[Music] Welcome to Derms on Drugs. A video podcast brought to you by Scholars in Medicine. Derms on Drugs is where cutting edge derm meets so, so comedy. I'm Matt Zeyers in each week. I'm joined by my residency buddies, Laura Ferris and Tim Patton. 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 cutting edge of dermatology and it'll be the most fun you've ever had while learning something useful. New episodes drop every Friday, so make sure you set your calendar. And let's go ahead and get into it this week. We've got one of our patented six pack episodes where we're going to talk about six of the coolest articles that we've seen recently in the literature. The same way we would talk about them if we were sitting on Patent's back porch having a six pack of beer. So I don't know if Ferris drinks beer, but she's a little snooty, but Patent and I certainly would be. So Dr. Ferris. I have one who haven't saw me on blog, but that's okay. There we go. There we go. That sounds right. Yes. All right. So I'll start with my first paper. So this was in JAMA dermatology, immune checkpoint inhibitors and field cancerization and keratinocyte cancer prevention cocks at all. So this was a clinical trial that was really not an intervention to treat AKs with immune checkpoint inhibitors because that would be a little bit over the top. But what they did was they took 23 adults who were immunocompanied who were starting a P.D. one or P.D.L. one inhibitor for another cancer and who happened to also have AKs. So these are people who are going to have it for at least six months. They had to have AKs on their forearms. They couldn't have had like recent topical five FU or anything like that. And what they did was they basically did account a forearm AKs at baseline and then at months three six and then 12. And so these people were pretty, you know, AKE. They started with about 47 mean number at baseline and then it went down to 14 at 12 months. That was statistically significant. So, you know, AKs, that's nice that they decreased the numbers of AKs. How about keratinocyte carcinomas? So what they did was they looked in the 12 months before they started their checkpoint inhibitor and the 12 months after they started it. And their, you know, total numbers basically decreased from 42 across the 23 people in the 12 months before to 17 in the 12 months after. So the number of, you know, SCCs decreased from 16 to five. These really didn't reach statistical significance, but realize this was 23 patients. So kind of interesting. You know, are we going to start doing this for AKs? Like I thought this clycery was an expensive AK treatment. Like I can imagine that a PD1 inhibitor is probably going to be a really expensive AK treatment. Maybe probably not, but like, I mean, maybe at some point, like in those terribly sun damaged, you know, everything's in SCC or an AK maybe you only need to, you know, maybe you don't need six months, maybe you need a dose or two. You know, these will eventually go biosimilar. This cost will come down, you know, maybe that would make sense. So I thought it was interesting. If you look at the picture, there's a nice photo in the, you know, in the, as a figure. I mean, you could see markedly improved AKs. Did it, did it affect their BCC numbers to the same extent as the SCC? Like I think of BCCs is pretty non-immineogenic. I don't know if that's true, but that's why I think of them. Yeah, it's interesting. If BCCs, they have a high tumor, mutational burden. I think that the biggest reduction was actually in squading the cell carcinoma. So I have to go back and look at the actual numbers. Did it say anything about if there was any correlation between adverse of the, so, you know, I think of with with a mikwamad, right? Or customer trying five, a few other things, and I think it was immunotherapy for AKs. I think of it as being the worse their symptoms are the better it works. Or did they not really even talk about like did their AKs get inflamed? Or did they just go away? They just went away. There wasn't a lot of inflammation. So it sort of looks like it's mechanistically different than what we see, you know, remember in residency, because like you don't see a lot of people getting, you know, systemic five, if you anymore, but remember, we would see patients who we get put on systemic five, if you for like, have neck cancer and then they come in and their AKs were all let were all lit up. It seems like it's a little different from that. So it looked like in the photo and maybe I was making this up. Didn't it look like he was developing bit of Lego as time went on? Did they, did they do any sort of association of you got a better response? It was probably too small of a study, but did you get a better response if you had like a cutaneous side effect like you do with maybe, you know, like melanoma, things like that? I don't think that there was it was powered enough to see that all that I really, and I have to go back and look at the paper again, but what I kind of noted was like the adverse amount profile looked like every adverse amount profile. And you know, PD one inhibitor studies. Big drawback to treating AKs. Now you have diabetes and adrenal insufficiency and hypothyroidism. And you may have died from colitis, but otherwise it's all good. Your skin's not smoother. Yeah, most most common adverse events were rash of 30% of patients had macular, popular rash. One person actually got bullies, Pemphagoid in the study. Yeah. And they didn't really correlate it. There was no difference in the clearance of AKs and those with cutaneous versus noncutaneous adverse events. So that's right. The outcome that they used was did you like they sort of said, like good response was greater 65% or more of AKs cleared. You know, not good response was less than 65% and the people who had cutaneous adverse events weren't more likely to clear their AKs. Okay, we're about to give you guys a $3 trillion idea here. You ready? Okay. Yeah. Topical PD one inhibitor. Could have a tube of that stuff for $24,000. And we get ready for your AKs. Yeah. So I think it would have to be not an antibody. That's not going to do well. Which is what these are. Oh, I didn't really feel like you can have inhibits small inventory RNAs that could do it. So maybe we need a cosmetic chemist back. Okay. All right. Pat, let's let's move on to article number two, Pat. All right. So I did a intradermal Botox for melasma. It was intradermal botulinum toxin A for melasma, a randomized split phase study trial and in vitro study. And it's anti-malanogenic effect. It was by Thann. No, I got this. Thannis Sarnixorn at all. And the January, 2012 edition of Derm therapy. It had two main parts in vitro data of abobotulinum toxin. So this is this board effects on melanoma cell line and the clinical trial data details of the M.V. Tro stuff. Basically, it seemed to decrease UVA induced melanin content and tyronosinase activity. And yet it was not cytotoxic for the clinical effects. 12. Did they have any explanation for how that like I think of both the botulinum toxin as so. I don't remember what the hell it does. It cleave something. It's the yeah, it prevents a subtle colon release from the neuron. So a subtle colon doesn't go and bind to the neuromascular junction. Right. I'm the same way. I was looking. I mean, these cells do have if AI is correct. They do have the capability of releasing a subtle colon. And then I'm like, well, but is that so does the acetylcholine then bind to the cell and make it make melanin? I don't think they know. Yeah. The mechanism here. Okay. I mean, I think they're like, well, maybe Botox has tyrosinase activity, like every other thing that can potentially lighten the skin or not tyrosinase, but inhibiting tyrosinase. Yeah, that's that I thought the same thing. I'm like, why would this work? If you put Botox in with a melanoma cell line, why would you expect any effect on these? And I think they kind of were like, maybe it does this. Yeah, they didn't really get into it. Okay. Is it like the release of like low granules or something? I don't know. Like, yeah, I don't know. Transport. Yeah. All right. I don't want to go into details of that because I didn't know the details. So let's move on. For the clinical effects, 12 women were enrolled and they received disport on one side of the face and normal saline on the other. Constration to Disport was 66.67 units per mil. That seems like the similar dilution for if they're doing it for fine lines and wrinkles. It was injected intradermally. You would achieve a two millimeter wheel and injections were placed two millimeter apart. So three months, they had different
measures of malasma, the MAZI, the PGA, and patient satisfaction scores were all statistically significantly better for the side of the face treated, but this board compared to controls. So now, right, we talked about skin-lightening agents for malasma. We have hydroquinone, our mutant systemine, licorice, tretenone, vitamin C, caujic acid, thiamadol, four-end butyl resourcinol, azaleic acid, tranixemic acid. So we have more things to treat malasma than melanoma, and no one should ever have malasma ever again. That was my trick. None of them work like shockingly well, right? Well, yeah. I mean, like, they all scored facial drooping, right? Yeah, they all scored well, but you look at the pictures and you're like, it's a little bit lighter. I look at the pictures and it was like the pictures where you're like, I think that's just blurry. I think that's blurry. But they did use, you know, scoring and people, the assessors were blinded to treatments. Was I blown away by the pictures? No. I mean, given that we have 37 other things to lighten the skin, I think Botox is way down on the list for me because, right, you will get a droopy face like Ferris when she got her rosacea treated with Botox. I was a good residency story. I did try half of my face treated with Botox. Yeah, you didn't have to. It did not work for the rosacea. I did have facial hemiparesis. The longest acting Botox I've ever had in my life. When you didn't have to count my scratching their ears. I did not. Yeah, just do that. And then I published myself. It was good. Did anybody make you wear a collar of shame? No, fortunately. I couldn't need a sandwich for like six months because I couldn't actually like open my, get my lip up enough to eat. The food would just fall out of your mouth. It was really attractive. It was very attractive. Never to be done again. All right, all right. We're moving on to our next one, which is I got to say, this is an early contender for worst article of the year. And so title is article Unmet Needs of Effective Advanced Systemic Therapies in Moderate to severe atopic dermatitis patients in the target derm A D registry. And the main takeaway for this article is I am going to be ignoring everything that comes out from the target derm A D registry because this data is just crazy. It's ridiculous. So the takeaway was that that do PICSIN doesn't work. And so their takeaway was that if we look at how good their rash is doing, IGA times BSA. So VIGA times BSA, multiple studies have shown that that's a good determinant of efficacy. According to that, half of people did not improve on, on do PICSIN. And when I say this is ridiculous data, it is just so different from the clinical trial data and from every single dermatologist who's ever used do PICSIN's data, who's ever used do PICSIN. So in a half of them, they're, I'm sorry, I got, I actually was looking at the wrong thing. Two-thirds of people, their skin did not improve on do P. In terms of quality of life, half of people had lacked improvement in their quality of life whenever they went on do PICSIN for their monitors, a very top-it-ermatitis. When we look at itch mood and sleep, 85% of people did not improve. We look at depression, 80% of people didn't improve. We look at anxiety, 80% of people didn't improve. Like it's, I found this so unbelievable that I actually reached out to one of the authors and was like, how do you explain this? This is crazy. And their answer to me was, well, you know, germs are just satisfied with people not having very good results. I was like, this, like I'm speechless. Patients would come back to us and say, I'm not really much better. And we would say, yes, you are. I mean, that's just, it's, the numbers were just not believable. Is there, is there a problem with, like, what's the problem? The registry? What, I think- They want to severe it, baseline, so it's harder to measure it because it's like more of a real world setting, right? So, like, it was that what it was, like, where they not, like, washed out from other drugs. So there wasn't as much room as like when you put something in a clinical trial, and your numbers look really good, right? That's kind of what I was hoping for. Yeah. It just, it didn't, I can't explain it. And that's what, that's why it makes me say, like, if this is supposed to be a real world registry, this is not real world. Yeah. Like, it just, it didn't, and so it, it makes me say, however they designed this registry, like, it's, it's, any data that comes out of it, I can't, I can't believe it all because it, if it's saying that 80% of people, Dupy doesn't help their itch or sleep. That's just ridiculous. Yeah, I wouldn't, I'm the same way. Like, you just put the paper aside and say, I'd never reading another paper coming from this registry because this is clearly not accurate. Like, it's- Or the way that they measure that they looked at data here didn't give us like the, the, the, the real view into like, what happens? Like, we know when you have somebody who starts, like a lot of times when you put people in registries, they're your long-term patients, you know, they're on their third drug with you. They're not really washed out treatment naive. You know, they're maybe not that bad when they're switching over to Dupy, right? Like, that's, that's kind of was my take on it. Like, this is the issue with, you know, with registry data. So if you look at a lot of registries, they, registries like they pick out only those patients who have really severe disease. And that, like, the, you know, kind of clinical, like clinical trial inclusion level severity and then look at how they improve. But the reason that the people in so is essentially a hundred percent of people who went on advanced systemic therapy were people who went on Dupy. And that's because of when they were doing this registry, when they started enrolling people, it was before there were even other drugs available. So it wasn't like these were people who had failed lots of others. I can't understand. Like, I, and I don't also hate to say that I don't know how it's, it's so unbelievable. It's hard to believe it got published. Like, it's, it's just, I just, I don't get it. I don't, I don't understand. So yeah, that's the, that's my takeaway though is I'm not going to believe anything from the target Derm A D registry. Me either, man. I'm with you. Woo. Woo. All right, terms on drugs, not approved. All right. Let's move on to our next article, Dr. Ferris, what do you got? So this is switching gears. Frequency of androgenic cutaneous adverse events associated with Livo, Norgeastral, IUDs, and analysis of the FDA event reporting system database. This is Cousard, which is out of Cleveland clinic. So this was a paper where what they did, you know, we all think, I know that progesterone IUDs make like acne and hair loss. Like they have hormonal effects. They like, no, it's just local hormones, but we don't really believe that. We know that they make acne worse, right? So what they did, I thought was kind of clever was that they looked at spontaneous reporting of of AEs for these progesterone IUDs and for the copper IUD, right? So copper has no progesterone in it. And they said is there a difference. And so what they found was that if you look at odds ratios, if the copper is one, if you look at like marina and chalena and skyla, they are, they definitely have higher odds of having acne and alopecia and hair suitism. Now the little like kicker, like the odds were like, you know, sort of aggregating them all, like three times more acne, about six times more alopecia, about 15 times more hair suitism. The kicker of all this was that there was one that didn't seem to show it, which was Lilletta. And that is a 52 milligram, you know, IUD, leave on a gestural IUD, which is basically like identical to marina. And then the other two chalena and skyla are 19.5 and 13.5 milligrams. So they're lower and they have it, but for some reason, this one Lilletta was not associated with it. So, you know, I was like trying to look up and figure out why is this. You can measure the rate of release of leave on a gestural from each of these. And it's kind of the same, 21 milligrams per day with marina, sorry, 21 micrograms per day with marina, 20 micrograms per day with Lilletta, shouldn't be that different. You know, so I don't have a really good reason explanation for this. I just thought it was interesting. Maybe there's been, I don't know if one's newer and there's been more, you know, time for
reporting. I think they control for those things. But it does answer that question. You know, I'll, the OBGYN will be like, nope, there's no increased risk of acne and it does differ for IEDs for the, it's not just that you went off an OCP. There is a difference between a copper IED and a Livo norgestrol IED. And no, that was my, that was always my explanation. I thought I was so clever. I'm like, it's not the marina. It's that you're not on OCPs anymore. And they'd be like, ah, but now I can't say that anymore. I'll, I'll, I'll, I'm back to looking as dumb as I've always been. Oh, it just took one brief report. Yeah. Pretty much story of my life. Yeah. What's always interesting to me about these kinds of articles though is reporting bias. So, right, because if, if you got acne or hersotism or alopecia, you know, we, as the Derm, we always had, what did you, did you get a new hormone releasing? Oh, it's probably that. And then the patient calls and reports it to the FDA. Well, if, if somebody with a, got a copper one, I wouldn't be, oh, I would be like, well, wasn't your IED. And then the patient's not going to, not going to get online and report it to the FDA. It's, it's hard to fair it these out. But these are big numbers. I mean, you know, I agree. And the authors did say that was, you know, we, that basically made that exact point. Perhaps we just assume that it's not the IED when it's a copper IED. So, there, there is probably some reporting bias. But on the other hand, in, in all the years since these came out, I can't think of a patient I've ever, who's a, a female who I've seen and they've been like, oh, I got hormonal acne. And the top of my head, like, oh, did you get a marina? Like just because you heard it over and over and over again, never did somebody get a copper IUD before they, you know, got acne, wants that acne. So it's, it certainly fits. But, you know, I, I don't know. I'm not, I, I don't want to admit that patent might be right about the just coming off of the oral contraceptives, but I'm not going to rule it out yet. All right. Right about the scratching. I'm right about this man. Just don't, don't disagree with me. Pat next article, Pat, what do you got? As my second six pack paper was by Amar at algae, January 2025, British Journal with Dermatology, it was titled efficacy of duplibef for treatment, resistant grovers, a retrospective study single center retrospective chart review. The authors reported on 10 patients diagnosed with grovers on responsive to mostly topical therapies and treated them with dupli standard AD dosing. Did itching improve in everyone? Yes, it completely resolved in six of the 10, improved in two and wasn't reported for the other two, but their grovers completely went away. So let's just say that it got the itching completely resolved in eight of the 10 and improved in two. Did grovers go away in seven out of 10? It resolved. There was 0% BSA at follow up, which by the way, that's a weird way to judge grovers. Is it not? BSA. I don't even know how you did. It's mush together. The little. Yeah, it's like pinpoint. Yes, yeah. So I wasn't sure, did they just take a body, sir, area like, Hey, your whole stomach is covered with grovers. I'm just going to count your whole stomach is being affected. They didn't really go into that, but I thought that was so weird, because this is a retrospective chart review. Have you ever documented body surface and grovers? The grassy. The grovers area and severity. I do that all the time on microvers. Did you see? Are you going to have that? In three of the patients in whom it didn't go away, got better. Only one patient didn't really have a good response. He went from 15 to 10 BSA, which again, kind of weird. All of the patients with some sort of a topic. So maybe they had a history of asthma. One of the patients I think did have a history of a topic, Durham, had resolution of their grovers. You know, biopathy weren't available for every single one, but man, I mean, I grovers is pretty easy to clinically diagnose. So we have dupe for grovers. And I think, like, this is doable, right? It's not like this is a disease where you'll be like, I'm never going to be able to get dupe because you could easily call this just a manifestation of a topic. Which I think grovers, like I always thought of grovers as it was almost an irritant sort of contact dermatitis. And it just had a different morphology than your exemotist type of rash. It was just this popular sort of weird rash. But I always thought of it as yeah, pre-excessive and this is a reaction. I'm pretty sure they have now shown that grovers has some kind of a somatic mutation that affects your follicles. I feel like I read that somewhere a couple of years ago. I'll have to look that up and come back. But the chembiosis makes it I think harder for me that you see histologically to say it's just like a dermatitis, right? It's like histologically very distinct. A fair number of grovers. I mean, I think if you biopsy enough little lesions, you'll see sponge derm and eos on some of those as well. Now we understand why patent says it's easy to diagnose clinically because nine out of 10 cases diagnosed by patent were sponge sponge derm by up. Yeah, grovers. Grover. Right. So Emma Gutman is the senior author on this. So she's a very basic science-y oriented person. I can't think of why I could think of why do people help with the itch, but it's hard for me to think of why it would help with lesions going away. Did they do any you know, staining of the biopsies for I.O. 4 and I like was there any basic sciencey stuff in here? No, this is a very, very short. It was like a one page. It was it was a pretty lane paper for me to choose. Not that the results were lame, but it just there wasn't much to it. It was it doesn't make it lame. It's useful because these are I I didn't mean I phrase that wrong. Yeah, but it was a pathetic of me to be like, I'm just going to take this paper because it's like two paragraphs. After I did that J.I.D. paper, I needed a break. Will I use doopy for grovers? Of course. Why not? Well, and if they're itchy enough, it's you're right. You know, it's not unreasonable to call people with itch and a rash where you're like, I don't really know why you got this. All right, so there is a single nucleotide variant and ATP2A2 gene that is associated with grovers disease. There that's there is. Yeah. Yeah, so it's like a somatic mutation that for some reason localizes to like haryphalicals. Yeah, that's why you don't see grovers in young kids because you got to be old to get the mutations. Sure. And they were all C to G or G to A indicating it's potentially UV light induced mutagenesis. There we go. Unbelievable. What was going today? What was Grover's first name? What was Dr. Grover's first name? William. No. How's it going? Ralph. Ralph Grover. All right. Oh, you know, he actually did a follow-up study. So his original report was like in 1970. He was like six patients. He did like a follow-up report in the 80s where he took 375 patients with grovers and they did have, I think, a statistically significant higher history of like atopic diathesis stuff. So it was like in his paper that did seem to occur like atopic history did seem to occur more frequently in grovers. And it's interesting that they in this article almost everybody had some kind of an atopic homobidity. Yeah. Yeah. Okay. Maybe those are the people who respond. They did. I mean, everybody within atopic diathesis got better. Okay. All right. Let's move on to our last paper here. This one was mine. And again, this is this paper has such a great point. So it's discrepancies and patch testing, timing and outcomes, a retrospective analysis of the pediatric allergic contact dermatitis registry. So the, and this is by Sandler at Owl, but the senior authors, buddy of mine, Jeff, you who's at, I think he's at Harvard. And so they looked at this pediatric allergic contact dermatitis registry from 2018 to 24, 459 kids in there who had a positive patch test. And so the first, what they were somewhat looking at was how long does it take from getting dermatitis to getting patch tested? Essentially, they found out that people with skin of color, it takes longer to get patch tested. Okay. I kind of understand that just because it's a little hard to appreciate the air of them and some of the characteristics and maybe it's partially socioeconomic reasons as well. But what was that wasn't the interesting part of the article. The interesting part was this. So there are very, very few studies of outcomes with patch testing. So meaning there's kind of this assumption that oh, if I send you for patch testing and you're allergic to fragrance and there's fragrance in your body wash, that must be what's causing your rash. Well, there's very, very little data to back that up. And so most of the data, so one of the things have been talking about in lectures recently is that
Only about 10% of people who have a relevant positive patch test will clear. So about 50% will improve some and 50% won't improve at all. And so if your diagnosing contact dermatitis based on a positive patch test, you are misdiagnosing half of your patients only partially correctly diagnosing 90%. The gold standard for diagnosing contact term is people get better whenever they get away from something, right? So they looked at that. So this was an article where we did have this is the first ever data I've seen that's follow up data on pediatric patch testing and contact dermatitis. So of the 459 kids who they looked at, they stratified by improvement after allergen avoidance. In across the board, if you just look at all the kids, one third had no improvement, a half had partial improvement and then about 20% had complete improvement. So a little bit better than what some of the data shows in adults. But then if you look specifically at the kids with a topic dermatitis with a known diagnosis of that, numbers were pretty much exactly the same. A third got no better, a half got somewhat better and then 17% got completely better. So first what you would say there is 70% of them didn't have a topic dermatitis, 17% of them had contact dermatitis that was misdiagnosed as a topic dermatitis. But then the other really interesting thing, so there's a lot of discussion over the years about do people with a topic dermatitis or are less likely to have contact dermatitis? So there are a number of studies looking at race of positive patch tests and people who have a topic dermatitis and they've been kind of across the board, some have showed more, some have showed less. But the takeaway here is again, if you're using a positive patch test, you're generally going to be wrong because when you look at the odds ratios, kids with a topic dermatitis versus kids without, if you're allergic to fragrances and you had a topic dermat, your odds ratio was only 0.3, so 0.29. So 70% less likely to get better, meaning that probably 70% of the cases were false positive because you had a topic dermatitis in a bad skin barrier. With antimicrobial and preservatives, things like from out of hide and I so thysole unknowns, the odds ratio was 0.44, that was not statistically significant but still a pretty decent number. But then surfactants, so cocomitabral will obtain, which has been put out there as that's the one that's more common in kids with a topic dermatitis, your odds ratio was 0.03. So you were 97% less likely to improve than a kid who had a positive patch test who didn't have a topic dermat and then metals the odds ratio was 0.26. So 74% less likely to improve. So the takeaway for me was that in kids with a topic dermat, sure, it is still reasonable to patch test them and it is still totally reasonable to say stay away from your allergens, but it really looks like a huge number of these are false positives where the kids are not going to get any better whenever they avoid. Is that really a false positive or is it just not the whole story? So that's a great question. So it's a fault. I would describe it like this and well, I would call it a, I think they are false positive irritant reactions. Now it might be that they are, you're right, only partially getting better because they also got a topic dermatitis or whatever, but the main takeaway that I want people to have is if you get the kid patch tested and they have a positive relevant patch test, don't be like, oh, avoid this allergen and then come back and though you're no better. Well, you know, maybe you missed and maybe it's the laundry detergent or maybe it's the air freshener or maybe it's the they're using an air freshener at school and then they come back and through, well, maybe it's this or maybe it's that. Then they come, well, maybe it's this or maybe and so the kid then goes two years of try avoid this, try and avoid that where you just say, okay, we try to avoid in three months you didn't get any better, then you treat them with dupy, right? And then if they don't get any better than you treat them with dupy, then you go back and say, okay, maybe there is stuff that we missed. But it so it might be combo contact or a mandatopic term. It might be one or the other, but just don't think that a positive patch test is the end of the story. So how do we know that some positive patch tests aren't just sort of a like a worst skin barrier and an irritant reaction? And so it's almost like if you just do IGE arrest testing for allergies, right? Like, you get positive test of foods that people eat. So it's not necessarily a good test for like things that for clinically relevant, like clinically relevant result. Is that potentially the case for patch testing too? So if you would ask me that in 2016, I would have said no, no, no, it's a very accurate in the blah, blah, blah, blah. But once we got dupy, which I think works in a topic, derm, I think it rarely works in contact term because there's a lot of people who would get worse and then you'd fight when you put them on dupy, they're allergic to them. I think that patch testing is a very non specific tool. I think that there are lots of people who have a positive patch test, but they don't really have contact term. They've got a topic, derm, and a positive patch test. So you've been patch testing forever. 97% of patients with coconut or purple bettine, is that was that sort of your sense of stuff? Would you get these patients that would have that positive reaction and like, vast mature of time, they never got better? I would say that other than facial dermatitis, so face and hands routinely, I would see people like we'd find something coconut or purple bettine and they'd get better. Like that was pretty reasonable. But people who had like a widespread dermatitis really rare that I would, that they would get better whenever they would avoid the stuff in their body wash or the, this or the latter or the other. So the 97% didn't like blow you away. You're like, yeah, I get it. But more was like, oh my god, that's what I thought, but nobody's ever like, I'd say the 97% did surprise me. But also I didn't patch test a ton of kids, right? I don't really like seeing kids. So I didn't patch test a ton of them. So I, but yeah, it didn't blow me away. I was like, yeah, that makes, especially now that's only an atopic kids, right? So when kids who don't have at a topic, derm, it might be the, yeah, when you get a positive, it's really a high probability of getting them better. But that's the kind of the big takeaway is, is positive patch tests and people with a topic germ take with a huge grain of salt. And only call it contact germ. Once you've seen them get better with avoidance. If they don't get better with avoidance, then try treating them for a topic, derm, then they don't get better with a topic, for a topic, derm, then go back and look for, did we miss something, right? Did we miss an allergen? Did we miss an exposure? Whatever. But that's the, it just drives me. That's when I hear people say that a positive patch test is the gold standard for diagnosing contact germ. Every time somebody says that, I want to be like, you're a moron because if, you know, say you have a positive patch test, and you understand, I don't have to go through the whole thing. But if you, we got it, you do not have to. Yes. I take you to the majority of your income on patch testing anymore. All right. Well, guys, the, you know, I did want to mention one thing that Dr. Patten brought to our attention. The res pegaladousalookin from nectar therapeutics was designated as a high priority something by the FDA. It's just a cool thing. It targets the IOToreceptor complex and it stimulates T regulatory cells. And so it's rather than blocking something, this is one of the first times it's activating something to treat a topic dermatitis. It may give people a chance for a really long term if we get your regulatory T cells controlling everything. Maybe it really can give people a long term remission. So interesting that that was designated. I can't, what's the designation called your member? They asked for a more rapid approval path. Like a high priority or some there was. Something like yeah. Yeah. Fast track. Fast track. That's it. It was fast track. Right. Maybe we should have looked this up before going on on on the air and just making shit up. Yeah. It designated something. It's designated. It's important. It's important. That's it. It's going to be a long term. So I want to thank everybody for tuning in this week for another great and entertaining hopefully episode. If you've got questions, comments, ideas, for stuff you like us to cover on the show, shoot us an email at
[email protected]. Again, that's
[email protected]. I hope you learned a few things. I hope you laughed once or twice and hope 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.
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