting thing about this is when we first did it, again, it came from Alexei Grom in Cincinnati and Fabrizio DiBenedetti in Rome, who do just fabulous work.

And they've been at this, you know, like a dog on a bone. But their very first report, I think was 12 patients. And the idea here was to, the drug Gamafant, which is emapalumab, was approved for HLH, acquired or genetic, HLH, and very effective, you know, really nasty patients with horrible outcomes, including a high death rate. And the goal was to give it to stills patients with MAS, and maybe that would end up in getting FDA approved. Well, that happened last year, right?

The drug is FDA approved. Got FDA approved on 20 something patients and the prior application in HLH. But now they're up to thirty nine patients. And again, what's the profile here? There's thirty nine patients, the average age is 12 years.

They get one, two or three weeks of treatment. More than half the patients are MAS that occurs at the onset of Still's. And this is something different about this expanded cohort, over forty percent of them are patients with relapsing MAS, which is really kind of nasty when you think about it. So in the very first reports, they had really abrupt changes. You know, MAS is to be expected when in stills you have leukopenia neutrophilic leukocytosis left shift, and all of a sudden PMNs drop.

And you get other cytopenias. And you have a high, sed rate with Still's and it drops while LFTs are going through the roof and ferritin goes from 5,200, 5,000 to like triple 10 times the numbers. Ferritin is the biomarker that makes you worry about MAS. Ferritin is not the biomarker for Still's disease, although many people think that's true. And when that happens, you know, and you give this Gamafant, early on, everything got better right away.

Now in this story, the end result, was that about half to two thirds of patients have really a great response, a remission level response, to this intervention. And that's good, and that's very good and good enough to get FDA approval. But it also means when you start liberalizing who gets into the study, you bring in a lot of bad players, a lot of tougher patients, and treatment needs to be individualized. So, while I think there's an underutilization of emapalumab in patients with MAS, whether it's from Still's, kids or adults, or other diseases like lupus, or even vasculitis, or infections, or lymphoma, whatever, I think it's underutilized. There's still people using a lot of calcium inhibitors and etoposide and other things.

But, you know, the guidelines on systemic JAA and stills basically say, you know, steroids, starting IL-one or IL-six inhibitor, and then you do something to knock out those CD8 cells that are making all this gamma interferon, and that's how you get to a better outcome. So I still find this data encouraging, evolving, and another opportunity to teach about, that's why I presented it. Have any of you ever used it, Gamifant? Yeah. I've only used it once and I've been talking about it a long time, and I treat a lot of STOLS patients.

Well, personal experience was good with it.

Well, my experience was it was pretty rapid, you know, especially what I've observed in looking at other cases and looking at the data on this drug, from, Deepa Nnededi and colleagues is that when these people turn, they turn quickly and they turn bad and the numbers are going scary. It was scary yesterday, it's worse today. I'm not sure I wanna come in tomorrow. And what happens is that, if you do all those interventions, like I'm gonna start them on, you know, double dose, triple dose Anakinra, I'm going to give them a gram of Solu Medrol, I'm going to start them on, you know, cyclosporine, the turnaround isn't quick. It's actually quite prolonged.

It can be, you know, to fourteen days before you feel like you're going in the right direction. And my case and not all the other cases, but there really is sort of an immediacy to what happens. It's days rather than a week or two. And that might be the difference, you know, the mortality rate in adults with stills who get this is as high as thirty eight percent. It's a little bit lower, but it's, you know, anywhere from twenty five to thirty percent in systemic JIAs who get this.

So, the problem is it's new, it's, it's, expensive. I'm sure I've never done a cost analysis of it. But, you know, when we're talking life and death, I don't want to argue about the price of a drug that's sitting on a shelf somewhere that could save my life. And the other thing is, you know, argument, if you talk to Doctor. D.

Benedetti or Lexi Grom, they'll tell you about how you have to give the dose, give repeated doses. And then there's like this gameplay with continuing the therapy and knowing when you can stop. And again, I don't have enough experience like they do, but my suggestion is that at some point after a week or two, or no more than three for me with Gamifant, I'm switching over to a JAK inhibitor. Because in that situation, I've treated a lot of patients with MAS with just JAK inhibitors, And that's actually worked very well. And obviously a patient often can't go home on emapalumab or on etoposide on, and then, you know, everyone's worried about putting them on a calcineurin inhibitor.

We don't have worries about sending people home on any of the JAK inhibitors. But you do have to watch for a response there and see if they're maintaining their response. And don't be afraid to go up to the doses you don't normally use. You know, we use, you know, fifteen upadacitinib, two of baricitinib, you know, ten or eleven of tofacitinib. You know, I quickly double that if I needed to.

Watching labs, watching the patient, knowing I'm only going to do that for, you know, two to four weeks, and then they're to settle down into probably a normal dose for the vast majority of patients. But again, these people are so sick that there really is no script. Patients don't come reading textbooks. Gonna be off track on you and they're always a big challenge, which means for me why I think that this kind of addition is important. Anyway, we're going to go with one more round.

Let's make it a lightning round faster. Jeeha, what do you have?

I have poster number two ninety and this is something that very practical I can take back to my patients. I think it's actually the first RCT of looking at probiotics in psoriatic arthritis. So it's a small scale study out of Austria, but it was a true RCT. They enrolled about 60 patients and identified patients with actually moderate disease activity on some form of immunosuppressive or DMAR therapy. And for twelve weeks, they randomized to complex or combination probiotics versus placebo.

I don't know the amount of unit that they gave, but for twelve weeks, and they followed these patients and the endpoint was changes in the psoriatic activity disease score or addition or escalation in therapy. So both groups actually had decreased. If anything, was higher in the placebo group, sixty five percent against forty three percent in the intervention group, but it was not statistically significant. So I know my patients, I'm sure yours do as well, always come in preferring some natural or other routes like probiotics overtaking that. So at least now I have something I can reference and tell our patients like, this doesn't work, you're welcome to take it, but let's please have conversations about actual therapy that is proven to work.

So, want to go around and ask each of you, what's your take on probiotics? You can have none or you can have whatever you want. So, Nelly, do you have an opinion about this?

Yeah, so I was happy also to see the study and to answer to my patients. The problem with probiotics is that they are so heterogeneous and so many molecules and so it's so difficult. It's like the nutrition study where you have have difficulty in quantifying the income and the intake and the elements. But so far I didn't see any really exciting evidence to go and tell my patients to take it.

Sheila, what about you?

So I don't really have like a strong evidence base to support the use of probiotics. But again, I agree with what she has said that, you know, patients would, I think they would readily believe or follow you when you give probiotics or options than taking evidence based drugs like your immunosuppressives. But I think there may be a role as a supplement or as an adjunct to treatment, not just the main treatment in itself.

I don't think there is any data on psoriatic arthritis or psoriasis to my knowledge. I'm sure there must be, but I am familiar with a few reports in RA. There are two very positive reports of probiotics in RA, but they're uncontrolled. And if you look at the makeup of what was being given, they weren't quite the same. I know of one that was negative, and I'm sure that it's going to be a toss-up.

So I've had to look at this because people close to me are very homeopathic, very nutraceutical inclined, and they beat me over the head with stories of probiotics, prebiotics, and everything I don't know. And so I've done a little bit of work on this. And what my take home is, and I do prescribe them. I used to use probiotics, especially when people would have, I think major microbiome changes leading to problematic diarrhea as might occur with a premelast or with leflinamide, and using probiotics to manage that. But what am I doing?

Well, I'm being smart because I listen to my friends who read this stuff all the time, and it's not scientific. But the idea is you really need to have a requisite amount of, CFUs, you know, and how many units are in there and how many strains are in there. So I'm gonna do a pitch for a probiotic that I myself take that I think has benefits. GI wise, and that's PV8, it's commercially available, it's not expensive, doesn't have to be refrigerated, but they need to have 10,000,000,000 or more CFUs and they need to have five or more strains. When you go to the health food store, you you can go in there and spend $85 on a little bottle, or you can spend $19 on a bigger bottle.

Know, Cush Rule number six is the more it costs the less it works. So that's how I ended up with Pv-eight. And I think that I believe what Jeehaw said is true. I think that it's a negative story and that's the story that most doctors will believe but at the same time, if we don't smartly feed the proclivities of our patients, you will no longer be their doctor. And they'll be seeing someone who knows less than you about managing It's these a very delicate situation, I think, but it's always best to be on with the best data.

And I think that's why this was a appraisals report. Cool. Nelly, what do you have?

So I have POS two eighty eight, Doclavacitinib study, poetic study, was already published, but this is a POTOK analysis. They studied the impact of concomitant methotrexate in a pool analysis from the two pivotal trials of doclavacitinib. So this is a TYK2 inhibitors. They had two trials in psoriatic arthritis and this post hoc analysis, they studied only the patient who took continuous degravacitinib, so not the control arm. And they compared the efficacy at week fifty two, and the short answer is that there was no difference whether the patients were taking or not methotrexate.

So the ACR twenty, fifty, 70 were all the same range, so sixty three percent, forty percent, twenty six percent. They also found no difference with the antisitis, the spark criteria, the dactylitis, the PASI, and the disability questionnaires, facet fatigue visual analax scale, and also for safety. So just to say that this confirms what we know from other JAK inhibitors, molecules that are used, they are very efficacious as monotherapy.

Oral and monotherapy should be their calling card. The question is, do you get a sense from this that this is a drug that should be used in only mild disease or can be used in all psoriatic arthritis patients?

I think that it's like, all other similar drugs, it's mostly mild disease and I'm concerned there are there were a lot of reports in this congress about the safety also of JAK inhibitors. In axSpA it's not a big deal because these are young patients, but in psoriatic arthritis these are more, so the age is higher and they have more comorbidities, cardiovascular disease, obesity. So I'm really concerned about these molecules all in all in psoriatic arthritis patients.

Yeah, and my caution on that is that whether you're talking duclavacitinib or Prelacet, they're often considered similarly. And I think that's often ascribed to mild because it's oral, it's efficacious. Although the ACR 20 responses aren't as gigantic as you'd like them to be, so they get labeled as milder. But that just means fewer people achieve an ACR 20. I haven't done bucravacitinib trials.

I did a lot of Apremilast studies, and I can tell you Apremilast is not a drug for mild patients. It's a drug for anyone with bad psoriatic arthritis, whether you have three or 23 swollen joints, because I've seen 23 swollen joints go to zero on a Primalast. It just means that it only works in forty percent of people. Yeah. It's the response is mild, the patient isn't necessarily, have to have mild disease.

And again, I think they get pigeonholed in a marketing way, because marketers wanna say, well, consider it in these people, make it first, because if it's mild, then it becomes first line. Again, there's really no data that says it should only be used in mild, it should only be used first line, but those become marketing things that are trying to create some story in my prescribing head. So I don't know. Anybody else got a feeling about the crabacitinib and what we've learned from it since its release? Okay.

We can move on. Sheila, what's your second one?

So my second one is poster POS one zero six eight. It's actually a poster describing how the CRM SOE outcome measurement came about. So the process of how the consensus of the panel came up with the consensus on what domains will be included in the clinical outcome assessment. So it's the outcome measure is named treatment response measure for SLE. So I think it's an interesting outcome measure that we'll we'll still have to wait for how it fares in clinical trials.

But what the the study basically showed is that they came out with the consensus state. The consensus group came out with eight domains in SLE. So that's arthritis, hemolytic anemia, thrombocytopenia, pterositis, nephropathy, and then the, equicutaneous, manifestations of lupus. And then there, they came out with, so they came out with definitions of what a TRMSLE patient level response would be. So they came out also with definitions of what a complete, a partial or a no response would likely be or a definition of what it would be in these patients.

So I think what made me consider like discussing this poster is that it's interesting to look into how this would would affect or how it fares with its youth in clinical trials, especially since we know that the other response measures or the other disease activity measures are very stringent in that it doesn't really capture the entire SLE disease activity. Like for example, how about patients with thrombocytopenia? How do you how do you use, for example, this type of measure for patients with thrombocytopenia or, you know, so I think it gives a more holistic or a more broad chance for patients with these types of organ involvement to be enrolled in clinical trials in the lupus.

So they think, what is the projection for this? Will this be a practice tool or a trials tool only?

So based on what they reported, I think they're more targeting a trial tool first. So evaluations are still underway in how it fares in clinical trials, mostly clinical trials, I think. But, yeah, I've I mean, a big effort was made in coming up with all the consensus statements, mean, all the consensus domains particularly and how they also defined the different criteria for entry and then for response.

Yeah, yeah. Okay. You know, around thirty years ago, I was at a meeting in Portugal, in Lisbon, with a lot of the big names in rheumatology at the time. And Ted Pincus got up and said something brilliant as he often does. He said there's something wrong with rheumatology when the measures we employ in clinical trials are not the measures we use in practice.

Like isn't, I mean, agreed, it wasn't hard, but yet in SPA, in PSA, in lupus, and sometimes even in RA, we're playing some kind of game for the FDA and not for my patient. And it also doesn't help how when we share the same patient because the patient moves from Dallas to The Philippines to Israel to Michigan, that we can all talk the same language. I think it's a problem. And the problem is also that researchers in a discipline get very siloed and they have this sort of circular, incestual kind of thinking about things, without thinking about the patient. It's a little bit like today I gave a talk where the bottom line was teaching has gotta be about the learner and not about me the teacher.

You know, I got too much in my head, I'll talk forever. But if it doesn't really connect to an audience person, then why am I even on stage, right. I don't have a second one. I want to end with by saying, I'm gonna be a little controversial here and say, does anybody want to challenge me on the fact that I think today was pretty weak? I didn't have a lot to choose from here.

That's why I'm not going to talk about my next best abstract. I didn't find a lot, and it's you, Laura, a lot of the programming are not original new presentations, a lot of them are reviews of particular subjects and whatnot, we tend not to present that here. So there was plenty of educational things going on. But as far as research reports, both from the poster floor and oral presentations, man, I felt like the guy in the desert looking for water. So anyway, I just saw a few of you nodding.

So you don't have to say anything. I'll be the bad guy in this call and I'll take the negative email and I'll say that I'm sorry, I was forced to say that by those three nice women.

There were some educational talks, so I attended some of them. So it was not like waste of time at all.

No, no, no. Yeah, I think the educational stuff is really good. Yeah. It was

very strong.

Yeah, agree. But, you know-

I'm sorry, go ahead. Go ahead, Chia.

Oh, I was gonna say there were a couple of debates today, but I think I also, like that on the last day, they actually do seem to have very strong and interesting scientific content that they'll present. So I'm actually looking

forward to that

if So it was the last

it's something controversial there too. And I think this is gameplay by meeting organizers. Why are all the oral presentations at o dark thirty in the morning? They want everybody there. Why is everything held to the anything that might be interesting till the end of the day?

Not in day two or day three, but on day four, oh my god, tomorrow, there are so many really, really important guidelines and incredibly influential late breakers. They don't want anybody going home early.

Yeah. I think there's a little

bit of gameplay here. But, you know, I'm a

It's willing screening tomorrow, so it's okay. I will stay at the congress.

Okay. I do I do get I do get where you're coming from, Zach. So but they apart from the apart from the site the abstract studies, there were interesting sessions. I think the peripheral, the AxleSpA session was also good.

Right. I want to thank our panel for a great discussion and all their efforts in covering the meeting. You might want to follow them, after the meeting when we do, topic specific panels, like we're going do one on CAR T, I think we're going to do one on RA, I think we're doing one, I know don't what the other one is. There's a third one. We'll find out.

PSA? Okay. And that's gonna be next week. So people might wanna tune in for those. Alright.

Have a good evening.

Thank you. Bye. Bye.