Lasers, Scabies & Dupixent Dilemmas

Welcome to season two of Derms on Drugs, a video podcast brought to you by Scholars and Medicine the best educational platform of dermatology and provided no cost to medical providers. Derms on Drugs is where cutting edge dermis, yeah, interview is comedy. A med zyres from Dr. Dermatology in each week. I'm drawing by my residency buddies took to Laura Ferris from the University of North Carolina and Dr. Dim Patten from the University of Pittsburgh and we use our 60 years of combined Derm experience to discuss debate and dissect the hottest topics in dermatology. It is everything you need to know to be on the kind of edge of Derm and you'll have to put in listening new episodes drop every Friday on Scholars and Medicine Apple podcast, Spotify, and other major podcast platforms and just reminded that there is a video component that has the key figures and tables from the articles we talk about and this week we've got another one of our famous six pack episodes where we are going to go through the hottest coolest stuff that we have seen in the literature. I'm going to kick it over to Dr. Ferris to get us started. All right, so my first paper is Safe and Effective Acne Treatment Across Skin Types with the 1726 Nanometer Seabum Selective Laser, one year data from a prospective multi-center study. All right, Ferris, before you get into it too much, are you guys using this at the University of North Carolina? Do you guys have one? I don't think there are many of these in the whole city of Columbus. Is it taken on? We are not. Okay. I don't know how much it's taking off. It is not in a relatively poor state academic center taking off. Although I will say we actually do a lot of laser treatments. I know from training with you guys that none of us actually know a whole lot about lasers. Yeah, that's good. So, where is your opportunity to learn from people who don't know anything more than what's in the paper? I thought it was really, I thought this was really kind of interesting. Yeah, this thing is fascinating. Sorry, go ahead. Go ahead. Yeah. What's the brand name of this thing? I just thought it was clear. Avoclear. Avoclear. Avoclear. Avoclear laser. Avoclear laser. Okay, so that's 1726 nanometers. What does it do? It basically like fries sebaceous glands. So it's like if sebaceous glands are at the heart of acne, can you just zap them and get rid of acne? Okay, so this was a study where they basically looked at one year outcomes and they had published there, I think like 12 week outcomes previously. And I know you guys will be like, who cares, if it works, you don't need one year data. But I actually think if you're going to do a treatment for acne once and then stop it and you got to know if it's still last, right? Right. Okay, so there we go. So sometimes I get some hate for doing one year follow up data, I mean, 30 studies, but I don't know me. Sure. Yeah, because we're trying to write the idea with this is to replace acutate. And so we, you know, you went long term. This makes sense. It makes sense. Okay. I'll allow it. So thank you. I thank you, master. Okay. An open label study, 16 to 60 year olds, Fitzpatrick, two to six, they had a moderate to severe facial acne. So that's an IGA of three or four. There was like one mile to snuck in there. But and they had to have at least 15 inflammatory lesions. So this is kind of bad acne. And they had, you know, across the spectrum. So and they were, they had three treatments with the avoclear laser that were spaced two to five weeks apart. Now I was like, well, what else were they on? So they did have a 30 day wash out from other acne treatments. And then they could not be on any topical or systemic acne meds for the full year. And that was, you know, they did like fault. This doesn't let retrospective. It was prospective. So, you know, I thought that's pretty rigorous because in reality, like what I tell people, you cannot use treadmill in after this. No, I don't think I would. Okay. So, um, so this is sort of like the follow up. So between week 12 and week 52, basically there was no treatments. They were assessed. This wasn't COVID times. So they did like, there were a lot of this assessments were done by, um, by photography. So they had standardized photographs and they had independent assessors. But they were kind of blinded to like the study design and the time point. So, you know, they may see like they weren't like, here's the baseline. Then here's week two. So they just were like, here's some photos, give your IGA score and give your lesion count. So kind of a decent way to blind, I thought. If you look at the photo type of these patients, most of them were three's and four's. And if you look at their baseline acne, 77% were, were moderate, 22% were severe. And 89 out of 104, so decent size study completed all of, you know, all of the visits. 71 were like per protocol, meaning that they actually like had all their treatments and then follow it up. So what did they actually find? Baseline, mean inflammatory lesion count was 61, median 56. That's a lot of inflammatory lesions. And then it's 12. Yeah, a lot of pimples. That's like bad. I mean, I called that bad acne. And so, yes, on my IGA score. So these are people you would have put on acutane, right? This is 100%. Yeah, yeah. I would have put these people on acutane. At week 12, their lesion count was reduced by 49.4%. And then at week 52, it was down to set, it was reduced by 70%. And so if you called a responder, a reduction of 50% or more, at week 12, 79.8% were responders at week 52, 91.5 in the per protocol. Like that was a little bit of a twist. Like the ones who actually did everything, 91.5% were responders. But even if you didn't intend to treat analysis, and you counted everybody with missing data is a failure, 67% were failures at week 52. So they kept getting better. Now they also looked at non inflammatory lesions. They were down by 25% at week 12 and about 57% at week 52. IGA, by week 12, a third were clear or almost clear and by week 52, two thirds were clear or almost clear. And only like under 9.9% were moderate to severe. And there was like no difference in terms of subgroups of like this fits Patrick skin type, their baseline severity, age, sex. Safety and tolerability, it was like, you know, not surprisingly everybody had air theme up. Some people, most people had a DMA. There was some purging, which now we actually use as a medical term where like you get a little bit worse, after you start, we see that with a lot of acne treatments, 44%. I thought you meant that not like they didn't develop blemia as part of the treatment. Okay. Yeah. Okay. And, you know, there was some of that, but it was generally mild, 18% had mild dryness. There was like some itchiness, no blistering, no hyper or hypopigmentation. The patient reported outcomes at baseline, 56% felt a lot are very much embarrassment or self-consciousness about their acne. By 12 weeks that went down to 14.6% by 52%, 8.4% felt very or highly embarrassed. Whereas 90% said that they felt only a little or not at all embarrassed. So why does that matter? Because, you know, what acne really matters is like how do the patients feel, right? So all, you know, good stuff, pretty big. It was not a randomized control trial. You know, there was not a control group. So that's not, you know, great. Everybody knew, you know, every patient knew that they were getting it, but I think they did what they could to blind the readers. So, you know, how's this going to change clinical practice? Like, this is about $3,000, about $1,000 a session. So like $3,000 and it's out of pocket. You know, what I do this as somebody could find $3,000 in my pocket if I had to, what I do this for my kid, no, I would put my kid on acutane. But people, some people don't want to spend, you know, like, so, you know, I get that there are people who want to avoid acutane. I mean, interestingly, I mean, you know, North Carolina in the triangle area and like, there is this huge case of a kid with acne who went out and like had a psychotic episode killed five people. I mean, it's terrible. This was several years ago and the defense was not acutane, but menacicling because it can cause psychiatric effects. So like, there are going to be people who are afraid to treat their kids with drugs for acne. And I thought, oh, that's just acutane. But now I think we're going to have the menacicling, not that there are other things you can do. So interesting data, it's going to be expensive. And you know, just for fun, I was like, how is this, you know, relative to like cab trio, which we've done, right? That paper. So, you know, the sort of the best like apples to apples was that actually cab trio at week 12 had like a 75% reduction in inflammatory lesions versus this was about a 15% but cab trio didn't have like the one year data. you look at it compared to win levy studies. There was modest relative to vehicle. The inflammatory lesion was reduced by 38% with win levy. I think it's at 12 weeks versus 22% with vehicles. So you would say at 12 weeks this looks like it's better than win levy. It looks like it is maybe not quite as immediate as cab trio, but it has long term data. So I guess there is some long term data on out the six months with cab trio. But this is like three shots in your-- are three treatments and you're done. And I'm sure these were worse patients than any of us would use-- For average win levy. Yeah, if you look at win levy studies, those were mild to moderate. I don't think not moderate to severe. Would I didn't see that the pro-- I mean, they just they zapped your whole face. They didn't really go into the protocol and how long does this take and does it hurt. I mean, have you guys had laser treatment? I've done PDL and laser hair removal. My word. Wait, is that explain your hairline? Yeah, they were-- It was the worst. They got them back. They got them back. No, they got them backwards. They did PDL where he needed the hair removed and did the laser hair removal. I'm like, why are you aiming it up there? [LAUGHTER] There was not as much of pain as a side effect here. It was the edema and erothema. And I've known a few people-- I've known a few people have gotten it done. And it is in the same spectrum as like PDL. So painful, but people don't need, maybe topical numbing, but they don't need it for sure. And it takes-- depending on how fast the operator is, somewhere between 30 minutes and an hour, to do a treatment. OK. And so the thing that I've been surprised is that we haven't seen more of using it for reducing wholeness and subacius hyperplasia. Like those are-- if it reduces subacius hyperplasia and maybe reduces thickness of the skin and people who have a lot of subacius stuff, that I could see being super useful just because we got nothing else if it's to address those cosmetic concerns. I think it does work in subacius hyperplasia. I vaguely recall like somebody talking to me about this once and that it does. I was like, gosh, could this work for H.S. and I saw that they have some ongoing trials for H.S., so hyposubacius, you know, and everything. I'd be super interested in it if it worked. For that, particularly with only three, I mean, you could say $3,000 versus the course of Accutane, but $3,000 versus binxelks for life seems to start looking like a bargain. So-- Yeah, that actually makes a lot of sense. I had never occurred to me at all. OK. So Hanukul might make us learn about lasers all over again and are a step in such a far career. That's the thing I remember about this. And the reason I think it's so painful, because the key thing with this lasers, that that wavelength is more absorbed by sebum and sebums than it is by water. But it's like the absorption is just barely above the water absorption. So you're still getting a lot of bulk heating because of the water and your skin heating up. You're boiling your skin. Yes, but it's a little more heating up with the sebum than it is of the general water. That's the key thing about this laser. Oh, yeah. And then I was like googling like, what's the nearest wavelength of another laser to 1726? And so the device that has other acne is the 1450 nanometer. Don't ask me what that one is. But that is also like there's some data on that. But the result, like clinical results were apparently inconsistent. And one split-faced study showed no benefit over control. So it seems like there is something unique about really targeting the seabassite. So kind of cool. Yeah, makes sense. All right, Pat, and what do you got? All right, my first six pack was published online January 2026, clinical and experimental dermatology. The journal of the British Association of Dermatologists, case anyone wondered. This article was titled "Treatment with Microphinolate Moffatil" as an adjuvant therapy post where Tuxemab does not improve treatment outcomes and pempagus, so kind of a spoiler alert in the headline there. First author, Vich Van Nehdu, this was a letter to the editor. I like how they actually-- letters to the editor, you actually say deer editor. It was just to them. It'd be funny if somebody was like, I can't believe you published that. That was just a year. There's never any form of closing though. Like I want to see a letter, and then it ends with like with deepest adoration, and then the author's name. That's what we got. There's never-- Yeah. Never sign off. It's kind of rude. All right, so from back there-- The editor has a name for God's sake. Be like a deer dorge, you know? Yes, I know. I know. All right, we're going to change this next time. I'm going to be like deer-- You're trying to make it personal, but they don't make it personal. Either drop the deer altogether. We're not kidding anyone. It's not like you're writing the guy a letter, or just say deer dorge. All right. Yeah. OK, we're going to do practice on this. It's a movement. All right. So Tuxemab works well for pempagus and pempagoid for that matter, and is better than any other drug than allowing you to get patients to steroid-free remission. But patients relapse, relapse rates vary depending on the source, like 40 to 60. So I kind of tell patients, like, yeah, 50% of patients, like it comes back. But we'll address it then. Kind of similar thing for BP. I mean, the rate's really depending-- very depending on the source you read. So is there maintenance therapy that should be given to prevent relapses, right? This is the big question. Do you give maintenance or a tux to everybody? When and how much do you do low-dose pred? There is a study from Taiwan that suggested asithybrine could prevent remission. I'm sorry, prevent relapse. But I don't think that's a widespread practice. The authors of this study practicing at King's College in London say that they routinely prescribe either low-dose micaphenolate, 500 to 1 gram, or asithybrine, asithybrine, 1-megparchig, after Tuxemab therapy to prevent relapse. Like, that's kind of their standard. But does it actually help prevent relapse? They investigated. A retrospective review compared 33 patients that got low-dose prednisolone plus micaphenolate. Following Ruxemab treatment to 17 patients that got only low-dose prednisolone. So kind of a small study in the MMF patients plus prednisolone outnumbered the prednisolone patients kind of significantly. Length of follow-up, 36 months. Figure 1B, no difference in percentages of patients with complete remission, partial remission, or no remission. So there wasn't any difference overall. So it did percentage of patients in order to complete the relapse. So they're still on the Ruxemab. Like, is it ongoing through the Ruxemab? I would say no. And I don't think that they specifically when did we start this. So my guess is they got the two doses. And then they just started it right away. The percentage of patients in complete remission was actually higher in the prednisolone only group, but it wasn't statistically significant. Maybe the prednisolone only group relapsed earlier? No, that didn't happen either. Figure 1C shows similar durations of remission between the two groups. Were there any differences in anything that was measured between the two groups? There was CD8 T cell counts were lower in the group that received prednisolone plus micaphenolate, which led the authors to conclude they're not going to do this anymore. They're not going to give micaphenolate moffatil as maintenance therapy, 'cause it doesn't seem to help with remission rates. And by decreasing the CD8 T cell counts that authors hypothesize that may predispose patients to infections. So they did a study. They demonstrated their standard of care, so to speak, of maintenance micaphenolate may not be a good idea. It was kind of interesting. Do you use it or have you been using it? Are you going to stop using it? What's your. I don't do any. So the micaphenolate's interesting, 'cause it's low dose and that patients are going to tolerate that. Like, out there. You're going to run into many problems. But the other question is maintenance therapy at all. Do we have any really, really good evidence that there's a certain maintenance therapy that everyone ought to be using? I don't do any maintenance. They get retoximab, a pharynx-mer patients, you can taper off the corticosteroids. And, you know, the original retoximab protocol that was published in the Lancet, those patients got 500 milligram, like a touch-up dose, let's call it, at month 12 and month 18. And then the Vicky Worc study that was published in New England Journal of Medicine, I'm pretty sure she gave the two doses. And then at six months, patients got another two doses. So the study's kind of supported, hey, yeah, we should do this, but I do not. I mean, there's a fair number of patients where. Yeah, if you don't need it. And if you. Yeah, you don't need it. And it's not like, you know, maintenance, ruxilitinib with your atop third to keep it under control, right? Safe and whatever. Patuximabs are like an IV. Do you tell them. No, I don't do any maintenance therapy. Do you tell them like, okay, if you get one blister back, if you get one thing back, immediately let me know and let's get it moving, because you know it's coming. Yeah, right. I mean, the mouth especially, right? I mean, for whatever reason, skin clears really, really well. The mouth can be stubborn. So it's like, you notice blood on your toothbrush, toothbrush, you call me. We'll see where your titers are. If the titers are elevated and that they have the symptoms, pretty low threshold for getting them back to the infusion center. Okay. If the titers are normal and they're like, I think I got a blister, but it's not documented and then I kind of wait. Okay. Okay, and they didn't follow Desmagli in one and three titers. They're behind me. They're behind me, but I didn't see, but I probably didn't read it carefully enough. No, they didn't follow the titers. I'm pulling it up. I'm pretty sure they did not. Which do you think? It was a very, very short, I mean, it was truly a lens. It was a letter. Sorry, the editor has a very short attention. They should. He's the worst. Should have to go on that in calligraphy. And he never writes back. So really. All right, we're moving on to mine here. So first, first one was a hot topic. So, you know, does duplomab increase the risk of ketenitis T cell lymphoma in patients that get treated with it? Title of the article was duplomab treatment is not associated with changes in lymphoma risk in atopic dermatitis and other type two inflammatory diseases. Data from a large scale, retrospective cohort study, does in frontiers and medicines. So this is basically a genetic study. They looked at a whole bunch of people who got atopic dermatitis. They got duplomab or got some other drug. And then they also looked at people who had other type two diseases. And the basic takeaway first, that whether you get duplomab or not, you've got a. If you are diagnosed with atopic dermatitis, your probability of being subsequently diagnosed later with CT-T cell is 10 times higher than the background population. The actual number, and this is now across multiple studies I've seen this, is about one in 600 people who are diagnosed with AD will eventually be diagnosed with CT-T cell. Unknown if it is that it was CT-T cell the whole time. And it just looked like AD on pathology and clinical. Or if it was AD that truly turned into CT-T cell. We truly don't know the answer to that. But we do know one in 600 people who were diagnosed with atopic dermatitis are later diagnosed with CT-T cell. That is not a. There's not an elevated risk in people with other type two inflammatory diseases. And then so people with AD, you know, had a. With compared to people with other type two inflammatory diseases, had a similarly increased risk in the risk of. In the likelihood of non-hodgisins lymphoma, had a similar. But then also had elevated risk in T cell and natural killer cell lymphomas, and had a pretty dramatic increase in the risk of eventually getting cesaree. So it really is like AD predisposes to a later diagnosis of CT-T cell. So then the question is what about dupelemab versus other systemic treatments? Absolutely no increase in the risk of cesaree. I'm sorry in the risk of CT-T cell. The non-hodgisins lymphoma though, dupelemab dramatically reduced the risk. So hazard ratio of 0.44 compared to people treated with other systemic therapies. And it also dramatically reduced the risk of cesaree. So reduced the risk of cesaree by 92%. So a hazard ratio of 0.08. But CT-T cell risk no effect. So it really does look like dupe just. reveal CT-T cell, but it does not. if it does, it does not promote progression at all. But so the. this trinetic studies, you know, and always a little nervous with trinetic studies. But this was well done and these were high-powered authors. High-powered authors. So this goes with what I thought anyways. And again, it reconfers that dupe reduces your risk of hematologic malignancies overall and dramatically reduces your risk of cesaree syndrome. So. Okay, I have a question. Few people often say parrygonodularis and atopic dermatitis is the same thing. So patent tends to. When I see a pure. a pure parrygododularis patient, when I see parrygonodularis patient, and this was before. dupe even came out like. my pure agonodularis patient, so I'm like, okay, atopic dermat. I'm dealing with an atopic dermat patient and we're going to manage it like this. I mean, and when I still see PN patients, like I just get that feel from them. Like it just. like it smells like atopic dermat. So patent's doing five dermatology. Yeah, like. Yeah, man. Yeah. AD5. So there is some data that they've done biopsy studies of, you know, AD. People with AD, people with PN and people who have both. And they're. they're similar, but they are distinguishable. But it's. It really comes down to this question of like, where do you draw the line of. they're similar, but not identical. Like. It's a reasonable question. My belief is that there. there are people who have both. And there probably are people who have just the neurohypersensitivity and the rest of their skin is totally fine. But functionally, I don't care. Right. From the practical. This. I want to cut to the chase. Is this like shouldn't. do PN patients get CTCL more? I've never seen that reported. Not to my knowledge. I don't know if anyone's ever looked. They do. I'm making that up. I'm. with my knowledge. So why not? It's a vibe. It's a vibe of data. A vibe of data. A vibe of data. All right. Here's my other one. So this one is me announcing to the world that I was very wrong about something. So I'm. Wow. Yeah. When I'm wrong, I take. So I have numerous times said, "Hey, it's in the label for Dupy that it may increase your risk of parasitic and helmeth infections, but there's absolutely no data of any unusually or unexpected parasitic or helmethic infections." So that was theoretical, not real. I was wrong. Scabies. Dupy makes. of scabies worse. I don't. I don't know that you were wrong, but okay, go on. Well, but it's a parasitic infection and Dupy. I know. It makes it progress to be like Norwegian scabies. So people get crusted scabies probably because TH2 communities playing a role in fighting the parasite off. And it may be hard to identify. So there were. Several reports of this in the literature. But it may like reduce the itch significantly, not in all of them, but in some of them. But then people get like more phology of crusted scabies. And when I brought this up, like my. One of my partners was like, "Oh, yeah, that happened to my dad." Like, he had. We were my father in law. He had cancer and started to get itchy. We thought it was one of the checkpoint reaction inhibitors. Put them on Dupy. Then his rash started to look weird. And some of it going, it turned out he had scabies. But do you think that the Dupy made him to suffer the scabies? Did he get Dupy because he had scabies in the. Untreated scabies. Right. I mean, these patients have untreated scabies. I have seen this happen before. But they get. Some of them had scabies and they get put on Dupy. And. But the thing that was interesting here, that it turned into Norwegian scabies in normal people. Yes, because I could see that why do people get Norwegian or now what we call crusted? Just because the Norwegians are beating us in the winter or Olympics. Does it mean we need to name the scabies after that? No, we're bringing that back. We're going to bring it back. They haven't. You got the gold medal, but you also have the worst scabies, so. That's the worst scabies. So yeah, no. Part of Trump's foreign policy, that we're going to name a bad disease after your country. No, but I digress. Where was I going with this? But I do think that crusted scabies come. I mean, we've gone through this whole thing. Scratching is protective against parasites. If you're not itchy, you don't scratch. Say, their parasites are going to multiply. So. I could see it now. I will tell you, my personal. It's not personal. My experience is I have had a couple of patients who I put on Dupy who have gotten rip-roaring Demodex. Yeah, yeah, I've seen that a couple of times. Right, so. That's to me the parasite thing. Yeah. And yeah, that's an interesting, I think, Demodex and Scabies both. And it really goes back to me to the idea that if you put somebody on Dupy or any of these AD drugs and they don't like get dramatically better pretty quickly and stay dramatically better, you shouldn't just be like, well, it's still AD, let's try another drug. That's probably what's going on. But you should really like, if the first drug doesn't work great, you should really like think about patch testing, think about biopseeing. Let's say you have to do any of that, but you should really think about that, especially if they get 50% better, it looks to saying they just didn't get better enough. That's different. They didn't really get any better or changed or got worse. That's somebody that you really got to be like, what the hell is going on here? The most recent Scabies case that I saw that was it. He was on Dupy and it's kind of like, yeah, that's kind of weird. Like you're not any better whatsoever. Yeah. Any, yeah, it's Scabies. Yeah. And that's actually a reminder of the other thing for our listeners. If you haven't seen this before, the new thing in Scabies is that wood's lighting them works. So Scabies might fluoresce as like a little yellow dot and then the burrow behind them fluoresces is like a white, looks like a little smoke stack, a little smoke coming off of the Scabies might. So that's to me, that is now the most sensitive way to diagnose Scabies if it crosses your mind. And I have an AI answer. Larsen at Al 2018 cross sectional analysis of 695 PN patients from the Johns Hopkins Health System compared to 2.4 match, 2.4 million match controls for primary cutaneous lymphoma, which was predominantly CTCL. The odds ratio was 24.82. What? You're making that up patent. I mean, AI may be making you know, but I am just reading what AI told me. AI knows that it has to make me feel good. So this could all be made up like, yeah, Dr. Patten, you're right. It's true. And by the way, I'm, I'm coining a new phrase from now on that there's AI and BI, right? Artificial intelligence and biological intelligence, right? So that's we are just entities that have developed BGI, biological general intelligence. And now the machines are catching up with us. They're official general intelligence. There we go. All right, let's move on. Ferris, what do you got? Okay. I have from the JAD, hyper-caliburant incidents and females over 45 years old on Spurna Lactone for dermatologic conditions, a retrospective cohort study. And this was by Greg War at all. This is a Roshma Stigene and Jaren Barbieri who were the senior authors on this. Okay. So Spurna Lactone in, you know, your coolest acne patients, women over 45. And so we do know that, you know, we've got that this group has done a lot to say like, you know, we can, we can pull back on monitoring for a lot of things like, you know, we can thank them for not having to check labs on Ac, or for giving us the confidence not to check labs on Acutane. And then they've looked at Spurna Lactone, but the word has always been like fine for women under 45, but over 45 there's some risk of hyper-calemia. So the key question was, you know, for women 45 and older, how often do we see hyper-calemia, who's at risk? And what should we do about monitoring? And they also looked at like, what do people actually do? So this was a 10 year timeframe 2015 to 2025. They looked across indications. So it's basically acne, female pattern hair loss, here's tootism in H.S. and they had dev at least two prescriptions. And they narrowed this down to about 398 amalizable patients. They also looked at comorbidities like hypertension, diabetes, chronic kidney disease. And then if they were on like what they called risk compounding medications, so ACE inhibitors, ARBs, beta blockers, diuretics. And they looked at potassium labs at three points. So they've got to jump in for one second. There's one other one of our listeners actually after we talked recently about back from killing people who have, who get it for acne, especially young healthy people. One of our listeners emailed me that it, back trim also causes hypercalemia. And so if you have somebody who has been a lactone and they get back trim, it can cause them to get like severe hypercalemia that can even be fatal. That actually was from Dr. Dennis Newton at the University of Texas Southwestern. Oh, good. Okay. I did not know that that back trim, the time I was looking for them. No, I did not either. And that is a, you know, not an inconceivable thing that can happen. Yeah. Yeah. Okay. So they defined hypercalemia as a potassium oak five or higher because their lab upper limit of normal is five. Like, so I mean, 5.1, do I loose sleep over that? No. So it would be in their, you know, in their outcome hypercalemia. And then so mean age was 54. These 62% of them had no predisposing comorbidity and 70% were on no risk compounding meds. Most of these were acne 47.5% not most, but the highest use was for acne. And then hair loss at 37%. Most common starting dose 50 milligrams max dose, most common max dose was 100 milligrams a day. So, you know, and then 61% had at least one dose increase. So monitoring was like all over the place. So if you look at it, because you know, we're saying like, oh, we should do this. 70% of patients had a potassium within a year of starting post initiation within six months was 58.5%. And really, if you look at it, it's like the got the package insert actually says that you should have like potassium checked within a week. I don't think I ever knew that. So 19, only 19% had it within one week and only 30% had it within four weeks. 58% had potassium checked within six months or of reaching their maximum dose. So like in the real world, do we follow the label? We don't really. Okay. Incidents of hypercalemia, 10%. And among those with those baseline and interval labs, 13% developed hypercalemia after starting spur on a lactone. They were mostly mild 97.5% of these had a potassium of 5.1 to 6. The mean hypercalemic potassium was 5.3. There's one patient who had a potassium over six. When did it occur? On average, at 20.5 months after starting spur on a lactone. So it's not this like, oh, this happens within a month. There were only three cases, in fact, when it occurred within one to four weeks of initiation, which is like the window where we're supposed to be worried about it. Most common dose associated with it, 100 milligrams. There was no significant relationship between dose and degree of elevation. So who were the people most likely to have it? It was patients over 65 or older. Those who had one or more comorbidity. And the dose was not associated. And again, like if you combined all these things, like you were over 65, angiad hypertension, your risk went higher and higher. Most of the time hypercalemia was 85% of the time asymptomatic when it was present. That like the symptomatic was like fatigue or GI. There were like the only serious event they had was in one episode of Brady Cardi with QT changes. But they actually attributed it to the beta blocker and their calcium channel blocker and not to the spread of lactone. And most of them were like managed outpatient and that patient was not even star. It wasn't stopped. So 62% of cases, nothing about nothing change. They did not drop the dose, hold it. There were dose reductions and temporary holds like 12 to 17% of the time. Only 3.8% of the time did they actually like change their care, meaning that they, you know, that they did something different. So basically most patients did not have a management change. So what's the summer? Was there recommendation a cause it, it sounds to me like this, you know, as you know, fairs when you do trials and you're just checking labs like on a monthly basis and everybody you, you pick stuff up. So you know, without a comparison group, it wouldn't shock me if you saw this much hypercalemia in a normal group of like, so do they recommend? Do they give any, we should do it, we shouldn't do it. Like do they say anything? No, I mean, there wasn't like a strong recommendation, like they said still, you know, if you have women 45 to 64, you know, if they're on like rene and angiotension, rene, rene and angiotensin aldosterone system medicines. monitor them, maybe at baseline and one to four months after, for women who are over 65, especially if they have comorbidities, we should be probably following those women. Who's a 65-year-old who's still on SpurnoLactone for acting? I know, I was thinking about that. I have not had. I can't remember the last time I used SpurnoLactone on somebody over 65. Yeah, so basically it was like 45 to 65, you're healthy, maybe do like a baseline, one check and then just follow them. And if you have comorbidities and 65, then you can do some checking, probably it's baseline in that first month, and then maybe periodically, probably that age group to be honest is getting BMPs and CMPs kind of for other reasons. So I think we don't worry a lot about this, but yes, they did acknowledge because there wasn't a control group here, like how much of this was hemolysis in the labs or rechecking and then it came down to normal. So I don't think we got a lot of super helpful answers out of it other than it's still even in the higher risk older women group, it's still a list of things. Yeah. I've had older women who want to do everything for. Heralos. Female powder, Heralos. Yeah, yeah, yeah. And so they're like, I'm gonna. And I just had a patient like two weeks ago, she came in, she's like, my PCP is making me stop the Spurno. I'm like, okay. That's right, I'm like, do I care? Do I care? Do I care? I'm like, yeah. Yeah, all right. Okay. It's a good idea. You should listen to him. I'm sorry, Pat. What are you, Pat? What do you got? All right, my second six pack. I'm doing, I'm doing a third. You guys are doing thirds. I have a really quick. It's like a. Okay. Okay. Okay. So it was stuck that you're slowing it down. Just go. Go to the chase. Assessing disease progression in a early one, high-dried 90-subrotee of patients, a nested case control study by Roderie as Santa at all. It was available online in the Journal Dermatology February 2026 Retrospective Study. Two aims. Aim one. Follow herly stage one patients, determine the incidence of stage two and three disease. Aim two, performing nested case control study of stage one, to identify what factors, if any, were associated with progression. The study was performed at the Virgin de las Neadas. I'm probably butchering that. University hospital in Spain from 2017, 2024. 133, early stage one patients. This was based on clinical and ultrasound. All patients got ultrasound exams and every visit. Average follow-up was just under two years. The answer to the big question. How many patients was stage one disease at baseline progressed to early stage two or three? It was 50 out of the 133. So 37.7% of stage one patients progress. A Kaplan-Mire curve shows that the median time to progression was 308 days. So the patients who progress about half will do so within the first month. I'm sorry, the first 10 months. Okay. Okay. Only one patient progressed to stage three. Everyone else progressed to stage two. There's three tables with lots of numbers, table ones and two show baseline follow-up characteristics. Table three kind of interesting compares the patients that progressed to the patients that didn't progress. And according to multi-variate analysis, the factors that were associated with progression were the number of cigarettes smoked per day. So progressors smoked more cigarettes on average compared to non-progressors. If you were early stage one C at baseline, you were more likely to progress. I mean 80% of the patients were like stage one A. So stage one C like I didn't even know their words like what's this ABC stuff. Yeah, there was like a paper from a Dutch group or maybe Danish group and they're like let's break down stage one A, B and C. And one is like a few lesions but without tunneling. And three is like lots and then two is just kind of somewhere in between. It wasn't, I mean, it's kind of a honestly, I think the reason they did it was because these drugs are approved for moderate and severe disease. And if you have stage one, they're like if we call it stage one B, we can call that moderate and stage one C severe, which I think is actually like true. I would agree. But and you know, if that study came out of Denmark, we should now call it Danish hydrodonitis. Unless they give a screen, unless they give a screen land, then we'll let them off. That's right. So an increase in the number of abscesses but not inflammatory nodules was associated with progression. And finally, patients that had more punch drainages performed were less likely to progress and suggesting that this intervention punch drainages may help prevent progression to early stage two or three. I mean, that's you know, reading into it a lot. So focusing on some of these things, the authors say that encouraging patients to smoke fewer cigarettes, maybe a kindler, gentler way of broaching the smoking issue because we're all supposed to be like fluffy, happy, agreeable doctors instead of, you know, like we're not saying you can't smoke any cigarettes. That's right. Just smoke fewer of them, which actually I could see patients being like, okay, yeah, yeah, I'll try instead of being like quit smoking. That's not necessarily that's still too many. It maybe was a little interesting. BMI didn't differentiate progressors from non-progressors. So it's not like the non-progressors had statistically significant lower BMI. So the other area we're all supposed to be touchy-feely didn't really seem to matter. And then, you know, I guess drain the abscesses, right? Kind of important. It takes time maybe in a busy clinic. It's tempting to be like just take some doxy and hopefully those will go away. Maybe the drainage does prevent tunneling. I mean, you can buy it, right? You can leave an abscess there and then be a radically good tunnel. And I also think H.S. patients can be procedure averse, understandably so, because like a traumatic ER experience. And am I implying that ER practitioners don't know what they're doing? Yes, yes I am. What it comes to doing? Maybe discussing this paper like encourages patients like, look, there was a study at show this could actually be helpful. Everybody, maybe that's a little strong, but maybe this will help prevent like a tunnel to form. So yeah, that's all I got. What they, what they didn't, and they looked at, you know, progressors versus non-progressors, what percentage of them were given antibiotics. And it was about the same between the two groups. They did not do the same analysis for biologics, which I thought was strange. I just didn't know if maybe there weren't enough patients in there. Maybe it's hard to get biologics approved for early stage. What may there's one thing that is needed? It was weird that they did it for antibiotics and they did that analysis for antibiotics like percentages, prescribed this yes, no, progressors versus non-progressors. And they didn't do it. They didn't ask that same question for any other drug. That's the question we need is do biologics prevent? And then the topical ruxilitnib, which now has updated, right? Like that's what we really need to know is can you prevent progression? But wouldn't it have just been that they, if you're early one, you're probably not, they won't give you a biologian? Yeah, but they they had median duration of time on biologics. So the patients got biologics. Okay. Okay. Maybe like Ferris said, maybe it was such a low number that they didn't. Okay. All right. What's number two? Case report, zinc deficiency is a modifiable modifiable risk factor for nfortinab, vedotin, induced, cutaneous adverse events. So that's what's in fronters of oncology, November 2025, 10 patients treated with DV that developed either dysguzia skin rash. Four patients got zinc. And three of the four had the SD rifle at SD rifle like rash resolved. They were all low in zinc. And so I just this article popped across my whatever. And then we just had a patient with this rash. And I'm like check a zinc. And it was low. So we did see if they get better. And it was interesting. I saw that paper that the dysguzia did not improve with zinc. Disguzia did not improve. Drined has got a little bit better, but it didn't resolve with skin got better from the previous article of preventative topical cladators all in the susceptible areas that really seemed to work because that was a split study. It was kind of impressive. Yeah. So you give all these patients zinc and you slather them with cladators all. You know what would work great? You remember that old zinc cap? The it was the foam that was supposed to be just a zinc peritone foam. But it actually had the same clubatas all in it. I do remember. Yeah. Because it was it was like. All right. So I did I did three papers. I'm cool like you guys. Oh, all right. That's good. That's good stuff. All right. All right. My last two. Number one, Jack inhibitors and memory impairment and disproportionality analysis in the who World Health Organization, global pharmacovigilance database called Vigia base. So generally, I do not believe anything in in these databases. Because as soon as you say, Hey, you might get a side effect of XYZ. Then when people get XY or Z, whether it's related to the drug or not, they report it. So then it looks like there's more cases reported with that drug. This one matters a lot to me because nobody's telling people with a Jack inhibitor, hey, you might get memory impairment. So this is exactly how these are supposed to be used. and son of a bitch, it was significant. So like the risk of getting memory impairment, I was greatest with tofacidinib, the majority of these people were getting them for rheumatoid arthritis. But like tofacidinib had a res, an odds ratio or reporting ratio of like three. So and it was significant. These were most of the over half of the cases where non-altorally patients and a third of them were like serious memory impairment. Like, like meaningful cognitive impairment, the there's not enough data and vigilance to like really just like does it go away whenever you stop the drug. But in the case that these people had that triggered them to look at this, they stopped it and it did go away. And mechanistically it does make some sense because there are these neuroprotective agents that activate the jacks-tat pathway. And so whenever you block them, you may like not have these neuroprotective effects. So it was like a really interesting new thing that like if I think we probably need to start telling patients like, hey, if you notice your memory, like seems off, I still don't know if I'll tell people it would be like if they bring it up like hey. They bring it up, then we'll be like, "Oh, that's interesting." Yeah. But I remember this was reprimanded. I told you that when you started, don't you remember? For it. So yeah. But this came up, I remember this with like statins. Remember that was a thing with statins at one time and it was like, oh, this and then, you know, right now they have done multiple prospective randomized control. Like the statin thing didn't seem to be something that happened. They still say, you know, at rarely, yeah, that we don't know what that is. And so maybe it's the same thing with the jack. It would have been interesting. The case that they presented is pretty impressive. And it was one patient, but they said six weeks, the issue she was having completely resolved. Yeah. So they should have put it back on it and retested it. And it took a long time. The number of times. People were generally on the drug for like, I think it seemed like a year before this started. So it did seem to be like kind of accumulative toxic effect. Yeah, it's interesting. Like new unexpected. It's the kind of thing where you're like, well, with the new drug, you never really know well, son of a bitch, we didn't like maybe this, maybe it is a thing, maybe it's not a thing, but I'm sure a lot more stuff will come out now. Then my last one, this was just a great love it when this kind of stuff comes out. So development of a patient decision aid for a topic dermatitis, systemic treatments and adults. And so it's just a great example of how dumb physicians can be. So these were, I think a bunch of academic physicians and then a bunch of patients. And they was wanting to come over to the patient decision aid where like the patient, you give it to the patient and it helps them like understand the different drug options and whatever. So the doctors made it. The patients were like way too complicated. They can't understand it at all. Went back to the doctors, they made it more complicated. The patient said, no, this is terrible. Like we can't, and then they went back to the doctors and was like, no, we need to add more. There are not enough of the risks discussed. So they added, it was, they just kept getting further and further away if the patient's being like, please, we can't understand this. And the doctors being like, well, we need to give you more information. Like just the main takeaway, now there was one useful thing here and it was this that the best way to approach shared decision making with a patient is with staged decisions. And like that's what got me excited about this. And that's what I've been doing forever and trying to tell people to do. Like you give patients one question at a time. Like I always give them an A versus B. Do you want this? And so for me, it's do you want to pill little weaken your immune system or you want a shot that won't? Okay, well now if you say-- - The very unbiased question. - Well, but it's true. - It's true. - It's true. - It's accurate. Right? And then if they say-- - We don't get paid by regenerant at all. - Yes. - That's right. - Right? No, I mean, I do but not for this. - Yeah, if you get paid for that more than I know. - But right, and then if they say, I want a shot, then I'm like, okay, this shot is once every two weeks forever, but if you got allergies or asthma, it'll help. We have got other shots that you don't have to take as frequently, but they don't help with allergies or asthma. Okay, and then they-- Okay, and then if they say, wow, I want the one I don't have to take as much. Okay, this one might cause blood shot eyes. The other one doesn't cause blood shot eyes, which one do you want to do? Like it's-- So it's like A versus B. You always give people this or that, not like, okay, you've got five options. We could do jack inhibitors. We've got two of those. We could do, you know, do pill a mat. We could do-- Traveler, like here's the-- No, people cannot understand that. You give them one thing at a time. The other thing that that always reminds me is how-- And I'll be interested with you to do. I'll say what I do first. So when the patient's like, what would you do? Because some people are like, well, I always tell the patient that what I would do is irrelevant to what they should do. And the blood-- I always tell them, look, I'm going to tell you exactly what I would do, but just remember, this is like being at a restaurant. Like if we were out at a restaurant, I'd been there before and you hadn't. I might be like, oh, I would get the salmon here. And you could be like, I hate fish. So yes, the salmon's good here, but it's not what's best for you. Say the same thing with the drug. And then I say, OK, so here's what I would do, but I'm not saying that's what you should do. How do you guys handle it whenever a patient says, what would you do? I tell them what I would do. OK, Patton. It comes up with, like, kids. What would you do? Accutane, biologic, whatever. I mean, not like, I don't really see kids, but it's like, you know, with like 18 or 20 year olds of parents. We'll ask that or like, you know, yeah, people will ask that. I will tell them what I would do. Patton, what do you do? Kids with Accutane, that helps. Like, hey, my kid had this. This is what I did. And then I think they're like, OK, yeah, then that's what I want to do. Man, I don't know. I mean, in the instance of a topic, I'm like, the, the shots are safer. There's one that was FDA approved before any of them. And like, total conflict. Like I do the regenerative does pay me for like BP stuff. But so, but so you should know that. But I'm like, the shots just like the safety profile. You don't have to get blood work. You know, I don't care if your kidneys fail or you're like, it's just in so many patients are better and so many patients stay on it because it changes their life. And I strongly, strongly recommend that. Are you good with that? Or do you want to hear about other things? That's how I start off my AD. That's it. And granted, like, yeah, I'm pushing them towards Dupy. But I think there's good reason to do that. Yeah, there's just, there's the most patient years of exposure. Let's say like here are the risks that we know. And you know, I think, you know, when I read the package insert of Jack inhibitors for atopic dermatitis, it pretty clearly to me says you should start with a biologic. And that is a reasonable. It's hard for me to, unless somebody says like, I really can't see giving myself like I need olphobia is the primary thing that like I'll use Jack first line. If somebody is like, I can't give myself a shot. I don't want to give myself a shot. I don't want anybody else giving me a shot. I don't want a shot. I'll use a Jack first line there. But I agree. I mean, they are immunosuppressive. Whether they have other side effects or not, I don't know. But they're definitely immunosuppressive. And the shots are not. Yeah, I have come to appreciate like within the last three months that I never really thought about before. Wait, I mean, I do know beauty. No, I've always appreciated beauty. OK, that's a weird thing. Is that dupe, you know, hurts. Like I have talked to people that are like, yeah, I have given myself shots of other things. Dupy is very, very painful. Yeah, compare compare compared to the other drugs. Very true. I think dupe and then the I think, Lebri's less painful, Traylor, I'm not sure. And Nemo just done hurt it all. So that is my one like downsell with dupe is like, you know, here's what's been around long. And I will say this shot hurts. I've talked to people and they're like, man, it really hurts going in. Yeah. I thought that was interesting. Yeah, fair. Fair. All right. Well, that's that's it for this week's episode. I want to thank our listeners for joining us. I hope you learned a few things. If you laughed once or twice, mostly we're hoping you're planning to join us next week. And until then, I'm Matt Zyrus. I'm Tim Patton. And I'm Laura Ferris. And we are Derms on drugs. [BLANK_AUDIO]