The views and opinions expressed in this podcast are those of the hosts and their guests, and do not necessarily reflect the views or positions of scholars in medicine, or the guests or hosts institutions or employers. Content has not been reviewed to confirm accuracy of dosing or other recommendations. Viewers should confirm via independent research before implementing and recommendations in patient care. Welcome to "Derms on Drug" in a new video podcast brought to you by scholars and medicines. "Derms on Drug" is where cutting edge derm meets mediocre comedy. I'm Matt Zyres, and each week I'm joined by my residency buddies, Laura Ferris and Tim Patton, 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 actually learning something useful. So Tim, Laura and I have been buddies for 20 years, and what that means is that between the three of us we've got 60 years of experience. Laura is now the chair of dermatology at the University of North Carolina. Tim stayed at Pittsburgh where the three of us trained, and he's been faculty there for 20 years, and I'm a private practice dermatologist in Columbus, Ohio, who's spent 15 years in academia before making the jump to private practice. So we've got a diversity of wide experience, and we can't wait to tell you what we think about what's happening in the world of dermatology. So we are going to go ahead and get right into it. Now I do want to remind you tune in every Friday whenever new episodes are going to drop, but the setup of our show is divided into three segments. So the first segment, we are going to talk about the three articles that we thought were the most interesting things in dermatology for the week. We're going to call that the big three. After that, we're going to go into a deep dive where we're going to have a guest on who's going to talk about an interesting topic, something that we thought was hot and going on in the literature. This week we are super excited to have Dr. Ted Lane, who runs a meeting called the Science of skincare, and I'm going to tell you you're going to want to stay around for that interview because me, Pat and Ferris, we are not such believers in that there's much science behind skincare. So we're going to see if Ted is able to convince us differently. And then after our deep dive section, we go into the six pack where we're going to be talking about six more articles that we thought were interesting and impactful for the week kind of the way that we would sit around and share a six pack and BS about what's going on in the world of dermatology. So with all that said, let's go ahead and get into it. So the first article that we are going to talk about today is a really important one. And it comes from Abbey. This was published in the British Journal of Dermatology. It's the efficacy and safety of you, Pat, sit in it versus to Pilimab in adults and adolescents with moderate to severe atopic dermatitis. The week 16 results of an open label randomized efficacy assessor blinded head to head phase three, B/4 study. The primary author was Dr. Jonathan Silverberg. And you may have heard of this study from your Abbey rep. It's called Level Up. And so first, the big reason I really want to talk about this, Abbey is really making a big lot of noise around this, really educating us about it because the takeaway from the study is, Rinvoke worked better than DuPixen. Right? Now, so Abbey really wants to push that home to us. But I'm here to tell you that while this was a very well done study, it added approximately zero to our knowledge about these two drugs. Now, I'm going to explain why that's the case as we go forward. And really, it's because we already had a head to head study of DuPilimab versus DuPixen versus Rinvoke. It was done before Rinvoke launched into the market. It was called the Head's Up Study. That study showed us that Rinvoke 15 worked faster than DuPixen, but they got to the exact same point. They had equal efficacy at 16 weeks. And it showed us that Rinvoke 30 milligrams got about 10% more people to treatment success than DuPixen. So we already knew that Rinvoke 15 about equal to DuPi. We knew that Rinvoke 30 was a little bit better. Abbey redid this study, though, because they weren't allowed to use that heads-up data promotionally. So this study was really designed to be on label use of Rinvoke versus on label use of DuPixen. So, patients have moderate to severe, atopic dermatitis, yada, yada, the normal stuff. And then they were either started on Rinvoke 15 milligrams, or they were started on DuPixen. After four weeks, if they hadn't gotten substantially better on Rinvoke, both in terms of the appearance of the rash in the itch, they were dose escalated to 30 milligrams at eight weeks if they weren't doing really, really well on the 15 milligrams. They were dose escalated to 30 milligrams. And then we looked at our results at 16 weeks. So the reason this study didn't tell us anything new was that about 70% of patients dose escalated to 30 milligrams. And so more or less this study was again looking at Rinvoke 30 milligrams versus DuPi versus DuPi. And the real thing that we need to know is how to Rinvoke 15 compared to DuPi. Well, let me give you what the results of this showed. So first I already told you about 70% of patients dose escalated. Now of the patients who started this study, right? So 400 and some patients started the study on Rinvoke. About 10% achieved the primary endpoint, easy 90 plus worst itch NRSQR01. About 10% of the people who started on Rinvoke 15 achieved that endpoint on Rinvoke 15. Of the people who got dose escalated to 15 milligrams, about 14% of them achieved the primary endpoint. So we can really we assume that all of them, you know, people who would have achieved that is, you know, the fifth people on 15 would have also achieved it on 30. So we can really say about 24% of people on Rinvoke achieved the primary endpoint. But again, only 10% of those who started on 15 achieved the endpoint on 15. All right. Now for DuPi, it's about 9% of patients achieved the primary endpoint. So again, it looks like DuPi and Rinvoke 15 pretty similar to each other. There's a lot of issues with making that comparison that, you know, you could nitpick me on, but really ended up looking about the same. And again, Rinvoke 30 milligrams got a little over 10% more people to the primary endpoint. Okay. Great. So really didn't tell us anything new. Reconferring for us that if you're willing to go up to 30 milligrams of Rinvoke, you see better efficacy than you see with DuPi. The other couple of interesting things in here, it reconferms safety profiles as well. So Rinvoke, as we now know, there is no cardiovascular risk. There's no thromboembolic risk. There's no cancer risk. None of those things have shown up in the data. We've got like 30,000 years of patient exposure. And they didn't show up in this study either. But about 2.8% of people. So that's about one in 40. Got either zoster or XMH. And so a significant number of people, this is why everybody that I start on a Jack inhibitor for a topic dermatitis, I put on profile access with 500 milligrams of valley cyclovere. That's going to protect them both from shingles and from XMH. Now, if we look at the DuPi safety, first about 7, 8.5% of DuPi patients got an eye issue 1.5% of Rinvoke patients. So different to 7%. We already knew that 7% of people in DuPi get an eye issue. And then our througes. So 2% of DuPi patients got our througes, 0.9% of Rinvoke patients. So it was about 1% 1 and 100 people on DuPi got our througes. And we already knew that that number was in that range. And so overall, the study confirmed for us a lot of things that we already knew, but didn't really add anything other than solidifying those things that we already fought. So Tim, Laura, what do you guys have to say about this? You know, I guess you think they're about the same. Yeah, they're about the same. But I think you could argue this is more real world use, right? Because you start with 15 in the real world and then you dose escalate up to 30. I guess it gives you more safety. I would agree. I don't know if this is like the most illuminating study, but I think that if you asked Abby their argument would be, well, this is, you know, the way that it's going to be used in the real world. And so we could show that there's benefits to dose escalation. So how many patients with the two of you say in your real practice that you start on Rinvoke end up dose escalating? Patten? I have no idea. I've done it, but maybe I, yeah, can we get not most of them? Not most of them. Let's say that. Yeah, that's exactly it. Ferris, how about you? I'd say 10, 20% of the people I started on Rinvoke end up dose escalating. Is that about what you would say? That's about I would say 10%. Okay. Yeah. And so this writes 70% of people dose escalated. So it's not really real world use.
The other thing though that was really kind of interesting, about 2.5% of people on RINVOC got either X or a herpeticum or Zoster, 2% of DUPI patients got our througes versus 0.9% on UPA, so confirmed our througes for us, about 8.5% on DUPI got I-issues versus 1.5 on RINVOC. So about 7% of people got I-issues, we already knew all of that. So really didn't tell, give me a whole lot more information. And in the main reason I wanted to talk about this today is because Abbe's making sure we all hear a lot about this study, and I want people to really understand what it shows. It reconfirms for us, RINVOC is a little bit better of a drug if you go to 30, but we still don't really have a comparison of RINVOC 15 compared to DUPI. So let's go ahead on to our second fact, you guys want to say? Well didn't you think this was a, we're going to prove that RINVOC is better, and everyone's going to use RINVOC before they use DUPI because it's better. And I just, I don't think DURMS are going to do that. You don't have blood work, you don't have XMU, her pedicum, you give them a shot. It's only every two weeks. I, you know, they could say that it's so, so much better, but so many patients on DUPI, you might have come back and they're the happiest people in the world. I'm not going to go to RINVOC first, right? What I can't handle. I don't think you can handle label. I think you can. You can't. I think you can. They don't have to fail to biology. They can just add a shot at catalog. And I keep it, what I can, consult with Abbie, I keep telling them, you're barking up the wrong tree. You don't need to prove to people that RINVOC is more effective. You need to make people more comfortable with safety. And that, that's what's going to change behavior, right? Yep. But all right, so Ferris, let's go on to your article. Okay, so my paper is in JCI. And so this was a paper by Oka at all, and this was talking about TH2 cell-directed immunotherapy eliminates actinic carotocyte. So what was this? This was a paper looking at treatment of actinic carotoses with calcipatrial and 5FU. And so what they showed here was that this actually leads to the generation of resident memory T cells. And so I think that this is a very, very basic science dense paper that I cannot cover in three minutes. But kind of key takeaways here. So one, there was an open label study, 18 patients, six days of BID application of the combination of calcipatrial plus 5FU. And they showed reduction of, you know, mean number of AKs, 95% on the face, 82% on the scout, 65% on upper extremities. What I think was interesting is, you know, one, they looked at mechanism. It's actually TH2 mediated. That is not something that we think about as being how we protect from cancer. They showed that IL-4 and IL-13 were necessary. And also IL-24 mediated as well. Now what I thought was really interesting was they actually did this study five years ago, where they treated patients with either 5FU with Vaseline or 5FU with calcipatrial. And they, they only showed better efficacy against AKs. But they went back to those patients who had just been in that study. It not had a subsequent AK treatment. And then they biopsyed their, the AKs that they had. And they actually showed a big difference in the AKs and those patients who had had the calcipatrial, as opposed to those who just had 5FU alone. More resident memory T cells and, you know, upregulation of class 2. So, you know, I think that this is interesting because it would suggest that this is, and they also showed that with this combination that you reduce the number of squamous cell carcinoma is that form in a three year time period, better than the data that we have for 5FU alone. So, I think that this is really interesting. It suggests that this is really working differently. It's just shorter treatment for patients. And it also suggests that we can reduce the number of squamous cell carcinomas. There's this completely changed for me. So, I had, right, it's, we kind of known for a while, right? That 5FU plus calcipatrial was probably the most effective AK treatment that we've got. But I had always assumed that it was basically the calcipatrial was causing some irritation that then allowed the 5FU to penetrate better. No big whoop wasn't excited about it. Actually didn't do it because I was like, ah, I'll just have him use the 5FU for longer. I'll do whatever. This completely changed the way that I think about this therapy. And I think I'm going to actually start to use it. Like, what, is this what you've been doing for AKs? Is it what you're going to start doing for AKs? What, is this going to affect how you practice? You know, I have liked this for AKs for a while. I do think it works better. I think that the shorter duration of therapy is great for patients. I like that now I actually sort of had data. I thought it was interesting to call this immunotherapy, but I guess in a sense it is, you know, to me, the hardest thing is like my AK patients are older. This is a compounded medication trying to get them to a compounding pharmacy. It's silly, but that's like the biggest challenge for me of using this. But if I talk them through it, this is my first choice. And it's a very cost effective data-driven therapy as far as I'm concerned. Pat, and you use this? I've used it. I still use 5FUsed two to three weeks more often. I don't have a good reason for that. It's probably just a habit. The compounding, man, I mean, like a lot of them are just like, we'll call the patient, we'll deliver it. I haven't run into that being a difficult thing. They're part of our electronic records. We send it right in. It's actually pretty straightforward. I don't know. Old people are just hard. Old people are hard. I mean, you know, I get, because if they don't answer their phone, they're done. You're done. And they're not comfortable giving a credit card to buy something. I mean, these are like the times that I get, you know, hung up on it. But honestly, with the right patient who can, you know, navigate that, I think that this is a great option. And it's fast and it works. Yeah, I don't know why I'm holding on to my old way. Do they get alterations like a three week, five, a few thing? They get vigorous responses and it varies by person like it does with five. If you, I don't find that they get worse, like I don't find that they get less tolerable. All right, we're gonna have to get Ted's opinion on this when he comes on, because with him being in Texas, I would imagine he's treats more AKs. And a week than the three of us have treated over the course of our careers. But so let's jump on to our third paper patent. What do you got for us? All right, so paper by Sumer Eye at Al from October, 2024, issue of health affairs. It was a review of 11 studies that had various measures related to pediatric depression over a particular time period when the FDA issued an advisory and then a black box warning. So the advisory was in 2003, black box warning was in 2005. And what it says is that in children adolescents and young adult patients increases in suicidal thinking behavior can occur. A lot of those warnings do elaborate the patient should be watched closely for any changes in behavior. And so they were looking at things that happened around that time as it related to pediatric depression. The exhibit won depression diagnoses and visits for depression were slowly increasing before 2003. And then after the black box warning, they decreased. This I thought was the oddest chart. Why would black box change visits? You know, I could see it affecting prescribing habits, but actual visits to psychiatrists. So was there something else going on that maybe affected the second two charts? Come on, come on. Here's what happened. The pediatricians don't want to talk about the pray as soon as this came out, if they bring up depression, now we got to do something. They don't want to prescribe the SSRI. They don't want to say the patient's going to be like, I am depressed. And the guy's going to be like, I am not listening to I. I got like nine kids. You've got nine kids. There's no, he doesn't really have nine, but he might as well. They're not going to tell anybody they're depressed. Right. But the diagnosing changing, I just don't get it. Let's move on. Exhibits it. Okay. Okay. This was looking at rates of antidepressant treatment among pediatric patients. Now, the text of the paper says that antidepressant treatment and used declined anywhere from 20 to 50%. But what's weird is the one line, it's percent antidepressant use. It rises slightly before the warning starts to decline after the warning, but then it starts to increase again. And it's actually higher at the end of the graph around 2010. So the decrease, I guess, they were referring to those other two lines, which were prescription fills and percent antidepressant initiation. So maybe that's where they got the decreases. And then exhibit three finally was increases in psychotropic drug poisoning, which was a proxy for suicide attempts and suicide deaths following the FDA warnings. So as where's before the FDA warning from 1990 to 2003, when SSRIs became available, those appeared to be declining. So the visits and diagnoses don't make sense to me. I get what you're saying, Matt, but skeptical of that argument. What was most concerning, and authors conclude FDA should revisit.
at the black box warnings, it's actually harming patients, these warnings being present. What was most concerning to me, the article mentioned, fewer than 5% of pediatric patients were monitored in accordance with the FDA's recommendation, and there was no change in that. So the warning didn't increase appropriate monitoring, which I think the FDA thought, well, this will be helpful. But I also wanna say it's like doctors were kinda like, forget it, I'm not prescribing these medications. And that's like the doctor's fault. And yes, the FDA affected that, but I think of the black box warnings that we have. I mean, I think that was kinda the focus where we wanted to go with this paper, not to discuss pediatric depression the whole time. But topical calciner and inhibitors in risk of lymphoma, bardolumab and depression. I also, other IL-17s don't have that depression black box. Topical ruxolinib TNS with infection and malignancy. But my takeaway is black box warnings don't really mean a whole lot to me. They are there and you have to address them. And if you're a good doctor, you are aware of them and you address them. But aside from black box warnings, the internet and media and TikTok are saying, "Propel parabens and Sarave cream." And our sunscreens are gonna turn males into females. We have to deal with so many other things. The black box stuff to me, it's just, it's not a big deal. - See, Pat, you're in your ivory tower. You gotta remember that for those of us out here in the real world, we've got like seven minutes per visit. If there's a box warning that they're gonna get from the pharmacist that says, "This might make you think about suicide," or "This might give you a heart attack." Now, I gotta talk to him about it. Because if I don't, they're gonna get it and then call me. And so the box warning forces you to have conversations that you may or may not think you have to have. And in the real world, that's a big difference. - But so, you know, methatrexate, one of the black box warnings. - Yeah, you're right. - Death. - It's death. That's the worst side effect. And how much methatrexate did dermatologist use? - We use a lot of it. I mean, we still have to, unfortunately, because of the insurance situation. You know, before you want to pick sent, they have to fail methatrexate. I have never gotten a call. This can kill me. I don't specifically mention death as a side effect. I talk about liver and, you know, I mean, they sound bad. It's not like I don't address it at all. But I specifically do not say death is a potential black box side effects. Good luck. - No. - I don't feel as much as you think about. What do you think about that? - About black box, you know, I give some risk. I cannot go through the whole black box on every single drug. So if it has a black box warning, I will say, if you read about this, you're going to read about some of the risks that include blank. I almost never use the term black box unless I'm dealing with a very sophisticated patient who I think is going to need to know that. So, you know, it's, part of it is like, you know, they're going to go read things on their own. Part of it is I need to have some sort of medical legal documentation that I discussed risks. But I agree. I think it's still incumbent on us to make sure that we give patients the best treatment and give them appropriate counseling, put risk into perspective. It's a really hard thing to do. You know, I think where I come up with, you know, needing to do this is not a black box issue because I do a lot of psoriasis is IL-17. So I talk about inflammatory bowel disease. And you know, when I say this will happen with, you know, inflammatory bowel symptoms and about one out of a thousand patients. Like I try to give them a number, not like, oh, most people get this. I think, you know, if we have those numbers for things like misabents or lymphoma, that's helpful to put into perspective for patients too. All right, let's go ahead and move on to our, to the next segment of our show, our deep dive. And so I'm going to introduce our guest, Dr. Ted Lane, who practices in Texas. As I mentioned, this part of Sonova dermatology, Ted, great to have you on the show. It's a lifelong dream. Thank you so much for having me, guys. You got what, Ted, let's get right into it here. So you were in a meeting called the Science of Skincare. How do you say, what made you start that meeting? So to me, skincare isn't a lot of science. It's a lot of art. And that doesn't mean that it's like art is a big, like art's really important and hard to do. So that's not like a dig of like, blah, blah, blah. But it'd be like saying this science of, you know, Renaissance paintings, like, so why did you start the science of skincare and, you know, what do you guys talk about at the meeting? Yeah, so this started in 2021, right, during COVID, where I was, you know, at home, not much to do, thinking about my life. And I realized, you know, I had spent a lot of time with skincare just because it's a subject that's really interesting to me that we talk a lot about skincare in our medical practice. We use it for moisturizing cleansing, for our inflammatory skin disease. And yet we don't know much about it, right? We don't understand the ingredients. We don't understand the science behind the formulations, nor do we understand the layering and all the different science and chemistry that underpins topical formulations in the OTC space. So I just started to do some research on my own and realize how important it is and how nobody was really, giving us any education on this, especially during residency. I don't know, Laura, if you do at UNC now, or Tim, if at University of Pittsburgh, you guys have any formalized education on skincare. I certainly didn't. And it was not very easy to find it at conferences that were supposedly, you know, medical conferences or aesthetic conferences. You may get an hour here or there. And so I called up a buddy of mine who was Patty Ferris, who's kind of a worldwide expert known for many years, as one of the seven-year figures in skincare and nutraceuticals. And I said, "Patty, I think we should start a meeting." And she said, "Great idea. Let's do it." I didn't think she was going to say yes. So we kind of started right in the middle of COVID in New York City during their marathon weekend. And again, just so naive, we had no idea what we were doing. But it's kind of, you know, there was enough people that were interested in enough companies that were interested and they kind of gained a little bit of a footing in the science of skincare summit is, you know, we're entering year five in 2025. So look, I think to your question though, Matt, the idea of science underlying skincare is actually there. There's double-blind randomized placebo control trials done primarily by the larger companies, your L'Oreals, your Galderma, your Biosdorf, your Pierfabs, for example. But more and more companies now are finding the funding to do that as well, especially to young age. And furthermore, I think the science of skincare is actually outpacing the science of medical derm. So if you look at, for example, the regenerative area or longevity area, whereas previously we thought about kind of longevity medicine is at the fringes, my gosh, it's so front and center now as Peter Atias come out with his book and then we listen all these different podcasts and-- Well, there's that guy on Netflix who says he's never going to die. Yeah, that guy as well. Right. Brian Johnson, yeah. Let me jump in and ask you. So this is-- We patent in Ferris. So we trained with Susan Obaise. We trained with a very good aesthetic person. But what I have never been able to get answered. And I think Pat and I and Ferris, maybe as well, have always been like skincare is baloney because the key product that's always been around TNS serum with growth peptides, peptides cannot penetrate the dang stratum corneum. So nobody's ever explained to me how the heck that works because if it's more than five amino acids, it's over 500 Dalton's and it can't penetrate. So do they know how peptides work? Oh, such a great question, Matt. So TNS serum, let's take that for as an example, right? And remember, it's 25 years now. They've just celebrated the 25th anniversary of TNS. And they've advanced the formulation a couple of times. But TNS initially when it was out, they were talking about growth factors. And of course, growth factors are gigantic molecules. There's absolutely no way that they're going to penetrate the stratum corneum. And yet people were seeing a difference. I mean, people were paying $250 for this serum. It's going to work. It has to work. And it totally, it has to work. And we have some data to show it works. Well, now we're thinking that it works because not necessarily due to the growth factors, but there are exosomes in there as well. Exosomes are essentially liposomes. And they contain various things. But they can contain amino acids, very small growth factors. They contain microRNA. They can contain very small peptides, all of the above. And because they're at the nanoparticle size, they do penetrate. And now the thinking is, OK, this growth factor serum is actually an exosome serum. And that's where we're seeing some of these results. Now we have the flooding of the market of these different exosome products, which I'm sure you guys have seen from multiple manufacturers. It started overseas and now is kind of penetrating into the US market. And we're starting to see some interesting studies based on this. So you're telling me exosomes are a real thing. Because generally when I hear exosomes, but I mainly hear is, that sounds like crap. Do they really make chip penetrate? OK, so exosomes are a real thing. They have been shown to penetrate. We do know they penetrate. OK. They're liposomes, right? So we know liposomes penetrate. So that-- We heard a lot about liposomes like 20 years ago. [BLANK_AUDIO]
never turned into anything. - Yeah, so these liposomes, though, have biologically active ingredients. Now the problem is, you know, exosomes can be derived from various different kinds of mizankomal stem cells, adipose derived, platelet derived, umbilical, wortons jelly, you name it, and there's a company that has an exosome derived from that tissue. Now there's an exosome war out there to say, you know, my, because we're derived from mizankomal stem cells, we work better in the skin versus others. And there's plant derived exosomes as well. I mean, I could go on and on. - Yeah, yeah. - But I think what we need to do, though, is, you know, and study, and companies are starting to do this now, is just get more randomized trials out there, because it's, there's so much pseudoscience, there's so much hype behind it, we need to get the science behind the skin care, and we're starting to see that now. - Okay. - Pat, I'm kind of, I don't want to completely monopolize, talking to you, Ted, Pat, what do you, what do you got, Pat? - Ah, my most skeptical approach to these is, you know, I'm seeing immunobullus patients, and I'm trying to arrange for, you know, right, talk some ab, and immunobullus patient that his oncologist doesn't want to treat his metastatic renal cell carcinoma because of bull's pempagoid. And I'm like, I can treat this pempagoid. And then you have a patient that comes in, and is like, what do you recommend for skin care? And I'm like, I like, use gentle things and put sunscreen on, and maybe a retinoid at night, goodbye, and thank you. And they look at me, you know, you had the patient that looks at you in horror, and was like, I just moved here from New York, and my dermatologist there had me use a special wash in the morning, followed by three different creams, one of which use a natural sunscreen. And then I applied vitamins and acid and fish semen. And that's not a joke, right? There is a thing derived from salmon sperm. - Correct. - Right, here we are in. - Right, so yeah. And they look at you like, you are this horrible dermatologist, and my take is, the horrible dermatologist is the one who told you to spend all that money to put all this stuff on your face, to get what is probably clinically going to be a very little difference. So, right, I mean, that's my meanest, most skeptical take. Am I crazy for thinking that at all, or is there something there? - No, there's definitely something there. I mean, I think if you focus on the ingredients that have the most data behind them, so you've got your alpha-idroxy acid, your antioxidant, your retinoids, obviously your sunskins and your moisturizers, you're not gonna go wrong, right? Except for that patient who is so sensitive that can tolerate a retinoid, there are alternatives to that. What's interesting now in skin care, and this is why I say it kind of outpaces medical dermis, where previously we've relied on these legacy ingredients to affect change in the skin, what we're seeing now is a focus on the hallmarks of aging, particular cellular senescence, and if we focus on decreasing the load of senescent cells and the epidermis and dermis, not only do we achieve kind of improvement in the skin health and skin beauty, but we may also achieve an improvement in inflammatory disease. So, that's where that Venn diagram of skin care and pharma start to overlap, and you guys know this, there's no innovation in topical pharma right now, right? Nobody wants to. - Came to get a funny. - Yeah, aside from VTAMA and Zareev now, I don't know that we're gonna see anything else, because it's so difficult to get any payer to cover it. And so we have to turn to OTC skin care to help with these patients, and whereas we've tried these pharma drugs, now we're trying OTC skin care, and I think we're gonna get there, based on this novel mechanism of action and targets that skin care is going after. - Ted, are you in Houston or you in Austin? - I'm in Austin. - Okay, so see, Pat, and part of it is probably just that people in Pittsburgh and Columbus probably don't care as much about how they look as to people in New York and Austin and Houston. I think a lot of it's gotta just be driven by what patients want, whenever they walk in the door. - We still ask the question, and I just kinda feel like, you know, you start looking at it, and you see exosomes and antioxidants, and I'm kinda like, I don't know that this is gonna make it. Like don't spend $400, $500 on these products. - And it's less your a billionaire or a millionaire, and that's like nothing to you, right? - Yeah, you know, look, Tim, I hear what you're saying, this is why you should come to the conference, by the way. (laughing) - Okay, I just got an invite. - There you go. - But you know, these same patients are paying for NADH infusions and peptide infusions, and going to the wellness doctor, and getting all these unproven, you know, taking, you know, microdosing cereliamus, and microdosing GLP ones, and doing everything that, you know, taking that form and 500 BID, you know, everything that people are doing right now, right? - Yeah. - With little data, really. - Yeah. - And so, you know, people want to live longer, they want their health span equal, their lifespan equal, their skin span. And so, you're gonna get more and more people with all sorts of different diseases coming to you, worrying about their skin. And so, it's a, who's this skin specialist in mind, you to understand what's going on with skin care? Can I like the term skin span? Haven't heard that before. Right, Ferris, what do you got? What do you, what do you want to ask Ted? - So, I'll be the nice one here, Ted. I'm not gonna, not gonna. - Come at me, Laura. - I'm nice. I'm nice, I know. - Talk to her, you know. - I have a job. - No, so I'm gonna ask you like, what's up? - Ted's just skeptical. He's nice, but skeptical. - Okay, no, nice, but skeptical. All right, so I'm gonna leave us on a high note. So, you know, if for the person who, you know, maybe is sort of the average practicing dermatologist doesn't want to, you know, have to stock a lot of stuff or have a lot of upfront costs, wants to be able to, you know, say, I don't wanna do skin care all day long, but I wanna have some good options for my patients when they say, do you have any products, maybe be able to provide them. I guess my question would be, what would you say to those dermatologists? And then the other flip side of that is, how do you see like product sales evolving? So it used to be, you know, you had a cabinet, a glass cabinet of stuff in your office right into your window offer that, is that still how this is done? 'Cause admittedly, I've been in academia a long time. Like, do you walk in and people buy stuff off the shelf or are there, you know, things like Amazon type storefronts where you can have virtual inventory. Or how does that all work now? - Yeah, a lot of, okay, so there are companies out there which will put up a storefront for you on the web and then handle all the back office, shipping and keeping all their shelves and none of them on your shelves. So you're working capital is not tied up in inventory on your shelves. You can offload that to a third party. Of course, then you make less money on a sale, but it also solves for many of the issues that you talked about. Most of the time, patients come in because they're so used to purchasing on Amazon and again, this is why Walgreens and CVS are having such a hard time. They don't really expect to buy something in a brick of mortar and it's okay for it to be shipped. So you don't have to have that much inventory on your shelves. You don't have to have that glass cabinet. Although merchandising skin care is always helpful to especially if people are in your reception area and have some time on their hands. In terms of what products you should carry, again, Laura, I think that depends on what era you wanna practice in. If you are more interested, and I don't mean that in a pejorative way. I'm sorry if that sounded like that, not at all. - No, no, I'm probably the 20 years ago, ERA. - Okay, and that's where most of us are, right? - That we are. - That we still use this tar. - Yeah, call the time. - If you are interested in kind of the, what I call the legacy ingredients, and you would focus on your sunscreen, your antioxidants, your retinoids, your moisturizers, that kind of thing. If you wanted to practice more on the cutting edge and offer that kind of skin care, then you're looking more the regenerative techniques. And so you're looking at your peptides, your growth factors, your stem cells, your exosomes. So I think it just kind of, and then there come, obviously there's a gray area in between. - So, is there something that is truly better than if I can get them to get to 0.1% retinoin? - Yeah. - A good, you know, alpha hydroxy and good sunscreen, which the retinoin, right? The problem is their face just lights up. But if I can get them to that, is there something that's actually meaningfully better? You know, Matt, I don't have head to head trials, right? Which of course I'd love to do. But I can tell you that, you know, I'm lucky to be involved in a lot of different skin care trials right now. And so we have these different skin care products that are being made by both large and very small companies. And it is amazing to me what is happening to the skin with a novel compound with a novel ingredient. That is absolutely not a retinoid. - Okay, all right. Well Ted, I want to thank you for coming on. We will have for everybody on the scholars in medicine and the Terms on Drugs website, the link for Ted's Meeting, the Science of Skin Care. It actually does sound like a pretty cool meeting. And Ted, I really want to thank you for it. And I did promise I would ask, what is your take on calcifer trion flu or uracil? - You know, I was listening to that and it's interesting. I have been hesitant to offer that combination primarily for medical legal reasons, but also because, you know, as you guys mentioned, getting somebody in the Medicare population to answer a phone call or agree to pay for a compound of medication has been difficult in my practice. So I've steered away from it, but that data that Laura talked about in regards to those resident memory T cells and the decrease incidence of scrimal cell cancer three years later is compelling. - Okay. maybe you're going to be.
thing that I turned back to, although I really like PDT and I get along really well. Okay, fair. I know George Martin who lives on Maui and again, he's treated, I'm sure, 50 times more AKs than he's a big PDT guy as well. And so while it, I've not done much PDT, people who I respect do is the way that I would put it. Ted again, I want to thank you for coming out and joining us today. Really a fun conversation. Hey, I appreciate you guys best of luck with this. It's great. Thank you. All right. So before we get onto our final six papers here in our six pack, Patton, did you put together any trivia for us today? I did. And I tried to kind of stick with the theme, Ted, if you want to hang it up. And do three trivia questions before you head out. Oh boy, here we go. I was not ready for this. I think you'll kill it. Usually what we do is have the Gaston Ferris go up against Iris. He thinks he's the smartest dermatologist in the world. And we just like to prove him wrong. Thanks. Okay. There we go. First question. In their song, this is like a little - And their song she don't use Jelly, the Flaming Lip scene, that they know a girl that will make you toast, quote, "but she don't use butter and she don't use cheese, "she don't use jelly or any of these, she uses what?" - Vaseline. (laughs) - No, no, Margarine. - No, Vaseline, it is Vaseline. - All right. - Pat, you are making questions up just so that I will have no clue. (laughs) - I have a question in my head. - I had a follow up about Robert Chesborough and how he came to discover. It was the same answer. Vaseline was the same answer. I figured I would have to go on to that. Ferris, I'm impressed. - That question was like a random word generator to me. (laughs) - No idea what that is. - You were talking about it. - It was not. You got to follow along very closely. I need to practice it this. Maybe I need to do it. - I knew this song. - That's all I had going on. - Okay, I'm impressed. - I think the next two are more clearly asked. Okay, number two, Proctor and Gamble began to market cleaning agents on radio programs in the 1930s. These daytime drama radio programs eventually became to the whole world. - So poppers. - Yes. - So poppers. - So poppers is correct. - All right. - I didn't know we could answer the question before the question. - I think there's no way to do that. - I didn't do that one. - There's no rule. - I think you do that easily. - He's so cool. - All right. - That's cool. - You think you can do that. - That's cool. - These are off. Let's go, Patton. - It's all right. - There are no rules. - That's right. Okay, ready, final one. As a defense mechanism, the bombardier beetle, stick with me. The bombardier beetle can eject a hot toxic substance, containing a mixture of hydrogen peroxide and this skin-lightening agent. - Hydroquinone. - Hydroquinone, I think, Mac. I'm gonna call it a tie. So today's a tie. Okay, I was thinking about going Kojik acid. - I was thinking Kojik as well. So I'm surprised there was Hydroquinone. - Yeah, that's true. - What's the beetle toy to make me do? - I'm gonna have to try to make it. - When you practice 20-year-olds skin care. You know what I'm saying? - There's a baby. - There's a BBC video. He totally cooks and ant. It is something else. - See, I didn't know if he was trying to get rid of the dark spots and then the predators would be, go into the clubs and having too much fun. I had to do like that. - My kind of beetle. - Yeah. - Okay. - All right. - All right, well thanks for sticking around to it. - Thank you, too. - That was worth it. Thanks, guys. (laughing) All right, so let's move on to our next facts. So the first article that we've gotten here was one that I picked. So Jack inhibitors, it was from the International Journal of Dermatology infection risk with Jack inhibitors in dermatosis. I met an analysis and then a commentary called Jack inhibitors unveiling varicela and herpes risks in atopic dermatitis. And really the interesting takeaway here is that Jack inhibitors are not generally immunosuppressive. So you don't see a general increase in serious and opportunistic infections. You see very specific things. You see an increased rate of a respiratory tract infections. You see an increased rate of zoster and you see an increased rate of exema herpeticum. But only in patients treated for atopic dermatitis. In patients treated for rheumatoid arthritis, alopecia, ariata, whatever else with Jack, you don't see that. So that was kind of the interesting takeaway for me is that it's a very targeted immunosuppression. And the real clinical takeaway for me from this is that because of the exema herpeticum risk, 'cause it is not an insubstantial risk, I actually put everybody who I start on Jack inhibitor for atopic dermatitis on Valley Cyclovir. 500 milligrams once a day. Even if, no, they should be vaccinated for zoster if they're over the age of 50, even if they can get vaccinated after they're already on it. That's fine. But I put everybody on Valley Cyclovir because the zoster vaccine doesn't protect them from the exema herpeticum. That's kind of the takeaway that I had. Either you guys have anything you want to add kind of about Jack's and infection risk. - So, you know, one, you can actually give the zoster vaccine to people who are younger, who are going on, quote, immunosuppressive medications. So. - In theory. - In theory, but insurance sucks. So try to get that covered. - In theory, you can, and they should actually cover it. But, you know, in reality, it's two shots. I'm over 50, I still only got one 'cause I haven't bothered to go back. So it's hard to get people to follow through with it. You know, two, I still wonder about the exema herpeticum. I think most of that data is in patients who have inadequate response, like who have uncontrolled atopic dermatitis. So, did you see, was it related to the control of their AD? Like do the people have great control of their AD and still get exema herpeticum? - So I would say just my clinical experience, 'cause I haven't really seen the data presented that way. I've seen about 10 cases of exema herpeticum. And I would say that I see it in people who are doing really good, but not clear. So they are like easy, easy 80. So where you're like, oh, I'm really happy with how you're doing, but you're still using the topical once in a while. That's who I see get exema herpeticum. If they don't do that well, I'm not keeping them on the jack-long term. And if they're totally clear, I haven't seen it. It's in the people who are doing well, but not like spectacular. - Okay. - Yeah. - You know, the last case of exema herpeticum I had, it was she was a Chinese patient and she had come over from China where she got a patissette nib and she wanted to restart it. And I was telling her about depixant and that's that the other and how it's safer, whatever. So I put her on depixant and she got exema herpeticum. And then she said, why did you give me this drug that called me that? - Yeah. - I was like, no, this is the opposite. So, - Did her exema get worse? And did she get it because of her, like with the nexema flare? - It was one dose of the dupy. So she hadn't responded yet. - Yeah. - Yeah. - Yeah. - Yeah. - All right, let's go into our next paper here. So, Ferris, I think this one's yours? - Yeah, so this is the utility of aisle 23 intra-class switching in the treatment of psoriasis. So this was by Ren at all. And this was in clinical and experimental dermatology. So this was a retrospective paper, 43 cases. So there's not a ton of them. The vast majority were switches to risen chisimab. So mostly Giselchimab to risen chisimab. Some children are risen chisimab. - You're allowed to use brand names. People, there are plenty of people who are not gonna so. - Fine. - Switch into sky-rizzy, okay, Matt? I don't know what you're doing. - Have B is here. - It's not professional. (laughing) - Take a good note of the generic. - So third of these were primary non-responders. And these were also like, they were all multiple biologic failures. So these are kind of like the complex patients. Basically 81% of the time it was successful to switch to another aisle 23. And that success was defined as less than 1% BSA. They just looked at BSA. So I think it's interesting. So I like aisle 23's first line. I like the efficacy, I like the safety, I like the ease of dosing. A lot of times I think, gosh, I should switch them to another drug if they fail an aisle 23. But now I'm like, oh, I'll just try a different aisle 23. And it's still, even though most people were switched to sky-rizzy, people who were on sky-rizzy and switched to Trump via also had a high recapture rate too. There wasn't a difference. - I pretty much have always, if you failed one class, I'm gonna switch it to a different class. It sounds like you've generally done the same thing just 'cause intuitively. But so this is gonna kind of change your approach. - Kind of, I mean, in the end, like we have that data for aisle 17 classes too. So failing one class doesn't, you know, you often will still respond to another drug in the same class. I think we just, our gut reaction is it just makes sense, but they are different drugs. They're not all interchangeable because I like aisle 17.
I think I'm still more likely to say I'll switch from, you know, one aisle 23 to another than I am to say, oh, you failed your aisle 17. Let me do another one. Then I'll go to an aisle 23. Pat, and what about you use you generally switch classes or do you stick within class? No, I would switch if they were failing. Yeah, Risa and Kizzie, ma'am. It's also known as Sky Rizzie. I would say we're going to put you on. Now I can't even remember what Tulsa is called. So I'm going to have to go with. It's a kid's a ma'am. Oh my god. You're a pharma botan sold. Yeah. Yeah, I mean, are you going to, what are you going to do next time next time Sky Rizzie fails? I'll offer him Trump, I and I'll talk about we can go to a totally different kind of drug or we can go to Trump, I instead. And I never gave a damn about this because right, I do X-Sama, but now that we've got three aisle 13 drugs, the data is if one doesn't work and you switch to a different one. It's just as likely to work as if they never failed. It doesn't make any sense. It does not make any sense. That one's especially surprising, but I do think it's the, it's like the Stalara aisle 23 in heaven, right? How could a 12 and 23 that's doing both? How could that be worse? Or then if you're just inhibiting 23, did you just say worser? Worcer worse. Oh, you said worse or okay, fine. Okay, I get it except that there's probably something about the T-H1 axis that's impacting the disease. I don't know. Maybe there's X's own and we don't know it. Pat, Pat, let's go into your next to the next article here. All right, for an asteroid in Monoxidil versus Monoxidil alone, of course, they're talking topically. This was Assad at all in November 2024 journal the drugs and dermatology. Yeah, I mean, this basically the takeaway is the combination is more effective than Monoxidil alone, but man, there were just lots of issues with this paper. It said that FDA has approved topical finasteride for hair loss. This is not true. They use salt squaring for an androgenetic alopecia study, which I would say, like not do that. Like that. Yeah, yeah. You don't like this. You know, was it, did the patient have to put them on separately or was it combined ahead of time? They didn't really say. So they say that it's more effective. It was 86.7, you know, what do they call 86.7 versus 69.1 of the combination versus the monotherapy. I have no idea how they came up with those numbers when they they did the salt scores. The salt scores actually got worse like they they increased, which as we all know, the higher salt score is actually worse. So, man, I just, you know, if they took the time and to do the study, I think that a helpful editor could have gone back to them and said, you know, look, there's a better way to present this data. And it's like, I just thought it was kind of an editorial failure. I would say first, I agree with you that I think peer review often is lacking to a huge degree nowadays. The one thing that I thought was interesting here, if the data is believable, then the combo worked better on the vertex and the occipital area, but it was no more effective on the frontal and parietal areas. And that he did break it down by areas. Yeah. I was at power to look at that difference. I cannot imagine that this study. It's not asking intelligent questions, Ferris. I want to get that reviewer. That guy never reviews my positions. I'll use both. I don't I use both systemically. Yeah. All right. Let's go to my next article. So autonomic de-nervation dermatitis and easily overlooked dermatosis in the British medical journal case reports by Demali at all. Basically, I just want people to be aware that this exists. So the idea here is whenever you do a transcutaneous excision through dermis, you are cutting nerves and lymphatics. And then you can get a persistent dermatitis as a result of that. The mechanism is not exactly terribly worked out. There are a lot of different ways it could be happening. But why this is so important is the most common setting that you see it in is after a knee replacement. Because where they're cutting is right over some of the key cutaneous nerves. And then you can get this persistent dermatitis right over the surgical site. And as somebody who's done a lot of patch testing, I very regularly got patients referred to me. Because the suspicion was they were allergic to the knee that got put in. And then I'm, you know, talking to them, wow, it's not the knee. It's the surgery damage the skin and the blah, blah, blah, blah. But I had some people who by the time they got to me had had already had their knee their first need taken out a new knee put in because the people thought that this was allergy overlying the medic, the implant, which it was. But it really is this, this denervation dermatitis. And it's just useful to know about this. You treat it like you would any other dermatitis when I see this. I use some topical steroids. I use some derma leave. But it's just important to know that this exists as an entity. Probably not a whole lot of interesting commentary around this patent fair. She guys got anything. I got nothing. No, I'm glad that I'm glad I know about it now. Yeah, that's it. And I like said, I only knew about it because I saw it a bunch of times. Alright, Ferris, why don't you tell us about our next one here. All right, so this was in the New England Journal of Medicine. This is Jed Wollchock at all. And this is the final 10 year outcome of Navellumab plus if you limit map and advanced melanoma. I just thought this is like the final analysis of this incredibly long term study. I just thought we should know the Durham should know about it. So three arms, Navellumab plus if you limit map, Navellumab alone or if you limit map alone, about 315 patients per arm. So they looked out to 10 years because as we know patients can have their melanoma, you know, reemerge later in life. So, you know, when we tell patients, so the question is like, when do you tell patients, yep, that was bad. But, you know, you're, you're out of the woods now. So I think we always say it could come back. You know, they looked at overall survival and melanoma specific survival. And you know, definitely the patients who had who got Navellumab and if you limit map did better than the patients who got Nivo alone and both of those groups did better than the group that got in the if you limit map alone. So, you know, you are still you did not die for melanoma basically, you know, median survival with Navellumab alone 49.4 months median survival wasn't even reached for me for Nivo plus it be at 10 years, right. And survival is 50% of people have died of melanoma 50% have not so, you know, it was actually better to get the combination say you think well, gosh, 10 years, that's forever. But the median duration of treatment was like 2.8 months in that combination group, about 6 and a half months for the Navellumab group alone. And then the thing that I thought was helpful is can you predict who is going to do well. And so, you know, in terms of at 10 years. So if you were progression free at three years, your 10 year melanoma specific survival and the groups that got Navellumab is one of their treatments was over 96%. So, if you're a progress, if you've got, you know, a PD one inhibitor, your progression free at three years, you're probably not going to have recurrence of your disease also same for patients, so at least an 80% reduction in their tumor burden. So, you know, early good response may, you know, predict that you're going to do well. And maybe we can start pulling back on the frequency of surveillance or imaging on some of these patients. I know that's more an oncology issue, but our patients ask us about it too. And so, if there's these were people with melanoma that at baseline, at a minimum, they had a positive microscopic sentinel lymph node. So they had some kind of distant disease. Worst disease. So they had unresectable stage three or four. Wow. So, and so we could now say to somebody with disease, and they've got a positive clinical, you can feel a lump in their neck. We could literally say to them, hey, most people with your disease live at least 10 years. Right, that's technically accurate, correct? Yeah, with with the treatment with, you know, particularly we saw that in the, um, Navale, Mab and if you live in that group. Now, this is all kind of outdated, because if you have a patient, you know, we're going to treat things differently now. We've got different combinations. We've got neoadjuvant therapy that works even better. So this group of dead stage three disease.
They would have had their lymph nodes removed and then would have been treated. Now we know if you get people a couple doses of immunotherapy, then remove their lymph node disease, they do even better than this. So it's good to know the data, but it probably is not exactly how we're going to be giving care over the next, how are you to be treating patients over the next 10 years. But yes, these are people with advanced disease, patients who, when we were residents, we're like, oh, they're going to die. Yeah, good death sentence. It's going to be serious. Yeah. The death sentence. Yeah, I mean, I've got one guy who he got, his initial diagnosis was a met to his brain, like just collapse one day had a seizure, never found a primary on him. He got immunotherapy, you know, why these red metastatic disease? Got immunotherapy's not been my patient, like seven, eight years, doing great. And I'm like, good, like it's just shocking to me, but I guess it's not that rare. I'm going to see that now. Huh? Huh? All right. So Pat, once you give us our last one here, which is one that is actually pretty darn interesting to me. All right. Then topical steroid withdrawal is two papers. First one, I'll, I'll stir home at all and act a dermatovinearialogica January 2025. It was a questionnaire through a Facebook group of patients who had TSW and they just kind of, I think wanted to learn more about topical steroid withdrawal. So it was kind of odd because most of the patients that answered the questionnaire basically self-diagnosed topical steroid withdrawal. They didn't have like a physician diagnosis, which I kind of get, because we don't know how to diagnose this, you know, I think some, you know, the patients who have this do express a lot of nobody believes that this is a thing. And so I'm not even going to go to my doctor. So I think they just kind of wanted to get, the authors wanted to get more information. Figure one kind of shows all the things that summarize most of the findings. They describe the common signs of symptoms, air, theme, itching, birding, sleep disturbance, dryness, peeling, oozing, et cetera. And then they also reported triggers, mostly topical steroids, how often it occurred and the impact that it had on their life. So we know a little bit more. So after article one, this article, do you think it's a real thing? I do. No, I do. But I also think that, you know, a lot of these sufferers are kind of like physicians don't believe me. Well, if you walked into my office and you said, I have a history of atopic dermatitis. And it's really bad. And I used the steroid. And then I stopped the steroid. And my face got itchy red scaly. You couldn't fault me for saying, this could just be your atopic dermat. Yeah, this could just be your atopic dermat. And the fact that, you know, it's like, well, we don't believe them. I'm more than willing to accept that this is a thing. But how can we diagnose it? I have no idea how we differentiate it from other things that it can be. So how do we diagnose this? I mean, do you believe it? I didn't for a long time. But then the second paper here, the topical steroid withdrawal is a targetable excess of mitochondrial NAD plus. But senior author of this guy named Ian Miles at the NIH, who is brilliant. He actually did show that there are some physiologic mitochondrial alterations that they were able to define in the lab. So I do now think it's a real thing. But I still have exactly what you said. No idea how to differentiate it from your exomeflared versus you got addicted to topical steroids when we withdrew it. I mean, the other thing is parodermatitis that is induced by topical steroids. Like, we all would agree that that is a real entity. And it is in many ways different from regular parodermatitis with no history of steroid application. So to me, that also adds my clinical evidence of that's an entity. I know for sure is real. And so it makes sense to me that pathophysiologically, this is out there. But yeah, I still don't know how to differentiate the two. Just to -- Yeah. Yeah. Yeah. What's that? I don't know how to differentiate it. So what do you do? I mean, how are you going to treat this? So I think if -- you know, you could say, I don't know if this is your atopic dermatitis flaring. I don't know. Maybe you're using a face wash -- this is allergic contact dermatitis, which is going to flare pretty badly once you take steroids away. And throw in the possibility that, okay, this could be topical steroid withdrawal. We don't really know that much about it. That's really hard to treat. I mean, honestly, like, I've learned the most about topical steroid withdrawal, like, like, just going on these blogs and reading about these patients. And you're kind of like, all right, yeah, this does behave differently in the way they got it to go away. You know, did they just get better? Like, you know, did they have less stress in their life? And all of a sudden, they're atopic dermatitis get better because I've seen stress cause I atopic dermatitis go crazy. So, you know, reading those individual things, I'm buying it's a real thing. But I think patients have to be a little bit understanding that it's -- we don't know how to differentiate these things. That second paper, they went through -- right, all these different studies. I didn't understand 90 percent of that paper. A couple of cool takeaways. They offer maybe a diagnostic tool. So they put together major and minor criteria, three major, nine minor. If you have one or more major and three or more minor, that was 90 percent sensitive. So the major, burning, flushing, thermo dysregulation, I don't really know how that's defined. And then the nine minor, I'm not going to go through that. Just other symptoms. So, maybe we have a tool that take away was that TSW happens because, quote, there's increased expression of mitochondrial complex one and conversion of triptophan into kind of a remin metabolites. There it is. So now we know. And metformin and burberry, which is an ingredient in traditional Chinese medicine may be therapeutic options. So Matt, you have another reason to give everyone metformin. Give everybody metformin. So, thanks for joining us this week. If you've got questions, comments or ideas for topics you'd like to see us cover on the show, shoot us an email at
[email protected]. Can questions, just the word questions, @dermzondrugs, d-e-r-m-s-o-n-d-r-u-g-s, dot com. I hope you learned a few things. Hope to last once or twice. And I hope you're planning to join us next week. And I do have to tell you, next week is going to be kind of a mind-blower for you. So we're going to have a guy on named Richard Weller, who is a dermatologist in the UK, who has done some amazing work that really suggests that all of the sun protection that we're telling patients to do to prevent skin cancer may actually be substantially increasing the rates of heart attacks and cardiovascular death. So it may be that we are preventing skin cancer by telling our patients to stay out of the sun, but we may be increasing the rates of heart attacks and strokes and things like that. And I will give you the heads up. It has nothing to do with vitamin D. Totally different mechanism. You cannot give people vitamin D to counteract this. So anybody who says that, oh, Tom Steadasson, but take vitamin D means they don't know what they're talking about. All right. So I can't wait for Dr. Weller to come on and really see if he can convince us that this is real and maybe we've been overplaying the sun protection card. So join us next week for what is going to be a really cool discussion. And until then, I'm Matt Cyrus. I'm Tim Patton. And I'm Laura Ferris, and we are Derms on Drone.
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