Sunscreen Heresy & Other Hot Takes

Welcome to season three of Derms on Drugs. A video podcast brought to you by scholars in medicine, the best educational platform in dermatology, and provided in no cost to medical providers. Derms on Drugs is where cutting edge, derm meets, derm is comedy. Dr. Matt Zyrish from Dr. Dermatology in each week. I'm Dr. M. Dormamm, residency buddies, Dr. Laura Ferris from the University of North Carolina. Dr. Tim Patton 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 in a cutting edge, derm and you'll actually have some fun listening. New episodes drop every Friday on scholars in medicine, Apple Podcasts, Spotify, and other major podcast platforms. And I highly recommend that you download the scholars in medicine app to access the full podcast video archive, explore the best derm educational content out there, real, farming independent coverage of all of derm, supported by an amazing clinical consultant called Ask Simon. So this week we've got one of our patents in six pack episodes where we are going to go over the latest greatest stuff that we have seen in the literature, basically journal club on steroids. And let's kick it off, Dr. Ferris. What do you got? - All right, so today I thought I would go outside my comfort zone. And I am going to talk about the treatment of CTCL, something I do not do at all. I always have worked with smarter people and referred it to them. But this was such an interesting paper that I thought that I would talk about it. So this is a study in which patients, these are small study in which patients with CTCL lymphoma were actually treated with a drug called Brin Toxamab Vodotin Plus ultra low dose total skin electron beam therapy. Okay, so what was this? So patients with tumor stage MF, this is stage 2B or above, these guys have a pretty bad prognosis as we know. One of the treatments out there is a drug called Brin Toxamab Vodotin. And this is, it's an antibody drug conjugate or an ADC. So with the antibody target CD30. And then it has what's called a cytotoxic payload, which is MMAE, which sounds kind of like MMA, but it's MMAE. So I also like that part of it. So it's mono-mortal, what's that? Somehow I doubt you're a big MMA fan, Ferris. Or you would-- I'm not really. I'm not really. I'm on that. I'm surprised you can know what it is, but that's-- You always surprise me. You always surprise me. I aim to surprise. Model, methyl, or a statin E. So basically the drug binds to the CD30 positive cell. It gets taken in. And then it releases sort of its weapon, which is the cytotoxic payload. This is sort of a newer mechanism for chemotherapy drugs. And so this MMAE is an anti-mitotic agent that binds to tubulin. So it blocks tubulin, microtubule polymerization. It makes cells go become apoptotic. And so it's so toxic that you couldn't just give this free floating. You got to micro-dokes it into the exact cell. So kind of just like an interesting mechanism of action. And so what they did-- it's a radiotherapy, like total beam electron therapy is also sort of one of these treatments that is done for CTCL patients. So normally you do that in this 36, 30 to 36 gray range over several weeks. But then there's some studies that show that low-dose schedules, maybe 12 gray over multiple fractions, can be done. OK, so-- Pat and I almost killed one of our patients with this once. Oh, what's going on? Let's hear about it. Total skin electron beam was the lady who had bad terrible derriyes disease. Heria is disease. Was getting repeated just over and over and over MRSA infections that were only susceptible to vanco and they were getting less that said, rotovanko. So somewhere in the literature, there was something about electron beam for full body derriyes. And so we sent her over to Allegheny General. Wasn't she in the ICU for a month or something because it probably was that long? I think it was a week. But she did get better and we published it. Yeah, yeah. Have you ever seen her back? Like in the last 20 years ago. So I don't-- She died of metastatic ovarian cancer, not related to anything that we can-- Oh, no. I mean, I really liked her too. Yeah, she was good. Yeah, she was a good sport. So she stayed, but she stayed like long term was good. Yeah, her derriyes really never became a significant problem. OK. She was happy overall. I mean, she went through a rough patch there, but overall, she was happy with the response. Yeah, there you go. OK, all right. All right, Ferris, go ahead. OK. So what they did basically was this was-- so this was published in BJD for as Journal of Dermatology for those of you who aren't MMA, officiant, others actually doesn't have anything to do with it. And they-- so what they-- this is a retrospective study where they looked at 14 patients with stage 2B, MF, all of which were CD30 positive on average had about 5% expression. And these were people who had already had-- it leaked about on median three to three prior systemic treatments. And so they treated them with this Bruntuximabvedotin in addition to just two fractions of four gray each. So total of eight gray, very low dose total body electron beam therapy. So they're like-- Yeah. So they just went in twice, like literally two times. Wow. Two times for the total electron beam. And then they gave that concurrently with standard dose Bruntuximabvedotin 1.8 makes per gig. And so then they-- and then they look-- they followed these patients. And again, they received like a median cycle-- a median of nine cycles of Bruntuximab. But basically-- and then 79% of them went on maintenance therapy, which was methotrexate mostly. Clinically, so the overall response right here was 100%. So 64% of these patients had a complete remission. And 36% had a partial remission. And the median SWAT score, which is like the PASI of CTCL, as I like to think about it, it is dropped from 49 at baseline to three at three months. The median time to response 12 days. Now what's interesting is Bruntuximabvedotin was-- there was this large trial called alcanza. And so in that's where they gave systemic Bruntuximab, the mean time to response in that study was 83 days versus 12 here. And then they did follow these patients for on average about a year. Nobody at a tumor stage recurrent-- recurrent toxicity was pretty modest. Like 29% had a mild rash. 14% had great one to two neuropathy. There were no great three or higher toxicities. Bruntuximabvedotin, which I did not know, had one of their biggest toxicities is actually neuropathy. So about two thirds of patients in the alcanza study had neuropathy. So I thought that this was just really interesting. It was combining two therapies, low dose of the total electron beam radiation and what was a really quick response and a really good response. So I thought this was cool. It's not like, oh, we can go out and do those. Or people like me should start treating CTCL. We should not. But maybe this will be developed into a more of a clinical trial. So this is this paradigm of radioemino therapy, which is that you basically-- biologically prime a tumor. So you've got an antibody that targets that tumor that puts a radio sensitizing or some sort of cytotoxic payload. Then you hit those cells with radiation. And it's just like very targeted therapy. I know that this is being done in things like prostate cancer, for example. When you see that drug, pleu-victo advertise that that's being done. So I just thought that this was interesting. This seems like this could really be the next generation of how we treat these diseases. Don't ask me any hard CTCL questions. I looked it up why you were talking, because I couldn't remember what phase 2B meant or stage 2B. I mean, these people with real CTCL, this is not patch-black disease. These are tumors. Like no-- And they have failed three treatments on average. So-- Wow. Wow. Yeah. I thought it was really interesting. So-- That's a bad disease. It's like I get-- I, yes, send all of the med-- Ohio State's got a really good CTCL program that's co-run between onken-derm. So I send all of them immediately over there. But yeah, it's a bad disease. That's where the one's. As you should unless you. should continue to do. But yeah, it would be cool if this will be the next phase of where we go. Yeah, yeah. All right. Cool. All right. Can send them over and be really obnoxious and say, I were you. I really strongly think that they will really appreciate that. I'm sure that they will. I'll discuss it with the patient first. I'll be like, yeah, they're going to take good care of you. This is what they will do. Anything else say no. No, then they might send them back to me and I don't know what that. So I can't. Yeah, then you'd be stuck. Yeah. Then I'd be, no, okay. All right. Maybe this is really contact dermatitis. We're going to talk about test. It's what I did because I did diagnose a fair amount of CTCl. It wasn't rare that they would get sent for patch testing because you know, when that pre-diagnostic phase, it doesn't really look like a topic. Derm and a, you know, I diagnosed a pair of number cases of it. Yeah. All right, Pat. What do you got? All right. My first six pack is from the March 2026 edition of Qtus and is titled Malignancy Risk Among Suriases Patients Treated with Interluke inhibitors, a retrospective matched cohort study by Zariab Alam at all. So we recently just looked at that paper, DePilium Abuse and Patients on the mean checkpoint in Hiver therapy. And it affected cancer mortality like in a good way. And it made it look like patients taking Dupy had better outcomes in terms of cancer. I think we all came to the conclusion. We don't know if it's true, but at least we can feel better about prescribing it from a safety standpoint. So one of the theories proposed by us crackpots was blocking TH2 inflammation. You push patients down a TH17 pathway and that fights cancer. So one could reasonably ask, what if you blocked TH17 or if you blocked IL-23, which influences the TH17, would that make people more likely to develop cancer? A reasonable question, right? Yes. All right. Well, this paper maybe helps answer that. Maybe. It was a trinetic study. So they took Strysis patients placed on anti IL-17, anti IL-12, 23, and anti IL-23 therapies and matched them up with Strysis patients who were not on those therapies. Prepensiony mass scoring was done on sex, age, race, and ethnicity. 60,000 patients, like over 60,000 patients in each group. So you had 60,000 patients who got those biologics and 60,000 psoriasis patients that did not. And so after an average follow-up of just under four years, the biologic patients had lower odds ratios for lots of different cancers, lower odds ratios for skin cancers, Hodgkin and non-Hodgkin cancers, bunch of other solid malignancies. So, you know, it's another trinetic study, but I think it's another one where it reassures us on the safety of these medications and patients who are maybe concerned about developing cancer. I doubt, I mean, again, I doubt that it actually significantly prevents cancer, but I think we can say now we have more data giving us, there are safe medications. Yeah. So, yeah, limitations retrospective nature. Patients weren't matched on things that like would matter, UV exposure, ethanol consumption, HPV status smoking, family history, right? I mean, would that have made a difference? You know, if you have somebody with a family member that had cancer, they're probably extra cautious about using a biologic, so they won't do it. And then if they got cancer, like that would count against the control group. Yeah, I think most of the data supports the biologic medications, particularly those affecting 17-23 pathways. Don't predispose the malignancy, and now we have a larger trial. I'll be at a trinetic study and you can insert your own trinetics study disclaimer here. That shows the same thing. I don't think I'll tell patients that they protect them from cancer, but I will say that a study that looked at over 60,000 patients on biologics didn't detect higher rates of cancer compared to psoriasis patients. Not taking biologic, so just take the biologic damage to always share decision-making, take the drug, make them take it. So it's in did they so the thing I was forget about with articles like this, did they compare them to people who were on other biologics or just people who had never been on an eye, they could have been on something else, they could have been on a TNF, they could have been or just they were people who'd never been on any biologic. No biologics. Huh, so then that means like they don't have the same baseline diseases either. Yeah, I mean, I'm not against that, it seems like it would make it better. Yeah, well, it's in part of it could also be the idea that if you've got, if you're competent to get and stay on a biologic, you were also the kind of person who keeps up with your cancer screenings and sees your primary care doctor and all that kind of baloney. Yeah, they're just, I mean, that's always a confounding factor in these retrospective studies, just like use of the health care system. Yes. If you're a biologic patient, you're just a more savvy sort of health care consumer and so all of those things are going to be better. And you know, they have these odds ratios numbers which like look amazing, like for melanoma, it was whatever, 36% reduction in odds ratio. But like odds ratio are funny things and I just kind of went through a little bit of the statistics, but that's basically saying for if you had a thousand patients not on a biologic, a thousand psoriasis patients not on a biologic, you would see four cases of melanoma. And if you had a thousand patients on a 17 23 or 23 12 inhibitor, then you saw three cases of melanoma per 1000. Like that, that gives you that odds ratio of 36% reduction, but it is a teeny, teeny difference. So again, this is not like these are protective against melanoma, but I think it's very, very reassuring that you could say they do not seem to increase. Like you you you see very close to the same number of these sorts of cancers, whether the patient's on a biologic or not. And so that that's I think reassuring and hopefully reassuring to patients. Yeah, although I would argue so interestingly like, you know, a 36% reduction in cancer is massive. Like at a population level, that would be a massive reduction, even though, you know, at our how would we see that in terms of how often we see melanoma, I get it, that would not feel massive to us, but at a population level, it is. I would also say, utilization of the healthcare system is generally associated with the higher incidence of cancer because we detect, we know we detect lots of endolink cancers. That's like what we do. So the fact that you saw less and people we knew were high or utilizers, well, we assume are higher utilizers. We don't know. Yeah. To get into trinetics, you had to be an epics somewhere. So everybody was there was no non-utilizers of the healthcare system in there are non-utilizers in trinetics. So that's the, the screening thing reminds me of a, like a kind of an opiniony piece today about all of these full body MRI clinics that are coming, that are showing up and how much it's driving a increased diagnosis of incidentalomas that like you may end up getting chemo or surgery for something that never would have actually turned into cancer. It's a really fascinating, like, challenge because you think like, oh my god, I would want to know, like early, but like maybe, maybe nine out of 10 cancers that you get, you know, that you don't know about go away. Like we don't know, we don't know that number. We don't know. That's the huge, that's like my whole, you know, right melanoma. Academic interest was like, yeah, our a lot of it is like, what is, you know, what are the, really, really like the relevant ones and what are we doing by, I mean, this is what we do. We are like the full body MRI people of dermatology. We are screening and screening and finding and biopsying stuff without having the study, right? And if you look at like all of the studies of, you know, like mammography, they were done, you know, breast cancer. It was like, you know, mammograms done in a very defined population. And there was a, um, of, you know, women at a certain age. And there was a certain frequency. And, you know, this like kind of free for all of anybody can go out and get their whole body MRI. You know, we don't know the, we don't know, so we know like the mortality of most cancers when they are detected in the normal way. We don't know what number when they are detected in ways that we never studied in the past, right? Like, who knows? You know, they say, you know, if you, you know, I can career when they started doing thyroid ultrasound on everybody as a screening test, like their incidents went way up. The mortality per population stayed the same. The case based mortality plummeted because you just found a bunch of those cancers that weren't going to be. That's right. In this piece I read today, that was one of their like primary things that they discussed was that Korean thing where they just, yeah, ultrasound and everybody's thyroid or something. Yeah. Yeah. Okay. All right. Let's move on to our next, so I've I've got a couple. So first, so for any of our listeners, I've now gotten into being on X, by Handle is Matt Zyrus. And it turned out if you if you only engage with medical content, like nothing you'd never look at anything political even once, like it's actually pretty great. Like, there's a lot of like smart doctors on their posts and all kinds of stuff. I don't know if I'm one of them, but I knew. Yeah. Yeah. I had a quote. One of my posts went viral close to a million views that was about that I think the world of dermatology. the AAD in particular recommends to aggressive of sun protection, which we've talked about on here before that, you know, there's good evidence that sun reduces your risk of heart of text and strokes by 20 to 30 percent in that that far outweighs the, you know, the increased risk of dying from skin cancer. But as part of kind of doing research for that post, I came across an article that was recently, I think it was in JAD about oral photo protection. And it just is pretty cool. So the idea with these oral photo protection things is that there's a, they probably don't reduce the risk of skin cancer to any significant extent. But they definitely have good evidence for reducing the risk of sunburn. And we've got really good evidence around this. So in particular, the ones we've got good evidence for the polypodium, lucatomas extract, aka heliocare, that's got very strong evidence. And then a bunch of caratinoids. So lutein, beta carotene, and lycopene all have good evidence. And I was like, well, do you have to take so much that you like turning yellow and orange like the little kids do who eat nothing but squash? And no, it's not that the pigment is absorbing the light. It is that they are highly potent to antioxidants. And big part of the inflammation from sun is via, and is via reactive oxidative species. And then the third one was omega-3s. So omega-3s that have been studied for cardiovascular and all that other stuff. So take all those together. And it probably can have a meaningful effect on reducing your susceptibility to burns might have some benefits with reducing photo agent. So just interesting and you can stack them. So meaning the lutein, the lycopene, and the beta carotene, they all kind of are doing somewhat different things. So even though they're all carotinoids, they take all three of them is neutral squelches more antioxidants than taking just one of them. That just interesting stuff. And the other thing as you guys know, when I go out in the sun, I take, I've now, I've taken 16 heliocare before I, when I go on vacation, whenever I head out to the beach, then that I think it's not one 16 all at once. Then it gives you it's not constitute formal medical hero evidence. Do any of that? I love polypodium. I'm going to say there is heliocares one brand. There is one called inner glow that is actually made by a dermatologist, not one who I know, but I like it because it comes as a gummy. So it feels like a treat and sun protection together. So there are more than one, but you know, I guess I would say that there's not, like when you say that doesn't prevent skin cancer, we don't have evidence that it doesn't prevent it. We just don't have evidence that it does, right? Like that's true. Okay. Correct. But my, we're not like, oh, it's helping with photo-aging, but it's doing nothing for skin cancer. We don't have that. Okay. My understanding is that the, that it, it, it be relatively unlikely, that there, there isn't enough of it like in the nucleus or something. Because right, you get the the reactivative species in the nucleus or what's like getting your DNA. But when I look, when I kind of tried to dig into it, it's because I want it to prevent skin cancer, right? So I looked like, oh, can I say this prevent skin cancer? And it was the main takeaway I got was like probably not. But not a like, there was a lot of like, we don't know. A lot of we don't know to go with it. And then the other one that I looked at this week was about fungal acne, which we all hear about all the time. 119% increase in the number of Google searches around fungal acne. And the, the interesting take here, right? So fungal acne is pit or spore and polyculitis. Oftentimes it is non-inflammatory, in which case, they can look a lot like closed comatones, but they also can be inflammatory, in which case, they look more like popular acne. The biggest things that people talk about with it, trunk, more so than face, when it is face, it tends to be more like hairline. And people often talk about it being very itchy. That has not been my personal experience. Like whenever I see it in people, I've, it's not been like super itchy. It's just been like, Hey, your acne is going too far down your back. It has always been kind of my takeaway. And then that most of the stuff that we use for acne, a lot of it at least kind of works for this too. So benzoperoxide is pretty good anti-malacezia, salsylic acid is pretty good anti-malacezia. But then you also can use zinc, you can use dandruff shampoo, body wash, face wash. You can do weekly flu connozzol or itchriconazole, which is usually what I end up doing for these people. It's just long term here once a week, take a dose of itchriconazole. And that works really, really well for them. What do you guys take on fungal acne? Do you think it's like I have never seen a BHC, but I always read that it's itchy. I have not seen it be. I don't think of it as being itchy. I don't know. It looks like to me, it's like it's monomorphic and it seems to be people who sweat more and don't necessarily rinse off or wash after exercise. But maybe I've created that narrative. But I think I've had itchy. But the thing is when I thought it was malacezia, I ask them if it's itchy. And when I think it's acne vulgaris, I don't even ask. Maybe acne vulgaris is just as itchy as I don't know. Assyrcanemid bias. That's the, I don't know if I'm using that term correctly. That sounds really smart. I go with it. It's what was the term that Faris used the other week that abs abs scople? What the hell does that mean again? That's mostly used in radiation. What's it mean? It means that you treat one tumor and then treat tumors that you didn't treat go away. Okay. Okay. abscople. I got it. That's the word of the month. I'll keep people who know a lot about cancer so much that they can have viral expo. All that will add scople effect is going to say that. Faris, if you get on there and start trolling me, Faris, that's it. I'll be out. I don't think, yeah, I'll try to make an exhale. Yeah, somehow. All right. Let's move on. Faris, what do you got? What's your next one? Okay. So my next one is about Hs. And it's not about treatment, but I saw this paper and I was hoping it would give me more information, but I like this idea. So I moved from Pittsburgh, where everybody is obese, but there's some Hs, but it wasn't like mad Hs down to North Carolina, where people are also obese. I don't think it more obese than in Pittsburgh. And I'm like, everybody has Hs in North Carolina. So I'm like, there's got to be something environmental and, you know, Hs. And so this was a study that looked at this. So basically what they did was the four major academic centers in Boston, you know, which, and they between 2017 and 23, they basically pulled their Hs patients, about 3000 of them. And then they like geo-coded their, the patient's home address. And they got to the census tracks, the census tracks are like your zip, like the plus four of your zip. And so that is a way to kind of locate not just like you're in, you know, the five-digit zip code, which could have like, you know, really wealthy and really poor people. And, you know, but it does kind of get you down to a more narrow area. And you can correlate that with certain factors. Like, you know, what is the average income? What's the average education? What's the, you know, any like food and stability, all those kind of things. So they did that. And so then they said, like, are there Hs clusters? And so they did find that there were actually even within Boston clusters of Hs. So there are hotspots and south and central Boston, meaning like those, those census tracks had more than other areas. And so they postulated, you know, it seems like there is sort of location or place-based factors, you know, or neighborhood features that are associated or potentially drive, you know, Hs. And so then they could compare hotspots with non-hotspots. And so the four things that came out as factors that were more common in the hotspot areas were higher average afternoon temperatures, higher obesity prevalence, higher fine particulate air pollution, and then a higher percentage of black residents in that track. So, you know, interesting. So, you know, the obesity thing, not super surprising. We know that that is associated. But, you know, they reflect that, you know, potentially this means these are areas that have poor access to healthy food, or it's, you know, harder to have like safe outdoor exercise areas or green space. You know, air pollution and heat [BLANK_AUDIO] kind of interesting. So I guess like North Carolina versus Pittsburgh or Boston, like it is warmer, does like a couple degrees matter. I don't know, but I thought that that was sort of interesting, or you could argue areas of poverty have more obese people, and they've got more cement and fewer green spaces. And that's what's associating, you know, the temperature. But, you know, there is sort of data that like heat and pollution can promote through it, right? Like we've talked about this when we talked about catalytic converters being associated with the increased incidents of atopic dermatitis. So certainly air quality can influence like skin barrier and potentially microbiome. So there might be something there. And then, you know, racially, there's probably, you know, issues of again, like different socioeconomic factors, you know, structural racism, all the, you know, certain like, you know, areas that I don't know. Like there's probably all kinds of things that could be going on. So I wasn't, now if you looked at like what was the strongest of those four factors, the strongest association was with obesity in the areas of the highest of the highest incidents. And the lowest was the temperature. So does it really change anything for how we're going to practice? No, but I really think like there's got to be some environmental factor that is driving H.S. and certain areas that kind of confirm this idea that there's hot spots. And, you know, maybe in addition to obesity, there are other modifiable factors. So I thought that this was just sort of interesting. And, you know, you could only look at whatever is measured for each census track. So, you know, maybe this means we should be looking at other environmental factors. I don't know. Do you guys think there's anything to the like H.S. hot spots? Oh yeah. Like, yeah, okay. 100, yeah, 100%. I saw this because I'm very right into the AD being driven by air pollution. Right, the effect. I don't think it's as strong for H.S. but I think we're going to find that there are a lot of things that are related to sort of chronic ubiquitous exposures that are just kind of part of living in America. Air chemicals and clothing, blah, blah, blah. But yeah, I absolutely buy this. Absolutely, but Patent, what do you think? Yes, I buy it as well. No, it's, yes, it's going to be interesting as this data gets out there more. I need to send this on to Ian Miles, the guy at the NIH who figured out the atopic Durham and catalytic converter thing to just give him, hey, here's another disease you need to look at. Yeah. And there's like, you know, this whole field of like metabolomics, right? Where you look at, you know, things like microplastics or micronutrients or, you know, you can sort of look for these things now in individual people instead of trying to look at it at sort of a census tract or population level. So, you know, obviously not everybody in that area gets H.S. So what's different between them? Well, I don't know. I thought it was just kind of cool and I hope that this is maybe a direction that we'll as we can do more interesting, you know, like individualized studies maybe we'll learn some of the things we could do. Yep. All right, Patent, what do you got next? All right, my second six pack article was published online April 2026, dermatologic therapy and was titled Epigenetic Skin Aging and it's reversal to improve skin longevity. This is long across ethnicities and prototypes using a dihydro-miracetin-containing serum results from a prospective single cohort study like key at all. So my interest is Pete, I am a believer that this is how the air pollution is causing the I know I would have you at hypomethylation. But you know we're in a tent. Yeah, yeah, I mean, I'm like, you know, methylation. Yeah. Can you just apply at once and you're like because it like you got to keep it like what's the deal here? Okay, go ahead, Patent. Yeah. So fair number of the authors were from Beersdorf, AG says suggests maybe some commercial interest going on. That's the answer in people for those of you. You sure enough will pour. Yeah. This was a two part study. So the first part of study looked at epigenetic changes to see if those changes were preserved across different ethnicities. And then the authors looked at the effects on the skin of a natural epigenetic inhibitor dihydro-miracetin. So the first part of study was just to show that the method that the authors wanted to use to test the effect of their topical cream was valid. And I suppose it was I couldn't really explain what the hell the first part of the paper was about. Other than to say they validated their measurement tool that they used in the second part of the study. That's all you need to know. Second part of the study was taking a serum that contained dihydro-miracetin and having 60 volunteers apply it twice a day to the face and neck along with an SPF 50 plus sunscreen. Different measurements were performed. The epigenetic tape stripping clock showed a mean reduced epigenetic age of two years which that's like for eight weeks I think they did that. Yeah and 40% of patients showing a reduction of more than five years on that eight week twice a day. A bunch of other measures both objective and subjective. It's complicated paper for what might be some silly serum we all add to our skincare regimens. But the takeaway is that the serum seemed to improve a lot of stuff. The hypomethylating activity interested me. You know what sort of things did they measure. Let's see you know periorbital wrinkles improve skin surface roughness improved dermal density up 10.4% expert grading showed better firmness elasticity texture radiance and even neck wrinkles. They have some clinical photos. I gotta be honest I don't know how these cosmetic dermatologists do it like I don't see a damn difference. Whatever. It's like mildly better you know. It just if the patient came in and was like am I better I'd be like I don't know but I think the cosmetic dermatologists are like oh my gosh you're glowing. I can barely see your wrinkles like I just couldn't do that to the patient. It's a neat mechanism of action right? It's it's specifically looking at that you know. Methylation being a part of what we see with epigenetic changes and having a drug that specifically targets that. That that ingredient dihydramere acetone falls under like the bio flavonoid sort of family. Oh I so I knew I recognized it from somewhere. It is from the Japanese raisin tree and it there is some belief that it blocks speeds up alcohol metabolism. Yeah. But it helps with hangovers. It's the anti-hangover supplement. I've heard you can buy it on Amazon even as a pill. Turn. Um you know what I because like okay so here's the thing I actually went out to like be it buyers door for and humberg and I like saw their all their data. I actually have that stuff sitting I'm like too lazy to turn my age back two years by like to put a cream on my face twice a day but I haven't. And now I want to go back I don't go back and use it but I have it sitting in my drawer because they like gave some to me. It's not available in the US yet because the regulatory oversight here is greater than it is in Europe. So I think it's either available or soon to be available there. So there is all that but I kept wondering like you know the real reason why I have it as I was like couldn't I just take this as a pill then and get it systemically and then like not just you know demethylate the epigenetic changes in my skin but like anywhere right so like I mean I could maybe get myself to put this on my face twice a day but like I'm not going to put it on my body twice a day but then all my skin could look better. I've also been too lazy to take the pill to see if that is true but but that was my big question why couldn't you just take this orally it's a cheap supplement. You're you're ready to go when the good data comes out you'll be way ahead. I'll be running I'll be stockpile. Yeah. So it'll be in your survival trailer that's buried in your backyard. Exactly. What's not there there is so cancer cells are also hypomethylated. No it's I think it's believed that that the hypomethalation is a marker of cancer cell and it's not a cause of cancer cellness but Ferris you could look younger at the cost of increasing your risk of skin cancer. Okay maybe if I'm just lazy enough I'll just take a little bit of it and I'll get you in fact but not too fair and hypomethylate but yeah I'd love to see this study done with oral you know die had you. near Situn too. Sorry to the people at Eustrin who invested millions of dollars in this and I've given away my hack. It will be the oral reflumalast of anti-aging. In oral reflumalast we'll make you smarter too. Exactly. All right, let's move on to my last ones. So first one was a meta-analysis of azithromycin for acne. Basically the takeaway is we've got really good data now that azithromycin is at least as safe as doxy. It's way safer than doxy. Sorry. Way safer than doxy. Way better tolerated and just as effective. Like the part of the benefit here right now and I'm not a big antibiotics for acne person. I'm like playing everybody on acutane. But if I'm going to use an antibiotic for acne at this point it's going to be azithromycin. It's cheaper and there's less concern about resistance. So if we keep using doxy and minnow we're going to start to eventually we're going to start to see staff, community acquired staff stop responding to doxy and minnow. Azithromycin stopped working for staff forever ago. So if we're going to use something like this makes a lot sense to me the regimens that are out there 500 milligrams three times a week. But there was a more recent article that just looked at 500 milligrams once a week. So like just literally like once a week you take a dose of azithromycin and it was just as effective as doxy 100 milligrams once a day. I haven't seen any studies comparing it to doxy 200 milligrams a day. But doxy 100 milligrams a day is that thermycin just as good. 500 milligrams once a week once a week. Just as good as doxy right. What's the downside besides the dreaded Z-pack resistance? There there really isn't like there's no the GI up GI side because I you know I think of visit thermycin is causing like diarrhea kind of stuff to some extent. But the GI side effects were much lower. The photosensitivity was much like it was much better tolerated and just as effective. 500 milligrams once a week. I'm switching everybody. Starting tomorrow. It'd be now there's only one study looking at that dosing. Most of the studies were 503 times a week. What I'm probably going to be doing is 500 milligrams for like three days in a row and then 500 once a week after that. Try and make it on no study just sort of a install just get stoned. I just want to make sure I wasn't missing a study there. But yeah. So that's funny because I swear just today this headline came across about the European like a consensus acne update statement coming out of the Europeans publishing the journal or the European and they actually kind of discourage the azo thermycin. The guideline states should not be used routinely. Why? Did they look the rationale? It's sufficient evidence of efficacy negative benefit risk balance mainly due to concerns over promoting antimicrobial resistance. What which I was surprised because I'm right I just think yeah it already doesn't work for anything. What so they they are pro doxy and minno? Yeah pro that whole tetracycling what's that other one? Limicerecyling? Sericycling? Yeah they're pro those and discourage the use of either azo thermycin which I was surprised. I always use azo thermycin for carpe. No, always read like minno doxy. Azo thermycin 250 every other day for eight weeks absolutely wipes it out way better tolerated. They don't have to take it as frequently. So yeah I I it's just the nicer drug to give I you do get more drug interactions. No, because there are lots of meds. I mean young kids acne that's usually not a problem. But that is one thing where Azo thermycin interacts with a lot and that's probably the only drawback. I use I use it for perioral derm and rosacea at times again instead of doxy or minno. My favorite rosacea treatment though is the combination oral Ivermectin with oral metronidazole. I think that is by far the most effective thing for popular puscular rosacea. It's like miraculous and it's got a pretty good study showing that it's it is the most effective thing you can do to get rid of demodex. It's the big take with it. I'm a big believer that demodex is the big problem with rosacea which not everybody agrees with me on that but I'm I'm with you. I think it's a big driver. I'm sticking with it. All right and then my last one after that was a perioral dermatitis article and it was just interesting. So this was another trinetic study. So you know questionable how accurate it is but this one seemed pretty well done. It was basically looking at kids who get inhaled steroids. So either nasal spray or for asthma and they have a three times increased risk of getting perioral dermatitis compared to kids who get non-stereoid nose sprays in non-stereoid asthma inhalers. So didn't we know that? Didn't we kind of have that sense? Yeah I think yes I've always said that that like I said that it's a thing in adults like women who get perioral derm who are like not using topical steroids on their face and I was like oh and you'd ask them if they're using inhaled steroids at all but I don't know that I've seen data for it. It's been more like yeah that makes seems obvious. It falls into the category of seems obvious. Okay but now? Now we've got data to back it up and they said if you're but if your kid needs the inhaled steroid you can basically do the inhaler and then like 30 seconds later wipe wash their face and that because most of the exposure happens literally right after the dose whenever they're kind of breathing it in and out on their face. So if you need to use it and you're worried about this or your kid gets it just wash their face like 30 seconds after they do the inhaler. I do those clind of mice and wipes wipe it down. That's probably would work as well. That's not bad. That's not bad. We get it off of there. Okay all right that's it for this week. You know good good mix of practical stuff and challenging stuff. Ferris bringing the real medicine in making us talk about CTCL. I like it and so I want to thank everybody for joining us this week. We hope you learned a few things. We hope you laughed once or twice and mostly though we're hoping you're planning to join us again next week and until then I'm Matt Zyris. I'm Tim Patton. And I'm Laura Ferris and we are Derms on Drugs. [BLANK_AUDIO]