When Psoriasis Pretends to Be Eczema (And Other Problems)

Welcome to season three of Derms on Drugs, a video podcast brought to you by scholars in medicine, the best educational platform in dermatology and provided in no cost to medical providers. Derms on Drugs is for cutting edge dermis, the interim is comedy. I'm Dr. Matt Zyros from Dr. Dermatology in each week. I'm joined by Marizansi buddies, Dr. Laura Ferris from the University of North Carolina and Dr. Tim Patton from the University of Pittsburgh. And we use our 70 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. Does everything you need to know to be in a kind of a germ? And you're like, share some fun listening, new episodes of Dr. Dermatology on Scholars in Medicine, Apple Podcasts on the Major Podcasts, Plot College of Medicine, other major podcast platforms. And I highly recommend that you download the Scholars in Medicine app to access the full podcast video archive, explore the latest derm educational content out there. And we're talking real, pharma independent coverage of all of dermatology. It's part about amazing AI, clinical consultant called Ask Simon. And this week we've got another one of our patented six pack episodes. And let's go ahead and get into it, Dr. Ferris. What do you got? Okay. So I have a paper from the New England Journal of Medicine. I would say it's not the most earth shattering paper, but anytime dermatology makes the New England Journal. You got to know about it. Okay. So this is combined oral Ivermectin and 5% per methron cream to treat severe scabies. This was done in France. Senior author is Olivier Chosadau, who I remember working on slants scabies. He's like the world's expert in scabies. Okay. So what do we mean by severe scabies? It's what we would call crested scabies or back when we were less politically correct. When we all trained, we called it Norwegian scabies, but now we like the Norwegian. So we'll call it crested scabies. Okay. This was a study called the Gale Crusted Study. And so the question was, does higher dose Ivermectin make a difference when you are treating patients with crested scabies? So scabies. It was a blinded, randomized head-to-head trial. And they had to have crested scabies confirmed with dermoscopy or parasitology. You should have to parasitology. If you don't see a mite on crested scabies, it is not crested scabies. But they were randomized one to one to either Ivermectin 400 micrograms per kilogram or 200 micrograms per kilogram. And that was taken on day zero, seven and 14. And then, I need to interrupt for just a second before I forget. So for all of our listeners out there, if you've never heard this, because we always talk about scabies, dosen being 200 micrograms per kilogram, whoever came up with that is just sadistic and hates United States Dermatology residents. Because 200 micrograms per kilogram translates into 1 milligram per 10 pounds. So like that's so the 400 is 2 milligrams per 10 pounds for all of us Americans out there. All right, don't cave and start going to the metric system just yet. I know. Let's always throw this away. I don't remember that. I know. I'm just told the residents, yeah, I just told the residents, take their weight and pounds and chop off the last number. That's your Ivermectin dose. There you go. Okay, there you go. That'll be the most useful thing that everybody gets out of this. Well, now we got to double it. Now it's going to be. No, we don't. Oh, spoiler alert. Spoiler alert. All right, I'm just going to stop. Yeah. So everybody got also 5% per month in cream, day zero and seven. And then they got amolions and then like a caretale, like 5% salicylic acid for like when where they had the crusting. Okay, primary endpoint cured, cured, which is something that doesn't think we do very often. It's an infectious disease. It's an infection. Okay, it's fine. They have to have no mites or mite products under mosque or scrapings on days 18 and 21 and no active clinical lesions on day 28. Okay. So it's like, it's like whatever might and clinical cure. So I like the idea by the way, 32. What's up? I like the idea of somebody with crustacekabies and you're going with your dermatoscope like up real close to them. Like all these mites are jumping on you. Like I would not use a dermatoscope to diagnose crustacekabies. You want to stay as you want to stay far away from these people. The other thing I want to know is what the hell is going on in France? Okay. But you know how many people were in the study, 132? Right? It's not. Like maybe they all, you know, last week we did the study on, you know, the infection in the bath houses. I don't know what they're doing in France. I don't know. Yeah. Be careful. Okay. Media and age 67, but like a third of them were over 80 and about 60% of them were in the hospital. This is like, you know, kind of the people who you think about getting crustacekabies. And so what was the cure rate in the high dose group? It was 75% and in the standard dose group, it was 82% totally like odds ratio, 0.64, confidence interval across as one. No superiority. Wow. And then, you know, when they, like no matter how they tried to cut the data, there was really nothing. There, that like, there was no way to show that the higher dose mattered. And safety was fine. Like we know it is for both of these drugs. A.E.s were like eczema and skin irritation, which was equal among both groups. So you know, clinically just because it is crustacekabies does not mean that you need to go to the higher dose, combine ibure, mectin and permethrin, use of mallean and you know, the cure rates about 80% which is not a full cure. That's still, you know, that means 20% of the people are still going to have some scabies. So I thought that was kind of interesting. A.E. I mean, good for them for making New England Journal medicine, but I was a little surprised that that was a New England Journal paper. But it was a pretty large study. And if nothing else, maybe like it will remind the people who read the New England Journal, which is generally not dermatologist, but people who see hospitalized patients. Like what to look for to think about crustacekabies. Now, unfortunately, what they did not have in here was a picture of crustacekabies for people who have not seen it. Like it has such a distinctive look. If it looks like a gray powdery hypercarotosis, like you've never seen before, think about crustacekabies. I feel like when I've seen it with residents for the first time, they generally don't get the diagnosis. I would say it's like a gray powdery hypercarotosis and nothing else looks like it. What would you guys say? Yeah. Yeah. Yeah. I've got some pictures in my collection where I'm scrolling to oil. Oh, I remember that. It's like a very distinct. Yes. Yeah. Or go like Google a couple of pictures. You'll see it and then you'll never miss it. Yeah. And then you'll miss it because it is so contagious and you touch them and you are likely to get it. I've got a couple other scabies perl for people. Number one, if you treat people with permethrin and they get worse, permethrin is like the one product that has actual form out of height in it. So it has 0.1% from out of height. So if you give them permethrin and they get worse, you may have a concurrent form out of height contact dermatitis on top of the scabies. Number two, and I'm curious what you guys do. When I treat scabies, I always do weekly for four weeks because I'm like, why the hell not? Like I would want to be treated out the wazoo if it was me. So I do permethrin and I've remectin every week for four weeks, which is probably massive overkill. Yes. What do you-- But that's more than what they did in this study. Yes. And they only 20% of people didn't get cured. I know. No, but you're right. It probably is not. And I think that there's a lot of reinvestation, right? So people who get crustaceous scabies generally, they're not like-- Yeah. They generally have, you know, challenge, psychosocial challenge. Yeah, they're not going home and doing them all the laundry in the house. Yes. It's kind of the takeaway there. Yes. And surprising results, surprisingly alternating, like oral-yver-mectin, topical-mirathrin, than oral-yver-mectin, then topical-permethrin. Huh. Any theory or reason for that or just easier for people? No. Make it harder on the patient. It's not though, because you're only-- like the permethrin is hard. I think head to toe is difficult. But a fair number of patients with scabies, it took a long time to get there and they're miserable and they're like, I have to get rid of this. Like, can I do both? And I'm like, well, if you're going to do that, just alternate. And then, you know, I'm saving half the money. Saving $8. Yep. It adds up. So the cheap thing to treat. Yeah. And then just, you know, the pearl is that the Iver-mectin kills the mites, but not the eggs, whereas the permethrin is kills both the eggs and the mites. So that's why you never do one dose of Iver-mectin. It is one of the interesting things that whenever they've studied, if you use permethrin correctly, like if you get it in every corner of the world, you'll get it. crack and crevice and the whole thing. It is more effective than I ever met it. - Yep. - Yeah. - It's the Oversightle. - Yes. - You know, activity. - Have either you ever used those other ones, what the hell are they called? O-o-o? - Oh yeah, that new, no, because it's like too expensive and no insurance would cover it. - Yeah, there's the, the malathione one that has been around, that was the one that we catch on fire, yet to be worked on. - Oh, well that's for headlice. - That's for headlice. - Malathione is, yeah. So malathione, she's do a headlice episode. Malathione is approved for the treatment of headlice. It, I think it is highly effective. - Have I told you guys my headlice story? - Let's hear it. - So Margaret goes away for the summer, doing this overseas thing. She comes home a few weeks later, she's like, oh my scalp's itchy. And I look, she's got red, scaly, whatever. I'm like, oh, you got some rice. It's okay. I'm like, what's your name? There's all sorts of questions. What do you do? Who gets adjuvant therapy? Who gets image? Should Sentinel node be done? Do we change immunosuppressive? Like, it's a lot. So this was a study that wanted to address one of those questions. And they did a prospective study. Like, that's what we need. It was the lacunus study, which stands for something I didn't write down. Its goal was to compare physical exam versus CT versus ultrasound to detect nodal metastases and advanced cutaneous scrims cell carcinoma. performed in Spain 13 centers. 2022 2025 patients with advanced cutaneous SEC. So this was like Brigham and Young 2B3 and. - I have men and women's. - Brigham and. I always do. - This was the more. They did this one in the Mormon- - Fast and single section of print and stuff. - Why? I mean, it's a. It's, that is parietous. I can't. I always say Brigham and Young, bring them in women's. Thank you. They were like 2B3, Brigham and Women, and there were some two ways thrown in there, but they had to have something in additional to just being a 2A. Like they had to be immunosuppressed or something along those lines. - Well, they're all immunosuppressed. Isn't this a transplant thing? - It wasn't. It was advanced cutaneous, squamous cell carcinoma, close to half, like 40% of the patients I think were immunosuppressed. - And what's 2B mean? I have no idea. Like vaguely. - There's risk. There's four risk factors. Greater than two centimeters. Poor differentiation, parinural invasion and some, like invasion past fat or something along those lines. So basically there's these four risk factors. And so if you have zero risk factors, your stage like one, if you have one risk factor, your 2A, if you have two to three, your 2B, and if you have greater than three, your 3. - Okay. - They found that that discriminated a little bit better compared to the AJCCA staging. That's a, the same, squamous cell carcinoma is very, very complicated. Suffice to say these were advanced patients and the patients said, or the study said, "All patients are gonna undergo a clinical exam." So you examine their lymph nodes. You did a high resolution ultrasound in the lymph node, the draining lymph node area and a contrast enhanced CT. There's like around this time of surgery, plus or minus one month on the surgery. And then the patients were followed up for three months. So lots of numbers, weirdo statistical terms, like a mic nemar mid-P tests, like what? Anyways, 150 patients included in the study, 12 patients eventually develop lymph node metastases. Physical exam picked up one of these meds. So for all the emphasis, physical exam, so important blood, but not for nodal involvement with cutaneous squamous cell. Now, like bulky nodal disease was excluded for obvious reasons. So if they don't have bulky nodal disease and you do a physical exam and you're like, "Well, that's good enough. You don't have any, like don't do that." Ultrasound and CT were actually comparable. It's interesting 'cause it was like a review maybe in 2025 and CT was deemed the better test for picking up nodal disease. But in this study, the ultrasound and the CT were comparable. CT picked up six true positives. Ultrasound picked up seven. There were some good, there were some false positives that both the test picked up, but the sensitivity was pretty good. It was like 64% for the ultrasound, 55% for the CT. The huge difference was in immunocompanant versus immunosuppressed patients. So in immunocompanant patients, sensitivity was 100% for both modalities. They picked it up. I mean, they also picked up things that weren't, but you know, so what, you picked up the cancer. For immunosuppressed patients, sensitivity was 20% for ultrasound, 17% for CT. So the immunosuppressed patients, a fair number of them, the only reason they found out that they had nodal disease is that within that three month period, the patients were like, my next swollen, like a study did not pick it up. Wow. So if you were an implement-- Well, the theory they could have not had it, detectable disease. Yeah, but like in three months, right? Three months, let's not, I mean, bad cancer grows in three months. That's the point. Like in immunosuppressed patients, Cutaneous Quimisoccharinoma is a bad, bad cancer, where you did an ultrasound in a CT, and it was like, there's nothing. And then the patients came back and was like, this thing is growing in my neck. I still find it. OK, I thought you were saying it was there. Yeah, if you were to implement ultrasound CT, baseline to lymph node positivity, and immunosuppressed patients, it's just not a great test. So you just counsel those patients, like lymph node exam, and when you start to feel something come back, but ultrasound and CT were comparable at baseline. And given the fact that ultrasound is less expensive, and you're not subjecting patients to any sort of radiation therapy. And a lot of times in the ultrasound clinic, they're like, OK, well, if you can see a node, let's do the ultrasound guided lymph node sampling right then and there. Kind of an argument to be made for ultrasound. I'm sure there are patients like experts in Cutaneous Quimisoccharinoma that know way more than I do about it, and are like, actually, that's really dumb. But with this study prospectively-- You probably more subjective, right? Like user dependent. That's been the argument in melanoma that, you know, it's more subjective being able to identify metastases with-- Right, and the high resolution ultrasound, I don't think that's like your everyday run of the mill ultrasound. Like that is a different modality than what is used most of the time. So definitely, yes. And this was all-- I think the Europeans are just more ultrasound savvy compared to Americans. So a lot of caveats there. But I thought, these are the prospective studies we need, because we sit around in tumor boards and we're like, yeah, I mean, Sentinel node, OK, radiation, why not? I mean, And you can't point to a lot of prospective studies that's like, "Hey, this helps guide us telling us exactly what to do." So studies like this are nice. It was a good study. Okay. Did they use ultrasound in the ER like all the time? Because I've started watching the pit and it's like they're just ultrasounding everybody. If it's on TV, I don't know how you would argue that that isn't in real life. Must be what's really happening. It probably knows more about ultrasound in the ED than any of us do. So I got a lot better research than our opinions. I'm sure. All right. Let's move on to mine. I got two articles, but they were very closely related. So we're getting a lot more in the literature now about psoriasis, eczema overlap and people going from you go on a biologic and you get the other one and the blah, blah, blah. And some people like to say, "Well, it's just one spectrum of disease and I'm like you're an idiot." That is the dumbest thing I've ever heard. Because if it was one spectrum of disease, it would mean there was one cytokine pathway and it was like, "If it was too low, you got this and if it was too high, you got that." It's totally different cytokine pathways. Now here's what they found though. So they broke it into four different types. So first, the main clinical takeaway was with this, "Jack inhibitors work great." You should put these people on jack inhibitors, period. That's for all of them. Well, one group, there's one group that you should put an IL-23s, but other than that, everybody else should get a jack inhibitor. So there are four different types. Number one, there's co-existent disease. So co-existent means you have both classic psoriasis lesions and classic atopic dermatitis lesions. These people get the psoriasis first and then they get the top of your dermatitis as a separate disease. And so they'll have both, you know, centriobo and flexurobo both. And those people genetically have both the genetic predisposition to psoriasis and the genetic predisposition to atopic dermatitis. Disease number two is overlap. So co-existent means you have classic of both. Chloralap means the individual lesions, like you're looking at, those are the people that you're looking at. I can't tell if this is exomericurizes. I cannot tell. What they found with those people, and this was probably the most interesting thing to me in the whole paper, was that the biologics really did not work. So in the overlapping people, they put, so 5 out of 7 people did well on I/O 23s. They put a couple people on I/O 4s and I/O 17s, did not do well. And then in the other paper, they gave the treatment summer again. So when they put these people on biologics, psoriasis biologics, 18 people, AD biologics, quote, were often inadequate in contrast, Jack and Hibiter's always worked. And so I'm always with these people being like, "Ah, take a guess. Like if they're itchy or try dupy, if they're not so itchy, try psoriasis, try it I/O 23." And their takeaway was basically like, "No, it's very unlikely to work. You want to put these people straight on a Jack and Hibiter." And then the other two types, so those people as well have genetic predisposition, both diseases. And then the two other types, the people who get psoriasis should put them on I/O 17, and they go on to get ex-examinous lesions. Then you can switch them over to I/O 23, and the ex-examinous lesions will go away, and the psoriasis will do great. And then you got the people who are on dupy, and they get a psoriatric lesion with the, they get psoriatric disease. And whenever you see those people, you can actually switch them to I/O 23, I/O 13 only inhibitor, so that a number of those patients that they put on a trailow, and they actually did well also. And so it's, it's reasonable with those people to just get them off the I/O 17, get them off the I/O 4, and they should do well. But if they've got both diseases at baseline, then you want to go Jack and Hibiter. And so that was pathophysiologically, I think we, this was actually really useful because it did show that there is this group genetically that is predisposed to both both diseases. And it can be, they actually have both, and it can be an overlap where they just look the same. And some of them like flip flop from one to the other, but that there's people who like, they didn't, in this they didn't talk about that. There's a JEDV paper where they talked about that. Yes, about the cytokine, sort of the, the flipping. I'm not convinced that I like, like if the drug flips you, then I don't know if I really count that as flipping. Like I don't, I don't, I see people more like when I hear flipping, I want it to be like, I got psoriasis this week, next week I got a topic, derm, then I got certain, you know, that I'm not convinced exists. But I mean, but have you seen people, I've seen them not a lot, but where you're like, eh, it kind of looks like a topic, derm, you put them on Dupy and then they're like, bam, it's psoriasis. And then you put them on an IL-17 and you're like, bam, they're back to what really looks like a topic, derm. I have a couple of those people. Okay. And it's like, they just polarized one way or the other. And this study looked at that a little bit like the people who flip from one to the other. I mean, we'll go over that in another one. But I think IL-17s tended to drive the flipping from what looked like psoriasis to a topic more than 23s did. And then Dupyly, you map, drove it more the other way, but it's also probably that was the vast majority of biologics that were used to treat. I have not seen any of those people, but I could believe that I could believe that would exist. I could believe that would exist. This is four types. Like, do they have a town looking through the paper? I don't see like a table. Like, what are the four types? So it's in the it's not you're probably looking at the one that was like from career, Japan, or somewhere. There was a the other one was from Italy. The one that's in Italy has the four types. That's what I'm looking at. The dermatitis psoriasis overlap. So table number one is psoriasis exomecoexisting phenotype. That's on page two. Okay. Each table is a separate phenotype. Yes. Oh, okay. But so, bear said, I can buy that existing. And the the the yeah, and the answer would be put on a jack, right? Yeah. That would be or a methodorexate. Like, when I've had a couple of those people, they do well. They do better on nonbiologic. So a jack or a methodorexate. Okay. Okay. Cool. All right. That's it. Let's move on. Ferris, where you got? Okay. So this is efficacy and safety of ruxilitin of cream and patients with Lycan sclerosis results from a phase two randomized double blind vehicle controlled study goldstein at all, which was just recently published in the chat. Okay. So Lycan sclerosis tough condition. So it is kind of nice that there are now some clinical trials for things other than chlobatosol because you know, it is hard to tell patients stay in chlobatosol forever. So this was only in women double blind 11 sites 61 women, they had to biopsy confirm anogeneryl Lycan sclerosis. They had a BSA of less than or equal to 10% IGA of two or more. And then they had to have itching. So they had to have baseline itching NRS of four or more. They did stop all their other treatments. And then they were randomized to vehicle or ruxilitinib. And then everyone roll for up to for 12 weeks. And then everyone rolled over up to 24 weeks to an open label extension. So what's interesting is they made their primary endpoints. This is I think a big obviously thing for patients itch. They're like what proportion of patients have a four point improvement on itch NRS at week 12. And it missed its primary end point. It did not they did not see a significant difference in itch. It was like 35.7% in the rux group and 40% in the vehicle hit that four point improvement. So no likes to pain time to itch nothing, nothing did nothing. So you're like okay well whatever it's like a moisturizer. They also did look at like clinical signs. So they used there are two different measurements. One's called the clinical Lycan sclerosis score. And then the other is like the LSCA Lycan sclerosis clinical assessment that looks at both symptoms and signs. And what they saw actually was that when you looked at the change in the signs there was a significant difference. So you know when they looked at things like you know, Patekia or hemorrhaging and whitening and changes in architecture, ruxilitinib did work better and it was statistically significant. And so you know there was not like it wasn't power to look at this. So but it was for both of them. So I thought that that was interesting. There were like the adverse event stuff was actually kind of interesting too 'cause obviously like what we worry about are squamous carcinomas and patients with like inscurrosis. There was one patient who developed a vulvar basal cell carcinoma at an application site. So I thought that was kind of crazy. So you know, small study did not meet its endpoint, but you know, maybe this could work and I also thought it was interesting because they looked at, you know, at not just symptoms, but at signs. So if you look at the signs, I looked at it was petikei and echinemoses, whitening, fissures, and then structural changes primarily. So maybe this does have potential. The question is if it doesn't help the itch, how meaningful is that? But again, you know, maybe there are like, you know, again, this is another disease where you're not gonna just have one treatment. Clobate is all, it's great that it works, but it's not an everyday forever treatment. You know, if you can actually halt disease progression, could something help to, you know, maintain it. So I thought this was promising, maybe we'll see more in bigger studies. - It's a, so I was an investigator in this trial, I had a bunch of patients. They had all been on Clobate is all before. And like when I'm doing a trial, I'm sure you do the same thing, Ferris, I'll always be like, so I'm like, what do you think, you know, I don't know if you're in placebo or the real thing, but you think this is better or worse, and especially once you get into the open label, I think it's better or worse than what you've been on before. They universally were like, oh, this is working, but I think the Clobate is always better. - Okay. - That was what I heard from everybody. So I do think it works, but I don't think it works great. Which was surprising. If you had asked me ahead of time, I would have said I think it'll work for the itch and the burning more so than the structural changes and visible sides, but opposite result of what I was expected. - Yeah. Did you think you could see changes and people clinically are hard to say? - Yes, I thought I could. I thought I could. The assessments were difficult to do, just 'cause you're not used to like looking for petikei and looking for cigarette paper wrinkling, and is it a grade two cigarette paper wrinkling or a great, so the assessments were kind of difficult, but I did think I saw people get better. - Yeah. - We just had, we had the Lycan sclerosis physician on a few weeks ago. And she says like, Clobate is all in its lifelong, but she did say she tapers it out towards like once they kind of get a decent response, right? She's not using it every day. - Yeah, no, and I do that too. I'll tell them, I always tell them, don't go, like you cannot go below once a week with your Clobate is all, like you do need to. - So maybe something else to use on those days, or maybe it would decrease, maybe the long-term exposure to Clobate is all, I don't know. - Yeah, but interesting. - All right. - Compatent, what do you got? - All right, second six pack, International Journal of Dermatology May 2026, Cutaneous manifestations of vasculatists across sectional analysis from an international cohort by Micheladie at Al. I kind of thought this would be a paper that like took patients with acetylitis, skin vasculitis and would give us clues like what findings make us worry about what systemic disease, but it was like totally the opposite. And I should have picked a different paper, but I finally got to this while I was watching hockey last night, and I wasn't about to go find another paper 'cause I was watching hockey. This paper looked at patients with systemic vasculitis and asked what are the skin findings? So big study lots of patients over 4,000 from some sort of multi-national collaborative vasculitis thing. Skin lesions are very common in IgA, almost like a hundred, close to a hundred percent of patients with IgA has skin lesions, crowd-global and nemia. It's also pretty common around 90%. The Schetz and Polyureitis and the Dosa of skin involvement and around 60% of patients. But Schetz, that's mostly in the mouth in general, not really Cutaneous per se. MPA, GPA, EGPA, the ink of asculities, they have skin lesions in 2030 and 40% of cases respectively. How often is definitive vasculitis seen on biopsy? That was kind of a hard number to come up 'cause not everybody was biopsy, but in the patients that were, when a biopsy's done, it's like upwards of 75% for most types of vasculitis. Bipsy less often useful for Bichets, Takayasus and Giant Cell Arteritis, which makes sense. Table two, there's a short paper, there's a short paper. Table two had odds ratio of severe systemic disease based on the presence of skin lesions. That odds ratio was high for GPA and EGPA and it was lower for pain. So more severe GPA and EGPA if you had skin lesions, less severe polyuretis and Dosa if you had skin lesions. I don't know if this changes anything from a clinical standpoint. Vascularitis, like that, scares me. I missed a couple cases of systemic vasculitis because vasculitis wasn't present on the biopsy. So that's 75% is in Wagner's and things like that. Like I said, it was a little reassuring, but if you suspect vasculitis and the skin biopsy doesn't show it, that should not let you stop. That should not stop you from thinking, okay, this isn't vasculitis 'cause it's not always there. Maybe that's the point. I don't know. What did you guys think? Yeah. Yeah, I've missed some vasculitis cases because of that. And I feel like we talk a lot more about systemic vasculitis than you actually see. Like I can, maybe you've seen more being at the university. You know, I've been doing dermatitis for 20 years. Yeah. But you just don't see that much of it. No, and I mean, lucic, lucic, clastic vasculitis without systemic involvement, I wanna say that's the vast majority of what we see. I mean, like the vast, vast majority of what we see, or drug induced vasculitis where they don't have systemic disease, this paper didn't even have that as a category. Like LCV, Cutani's only was not even a category they looked at 'cause I think they wanted to start off like systemic vasculitis and working backwards to the skin. So yeah, like there were 1,000 patients with webinars. I mean, I've seen like four cases of webinars that I diagnosed from the skin, two of which I missed because one I thought was PG and there were a bunch of other people in the department that had seen the patient diagnosed them with PG and it turned out to be webinars. Sorry, we don't say that anymore. Granulomit is polyngiitis. And the other patient had like what we were just basically calling superficial pyoderminous, pyodermin gangrenosum that turned out to have GPA. So like 1,000 patients with GPA, I just like, it seems way, that's a bigger number than I would have ever suspected if you had 4,000 total overall. - Yeah, I mean, I guess the take home points from, I mean, your experience too is if it is, if it looks like PG do consider, you know, vasculitis and then what would you say? I think like for purls of biopsy and vasculitis sometimes like you miss it 'cause it depends what you biopsy, right? Like you want to biopsy more established lesions. You don't want the newest lesion if you suspect vasculitis, right? - Well, you kind of want in between 'cause you want in between. You don't want it to be all decimated and burned out, but you don't want the newest, I don't know. I think or like pick a couple lesions, I think there is a little bit to the timing and lesion selection for vasculitis. - I agree. - The other way. - I mean, there's a lot of hedging by pathology on vasculitis, like not definitive vasculitis, but suggestive of and then you're like, okay, why don't know, was that terribly helpful? Yeah, so. - And suspicion of systemic vasculitis, if you have a high enough suspicion, don't let a negative or sort of hedgy biopsy discourage you from working them up for systemic disease. - And then the two biopsies every time I think it might be, I'm hedging on vasculitis. - Yeah, that's a bad idea. - Just to get more lesions and different stages, yeah. - The other thing I have done here is telescoping biopsies where like you do a six and then you put that in the jar and then you do a four into the hole of the six to get deep enough, we're doing like a little wedge biopsy where you do a little, you know, a thinny lips, but that way you can get like a longer section that the pathologist can get better, you know, you have a higher chance of getting it. - Yeah, that's a good question. - So the top of the tape telescoping biopsies, I'm not sure I know a lot, but I guess because they can't. - Right. - And if I do. - Yeah. - Yeah. - And that's especially true for PAN. I think PAN, like don't do a little five millimeter punch if you think it's PAN, wedge it, like go down deep. - Yes, yeah. - Like it's the only time I've ever done that. It's like somebody with it's like horrendous, I don't know if this is PG or some horrible systemic vasculitis and like I'm gonna send in big chunks to try and find out. Like it's not like LCV, you like, it's gotta be kind of a scary patient. - Yeah, yeah. - All right, my last one, again kind of a cute one. So Ilvin inflammatory linear varuchus epidermal nevis, which I don't know what you guys think about this, but I always assume that these are kind of a blaschco's line following somatic mutation. - Yeah, they're like a mutation. - Vose act, type act. - And you got the psoriasis mutation there. - Oh, my God, I'm an indication there. - Like I think of it as somebody who thank God you didn't have a your whole body, you'd be covered in psoriasis. But it's always been super hard to treat. And so this was to Pineroff, so good old Fatama in two cases of Ilvin. Now once I actually pulled the paper and looked at the pictures, which we'll put in the video, it was like, I get like okay, it worked, but it wasn't like, oh, that was great. But like it, it worked, it worked. And so this will probably be now my, you know, if I see another case of Ilvin, I'll probably call it linear psoriasis and try treating them with Fatama. 'Cause it's just like-- - But one time I had a great response in Ilvin, it was the same thing. Like I was like, oh, we're gonna call this linear psoriasis, like a biopsy psoriasis form. I tried like every biologic, every topical, methatrexate. And then finally, I was like, I'm just gonna do so tick two. I mean, it melted the whole thing away. I was pretty impressed. - I have three patients on psotic two and I am absolutely like blown away. How good they responded. So tic two, like they did get killed in the market. It's a really, really good drug. - They were, they were just, they never communicated well, like okay, assess people for TB. Doesn't mean you have to do a TB, like do you have a cough, do you work in a prison? Like that's good enough. But they were, they were, I don't know, who was advising them, I don't know what their deal was. Hopefully, Takeda will do a better job of communicating the actual risk profile. 'Cause that's an even better drug than psotic two. - Yeah, we should have three new tick two, potentially three new tick two inhibitors that are seem like they are better relative to de-cravicinibs. So it'll be interesting to see. - Had you guys seen any, or had anybody tell you they've been using my coat with Ica-tide? - Ica-tide, I did the trials in it. I have not actually had anybody on it. - Or did anyone on it? - Clinically, yes. - Did you, what was your tape from the trials? Do you think it's, - Oh, that was pretty good. I'm really about good, yeah, good responses. You know, it's, you know, I could go, like do patients really want pills? Do they really want, like do they really not want shots? I don't know that they do, but I will say I had some excellent responses. And again, I don't know who was on what dose, but I think it is impressive if you want a biologic and the patient really doesn't want a shot. I think it's a good option. And now what was interesting to me and like the trials was I thought, oh, this is going to work in like, pulmonary plantar disease or whatever. It really wasn't that great. So I'm very curious to see the PSA data. - Yeah, yeah, 'cause right, there's that theory that like, oh, since it's a smaller peptide, it penetrates better into stuff in the blah, blah, blah. And then it's not dry from a camel. Is it, that's not the one that came from a camel. - No, that's so-no-lockamab. - So-no-lickamab, okay. - Yeah. Yeah. That was AHS, right? Is so-no-lockamab being actually studied in, so it's been studied in, yes, psoriasis or psoriodiatric arthritis as well as AHS. I think that primarily psoriodic arthritis, but there's some psoriasis data for it too. - Okay, that's it. All right, well that's it. I won't thank everybody for joining us this week. Hope you laughed once or twice. Hope you learned a few things, but mostly I hope you're planning to join us again next week. And until then, I'm Matt Zyrus. - I'm Tim Patton. - And I'm Laura Ferris, and we are germs on drugs. - Thank you.