Dermatology Update: The New, The Old, The Common and The Rare

Welcome to season two at Derms on Drugs of 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, hitter miscomedy, a Matt Zyris from Doc's dermatology in each week. I'm joined by my residency buddies, Dr. Laura Ferris from the University of North Carolina and Dr. Dim Patten from the University of Pittsburgh. 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 cutting edge of dermatology and you'll actually have fun listening. New episodes drop every Friday on scholars in medicine, Apple podcasts, Spotify and other major podcast platforms. And a reminder that there is a video component that has some of the key figures and tables from the articles we talk about. This week we've got another one of our patented six pack episodes where we are going to talk about the stuff that has caught our eye in the literature is the most interesting and useful over the last few weeks. Let's go ahead and get into it. Dr. Ferris. All right. So I am going to start with a paper that was pat published in JAMA Dermatology and this is by Breglio at all. And this is looking at everybody's favorite vitamin, niacinamide, sorry, nicotinamide, niacinamide, nicotinamide, vitamin B3. So this was, you know, we've had a few papers that have been small, randomized, controlled trials looking at nicotinamide and the prevention of skin cancer. And you know, the first one like made it into the New England Journal of Medicine, then there has been some, you know, thought that well, other studies have maybe refuted it. But this was one that was looked sort of done on a really big scale. So they looked at 33,000 patients from the VA system. So what does that mean? They're all going to be like male and older and they're mostly going to be white, but that's okay. So they pulled 12,000 patients. So first of all, they picked people who had had at least one skin cancer. And then they pulled, they found 12,000 who had been on at least 30 days of nicotinamide 500 milligrams twice a day and then did like propensity score matching. So matched controls about 21,000 people. So then what they could do is then look at, you know, incidents of skin cancer over time. So who are these people? Me and age was 77. They were 98% male, 95% white. They were pretty similar in terms of those demographics. The nicotinamide group was more likely to have had CLL, to have had a solid organ transplant, although this was definitely the minority of patients and to have been had acetretin treatment in the past. The median number of skin cancers before starting nicotinamide was three, but 15% of them actually had 10 or more skin cancers before starting or before going into this cohort. So what's the top line result? So we make sure here. So again, they only looked at people who had had at least one skin cancer. Yep. Okay. Yeah. So you couldn't, it wasn't like anybody went on nicotinamide for anything. So I think the idea was like they were hoping that actually like they were on it for skin cancer prevention. All right. So top line result, 14% reduction in skin cancer risk and the nicotinamide group versus the group that did not receive it. So you know, that's not insignificant given the size of the VA, the number of non-millanoma skin cancers. What really drove it was cutaneous quam muscle carcinoma is 22%. Reduction overall, there really wasn't protection from basal cell carcinoma. That was sort of overall. However, if you looked in the group that started it early, like they only had one, there was actually a little reduction there. So biggest bang for your buck was, you know, if you started it right after you had your first skin cancer and that group, the risk reduction was 50%. So I thought that that was interesting. In the solid organ transplant recipient group again, it was like a couple percent of the population. They did not see a significant benefit. But if they looked at people who started it, who had had a solid organ transplant, if they started it once they had just one or two skin cancers, then they actually had nearly a 50% reduction in subsequent squamous cell carcinomas. So I thought this was helpful. So this was good. They matched to the number of past skin cancers, the timing of their primary skin cancers. They broke down the results by like, you know, did they start it after 1, 2, 3, 4, you know, 10 skin cancers, etc. So, you know, I think like the take home point is if you're going to do it start early, you get more bang for your buck if you start after that first skin cancer. And so, you know, I thought that was good. It's the VA. So, you know, what are the limitations, right? So you don't need a prescription to start nicotinamide. Anybody who's worked in the VA knows that the vets want a prescription for absolutely every over the counter medicine like Tylenol that they might possibly take. So you actually probably have some decent records where as if you tried to do this in one of our health systems, people might not put down the nicotinamide. So probably better, you know, accounting for it, but you know, their point was even if people were taking it outside, that should bias you toward the null. So if they didn't get it through the VA, you know, you could have people in the control group who were taking it, but that should bias toward the null, not sort of bias you toward nicotinamide being productive. So have you, are you guys already using this? Have you been, do you, do you routinely recommend nicotinamide to everybody with what? Like, what is your thing? I was and then I kind of was like, well, then the transplant study didn't show it worked and those are the patients I worried about. Then I was reading other studies. I was like, maybe I, maybe I shouldn't do this. And then, you know, I think the problem is then when I do it, I'm like, oh, God, you've got like 85 squames. I mean, try nicotinamide, but that's actually the wrong approach to take. You should be like, you've had a skin cancer. This is a vitamin. It's pretty safe. You know, why don't you, why don't you do this? Yeah, I am not as good as I should have been and I think I'm actually going to be even better now. I mean, I had a guy yesterday who had like history of AK's, lentigienes, never had a skin cancer. And he was just one of those guys like I like to keep a close eye on things. I want to keep coming on a regular basis. And I actually brought up nicotinamide to him. I mean, right? If you started after one and it's better, maybe if you started before even get one, it'd be even better. But when I had high enough risk, yeah. Yeah, but then I kind of want to say we're going to be like just recommending this to everybody because it's in a ton of the skin health supplements along with collagen and vitamin C like nicotinamide is in a lot of those overall. This is for your healthy skin. We're just going to be recommending this to everyone. Is that me? Yeah. I mean, I thought this paper was helpful. The other thing my pearl that I do, I'm better at this with skin cancer patients. Look at their med list and make sure they're not on hydrochloroethyazide. That is a so terrible at that too. Yeah, I've gotten better at that. So, clear association with cumulative use of hydrochloroethyazide, new scue misocarcinoma risk. So I do a better job of looking for that. But now I'm going to like, I have a resolution. I'm going to do both. One of the things that's always interesting to me is why are all the studies 500 BID? Why can't it be 1,000 once a day? People are much more likely to take 1,000 once a day than they are to take 500 BID. I wondered that too. The other thing you said nice in a mind at the beginning then said, oh, no, nicotinamide. Those are the same. Yeah, they are. They're the same thing, but I have a case to put up there. But then we'll give niacin, which then yes, causes flesh and flushing. And nicotinamide makes it much more clear. If you just say nicotinamide, then they're not like niacin niacinamide. But yes, they are. They're BID. I had a patient who we worked about the wazoo for flushing. And she bid, you know, I'm a niacinamide and blah, blah, blah. And I finally had her bring her meds in and it was niacin. And she was like, oh, no, the pharmacist told me that was niacinamide. And I was like, oh, yeah. So yeah, that's a, it's worth being very, if you get somebody who's flushing definitely, if they say they're a niacinamide, definitely make sure of that. All right, let's, let's move on. Pat, and what do you got? All right, my first six pack was from the July. August, 2020, 25 edition of dermatitis titled new and emerging pharmacotherapies for pruritis, a systematic review and network met analysis speaking of network metasus. By Lee at all, authors wanted to compare the efficacy of medication studied to treat paritis using just one measure. And it was the four point reduction in the peak paritis numeric rating scale. Also sometimes referred to as ppnrs. The numbers are confusing. Figure one says that 48 studies were included. But then table two says only 31 and it seems like they finally settled on 20. and it wasn't 100% clear how they whittled that down. 15 studies in atopic derm tendons rise is four in pyroagroinodularis. So, you know, four studies in a meta-analysis is that helpful. Figure three has kind of three separate fours plots, one for each disease. For atopic derma patacitinib was the most effective itch reducer. I wanna say that they combined the 15 and 30 milligram dose data. That's what I gleaned from going through the supplementary material, which is what dedicated and conscientious podcaster does, we go through the supplements. Avroberry, Dupy, they were around the same lebri and trail-o rounding out the rear, so to speak. For psoriasis, 10 studies were evaluated, exochismab, Ustekinumab were the winners. They didn't go up against like the big boys, like the 23s weren't really in there. Did they not focus on itch in their studies? You guys did clinical trials for the 23s, was itch not a huge component of that? - I feel like that's a question in all of them. But I don't know, I don't remember. - But maybe it just wasn't NRS, like they didn't do NRS for, like that was what they, the, so I don't know. For Pyrago Najalera, Pyrago Najalera, you know the trail with that word, Pyra, pruratus was I saw the P and then the U in the R. And so for me that was pure. And then you tried to throw an R ahead of a P U in an R and you can't say, you can't say prurir. And so I just, I ignored the first R and went with pure, pure, pureitis. That was how I said it, because I just couldn't get past the fact that really just ignore the second R and think of the word prune. And that's pruritis. But man, that, that I really had to rework my brain network. - Just for anybody who's wondering, we have been making fun of Pat and since residency for the way that he's always said, pureitis. - Well, I just wanted to explain why. I think maybe you've gone a little bit more sympathy. - You didn't need to explain why. It's just that you're an idiot. - Oh, that's the short story, fine. All right, I'm just gonna call PN. Can we just go with that? - Okay. - Nimo was the most effective at introduction. Doopie, next most effective sir Loppetent. And I'm sure if I'm saying that one right. And Vixirilla Mab, so Sir Loppetent was a neurocine in one receptor blocker, substance B, binds to NK1, we itch, they halted that trial. Vixirilla Mab, it's an oncostatin em receptor blocker. I think they halted their PN studies as well. So I, this didn't really add much, right? Oopa's good for AD. Xochismab being like, I guess if you have your itchy, itchy, psoriasis patient, maybe Xe. - I think that's-- - That was a hundred things for a while when it came out. Remember the itch of psoriasis? I feel like Xochismab really like pushed that when they came out. So I think they asked better and more questions about it. - So yeah, my sense is that Risen Kidging Mab is probably just as good for it. And maybe they just didn't look at it. I don't know. - So I am a, I'm gonna use this as my moment to wax poetic about itch a little bit and itch measurement because it drives me nuts, right? So when you look at the studies about NRS scores for psoriasis and atopic derm, they say that psoriasis is just as itchy as atopic derm, right? And that is just crazy talk, right? It's crazy talk. The patients with psoriasis don't complain about itching like patients with atopic derm. And here's the reason why. So if I said to some of it, it's easier to think about it with a pain scale. If I said to somebody who's never had a major injury in their life, nothing terribly pain was ever happened and I squeezed their finger in a little vice and said, okay, rate that on a one to 10 of how painful it is. And I squeezed it really hard. Oh, oh, oh, oh, oh, oh, oh, oh, oh, oh, oh, oh, oh, oh. And let's say then though that that was a 28 year old woman. And then after that she got pregnant, nine months later, natural childbirth, no pain meds at all. And then after she gave birth, we gave, we came back and gave her the same test and squeezed it again. You think she's still gonna call it an eight? No, she is not, right? So any kind of a scale like that is very susceptible to anchoring. And right, the itchy issue can imagine being is based on largely on how itchy you've ever been. Any of these 10 point scales, I'm very suspicious of because I, you know, I don't know if most people know this, that the pain 10 point scale is the main bad guy in the world of like what caused the opioid epidemic? Forget Purdue pharma. If they, if somebody could sue the 10 point pain scale because at one time it was, if somebody said their pain was a seven, like quality indicator was you gave them an opioid, right? And like we should, like where you make, like you have to pick which face looks the most one. I think those guys are, they should go to jail. And this is why for both itching pain, they should be functional questions, right? So for itch, what I basically what you wanna say is, okay, like is, are you so itchy that like you notice it, but it didn't really bother you, you can go about your day, are you itchy enough that like you're thinking about it a lot, but like you can still do stuff, or are you like so itchy that like you're just thinking about it all the time? Like it's hard to, like cause it should be functional, right? So either no impact on function, some impact on function, or a lot of impact on function, right? Which is why like this is that is the sleep disturbance, right? Is it like, that is a very reasonable, yeah. Scratchy things, the things that you know, measure if you're scratching. You should give everybody poison ivy and scabies the month before they go into the study. And then it'll be like, how would she are you? That's, you might have some trouble getting that through the IRB. You think so? I do not think so. Maybe I'll be in Canada, maybe Drucker can do it. Yeah. The biggest thing that I would say also about this that was kind of of interest to me, you know, that Nemo is so much better for prognogilaris. But I don't think it was even in the network meta analysis for a topic dermatitis. Is that correct? That's correct. David wasn't included in the atopic term part, at least in the little forest plots they did. And I don't know, you know, they talked about, oh, there was a really quick onset of itch improvement with topical rexolidin. But for whatever reason or another just didn't make the final cut. And I don't know if they explained that well or didn't. Yeah. It's a, it's hard any, it's always hard to compare anything that's topical and systemic. But you know, I'd say this was, you know, the, the psoriasis ones I don't care. I think that was kind of silly to put in. But I would say in general, this, this was in line with, with my experience, of which drugs work the best. Nothing really, you know, okay, great. Neemolism abs probably the best drug we've best biologic we got for itch. Jack inhibitors are probably better than Dupy Dupy and the other biologics for itch. But you know, okay, great. That's what we got. Yeah. Yeah. Wasn't, wasn't anything earth-thrattering? Sorry. Sorry, man. That's, I'll, I'll, I'll forgive it. I'll forgive it. Let's, let's jump on to mine. And so I am now doing a couple of articles to this week instead of my normal three. Number one was interesting. So a randomized double-blind trial of Oromanoxidil 2.5 milligrams versus five milligrams for male endogenic alopecia. So title of the study, Oromanoxidil 2.5 milligrams versus five milligrams for male endogenic alopecia, double-blind randomized clinical trial. This was published in JAD online so far. What was interesting is that whenever you look at the dermatologist assessments, there was no statistical difference between 2.5 milligrams and 5 milligrams. However, whenever you look at self-assessed clinical improvement and the patients were blind at as well, there was a significant difference. And it was interesting. So when you look at, you know, how many patients said they had great improvement, the people who got 2.5 milligrams, it was 46%. So about half, people who got 5 milligrams, it was 72%. So about three quarters, meaningful difference. When you look at great improvement from the dermatologist perspective, the Raiders perspective, they said that in the 2.5 milligrams, it was 25% and in the 5 milligrams, it was 32%. So just a big discordance between the dermatologist assessed improvement versus the patient assessed improvement. That was one of the biggest things that I took away from it. And also that this was a relatively small study, so 50 people in each group. I would bet that if you redid this study with 200 people in each group, there would be statistical, statistically significant differences. That was my other takeaway from it. But, you know, so it suggests to me that the 5 probably does work better, but that the 2.5 works pretty pretty well also. When you guys use orminoxidil, what do you usually do for dosing? Start with males, 2.5. With females, I start with 1.25. Okay. Pat and Sam. How often up to 2.5 in females? And I had one female patient, I think we talked about this before. She wanted to go to five because she was tolerating it. And she wanted to see if it would be better. So I took a female patient up to five. I routinely take guys up to five. Do you see much hypertricosis at five, fuzzy faces? Now, that's just not a frequent reason for discontinuation. It's not like I've never stopped it because of patient calls and they're like, no, they don't want to try it. I'm seeing them for the first time and they don't want to try it because they got it with it. But it's not a lot. It's not high. It's got to be less than 5%. In men or in women, are you talking about? Like, well, nobody, no guy is going to complain about that, I don't think. But females, yeah, it's less than 5%. I just don't get that complain all off. I see it in women. Maybe I have horrible follow up and they're quitting it and I don't. No, it may just be the patient population. I gave one woman when I first started using it. I was like, didn't know where to stop. And I think I went up to like 7.5 or something and it's poor woman. Like came in with comfortable hypertricosis. It was like, sorry about that. Go back down to half a pill. But yeah, now I do see it in like, you know, sometimes it's just like, it's just like a little bit kind of along the lateral cheek. It's like, I have to ask about it or look for it. But now that I've been more diligent about that, I do see it. Yeah, and I mean, then don't care, right? If you're going to shave anyway, you don't care. Some like it. Well, unless they're getting it like on their forehead or something, I mean. No, but in men, it's always in the beard area. I've never seen it on like the forehead. Pat, and how long have you been taking it? I don't need such things. Yeah, it's obvious you think so. I had a hair transplant in Turkey. All right, let's go out to my second article. This is just a case report. But it was a premalast in the treatment of pitoriasis like anoidis, et varial laforma secuta, a case report, pretty like pretty bad, believe it. And initially treated with 80 milligrams a day of prednisone plus atheromycin, 500 milligrams a day, then they stopped the steroid after a week due to steroids, I had to fix, put them on acid, treten, that didn't work. Then they put them on a premalast and it worked really well. And the main takeaway here is I'm always looking for new reports of PDE, systemic PDE4 inhibition working. So now, reflumalast. Yes. PDE, a go to drug for pleva and probably for PLC as well if it requires treatment. That was my takeaway there. I cast should be changed to derms on reflumalast. Exactly. It's not a bad idea. We really do talk about it every day. I want to make it sponsor us. I doubt it since it's $6 a month. All right. I'll take anything. I'll take five cents. Okay. All right. Let's move on. So Ferris, what's your next article? What do you got? All right. My next article was just came out in the Lancet and was this was just special journal. It's very special. It's a very European kind of experience. It was also presented at EADV. One stale oral, Icochricin reverse was placebo. And one stale oral, de-cravicinib and patients with moderate to severe plaque psoriasis. This is iconic advanced one and two, two phase three studies. Linda Stein gold is the lead author on this. Okay. So what was this? So this was basically a head-to-head, you know, active comparator study of two of them. So hang on. Trying to get my numbers in front of me. Okay. Iconic one and two over about 1200 adults, moderate to severe plaque psoriasis. What does that mean? 10% BSA, IgA, three or more, Pazzy score, 12 are more. 20% about 20% of the patients were severe at baseline. Most of these patients not surprisingly in this day and age had tried systemic therapy, two thirds. There about 25% were biologic experienced. And so co-primary endpoints were Pazzy 90 and IgA zero and one week 16. So Icochir kinra, 70% of patients achieved IgA zero, one versus 10% on placebo. And if you look at and then Pazzy 90, which was the other end point versus placebo, like 55 or 57% versus like 1 to 4% on placebo. So we already kind of knew that from previous studies. Now, how does it do, how does Icochir kinra do compared to do kravacitinib? So Pazzy 100 was 30% in the Icochir kinra group versus like 12% in the, in the do kravacitinib arm. And Pazzy with, you know, with Icochir kinra and do kravacitinib, some keep improving through week 24. Safety, so you actually had active comparator to safety. So they were numerically lower in the Icochir kinra group compared to the do kravacitinib group. So about 50 adverse event rates of like 57 versus 65%. So, you know, I think like if you want to do the non-official network meta analysis, we know that do kravacitinib was superior to otesla and head to head studies. So I think that this would say then, you know, we can say Icochir kinra once a day is going to be superior to both otesla and do kravacitinib. The interesting thing is going to be we've also got two second generation, two inhibitors coming out the Zasso sit nib and I forget the name of the other one and to see how those and we're not going to have any head to head trials of those, but we should have head to head trials of those versus do kravacitinib. Yeah. So it should allow for a assessment of, you know, how do they compare to Icochir kinra. Right. So just a little reminder, what is Icochir kinra? It is a peptide that is taken orally that binds to the IL-23 receptor. So it's a pathway blocker, but it works a little differently than the, you know, skyrisee trumphia. So, you know, I think it's interesting. I'm very interested to see like, you know, what it's like when this drug comes to market. You know, it's an interesting technology. We're going to see this. So, you know, I was looking a little bit at the history of it. So, you know, it started out as a peptide that had like enhancers in it that you, it started out being looked at just for like IBD, right? So you can imagine it's going to sit in the gut and actually they do have IBD studies ongoing for this drug. So, but it turns out that like they, when they optimize the drug, they don't even have to put anything in it that makes it, you know, preferentially go into systemic, into circulation. It's actually just that the drug is absorbed and goes right into circulation. I like the idea that, you know, just like when we talk about like nanobodies for HS, we think about small molecules might be good for penetrating tissue that's inflamed. And so, you know, I'm really curious. I'd love to see like if you labeled this peptide, does it penetrate into the skin differently? You know, I think it's going to be, I think it's really interesting. So, and I think it should be something we can use across diseases. And then to that effect, like what's it going to do in the joints, right? So maybe getting into synovium is going to be easier if you're a little peptide versus a big antibody. And is this going to be like an IL-23? Again, this is all complete speculation. I have no idea. But, I always feel inflamed tissue has higher vascular permeability to begin with. So, I always feel like that whole small molecule might get into the tissue better. It doesn't always seems like baloney to me. Maybe in the joints. How about non-inflamed tissue? Yeah. And maybe synovium might be different as well since that's in a vascular space. Right. Maybe. Yeah. I don't know. So, I think the big question is going to come down to patients want to pill or to patients want to shot. And I think that's like a big topic that companies are really interested in and looking at. I think to some degree want to have that narrative like to patients want pills or shots. I think that there's patients who want pills and there's patients who want the least frequent dosing that they can get. Yeah. It's not just like a shot, right? It's like once every three months, you have to remember to take it. Right. Because of every day. So, it's going to be tough. Fair. Fair is just I wanted to give you a heads up that after the end here. I'm going to be asking you what was the biggest scuttle but at the EADV? Was there anything that people were like, who are really talking about? All right. Well, I was barely there. I flew in, gave my like my flight got delayed. I was on the ground for like 24 hours. So, I'm not scuttle but. Okay. Absolutely. it up alive. All right. All right. Pat, what do you got? All right. Second six pack was September 2025 edition of allergy asthma and clinical immunology was titled "Ava Prittin and Reduces Symptoms and Mass Cell Burden and Systemic Mastocytosis." I have got to stop letting you pick your own papers. This is so interesting. Listen up people. Macchulo-popular, cutaneous mastocytosis has always been kind of interesting, right? Impressive clinical findings. You make the diagnosis with a biopsy. You work them up for systemic serum, triptase, CBC, LFTs, maybe send off a C kit. And it's all negative and then literally there's nothing you could do for the skin. Nothing ever worked for cutaneous mastocytosis. Well, now there is. So low dose, Ava Prittin and 25 milligrams a day. Is the S is a report out of Germany. Is that a drug that's on the market? Yeah, it's FDA approved to treat indolence, systemic mastocytosis, metastatic gastrointestinal stromal tumor that has the PDGFRA mutation. It's approved. It has a brand name. I don't remember it. Okay, but so we could send these people to like a hemalk doctor to get this. Yeah, so they talked about two patients and they had like sort of indolent disease. They had pretty impressive cutaneous disease. There's photos in the before and after. But they also had elevated triptase and they had systemic symptoms. And so it wasn't just like, hey, you have macular, popular, cutaneous mastocytosis. But the skin did get better. And I was just amazed at that. And so that's why I picked it because clinically it's very impressive for disease that literally we had nothing for these patients. And now we have something. I mean, their skin is kind of clear. I have a feeling, you know, the next person I see, I'm really going to be like, but isn't your stomach hurting too? And don't you have brain fog? And then I think this will end the endolence. And then I'm going to get them have a prittinid. Okay. I mean, I feel like everything I open, they're like, let's talk about endolence systemic mastocytosis. Yeah, that was a thing. I am getting emails once it's not I do compare this. I know you guys are going to yell at me. It's like the emails that I get every week for GP. I have seen one GP patient ever. I know that spesalism have worked really well. And I know that you actually want to give it subcue low dose long term because that spends more money. No, I think that's a more effective way to manage GP as opposed to waiting for them to flare. I'm just kidding spesalism. Don't send me hate now. But man, like the proportion of how many GP emails I get compared to how many patients I have, it's a million to one. Stop sending me GP emails. Wow. Million to one. That's a lot of emails. Okay. Yeah. I'll forward them to you. Okay. No, please don't. Okay. All right. So we had a new drug for even indolence cutaneous mastocytosis. All right. Good to know. Good to know. Are you going to really pick my papers from now on? No, I'm not on probation. No, that would take too much effort. And now that I know that it's it is a drug on the market, then I'll it's allowed. It's allowed. All right. So my next one was psoriasis and atopic dermatitis overlap pathogenesis and therapeutic considerations for the clinician. So it's in dermatitis. The senior author on it was Peter Leo who the dermatologist drugs know and love. And basically the takeaway here is, it's that they go through kind of the pathophysiology of, you know, is this a real thing? Right. So is is it that there's some eczema that has some psoriasis or psoriasis that has some dermatitic components where psoriasis form dermatitis or is it or eczema that is psoriasis or is are the people who really do kind of have both. And they're making the argument that there are people who do really kind of have both. And they're they're takeaway is that in somebody who's got real clinical manifestations of both diseases, our first line therapy should be a jack inhibitor. That the drugs that make the most sense, if that didn't work, if you think it's more psoriasis, you should go IL-17. If you think it's more atopic dermatitis, you should go IL-13. And then if that didn't work, you think about doing a combination therapy with an IL-17 and an IL-13. Essentially, the all common sense would be my main takeaway that if your main issue is, I just want to get them better, you put them on a jack. If you don't want to put them on a jack, then you think about, okay, which one do I think is more likely and you try a drug and if it doesn't work, you try the other class. And that if none of that works, you can either put them on both drugs or you can try a jack at that point if you haven't already tried one. But just in useful article, because this comes up a lot, right? Because then people. I think also, these are the patients I like, method trexate for sometimes. Cheap and it can work for both. I have seen patients where it's like, I remember one patient. It was like, you put them on, do picks in and they break on horrible psoriasis. You're like, all right, it's clearly psoriasis. They put them on, like, I don't know, humeraracosamtics and then they were like, examinist, you're like, all right, it's clearly a topic. I think the cytokine inhibitors are so targeted and polarizing that you can. you just sort of make them flip back and forth, whereas a little bit more. this is the time when non-targeted can be helpful. So, yes, the jack inhibitor is good. Sometimes, pathotrexate is still a useful drug, even though there are jack inhibitors out there. I think that that. I'm sure you could try a roflimolasmap. There you go. I was waiting for you to get on the right path. I knew you were a pathfirus. All right, Pat, in any comments? My experience has been that it's more often I'm looking at them and it's spungiotic, like, more heavily spungiotic. And I put them on dupe and it gets worse. Is that what happened more frequently with you guys? That's hard for me to say if I think of. I don't know. Yeah. I was just curious. Like, do you set. like, the psoriasis that becomes eczema-dus with a 17 or 23 or 12, 23 TNF? I don't know if I've really ever seen that. And it's certainly according to the literature, happens more commonly with I/O 17s than with 23s or TNFs to get an examinous reaction. That's interesting. Maybe I don't need enough of those. Okay. Okay. All right, my other article was just since "Obsulara" got approved just, I think, last week, down to age two. The article just came out, "Efficacy and Safety of Ruxilinative Cream and Children Age 2-11 Years with Atomic Girmiditis" results from true AD3, a Phase 3 randomized double-blind study, main takeaway actually worked even a little bit. this is milder, a day-topic dermatitis randomized double-blind and pseudo-trial, numbers were actually even a little bit better for IGA treatment success with kids than it was for adults. So 56% that number is more like 51% in adults, but really effective in kids. Obviously, the challenge is talking to parents about the boxed warning, and there is a little bit of systemic absorption. So we can't say like, "Hey, you don't need to worry about this at all." Like, "Well, it's below me, the blah, blah, blah, blah." Like, there is a little bit of systemic absorption. You know, is it enough that it should have any immunologic effects or anything? No. It shouldn't be. But there is some systemic absorption. And is it imaginable that if you use it over a big enough body surface area, there will be some kids who get a high enough level that it could do. imaginable. It's unlikely, but it's imaginable. So it's, you know, that's going to be the challenge just talking about the box warning, you know, with parents. You know, what do you guys think? You think you'll be using much. Abselura in the 2 to. 2 to 12 age range. I don't see. Try very hard not to see kids of that age. I. You know, that's a great question for. Because if you're putting it over that much body surface area, given that Dupy's approved down to six months, why on the world would you not have that little kid on Dupy? Other than they may scream their head off when you attack them with a needle every two weeks. But still, aside, my kids would scream and cry at me, and I didn't give them Dupy. So you're that just part of childhood. It can be a big like. There are kids who it's like a huge, you know, four-year-old, who you can't really explain anything to them, and it's just. No, I share an office with pediatric dermatologists, and so those kids do come I mean, it's heartbreaking. - It is, it is. Yeah, it is. - I mean, I laugh a lot, but my first response was, oh, that's really heartbreaking. - Yeah, it sucks. It sucks, yeah. - It sucks, man. - Yeah, it sucks. All right, well, that's it for our six pack for this week. I'm gonna sign us off here. So for all of our listeners, thank you for joining us. I hope you learned a thing or two. I hope you laughed once or twice, and mostly we're hoping you're planning to join us next week. Until then, I'm Matt Zyrus. I'm Tim Patton. - I'm Laura Ferris, and we are Derms on drugs.