PsA: The Derm Version

Welcome to season three of Terms on Drugs. A few podcasts brought to you by scholars and medicine, the best educational platform of dermatology and provided in no cost medical providers. Terms on Drugs is where cutting edge dermis, interview, miscommittee. Dr. Matt Zeyer, some Dr. Sturmatology in each week. I'm drawing my residency. But he's such a lawyer affairs from University of North Carolina. Dr. Dim Patten from University of Pittsburgh. And we use our 60 years of combined dermic spirits to discuss debate and dissect the hottest topics in dermatology. Is everything you need to know to be on the cutting edge of derm. And you actually have to fund listening. New episodes, Dr. Poverty and Scholars and Medicine, Apple Podcasts, Spotify and other major podcast platforms. And I highly recommend that you download the Scholars and Medicine app to access the full podcast video archive and explore the best medical, derm educational content out there. Real, farming dependent coverage of all dermatology, supported by an amazing AI clinical consultant called Ask Simon. And I want to thank Johnson and Johnson for sponsoring this week's episode. And I am so excited this week. We've got another one of our patented deep dive episodes. And we are going to get into psoriatic arthritis. But we're going to get into it in a much cooler way than you're used to getting into it. To help us do that, we've got with us a fantastic derm room, double-borted physician from Mount Sinai. Dr. Sakshi Katri. Sakshi, tell us how you got into room derm. And what your path is, the idea of being double-borted in room and derms. He did internal medicine, then rheumatology, then dermatology. So you were resident until you were 47. Is that-- you don't look 47, though. Well, that's all the botox. That's interesting. That's all the botox. Right, so I was a room fellow in Einstein. And I just-- well, first of all, thanks for having me. Excited to be here. So I was a room fellow at Einstein up in the Bronx. And there's just so much of skin that we would see in our patients. And we knew nothing. The most that I would do is prescribe probera sulfur everything. And that was the extent. And even my room attendings didn't know anything about the skin. We just didn't get that much of exposure. So I'm said and dipitously at that time, there was a joint combined round between the dermed department and roomatology, the first of its kind. And there was a speaker who was both a roomatologist and dermatologist. And that was it. It was like a light bulb moment for me. And I decided that I wanted to pursue dermatology. And so you did an extra three years after finishing room or did you-- did some of the room count towards derm? Like, how did it work? I wish. No. So I did. I was in attending for a year as a roomatologist. Then I actually had to do research in derm for two years, because derm is extremely hard to match. And my room training was not giving me any brownie points in my application. And then I did a three full year of derm residency. See, that's the problem with New York City. If you had been in Columbus, so our guest a couple weeks ago was one of my former residents in Ohio State. She was an OBGYN and called me and was like, hey, I feel like we don't know any stuff about the skin. You guys don't know anything stuff about the bulb. But can I come spend six months and hang it out in clinic? And I was like, no, god damn it. You get a residency spot. You can't come to clinic. You've got to start residency. And she was like, OK, man, if a roomatologist came and asked me, man, you know what? I did not get the memo. I'm going to tell my room colleagues of the interest in derm through each out of the year. Oh, I will get him a spot. I will get him a spot. But all right, let's go ahead and get into it. Dr. Ferris, let's kick it off with our first paper. What do you guys? OK, so I'm going to go over the apex study. So the title, this was published in the annals of rheumatic disease, a very rheumatology official journal. So this is inhibition of structural damage progression with the selective IL-23 inhibitor, gazelchimab, and participants with active PSA, 24 week data, phase 3B, randomized double blind placebo controlled study. OK, so what-- why did they do this study? I think, like, for all these companies that make drugs, you know, first you get-- you get me your psoriasis indication or you get your psoriatic arthritis indication. Then you get your psoriasis one. But you know, then it becomes like, well, you work in the skin, but how do you work in the joints? And then it's like, oh, it looks like it works in the joints. And then it's like, do you have-- what about radiographic progression? We get terrified in dermatology that if we don't refer to rooms that we're going to miss radiographic destruction and everybody's going to basically be like disabled within a year because we didn't send them to room and that this is the holy grail. So actually, one, I can't wait to ask to actually about this one. We're done. But how did they do this study? So you know, gazel-- this is like up until this data came out. There were no IL-23 inhibitors. While they were FDA approved for psoriatic arthritis, they did not have data showing that they prevented radiographic progression of disease. And there was even an earlier gazelcumab study discovered too that did not get them that indication. So APEX, multi-center phase 3B study. So patients had dead PSA for at least six months with active disease. And so one of the things I think is like important for us is dermatologists is what is active disease? It's like three or more swollen and three or more tender joints in an elevated CRP. And then they had to have at least two erosive joints on baseline radiographs. So like this is not just the, oh, I maybe get some back aches in the morning. This was like people at pretty active PSA. Then they were randomized. They either got gazelcumab 100 milligrams every four weeks, or 100 milligrams after the loading dose every four weeks or every eight weeks or placebo. And then they would cross over at week 24. So who were these people? They're a biologic naive, they're a jack naive. They had to either have like two centimeter or a paper plaque or psoriatic nail changes. So this was not just like they had to have some skin disease. They could be on concomitant, the tracks they hydroxyploric when La Flutamine and said even Lotus prednisone at like 10 milligrams or less. And then there was an escape arm that they could have, like their D-mards, their conventional systemic D-mards tweet. And then everybody got radiographs of their hands and feet at baseline in week 24. And then they were scored centrally, meaning like it wasn't the investigator doing it, but a central, you know, I guess radiologist, looking at the modified Vandar Heidi Sharp score, looking for erosions and joint spains narrowing. Two readers, you know, so pretty like rigorous. Primary endpoint was ACR 20 at week 24. Secondary endpoint was change in total, PSA modified Vandar Heidi Sharp score at week 24. Okay, so this was, you know, a multi center study, basically over a thousand participants, 370 ish in the Gisellek in H Gisellek imab arm or placebo arm, mean age was 53. Okay, mean swollen joint count was 12, tender joint 21. So that's actually, you know, pretty again significant PSA. And they had, you know, Vandar Heidi Sharp scores in the high 20s, meaning that they did have erosive disease. And about 60% of them had a BSA of 3% are more meaning, that's the reason that's gonna be important is that like you could actually see, you know, skin changes as well, 40% had dactylitis or enthocitis. And most people were on some sort of demar and mostly met the trixate. So, you know, that's sort of the population that you're talking about. Okay, so how did the Gisellek imab do? If you look at ACR 20, which is, I think maybe a low bar right now in PSA, two thirds of them on Gisellek imab reached ACR 20, whereas about 47% on placebo, ACR 50 responses were in like 40% range versus 20% on placebo, ACR 70, 22% in Gisellek imab arms 11% on placebo. Across these, I think one of the things I noticed is that it doesn't really seem like there was a better response to the Q4 versus Q8 week dosing. Okay, radiographically the sort of meat of why they did this, what did they see? Okay, so mean change in total, Vanderhide sharps grant week 25 was 0.55 and 0.54 in the Gisellek imab group. And verse is, it was 1.35 in the placebo group. So what does that mean? Lower means like less progression, less joint damage. So there was more joint damage in the placebo group. You know, the group of Gisellek imab for six months versus the Gisellek imab. So, you know, that was a statistically significant result. Okay, how about the skin? You know, it was sort of what you would expect, Pazzy 90 rates at week 24, were like 69%, 60% versus 22% on placebo. Pazzy 100 responses around the 40% mark. and then nails, they actually. did see modified NAFC improvement of about 40, 36 to 43% in the active arm and it actually got worse in the placebo arm. So did get improvement in nail disease. They did look at things like composite outcomes, like minimal disease activity. And that was achieved by 30% in the roughly in the Gisellumab arm versus 13%. So that was like that's sort of a combination of both skin and joint and lab changes that showed minimal activity. Safety, there's kind of nothing really to see. It was what you expect with an IL-23 inhibitor, so I won't go into that. So I think what's interesting, this is now the only selective IL-23 inhibitor that has been shown to significantly inhibit structural progress. So this is the question of PSA. You know, it's only weaknesses, this is only at 24 weeks, right? This is like a long-term disease. This is also a biologic naive population. So what does this mean if this is somebody's like, you know, fourth biologic. And then this wasn't a monotherapy study. So, you know, I am super curious actually to see, you know, I've got all these questions. So A, what do you think? B, how important is inhibition of radiographic progression? Is that a marketing thing or is that like the real deal something that is clinically meaningful? Right, so I will say that, you know, IL-23 blockers are excellent drugs, you know, they're excellent in their dumb space. So to have radiographic inhibition from a rheumatologist perspective is super important. Because we in the room space sort of think of can we minimize progression of joint damage that patients have accrued prior to starting systemic therapy. And having an IL-23 that's used so much in the dumb space, now having that inhibition of radiographic progression is certainly helpful. That being said, we also have to understand that you are looking at patients who have radiographic damage from get go. The question about, you know, what if somebody does not have radiographic damage? Can this drug potentially prevent new damage from happening? You know, because in today's day and age, not often do I see patients walking into my practice, whether I'm seeing them from a room perspective or a dumb room perspective with 11 and 20 small and joint standard joints. You know, they tend to be oligarchicular, a lot of dead-outness. When was the last time you saw a telescoping joint? I saw one of the, whatever I was in a resident at the VA, a guy with a thumb. So for anybody who's not like done a lot of this. So telescoping joint is when the finger is like so degraded that the best finger becomes like a little nub. You can grab the end and pull it out like a telescope because the skin is all still there. What was the last thing you saw when I one of those? So I do have a couple of patients that have telescoping joints but mind you, these are patients who've had PSA before the advent of systemic biologic therapy. I have not seen that happen since having these biologics for PSA patients. So I think that telescoping fear is all pre-biologic. All right, all right, all right, go ahead. Sorry. So these are people with bad disease. Exactly. So you're selecting a population with bad disease which perhaps it is not representing the patients that we see in our tractors. I mean, that being said to have that inhibition of radiographic damage is super important. Especially the patient has radiographic damage to begin with because in that scenario, I will reach for the systemic therapy that has that inhibition of radiographic progression as opposed to other MOAs which might not have that. So do you first do we have so, all right, let me let me start by tell you where I'm coming from. I'm like, look, I'm a dermatologist for God's sakes. If your joint hurts, I'm going to be like, okay, like here's a drug that I think is going to help. If your joints really hurt, I'm going to say go see somebody, go see the rheumatologist. But so from a, I don't follow psorheoric arthritis well. Do are there any head to head trials? Like do we know? When they look at inhibition of radiographic damage, the answer is no. I mean, they're just some head to head. Well, there are some head to head trials looking at different MOAs, but generally these are molecules that are produced by the same company. And they look at non inferiority, not necessarily superiority. There is a head to head, but it looked at a composite score of skin and joints with superiority at the primary end point. But again, we have to understand that the sort of driven by skin, right? So it does seem like perhaps with the most part our MOAs are non inferior to each other. So that's so that's what I was kind of getting at. I still hear people say like, well, if they've really got joint disease, I'm going to go to a TNF and because I think they were not. And I hear that, like that sounds crazy. Like if you had to rank them, not like particular drugs, but 23, 17s and TNFs for people with meaning. I mean, TNFs, TNFs are like like my lowest priority or go to, I do not use them. Unless of course their patients were just grandfathered in and are doing well. Or if there's any other reason for me to consider an TNF, which again from the top of my head is not that many either because we have the acenabitors that will treat multiple different, you know, immune diseases and so will an IL-23 blocker. So really, I mean, I was going to ask you which rheumatology are you talking to? Because I bet you probably the younger ones. This is germs. This is germs. So that don't know anything about it either. They don't know anything about it either. That's why I don't believe them. I'm like, I cannot possibly. And I think that's all it's going to be. So do you think 23 or 17s are better? That's a hard question. I think my answer would favor a 23 if I was looking at a patient with maybe early disease and I know we'll be talking, you know, I mean, there's a lot of chatter around 23 inhibiting the incidents to PSA, in patients that have psoriasis. And then there's also data within the room space looking at retention of 23s and, you know, perhaps these patients don't switch to a different MOA that often are that frequently. So I do think 23s are excellent. Certainly for a patient that has psoriasis and certainly for a patient that has psoriasis. And, you know, you're like, is this subclinical PSA or LEPSA, you know, mild disease? Where, you know, the infrequent dosing and, you know, the safety, the skin clearance, the fact that it has an ACR 2050 70 response. And now with the 23 having inhibition of radiographic damage, I think it's a win win for 23. And deep, it's germs, you know, there was like this time in marketing where everyone's like, do the pest. And if they might have psoriasis arthritis, you must send them to rheumatology. Otherwise, they'll all have telescoping joints in a year, right? And like, we all know that's kind of crap. Not gonna happen on the ass. Yeah. And I, like, my feeling, and you tell me if I'm wrong, as a dermatologist is, if I get a history, I can get a history that is relatively consistent with psoriasis arthritis versus I know that's OA, right? I'm not going to be able to be like, there's no vandal hearty sharps going going on in my clinic. But there's like, oh my God, that's not even happening in a room clinic. Let me just tell you okay. That I don't feel so bad, but you know, so my feeling is if I suspect this is PSA, I can give them something that will help their skin and their joint. And if they feel better, I don't know. Yes. Send them. Okay. And like, and the other thing is when you look at those patients, like 20 swollen joints, those are not the patients, you know, when they're like, whoa, send them to room. Like, that's not who comes to see us. Exactly. What would like one or two maybe three four max five, right? Beyond that, these patients are presenting to a rheumatologist just because they have, you know, impairment of their activities of daily living with their bajillion, dozens, swollen and tender joints. So I totally hear you and I agree with you. And I completely second that thought as well. I think again, you know, in every, like depending on where you are, how soon can you even get your patients to see a rheumatologist? I can't. Like, I mean kids. They get like, yeah. Exactly. So if we have data that's published from like way back when saying that six months of diagnostic delay results in repair or joint damage, then that patient can't, then you wait nine months to be getting an official diagnosis from a rheumatologist. So I think it should be more like, you know, start the systemic therapy as long as it's covering PSA, that's good. And then patients, if they improve, then that's great. If they don't improve, then see a rheumatologist. A lot of times insurers just say like we're not giving you a 17 or 23. We have these very inexpensive adalimamabyle similars. And my sense is like most of the head to heads, like you said, yes, when you combine skin and joints, there are, you know, superiority. But for the most part, when they look at specifically like ACR 50 scores, the TNFs actually still do okay. So if that's what my patient gets because that's what the insurance says, is there an obligation on our part? If we think psoriasis is going on to say, no, no, no, look, we need to get this person on a 17. We need to get the person on a 23 or like TNFs are actually okay in that situation. Like I don't see myself fighting with an insurance company over arthritis because I'm not a rheumatologist. And I think that's what a lot of germs are like, do we need to put that put up that fight? Like if they have joint pain, we're going to say okay, maybe it's psoriasis arthritis. The adalimamabyle similars are what I can get you or you stick in you, Mabyle similars are what I can get you. That's actually, actually okay. - So that's an interesting point that you raised because I think coverage for systemic therapy is a lot different in the dumb only space where you're just, you know, coding for psoriasis as opposed to in rheumatology where you might even be forced to giving them methodorexidous first step before they agree to giving a biologic. So I cannot, like my cheat sheeters, I tell patients that I'm gonna just try to get everything approved for psoriasis diagnosis because that opens my ability to get you a lot of different MOAs and are perhaps go with my shared, sorry, let's call it shared decision making, our shared decision making with regards to a particular MOA and I don't get unplisted that often into giving methodorexid or an anti-TNF as well. - So you get a more sort of leeway in prescribing to some extent from psoriasis then from psoriatric arthritis? - Yes, yes, yes. Because if I just use PSAs often I'm told, I'm supposed to give them methodorexid and that's the reason why if you have rheumatologists in the community that you're sort of sharing patients with, you'll hear this sort of, oh, they started me on methodorexid, it's always starting them on a convention synthetic demy. - Yeah, that's answers a lot 'cause I always wonder, like what the hell are those rheumatologists doing? - Yeah, thinking, exactly, exactly. Methodorexid is not work, it's not even approved for ps, they're like why? - Yeah, so you did mention jack inhibitors and so I'm curious here, the first time we've had a room on the show, I think of, so I took pretty regularly that I look at the Zell Jans or a surveillance trial and say, Zell Jans didn't cause any events, Adalina Mab just made the events go down. Is that the general take in the room world? Like do you guys, what do you guys think of jacks? Are you guys like a third of the world? - So we like our jacks, it's just that we cannot use them first line and we have to use them after using an anti-TNF. - And that's insurance meet, like if you could use them first line. - No, you can't. So the FDA approval for say PSA says you have to have tried an anti-TNF before you can give them jack. So it's never gonna get approved without them having tried an anti-TNF first. So we don't have any issues with jacks in the room space. But then I think as a rheumatologist, then forces me to then do the whole methodorexid anti-TNF and then a jack pathway or cycle, which when I put my room dumb head, I'm not like comfortable with because why should I do that? - Well, I always wondered like the, I wish there was a way to like, I feel like it's not unreasonable to try somebody on like, Adalina Mab plus 10 milligrams of methodorexid that's gonna cost like nine grand a year. And if they're the 50% of people that like that happens to work great, okay, we just save society like 50 grand. But if it doesn't work, but then I'm like, I would wanna try it. - Exactly, I was, I was gonna ask you that, would you do it for yourself? - Yes. - For 30 grand to go on the cheap stuff, I'd be like, I'll take the 30 grand and I'll try the cheap stuff. Like we should pay people to take the cheap drug. - No, but put yourself in the insurance companies' shoes. I would never wanna do that. They're making millions. They're CEOs, make millions in profits. So no, thank you. Absolutely not. - But it's not probably, if you were to say to me, no, no, this has to be 17. I'd say show me the study where 17s or 23s went up against Adalina Mab and showed superiority in arthritis. - That isn't. - There isn't. - Right. And it's not like those head to head haven't been done. They've been done. - It's the same. - Patent is an insurance. - It's always an insurance. - Oh, that's right. Exactly. Are you okay with an insurance? - I'm not and I hate it. I hate the insurance having to fight them. But when you sit back and think about it, I'd be like, you know what? I would deny this. I would deny this and I'd make them do the biosignular. - Right, so that for the next time, next time he's fighting a higher off, they're gonna be like, hit play. And he's like, I would deny this. - That way. - So never get released now. - Yeah, but the thing is that I don't think that's the same issue in dermatology. So if you're using a psoriasis diagnosis, I am pretty certain that you can get a 17 out of 23 before and anti-TNF. So just use the path of these resistance, which is psoriasis. - I think that depends where you are and who your coverage is. Well, in Western Pennsylvania, the coverage is horrible and they're like, no way. Like if you go to 17 or 23 first, they're like, no. Here's the will to be, it'll be amgivita. There you go. - So when you're Pennsylvania, they only have like two insurance products and they're both like super pain in the butt. - Oh, that's the normal. - Like one even further. So this Giselleke map, so the joint progression, on probably the biggest cover, the insurance person in Western Pennsylvania took Giselleke map off the formula. It's not an option. - It's crazy. I think Tim, you should definitely move to the upper east side. - Yeah. - I'm doing it. - I'm the upper east side. - My internet connection may be better. - Yeah, you might have to. And you'll be able to prescribe an I-17 or a 23 first line for your patients without pushback. - I'm talking to your back. - It is remarkable, but because I used to work at that place, it is absolutely true, that they just said, we're just not gonna let you give Giselleke a map at all. You're like, oh, you mean like it's not preferred? No, you cannot give it at all. You mean after they failed two things, I could give it. No, you may not, we will pay for it under no circumstances. Isn't that just absolutely crazy? - Okay, I'm gonna remind myself not to look for a job of Megan Vessent, that's a lot. - Yeah, yeah. - It's one to North Carolina, it's much better. - All right, so let's move on here. So I think we've established that there aren't really head-to-head trials, but we would not want to be, if I suddenly got psorianic arthritis, I would not want to be on a TNF. - I don't get it, yep. - And we've also established dermatologists can on suspicion of PSA, treat it with a drug that we know works for the skin. - Absolutely. - We don't have to send everybody to room. - 'Cause you don't have to, and if the patients are doing well, then that's about it. If they are not doing well, or if they start doing well, then send them to room. But I do think making them wait for nine months makes no sense. - I agree. - I would still send them to room though. Even if they got better, I would know like, okay, nine months, I'm not gonna worry about that. But look, there may be subtle changes in the joint exam that has a dermatologist. I'm not gonna pick up that a rheumatologist would. And so with arthritis at the outset, even though you're better, I think a rheumatologist should be seeing you somewhere in your care. - See, that's why Pittsburgh has to keep care so cheap, because Pat and is doing all of these unnecessary referrals that are running up the cost of care. - That's, yeah, that's it. - So you can either get rheumatoid. So basically it's like you can either get rheumatoid and see a rheumatologist or you can get an anti, you know, I 23 or a 17 and just stay with me. - Yeah, that's a bad thing. - No, but either way, either way, it'd be like you had arthritis. I just wanna make sure that it's being followed up. It doesn't have to be right away 'cause you feel much better. But, - And then you know what happens? The rheumatologist doesn't A and A, and it comes back positive. - That's what happens. - Because that's what it always do. - I know, exactly. I check A and A's in all my psoriatic arthritis patients. You don't do that? - No. - Is that a mistake? I don't see. - He's being sarcastic. I hope he does not do that. - Let's move on to your, where do you got that? - You know what, because we started late because of me, we can skip mine. I mean, it was an interesting paper, but there's so many overlaps with the one that you had. Basically it was, you know, interception of disease. When patients have psoriasis, how can we design trials to detect what's the best drug that's gonna prevent the development of psoriatic arthritis? And, you know, the conclusions where we don't really know, here are the factors that we take into account. But it was more of just a descriptive, we don't really know what's going on. Here's some great ideas, and that's kind of how they ended it. So there's my paper. - Okay. - It was a pretty data dense paper. And I would say that perhaps the only thing from the paper is, you know, just to shout out to BAMPAR trial, hopefully we know if early treatment with a biologic changes outcome. So, to be the target. - Yeah, so the panopropial, yeah, real quick, is Giselle Kimab again, versus placebo, patients with psoriasis, and they have to have ultrasound findings of inflammation. And that's the inclusion criteria. And then they're gonna do Giselle Kimab versus placebo. And are they going to prevent the onset of psoriatic arthritis? So inflammation is not necessarily psoriatic arthritis. Inflammation is inflammation. psoriatic arthritis is like synivitis. And so is Giselle Kimab going to prevent a versus placebo? And kind of an interesting arm where, you know, because a placebo group is gonna cross over, I think at week 24, but there's also this, this observation, observation arm, those patients aren't going to go on any biologics. So topicals in narrow band UVB. And so we'll have a nice comparison of like at one year to year, probably like what percentage of patients were we able to prevent the development of psoriatic arthritis? Are they going to enroll like 157,000 people into this trial? Like, that was one of the points, that was one of the points brought up in the paper. Like, look, if we want to show a 30% reduction, we're going to have to enroll 1,000 people in each arm. I mean, yeah, it's, it's, that's a challenge. It'll be interesting to see what, what that study shows. Yeah, may, yeah. All right, let's, let's move on to the one that I had. Because, and I, I picked this one because it, I think, gets at a really difficult question that we've kind of been alluding to here. So it was looking at a claims database and saying, how many people, so first, how many people who show up with psoriasis have musculoskeletal complaints? Like, period, not like psoriatic arthritis, like have back pain or arthritis or fatigue or whatever. And does that predict who's going to get a formal diagnosis? So yeah, arthritis going, going down the road. Now, first, for people who haven't, and I've assumed the vast majority of our listeners have not done health outcomes based research with claims databases. The first thing is like, you have to take this with a huge grain of salt because it's like, how, how rigorously did people make the diagnosis of psoriatic arthritis versus not make it, right? And how rigorously do you document and code things like back pain or, yes, you know, yeah, it's, it's so much. So you got to take it all of the grain of salt, but the big pictures here number one, half of people who got diagnosed with psoriasis had musculoskeletal complaints. So things like back pain blah, blah, blah, which right. Okay. So as the back pain exular arthritis is that early psoriatic arthritis, they're more likely to get diagnosed subsequently. The answer there was interesting. No, back pain was not a predictor. A formal diagnosis of enthocytis was not a predictor. Now that's no probably one that who the hell's diagnosing people with enthocytis other than if you're like, I think you maybe have psoriatic arthritis. Like so it's that one's a little iffy. The back pain one was kind of surprising. But in general, the people who showed up with musculoskeletal complaints or througes or arthritis, that kind of stuff had an increased rate of getting eventually diagnosed with psoriatic arthritis. And so I think it gets back to what we're talking about earlier that like if your psoriasis patient shows up and you're like, Oh, you got some back pain. Oh, your ankles hurt whenever you wake up in the morning. Just put them on a 17 or a 23. And if they get better, it was psoriatic arthritis. And if they don't get better, then it was probably osteoarthritis. That's like, is that a reasonable takeaway of it? Like it's if they get better than unless you're seeing a worse like Dr. Patton, they don't need to go see rheumatologist. But if they don't, can serve it of medical care, it's you say, whoops, I object to that characterization. Thank you very much. So is that that general approach seems very warranted to me? And that's again. So absolutely. And I do think that I would probably add another layer of like age because I give it a patient that's skewing younger and they're talking about our trials and sort of just non-specific joint pains. My index of suspicion for these patients is possibly having PSA is a lot higher because you know, you don't have like that osteoarthritis mechanical component. You know, anybody who's like 70 who gets sent to me for like rolling out PSA and they've had psoriasis for years and they might even be a systemic therapy for the psoriasis. I'm like, the odds if you're having OA are a lot higher than active PSA at this point. So I do think as like that age should sort of be also used as a form of stratification in some ways. All right. So do the tick two drugs or PDE for drugs? Do they work for psoriatic arthritis at all? They are a proof of PSA. We do have one tick two and we've had a PDE for for the longest time of proof of PSA. Again, if you're asking my opinion as a rheumatologist, I do think it depends on where in the PSA disease paradigm you're starting that medication. If it's super early, yes, if it is more established, I don't think them by themselves potentially take care of every same. Do you think they're as good as the 17s and 23s? Oh my God. Well, there's no head to head. So it's like an clinical experience. I would say probably not. But then again, if it's a patient that has like some morning stiffness, you know, like weak joint pain and they are, they don't have a swollen joint tender joint, then they could potentially respond to a tick two and a PDE for just because they probably had a remile. I mean, I don't use the word mild, but perhaps they do have mild disease. But I'm not going to consider it for a 20, swollen, tender joint irrespective of what their inclusion criteria might have stated because I don't think that they by themselves will be helpful. So really whittling this down, like to the fundamental question for me, does joint pain ever really play a role in your therapeutic decision? Like is there ever a time where you're like, okay, I'm going to, I'm going to, I'm going to sound like an ages when I say that younger patients, perhaps yes, older patients, perhaps no, just because there's just so much of mechanical O A that comes into play and pain is pain. The body does not cannot differentiate between pain from inflammatory arthritis and ferrostia arthritis. Certainly we can ask about morning stiffness to help distinguish between the two. But sometimes patients have both and pain is just a catch all that being said, you know, we probably should not start to go and discuss fibromyalgia because fibromyalgia can be a thing that can be contributed to pain and our PSA patients certainly have fibromyalgia. So it's not a very linear yes, no, but younger patients, I'll still give pain sort of that importance because I do think it's probably inflammatory. Unless of course, you know, they were a division, what football player or they've had some good, you know, trauma to their joints and or they've like physically exerted themselves. They're less likely to have O A. So that means in a younger patient who's got some joint pain, you're more likely to go 17 or 23 and not go tick to PDE for. Is that is more likely to say that maybe this is a play pain is indeed sorry, I take arthritis as opposed to an older patient who has long standing psoriasis and just like and they have like some knee pain and their dermatologist happens to ask them now about arthritis symptom, which is because that is in work and now because they complain of knee pain going up and down the stairs, they get referred to me for rolling out PSA. That patient is perhaps less likely to actually have PSA than the younger one. Okay. Fair. Right. And we've done some stuff with psoriasis and interclass switching versus intraclass switching is there similar studies in the room world with psoriatic arthritis and when do you make the determine what's a good like three months, two months, six weeks? Right. So in the room world, you know, a lot of data has been taken from rheumatoid arthritis where treat to target is a big thing. And unfortunately, you know, the RA data also talks about triple therapy with demards being comparable to an anti TNF. Right. This was like when I was in room fellow. We this was all. Oh my god. It's in a blow your mind. A message. Say it. Self-assalacy in Placola. I thought you've seen a might was in that. I, well, I, I, but either of these three, but you know, it's a combination of these three, you know, try to kill people exactly exactly. We're trying to give them SGS from self-assalacy in yes. Right. They didn't come back. They must be better. No, they're dead. Now they need an actual doctor who's a dermatologist. I'm kidding. So in the psoriasis space, it's a little hard. It's, it's not clear because historically everything that they did for RA, they sort of co-opted to PSA and that's why, you know, everybody would get demar therapy. I sometimes even see patients in 2026 on self-assalacy for PSA. And I'm like, what are you talking about? This is crazy. But you know, I think rooms tend to be more change averse. So they do like, you know, let's do a demar. Let's do a combination demar. Then they'll go to an anti TNF and they'll cycle between anti TNFs before they even think of a different MOA. That's just because they have the trait of doing that from RA. And then the, the EULAR did come up with some guidelines a few years ago where they did say that, you know, what you could consider a switch within the same class, you know, like you could go from one anti TNF to another anti TNF, but that is. There are more switching class before you want to the next one. Yeah, yeah. Or a lot more like let's do a different MOA. Yeah, yeah, yeah, yeah, yeah. And the data, I mean, there's, I haven't seen it like I have respect. Yeah, there isn't a data now. Yeah, I mean, whatever data that's there is, it's sort of, we have data in the PSA space, which says, you know, as money trees for the most part patients for, you know, you retain on them in the real world, you know, in registries and sort of claims databases are a lot longer or they have the least amount of switch. Now again, you take that information with the brain of salt is it because these patients, you know, prefer, you know, the infrequent injection safety and their skin is doing well and they're willing to sort of be fine with a little bit of arthritis that's left behind. Who knows? But it does show that I have 23s tend to have the most retention and the least amount of switch. So I guess that means something. All right, to change subjects a little bit here since we've got a rheumatologist. Change, we got to move on to, we got to get, we got to do trivia. We're going to know. We're going to save time. We've got, we've got like three more minutes here. All rapid fire for rheumatologist. Which drug are you most excited about in the connective tissue space? Repo or lift, lift, let a little bit of that. I mean, I'm a little excited about lit full of map just because of the MOA being so different. And you know, it's kind of like to spice things up. So I would say I'm pretty excited about that. So because, you know, the loopers, the loopers space is heating up and that's, you know, it's about time. And do we, do you think that they will work for each other? So right now, right, it's Brepo's coming for Dermato and the little is coming for loopers. Yes. Do you think Brepo will also work for loopers and the little work for Dermato? Of course. There are always overlaps between the two diseases. So I would say yes. Okay. And then last thing before we get to trivia, fibromyalgia, I think it's a real thing that it's neuro, that it's the equivalent of neuropathic itch. Yeah. But it's neuropathic pain. Maybe we should maybe we should try giving them Neemolism, I've been thinking of that. And so, if you're just trying something, is to rooms think at the real disease at this point, like because when I was in medical, it was like fibromyalgia just might be whiny people. And I'm like, I'm pretty sure that we don't think that anymore. Now we're pretty sure that it's like a real, a real thing. So I think it comes down to who you're talking to if they have sort of person research academic interests in fibromyalgia, but I do think with the most part, we used to be like, oh, it's kind of like this catch all for you just have pain. You just get pain, you have stuff hurts. Yeah. Life is like, you know, you don't like it anymore than we do. Oh, I sort of joking say that fibromyalgia is like a drug word hair loss. I mean, thankfully now we do have options for like inflammatory hair loss, but like just hair loss in general. Yeah. That's what's a hair loss, the hair loss of room. Yeah, it's the hair loss of hair. I like it. I like it. Okay. All right. Let's move on to trivia. So actually, so the rules, just to, you got to let pet finish this week, you don't have to let me finish because it's these longer questions and as soon as you know the answer, you shout it, but once you give your answer, you're out. Okay. Sound good. All right. All right. It's a competition between the three of us. Oh, yeah. We don't keep track. I'll give you your nine, I'll give you your nine dollars back that you gave me to buy that. I did. I did not draw in America. We don't believe in trivia in India. So I'm definitely going to fail this, but okay, go ahead. You'll get this. All right. So these are the category room, derm epinems. Got it? Okay. All right. First one, this French medical student described his eponymous condition in 1862 as part of his doctoral thesis, the title of that thesis, and this is obviously translated because I'm not going to massacre French for everybody. Local asphyxia and symmetrical gangrene of the extremities, the white, red, and blue of the different phases of the conditioning. No, I know. Yes. Yes. Fair. I can't. Part of it, but I couldn't. I mean, I heard asphyxia and I'm like, what are we talking about? And he's got to go out asphyxia. I was thinking, right? It must have been weird stuff. Yeah, it must have been like the worst rain odds patients in the world. I mean, gangrene of the extremities, that is not rain odds, but hey, I don't know. It was just doctoral thesis. So that was always an impressive thing that that's where he described it in his name after him. All right, ready? Second. You said it'sphyxia. I immediately went to thinking you were going to now talk about auto asphyxia. I mean, I was thinking and then there's lines in the gutter, you people. That's weird. That's where both of you went, but that's. That's French. He's also French. What do you expect from them? Yeah. Right. Oh, man, the letters, the letters after this episode. All right. They don't speak English. So we have five. Five or my algae doesn't exist. French people, auto asphyxia, we're doing real well. We're good. This physician's description of his eponymous disease in 1937 was initially met with skepticism. Medical professionals at the time felt he was merely describing a constellation of findings seen in patients with syphilis. Rager syndrome. No, you're out. The Greek physician, Adam Manteadees, had described the disease six years earlier, leading some to suggest that his name should be added to the name of this disease. That being said, most of us know this disease only by the name of the Turkish physician. Who describes it? What's that? Bouchette. It's Bouchette's. Oh, Turkish physician. You knew because of the little thing that hangs out off of the country. That's right. The only Turkish thing. I don't remember from the Turkish guest. All right. Number three, this physician completed much of his foundational research in Sweden in the early 20th century in an era before autoimmune disease was a well understood concept. His 1933 thesis was largely ignored at the time, but has now considered a landmark document in room. The condition he described is now one of the most common autoimmune conditions in the world and consists of the classic triad of kerato conjunctivitis sycoc. Zero stomial. Children's. Children's. You show. There was a thing. They're about to try. Matt knows all the answers. It just doesn't get to his mouth, which from Matt's mind to his mouth, usually that's a split second. Yeah, it's a short track. Yeah, somehow with trivia been more. It's really the frontal lobe to his mouth. That's the story. Yeah, different. Different part of the brain. That makes sense. All right. Well, so she it has been so much fun having you on today. This was really, really a fun episode. I want to thank you for joining us. I want to thank all of our listeners for joining us. Hope you laughed a few times. Hope you learned to think or two, but mostly hope you plan to join us to get next week. Until then, I'm Matt Zyrus. I'm Tim Patton and I'm Laura Ferris and we are Derms on drugs. [BLANK_AUDIO]