In this episode of Derms and Conditions, our host, Dr James Q. Del Rosso, reflects on the past year of podcasting, offering a rich summary of key dermatologic topics discussed throughout 2023.

In this episode of Derms and Conditions, our host, Dr James Q. Del Rosso, reflects on the past year of podcasting, offering a rich summary of key dermatologic topics discussed throughout 2023.To start, the episode delves into highlights from an interview with Dr Shane Chapman, who specializes in skin cancer. Dr Chapman shares insights into nonsurgical options for treating nonmelanoma skin cancer, focusing on strategies for cases of squamous cell carcinoma and nodular basal cell carcinoma that may not be amenable to surgical treatment for a variety of reasons. &nbsp;Next, Dr Del Rosso features an episode with Dr Adam Friedman, who explores the topic of sensitive skin as a standalone entity. They highlight the prevalence of sensitive skin and the need for dermatologists to acknowledge and address this poorly understood condition with an open-minded approach.In another segment, Dr Del Rosso revisits the work of Dr Matt Zirwas, who specializes in chronic dermatitis and inflammatory skin diseases. Dr Zirwas shares valuable insights on diagnosing scabies and addresses concerns about the differentiation of cutaneous T cell lymphoma from atopic dermatitis in older patients.Dr Del Rosso concludes with a review of a 2-part series featuring Dr Jeff Donovan, who provides comprehensive insights into alopecia areata. Dr Donovan discusses the many mimickers of alopecia areata and when and how to conduct a biopsy. He reviews treatment options for alopecia areata and discusses the efficacy of newer agents, such as JAK inhibitors, to treat severe alopecia areata. The use of dupilumab in selected cases, especially in children with both alopecia areata and atopic dermatitis, is also reviewed. Other relevant suggestions from Dr Donovan include his perspectives on both clinical and laboratory assessments, his discussion of other inflammatory hair diseases, and tips on differentiating these other hair disorders from alopecia areata along with suggestions on management approaches.Overall, Dr Del Rosso provides a comprehensive review, sharing insights and practical tips from featured experts. It was a great year for the Derms and Conditions podcast, mostly because of those who listened in and the expert faculty who shared their expertise so openly. In conclusion, Dr Del Rosso encourages engagement and feedback from the audience to help shape the direction of future podcast episodes.

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Final Thoughts from 2023: Highlights from Podcasts Past…

Dr James Q. Del Rosso, sits down again with Dr Jeff Donovan, a board-certified dermatologist who practices in Whistler, Canada, with his dermatology clinic dedicated solely to the management of hair disorders, for part two of their discussion on alopecia areata and other hair loss conditions.

In episode 67 of Derms and Conditions, our host, Dr James Q. Del Rosso, sits down again with Dr Jeff Donovan, a board-certified dermatologist who practices in Whistler, Canada, with his dermatology clinic dedicated solely to the management of hair disorders, for part two of their discussion on alopecia areata and other hair loss conditions.Dr Donovan begins the discussion by addressing autoimmune thyroid disease associated with alopecia areata and the appropriate laboratory interpretation and monitoring for these patients. He discusses the comprehensive baseline laboratory tests he collects before initiating JAK inhibitor treatment as well as how he approaches laboratory monitoring during the course of therapy.Next, the pair addresses how to tackle low laboratory values, such as vitamin D and ferritin, that are associated with more severe alopecia areata. Dr Donovan emphasizes that when treating iron deficiency, patient comfort and adherence are paramount. The pair notes that patients genuinely appreciate a thorough and concerned clinician and how important it is to set appropriate patient expectations with treatment.They then transition to the use of dupilumab in atopic children with alopecia areata who experience hair regrowth and how to determine which patients are more likely to respond to this treatment.Next, Dr Del Rosso describes a difficult case of lichen planopilaris, and Dr Donovan shares key clinical and dermatoscopic findings and encourages clinicians to have a low threshold for biopsy when suspecting lichen planoplilaris or another disorder other than alopecia areata, some which may cause scarring. He discusses treatment with topical corticosteroids, intralesional triamcinolone injections, doxycycline, hydroxychloroquine, methotrexate, and cyclosporine in isolation and in combinations and what would constitute an appropriate trial on these therapies. More data are needed on the use of JAK inhibitors for causes of inflammatory alopecia other than alopecia areata.Dr Donovan concludes by mentioning education opportunities available in hair loss and his final words of wisdom regarding alopecia. Tune in to this episode to learn all the details from a true hair expert! &nbsp;

Jeff Donovan, MD

Untangling the Questions and Challenges in Patients with Hair Loss: Part 2

In episode 66 of Derms and Conditions, our host, Dr James Q. Del Rosso, sits down with Dr Jeff Donovan, a US and Canadian board-certified dermatologist specializing in the treatment of hair loss. In part one of this series, the two discuss how to approach patients with alopecia areata.

In episode 66 of Derms and Conditions, our host, Dr James Q. Del Rosso, sits down with Dr Jeff Donovan, a US and Canadian board-certified dermatologist specializing in the treatment of hair loss. In part one of this series, the two discuss how to approach patients with alopecia areata.Dr Donovan starts by discussing conditions that can mimic and easily be confused for alopecia areata, such as cutaneous t-cell lymphoma and lichen planopilaris. Dr Del Rosso asks when a biopsy should be done to confirm the diagnosis of alopecia, prompting Dr Donovan to share his suggestions on biopsy caliber, appropriate sites for biopsy, and the ideal pathologist review of the sample. However, he notes that with strong dermoscopic confirmation, a biopsy may not be necessary.Next, Dr Donovan notes the potential topical treatments for patchy alopecia areata, including topical clobetasol, topical minoxidil, and steroid injections, which are effective treatments for the vast majority of patients and should result in hair regrowth within a few months. Dr Del Rosso then asks about the use of baricitinib and ritlecitinib in patients with severe alopecia areata, defined as having a Severity of Alopecia Tool (SALT) score greater than 50 (indicates 50% hair loss). Dr Donovan notes that in the studies on baricitinib, patients had a severe mean SALT score between 85 and 90 (between 85 and 90% hair loss) but still experienced significant regrowth. However, Dr Del Rosso mentions that the studies have earlier endpoints, which fail to capture regrowth that happens with longer term use, and Dr Donovan agrees that the data is promising and more long term data will help capture the longitudinal effect.Dr Del Rosso transitions to the use of JAK inhibitors for alopecia areata and the favorable safety data around them in this population. Dr Donovan agrees that for younger patients with few to no comorbidities, JAK inhibitors have had minimal safety concerns. However, he notes that he counsels patients that the longer term side effects of baricitinib are currently unknown, as the data only extends to 2 years. He also states that he likes to have patients be on baricitinib for at least 6 months before considering switching to another JAK inhibitor or making a modification like adding oral minoxidil.The two finish by discussing the use of minoxidil in alopecia areata, and Dr Donovan states that the anecdotal evidence is promising, and the drug is well tolerated, but more studies examining the effects are needed. Dr Donovan then mentions that patients &nbsp;with chronic alopecia areata who experienced regrowth on JAK inhibitors should continue therapy to maintain their results, as the chance of spontaneous regrowth is quite low. However, he states that it may be worth waiting to start a JAK inhibitor in a more recent onset alopecia areata, as there can be a high probability of spontaneous regrowth. Tune in to find out more!

Untangling the Questions and Challenges in Patients with Hair Loss: Part 1

In episode 65 of Derms and Conditions, our host, James Q Del Rosso, DO, chats with Ted Rosen, MD, Professor of Dermatology at Baylor College of Medicine and Chief of Dermatology Service at Michael E. DeBakey Veterans Affairs Medical Center, to discuss new developments in psoriasis treatment.

In episode 65 of Derms and Conditions, our host, James Q Del Rosso, DO, chats with Ted Rosen, MD, Professor of Dermatology at Baylor College of Medicine and Chief of Dermatology Service at Michael E. DeBakey Veterans Affairs Medical Center, to discuss new developments in psoriasis treatment.They begin by discussing the current psoriasis treatment landscape and the perception that with effective biologics now on the market, there are no longer any unmet needs in psoriasis treatment. They reflect on the importance of having a variety of treatment options with differing mechanisms of action, which can address variability in patient response. They highlight the novel mechanism of action of bimekizumab, which provides dual inhibition of both IL-17A and IL-17F.The pair then discuss the relationship between IL-17s and candidiasis, noting that while there is a broad spectrum of risk, it is usually minimal and manageable, typically presenting as oral thrush rather than serious systemic infections. Dr Rosen discusses how he counsels his patients about the increased risk of candidiasis when on an IL-17A-F blocker and the importance of balancing risk with the potential benefits.They also delve into the data on bimekizumab, highlighting the favorable PASI 75 results seen at 4 weeks and how it compared to adalimumab, ustekinumab, and secukinumab in pivotal studies. Dr Rosen also discusses how the patient conversation can differ when counseling a patient on an IL-23 blocker compared to a drug with a simplified dosing regimen with an early onset of action.The pair concludes by discussing the dosing regimen for bimekizumab, noting that it’s possible to reduce injection frequency after the initial 16 weeks of treatment and still sustain the same level of efficacy. They also discuss evidence that may suggest adjustments to the bimekizumab dosing regimen may lower the risk of candida.Tune in to this episode to learn more about bimekizumab and its impact on the psoriasis treatment landscape! &nbsp;

Ted Rosen, MD

Does Bimekizumab Raise the Bar of Success for Moderate-to-Severe Plaque Psoriasis? Perspectives from Dr. Ted Rosen

Learn about a new treatment for moderate to severe plaque psoriasis from expert voices in dermatology, go to purespectivesinsriasis.com. That's peer spectivesinsriasis.com. You're listening to the Derms and Conditions podcast. Hi, I'm Dr. Jim del Rosso from Las Vegas, Nevada. And I'm going to be talking to someone that brings me back to the early 1990s when I first met him, when we met at a meeting talking about antifungal therapy and onicomycosis. It's been some time, and that's Dr. Ted Rosen. And anybody who doesn't know Uncle Teddy, I'm not sure what planet you're on, but anyway, Ted is professor and vice chair at Baylor College of medicine, dermatology, and he's chief of dermatology at the VA hospital in Houston. You've been at this position for quite some time, right, Ted? 40 years. 40 years. So quite a bit of experience. So, Ted, we're going to be talking today about anti IL 17, primarily as it relates to, or IL 17, the cytokine, as it relates to psoriasis. But we also know that diseases don't own cytokines. That cytokines play a role in many situations. They have normal physiologic function, but when there's dysregulation, they contribute to disease. And hydratinitis, operativa and some other ones have been identified with IL 17. But one of the things that I've heard a lot of people say is that we have gotten so good with our psoriasis treatments, especially some of the newer biologics. Do we really need anything else? We're pretty much where we want to be. Could anything else be an improvement? And the issue I have with that is we're not getting everybody to pazzi 100 and keeping them there. But what's your feeling about that when you hear that from people? Well, I think we have a nice library with different mechanisms of action. Tnfs, IL 12, 23, 23, Il 17. It's nice to have multiple drugs because no drug is 100% posi 100. I think some of the more new agents are getting close. Certainly, if you look at posey 90, we can get pretty close to that, and we have good persistence of effect, but there's always someone who's going to need a different moa in order to get them well. And the other thing is, even though we have pretty good persistence, you have people who do great on any given drug, and after a long enough time period for whatever reason it is their disease starts to come back, and it probably is good to have a different mechanism of action to use on them, too. So I think the more the merrier. Give us choices and let us use them as we need them. I agree. I like when there's a lot of choices on the menu and there's some evidence. I remember I was with, talking with Jen Cather. There's some evidence that the individual's transcriptome can actually change over time, and the patterns of their response to different treatments might change. So that might explain why we see some differences. But I have some questions for you, because you're a lot smarter than I am. You always have been. I always learn some stuff from you. But anyway, among the several advances we've had with biologic agents for psoriasis, agents that inhibit IL 17 have been major breakthroughs, and we're very happy that we now have a new agent, bimikijimab. Just recently, FDA approved, that inhibits IL 17 a and IL 17 F. Well, I think this. I think we have primarily had IL 17 a blockers in the past. Bridaliumab is a little more broad spectrum because it's the IL 17 receptor rather than entrapping the cytokine itself. But we've had mostly IL 17 a, and they're good. I'm not going to complain about them. But I do believe that IL 17 F can contribute by itself. And I think we have to remember that. Like you mentioned, there are physiologic purposes for these things. And one of the ways the IL 17s work is they can dimerize. So you can have two IL 17 A's, two IL 17 F's, and you can have IL 17 a and f. And all of those have, when they're in excess, may have deleterious effects. So I think that by blocking the f version along with the a version that we'll probably have, and I think this is borne out by randomized clinical trials, we'll have extended efficacy. It's not that the other agents aren't good, it's that we can take a good thing and make it better. I think that's a Beatles song, but at any rate, that's my point. We'll start singing hey, IL 17 instead of hey Jude. Right? Right. But one of the things that I've also had people say to me is that when we inhibit IL 23, IL 23 is what stimulates IL 17 production downstream. Why wouldn't just having anti IL 23 get the job done? But there are other sources of IL 17 like innate lymphoid cells and other types of t lymphocytes. Not all the IL 17 is dependent on IL 23, correct? Correct. And that's why you need to address the cytokine itself in all its sources, and no inhibition is 100%. So if you're blocking IL 23, you're not blocking all IL 23 either. So because 17 is an important downstream. It's an important downstream cytokine for things like psoriasis. And I think, as we've seen clinically now by trials for hydradnitis, you really need to get after it. Right. And psoriatic arthritis and axial spondyl arthropathies. And I think the list is going to get longer and longer as we learn more. So, to me, the take home point here is that by inhibiting IL 17 directly, you're not as concerned about what the source is and only blocking that one source, you're inhibiting it on multiple levels. Correct. That certainly makes sense. Now, what about this history that anti IL 17s have of predisposing patients to development of candidiasis? What I've read is usually it might be oral, maybe sometimes superficial mucosal candidiasis. Rarely is it something that's systemic or a serious adverse event, though I guess that's possible. What's the story with IL 17 and Candida? So, as you know, and I think most people identify me with infectious diseases, this was really my major concern. And so I have a couple of points. It's a great question. So, yes, it is of concern. However, as has been proven with previous and recently approved IL 17 blockers, blocking IL 17 sufficiently to give you very high for psoriasis. Posey 90 and even posey 100 numbers, there really is, if any, minuscule risk of candidemia, something that's serious in the bloodstream, and then it is extremely rare to cause cutaneous candida, and then it can, but not quite as often, cause vulvo vaginal candidiasis. But what it really tends to cause is thrush, oral mucosal candidiasis. And that's because the actual defense mechanisms we as human beings use is different in these sources. So IL 17 plays a very central role in the oral defense against candidate. We all carry candida, so we don't get oral candidiasis because IL 17 does its thing. Candida releases a compound called candida lysin, which stimulates IL 17. IL 17 then makes forward chemo attractants, which call in particularly neutrophils and mononuclear cells, and also upregulates certain other molecules, like beta defensins, they poke holes in the candidate membrane, but in the vulvo vaginal tract, it's actually a totally different mechanism where il one beta is the major defense against Candida there. And that has very little, if anything, to do with IL 17. So if you look at the numbers from all the randomized controlled trials using IL 17 blockers, most of the problem is going to be thrush. It's not going to be vulva vaginal, it's not going to be cutaneous, and it definitely is not going to be systemic candida. And even though it may cause oral candida, it tends not to cause candida esophagitis. Okay, then my next important point is, how do you quantify this? And when you try and quantify it, there is an incredibly broad spectrum of risk. And yes, there is a risk. I will not deny that for 1 second. But let me just give you one example. If you look at the head to head study of bimikizumab against secukinumab. Bimikizumab was responsible for candid infections, virtually all in the mouth, few vulva vaginal, but 21.2%. The risk of candidate infections with secukinumab was only 4.6%. But if you look at secukinumab's own phase three randomized control, the critical, the approval studies, the risk was 13.5%. So you have wide ranges, so you're not going to always see this. And when you do, it's going to be mostly oral. Also, my other point is there are other things that make candidate infections, whether it's with or without an IL 17 blocker, more likely. Right. So if you're going to give an IL 17 blocker, if someone's diabetic, make sure they're in good control. If they drink alcohol, which suppresses the local response, tell them they need to knock off or at least mitigate against that. If they're taking steroids for any reason at all, maybe they have concomitant arthritis, they really should be off the steroids or other immunosuppressives for any other reasons. Just get the patient in a mode where they're less likely to have candida and watch out for it, and you can treat it. We can talk about that if you'd like. Ted, I'm going to ask you to hold on for a second because we're going to get a word from our sponsor, but I have some thoughts and questions for you, so hang on. Visit perspectivesinsriasis.com to read about a treatment for moderate to severe plaque psoriasis. Created in partnership with dermatology experts for dermatology experts, this hub is your one stop educational platform, delivered by respected voices you trust. That's peerspectivesinsriasis.com. So, Ted, I have a question for you. You're in the room with a patient and you're getting ready to write anti IL 17, let's say an anti IL 17 a and f, both being blocked, where you seem to have some increase in the risk of candidiasis. What are you going to tell the patient before you start the treatment? So, as I mentioned, I would just ask about drinking habits and are they taking steroids? So just are they diabetic? Are those things I need to mitigate? Then the next thing is I'm going to tell them, advise them that there is a risk of yeast infection. I'm balancing that risk, which is small compared to the likelihood that an IL 17 a and f blocker is going to give them substantial relief from their psoriasis. And then I'm going to advise them to call me if any of these things happen. I. E. The symptoms of oropharyngeal candidiasis. If you have a white coating anywhere in your mouth, if you feel any, it's usually sort of stinging, burning. It's not usually pain, but it could be, but stinging or burning, any problems at all, even though I don't expect esophageal disease, but any problems at all, swallowing. And if it's a female, most women have had at least one episode of vulva, vaginal. Can they know what it feels like? And the major symptom is itching down below. So if you feel like you're having a yeast infection, let me know. So I'll warn them about the risk. I'm going to tell them that the benefit far out exceeds the risk and then give them some rendition of the symptoms I want them to watch out for. And that's when you holler at me. Sooner the better. And I might just add that in all the Il 17 drugs, all the studies, all the candida infections that have been seen have been amenable to therapy. What's been the typical therapy that's been given? So for oral candidiasis, nystatin suspension, swish and spit, or even swish and swallow. Doesn't matter. Four times a day. There used to be a nystatin pastel. It dissolved in the mouth, but it's off the market now. Clotrimazole troch, which you just let it dissolve in the mouth five times a day if need be. Usually that takes care of it. And if worse comes to worst, oral fluconazole is still a very good drug. And of course, it's the drug of choice for vulva, vaginal candidiasis, a single 150 milligram. And if for some reason fluconazole doesn't work and the topicals haven't worked, we all should be aware that there are at least two new drugs approved for candida. They don't seem to have penetrated much into the derm market. But there's abrexafungirp and otasaconazole. These are great drugs. Or if you want to use an older drug, posiconazole. And even voriconazole should work. But for oropharyngeal disease, most of it responds quite nicely to nystatin suspension or gluterimazole troch. So, Ted, one of the things that really stands out to me when I look at the data on bimikizumab, which there's been a lot collected, both short term, the pivotal studies up front over 16 weeks, looking at Pasi reductions and global assessments, but looking at the longevity effect also. But one of the things that really stands out is, first of all, you have a set dose of 320 milligram injection. You don't have to give multiple doses up front and load it. You started at 320 milligrams injection every four weeks. And we'll get to maybe adjusting that, even spacing that out. But after one shot, after four weeks, the Pazi 75 is about 70% to 75%. And that was higher than when it was compared with some of the other drugs, anti tnfs. It was compared with adolemab. It was compared with eustachinumab 1223. And it was also compared to, as you mentioned, secuchinumab, and was superior, significantly superior to all three of those. But that seems like a very favorable response for just four weeks. Sure. I mean, rapidity of onset is important. It's important for us, it's really important for the patients, of course. But I think you can always tell a patient, look, just bear with me, which I often have to do with the IL 23s. You're going to be okay, you're going to get a response, but it's going to take a little while. And you can usually put the patient at ease in that way. But it's so much more helpful if it works up front. It's also helpful to have a simple dosing regimen. I cannot tell you how many times I've had patients where you have to do multiple loading doses, and they call, how many am I supposed to do? Again, it doesn't matter. They lose it. They forget it. A nice, simplified dosing regimen with an early onset of action is optimal. And then if you look at down the road and you look at years later, you have really unparalleled posi 90 and posey 100. And I'm not a psoriasis guru, but I think many of them now talk about treat to target, target being clear or pretty darn close to clear. You're not going to get another drug that will get you this far towards clear and keep you there. Yeah, especially looking at the bell curve. You may get some outlier, but looking at the bell curve, this drug has substantial efficacy. But one of the things that was also interesting is looking at getting to week 16, the patients that got to Pazi 90. And if you extended it to every eight weeks with that 320 milligram injection, you were able to sustain efficacy very similar than if you continued on every four. So you're now decreasing the amount of injections that the patient's getting. So there's a lot to be learned here. And, Jim, there's another important point. Right there is for all the biologic drugs, and especially for the Il 17s. Although this hasn't been explored in depth, it does appear that there's a dose response in terms of candida. So if you give a lower dose by decreasing the frequency of injection, that's a lower dose, you will, in fact, lower your risk, almost certainly of Candida. So I like that option very much. So, Ted, I think you answered all the questions that I have, and looking forward to seeing you at an upcoming meeting. I know we'll definitely run into each other, but I have one important question for you. And what's that? Do you like your matza balls soft or hard? Oh, my God, I like them soft. If I wanted them hard, I would play softball with them. Or baseball. No, soft. It's funny because Brad Glick and I agree on soft. And Mark Kaufman said hard. And we told him if we would have known that, we would have never voted for him to be president of hard, hard matza balls. Anyway, Ted, it's great to see you. Thanks a lot for sharing this information. You always shed light, especially on the infectious disease area. Nobody does it better than Uncle Teddy. You take care. Thank you very much. Thanks for having me. Thank you for listening to this episode of Derms and conditions if you have any questions, please email us at podcast@dermsquared.com that's podcast at D-E-R-M-S-Q-U-A-R-E d.com. Podcast@dermsquared.com with so much to learn in the field of dermatology about treating moderate to severe plaque psoriasis, we've developed an ondemand resource hub that offers providers like you a collection of relevant educational video content, all delivered by your respected peers. Visit peerspectives in now that's peer spectivesinsriasis.com.

In Episode 64 of Derms and Conditions, our host, Dr James Q. Del Rosso, sits down with Dr Shane Chapman, Chairman of the Department of Dermatology at Dartmouth Hitchcock Medical Center, to discuss nonsurgical approaches to treating nonmelanoma skin cancer.

In Episode 64 of Derms and Conditions, our host, Dr James Q. Del Rosso, sits down with Dr Shane Chapman, Chairman of the Department of Dermatology at Dartmouth Hitchcock Medical Center, to discuss nonsurgical approaches to treating nonmelanoma skin cancer.Dr Chapman begins by discussing topical treatment options for nonmelanoma skin cancer for patients in which surgery would be untenable. He notes that intralesional chemotherapy can be an effective treatment option for keratoacanthomas or squamous cell carcinomas in poorly healing areas, such as the legs, or when multiple lesions are present. He then notes that 5-fluorouracil at 50 mg/cc is superior for treating squamous cell carcinomas, while intralesional methotrexate at 25 mg/cc is preferred for uncomplicated, nodular basal cell cancers, with the potential for reduced scarring. The chemotherapy agent should be injected into the center and around the periphery of the lesion, with 2-5 treatments needed for resolution. In addition, he states that 10 mg of oral acitretin every other day used in conjunction with intralesional therapy can decrease skin cancer growth with minimal side effects.Dr Del Rosso transitions the topic back to intralesional methotrexate, and Dr Chapman mentions that lab monitoring with this therapy isn’t necessary as systemic absorption of methotrexate is negligible. He also states that methotrexate and 5-fluorouracil can be interchanged or used in combination with PDT to treat keratoacanthomas/squamous cell carcinomas. Dr Del Rosso then presents a case of a patient with a nodular basal cell carcinoma on her nasal tip who refuses treatment with surgery or radiation. While he would initially have a discussion with the patient that Mohs would be the ideal therapy, Dr Chapman says that intralesional therapy can be employed with potential enhancement with topical imiquimod or light therapy. He also discusses superficial radiation, which is primarily used as an adjuvant therapy in the treatment of squamous cell carcinomas with perineural invasion and is avoided for lesions on the nasal tip due to the risk of cartilage necrosis. However, he believes that flash radiation, which minimizes exposure to surrounding tissues, will be used more for treatment in the future.Next, Dr Del Rosso asks about the treatment of broader skin lesions, such as superficial or multifocal basal cell carcinomas. Dr Chapman explains that imiquimod and 5-fluorouracil are potential treatment options, and both red and blue light PDT can be used for superficial basal cell carcinomas and larger lesions. He states that red light PDT penetrates deeper and is more effective, but red and blue light can effectively be used together to treat nonactinic keratoses. He applies aminolaevulinic acid nanoemulsion for 30 minutes with 10 minutes under the light for the first treatment and the levulan solution for 1 hour with 15 minutes of light. For second and third treatments, he says that the incubation and activation can be increased if the initial treatment was well tolerated.To end the discussion, Dr Del Rosso asks Dr Chapman how he manages brisk imiquimod responses and how that impacts treatment duration. Dr Chapman will have the patient use a retinoid for 14 days and then start imiquimod for 5 days a week (Monday to Friday) for 4 weeks. Depending on the appropriateness of how brisk the response is, he will either maintain the imiquimod regimen, increase to 7 days a week, or decrease it to 3 times a week. He stresses that imiquimod can be discontinued temporarily if the reaction to application is significant, but the goal should be 12 continuous weeks of treatment for effective results. Tune into this episode to hear the full details and learn more! &nbsp;

Shane Chapman, MD

Beyond the Knife: Practical Nonsurgical Options for Skin Cancer

In Episode 63 of Derms and Conditions, our host, James Q. Del Rosso, DO, sits down with Adam Friedman, MD, to discuss some important topics in dermatology, including a comprehensive resource for portraying skin conditions and his research findings relating to sensitive skin.

In Episode 63 of Derms and Conditions, our host, James Q. Del Rosso, DO, sits down with Adam Friedman, MD, to discuss some important topics in dermatology, including a comprehensive resource for portraying skin conditions and his research findings relating to sensitive skin.Dr Friedman begins by describing his atlas project, created to address a gap in dermatology in the limited way textbooks and atlases portray skin conditions. The Full Spectrum of Dermatology: A Diverse and Inclusive Atlas is a comprehensive resource that depicts dermatologic conditions across the full spectrum of skin tones to help dermatology professionals visualize the nuances in skin conditions.Next, Dr Friedman discusses his research on sensitive skin and how he puts his findings into practice with his patients. He details his global study that looked in-depth at sensitive skin and what factors trigger and exacerbate it, highlighting the importance of dermatologists having tools to assess the condition and provide management strategies. The pair also touch on guiding patients on the use of products for sensitive skin and utilizing samples.They conclude by discussing the importance of early intervention to prevent disease progression and the benefits of initiating more advanced therapies in earlier disease.Tune into this episode to hear more about what’s on Dr Adam Friedman’s mind!

Adam Friedman, MD

What is Dr Adam Friedman Up To Now?

In this episode of Derms and Conditions, Dr Jim Del Rosso and Dr Gary Goldenberg discuss some of the highlights from the meeting. These include recent FDA approvals such as bimekizumab for psoriasis and the triple topical combination for acne vulgaris, the newer nonsteroidal topical agents, tapinarof and roflumilast, and their relevant clinical use, the significance of narrow-spectrum oral antibiotic therapy with sarecycline as compared to other oral tetracycline with regard to antibiotic resistance, and physical devices such as laser systems used to treat acne vulgaris.&nbsp; &nbsp;

Gary Goldenberg, MD

Live From Las Vegas! Greatest Hits from Fall Clinical Dermatology 2023

Now a message from our advertiser, Bristol Myers Squib Sotiktu, to kravacitinib. It's showtime. To learn more, visit www. Dot sotic two hcp.com, spelled www. Dot so tyktuhcp.com, or visit us at the Bristolmeyer Squib booth. Derm. You're listening to the Derms and Conditions podcast. I'm Dr. Jim Dorasso, here with derms and conditions, live at the fall Clinical Dermatology in Las Vegas, 2023. And I have with me, Dr. Gary Goldenberg is one of the course directors, and we're going to be talking about highlights from the meeting. We're thankful for Bristol Myers quib, for supporting this particular podcast, derms and conditions, which hopefully you're listening to every episode, but this is going to be the best one yet, right, Gary, ever best one? Absolutely. So one of the things that was exciting that just happened this week is the approval, the FDA approval of bimbicizumab for the treatment of moderate to severe psoriasis in adult patients that are candidates for systemic therapy or phototherapy. We've been waiting for this for some time. What is different about it is it's an anti 17 IoT, 17 a and f, which adds some punch to the efficacy of the drug. So what do you see with this particular agent as far as advancing or improving the responses in psoriasis? First of all, I want to say that I'm happy to be here with you. I'm always happy to talk to you about various topics, but especially dermatology. I think we're living sort of in the golden age of dermatology, and our patients are very fortunate. And this new drug approval is just a testament to the investment that industry is making in our specialty and in our patients. And I think my kind of thought process on biologics in general is that they just keep getting better and they keep getting safer. So if you look at the data of this new medication, the data looks incredible. Patients are getting really good clearance rates. They are clearing fast. The safety looks very advantageous. And I think it's great to have another tool in the toolbox for treating patients with severe, moderate to severe psoriasis. When you have one out of three patients after a single dose getting to Pazi 90, clear, it's essentially clear. And so the results are, in terms of the efficacy, are excellent. But when I just look at the simplicity of it, it's the same dose. It's great every injection. And I think, look, I think we get really kind of bogged down with these measurements. Passy 90, passy 100, passy 75. When I see a patient with moderate to severe psoriasis, they just want to know that they're going to improve. They just want to know that they're going to get better, that the drug is safe, it's going to be efficacious that they're going to stay better for a long period of time. Because all of our patients that have had various therapies before, they would kind of go back and forth. They would get better, and then they would get worse. They get better and get worse. And some patients, that's even worse than not even improving. I think the fact that they're going to be clear, almost clear, at a very high rate, quickly, with good safety, I think it makes my job so much easier, because the conversations are just. It's a friendly conversation. It's not like the commercials you see on tv where there's a laundry list of potential horrible side effects. And when you go through that, the reality is the other we have are excellent, but this is a significant increment of greater improvement and faster improvement. And as far as the safety, there is a higher risk of candidiasis. But it's typically oral candidiasis that's very manageable. And look, I think no drug is for every patient, and if we had only one medication approved, it would be really a terrible situation. Right. But we now have a long list of highly efficacious and safe medications, and there are going to be some patients who don't get better with every drug where maybe the efficacy wanes. So it's always nice to have something new that you can offer to your patients that has high efficacy and good safety. So it's nice to know this is available. There are some warnings in the product manograph that are important to address. They're all things that we often deal with on a regular basis and are pretty easily managed. Another update that actually came from the EADV, the European Academy meeting in Berlin, is we now have three year data with ducravacitinib, a six milligram tablet given once a day. We now have data to show that the efficacy once you get the patient, and these patients actually do very good. We're talking about Pazi 75, Pazi, 90, and occasionally Pazi 100% clearance with an oral drug, which is better than what we've had in the past, that once they get to that point of the improvement that they're going to get to, which is usually very high, they stay there. They don't drop off in that effect. And in looking at the adverse event profile. Gary, I have a question for you in a moment. In clinical practice, did not get the box warnings that the other Janus kinase inhibitors got. It's a tick two tyrosine kinase two inhibitor, which is a very different profile. And going out three years, there's been no change in the safety signals, so still carries that no box warning, because if there was an increase in those adverse events, that label would be changed. So, Gary, I have a question for you. How often does it come up in discussion from patients that they ask about box warnings or how do you discuss box warnings with your patients? Yeah, first I just want to briefly talk about decrevisitinib because I think it's a great improvement in oral options that we've had in the past. And look, not every patient is the right patient for a biologic. And some patients want to try an oral treatment before they go in an injectable. And I think having something that has really good efficacy and now three years of safety data makes an easy conversation. And what I think we see with a lot of medications, especially some of the newer drugs that have come out in the past, let's say five to ten years, is once the safety is established short term, it appears in a lot of these drugs, this one included, that they continue to stay safe where some of the medications that were approved, let's say, 1520 years ago, that wasn't always the case. So here I feel a lot more comfortable giving a patient something that I know has good safety for a long period of time. And look, the fact that it doesn't have a black box warning is certainly helpful. Having said that, I'm also comfortable using drugs that have a black box warning. And you just have to sit down and talk to the patient about the warnings. And look, our patient population is fairly healthy. We're lucky overall. And a lot of these warnings come from other specialties. Some of our colleagues take care of patients that may be on multiple immunosuppressants or immunomodulators. They're older, they're older, they're more sick, they have more comorbidities, they're on other medications. They may also have some immunosuppressive or other adverse events. So I think once you talk to the patients and say, look, if you just look at the data in dermatology, patients like you that are not also going to be taking other medications systemically that can affect your immune system, I think patients are more likely to understand, and there are recommendations on how to monitor the patients, what blood tests you need. And we've done that in the past with many other medications. At the end of the day, we're doctors, so it's sort of our responsibility to make sure we're keeping patients safe. And look, if you can't interpret a laboratory report, then perhaps you should be doing something different. That's a consideration? Absolutely. Let's pause for a message from our advertiser, Bristol Myersquib. So tick two to kravasitanib. It's showtime. To learn more, visit www.sotictuhcp.com, spelled www dot so tyktu hcp.com, or visit us at the Bristolmeyers squib booth. So I want to move on to another area, and I think it's really a great time in the area of having other things than topical corticosteroids. And topical cordic steroids are very important to us. They can give us a quick impact when we need it to get a disease under faster control. But they're not something that we want to be using for long term. But when that was all we had, that's what we had to work with. But we have newer non steroidal agents, and I'm talking specifically about topical topinorov, which has a mechanism through aral hydrocarbon receptors, which was novel. Reflumolast, which is a topical phosphor diacerase four inhibitor that isn't associated with the stinging and burning of a previous agent that's in a different formulation, and it has different characteristics. I personally think both of these, they're approved for psoriasis right now. Refumoas just got down to six years of age for plaque psoriasis. They work extremely well. Some people it kicks in very fast. Some people it takes longer. But you can have them keep using it because you're not concerned about the safety aspects of it. So I use them frequently. I find them very effective. But what's been your experience? I'll never forget, starting in dermatology in 2003, Joe Yuritza used to tell patients all the time that topical steroids are fast to work, fast to come back, and non steroidals are slow to work, but slow to come back. I still use that in my practice. So if somebody comes in and they need an acute treatment, I will use a moderate amid potency to a stronger steroid to clear them, and at the same time, not waiting to stop the steroid. At the same time, I'm also adding a non steroidal absolutely. And once they're improved, let's say two weeks or whatever time it takes with a steroid, they transition off the steroid and they continue to stay on a non steroidal. But I start the non steroidal at the same time. At the same time. You have to. And then tell the patient. Correct. This is when you stop the corticosteroid. I do the exact with the corticosteroids. It's not how strong, it's how long. That's when you get into trouble. Right. If you use something for up to, let's say two weeks, four weeks, different drugs have different approval time periods because that's how long they've been studied. But I'm comfortable using a steroid for two to four weeks if it's necessary. Usually it's not even necessary. Sometimes it may not be, may not be. Right. But once they transition off the steroid, they stay on a non steroidal to continue to get their condition, to have their condition under control. Keep it in check, because, look, we know what happens if you stop it. It's going to come back. Right. It's going to come back at some point. And then I tell my patients to keep the steroid in their medicine cabinet just for an emergency use if they feel like their condition is getting worse. And conditions always get worse, it could be stress related diet, health changes, any of those things that increase your inflammatory milieu in your body systemically are going to make your inflammatory skin conditions worse. They can use that steroid as a rescue if necessary. I'm a little bit careful because it depends on the location of where 100% that might be happening. But if you educate patients properly, I think that it's very helpful. And this is the same conversation we just had about the black box warnings. I think if you actually take the time to sit down and talk to your patients and make them understand what the issues are, what's the right thing to do, what's not the right thing to do, and we write everything out for them. And I really believe that if you keep it simple, they'll kind of follow the instructions absolutely and do what they're supposed to. If you rush in and out, keep everything as simple as possible. The kiss principle works for just about anything. But I think if you're rushing in and out, I think patients, patients only remember 50% of what you tell them. Exactly. That's why I think written instructions, they remember 50%. That's high. Right. The other thing about these is they're both have great data for atopic dermatitis. They're very well tolerated. Not approved yet for atopic dermatitis. And reflumo asked in a foam rather than a cream. The phase three data is now out for separate dermatitis on the scalp, but also on the skin and other areas. Very, very impressive. I have to say that I look at these two new non steroidals the way I look at steroids. A steroid cream may only have approval, let's say, for psoriasis, but we know that it's also going to work for atopic eczema, for sebrique dermatitis, for contact dermatitis, anything that's inflammatory, if it has an anti inflammatory pathway, it might work for. So I've tried both of these off label for various inflammatory conditions, including the ones I just mentioned extremely well and look like any other drug. They work great for some patients, and for some patients, they may need something else. But I think we have the tools to really kind of expand the treatment algorithm for our patients, and that at the end of the day, we have to do what's right for the patient in front of us. Well, it's not that long ago that top of the corticosteroids, the package insert, said they're approved for use in corticosteroid responsive dermatoses. That's a very broad label. Right. But then they got specific. Oh, you only studied it for this? That's the only disease that's FDA approved. But we know that these will work in other areas. But I have another question for you, because we need to move on in the interest of time. What about in the cosmetic arena, what one or two things that really stood out at this meeting that you think are really important? I think acne is an interesting condition. We just had a triple combination therapy approved just this past week, and I think that acne is a condition continues to grow and change. In my practice. Most of my, I would say 90% of my acne patients are adult women, and some of them never had acne as teenagers or just had a few pimples, never really had severe acne. So I think it's important that we're continuing to develop tools specifically for that population. It is the fastest growing segment of the acne patients. And I think in my practice, I like doing procedures. I use more and more devices to treat acne, and I think that those are great tools to add to sort of what we're used to using for acne patients, such as topical retinoids and other combination therapies. Maybe some oral antibiotics. There are some that are more specific for acne as opposed to being sort of more broad. Even isotretinoin, I think, is still a very good option for some patients. But having a procedure, something that I know compliance is going to be 100% because I'm doing the procedure for the patient. You have the patient there. But on that topical therapy side, we now have benzoyl peroxide with tretinoin in a single formulation. The microencapsulation allows that we have the triple topical with quindamycin, adaptoline and benzoyl peroxide, but we also have topical closcoderone, which is the first time we've had an androgen receptor inhibitor that can be used in males and females. But if you think about utilizing benzel peroxide with a retinoid, or benzel peroxide with a retinoid and clindamycin, and now you're also using topical glasgodarone, you're hitting all four pillars with a topical therapy approach, which we've never been able to do before. But what about the devices? There have been lasers that have been approved more recently for acne, and I know, you know, you've done some work with those. Any thoughts on that? Yeah, I love the laser devices for acne. I think that there's advancements. We now can target the acne more specifically, and there are some devices that they can target the bacteria that causes acne. Acne is always a conversation. It's like the chicken. And what's the ones that have been approved now? The one that I've used the most is called aviclear and it's a 1726 pulse wave laser. And there's another one that's approved as well. And I also like the 1064 lasers for acne, for maybe more mild acne. And then I also like using microneedling with plateletrich plasma. I think for a patient that has both active inflammatory acne and some acne scarring, it's a really, really good option. So I'll end up with your discussion about the oral antibiotics doxycycline and minocycline, except for the extended release formulation of minocycline, were grandparented in. They're broad spectrum antibiotics, they work for acne. But saracycline, which is FDA approved for acne, specifically nine years of age and older, the primary data was on the face. They do have secondary evaluation on the trunk at work at both. But what makes it attractive, I think, is the side effects that we typically see and associated with tetracycline, whether it be GI upset, vaginal candidiasis, photosensitivity, were very low, but it has a narrow antibiotic spectrum, and it spares almost completely the organisms that are in the GI tract, the gram negatives, its activity is primarily gram positive. The GI tract microbiome is very popular in terms of discussing, not wanting to perturb that microbiome. So I'd like to end with your thoughts on. Yeah, I really love this conversation. In fact, there are some companies that are now developing drugs that specifically target the bacterial populations in the gut for inflammatory conditions, such as psoriasis. And I think that we're just scratching the surface with our knowledge of the gut microbiome, but we do realize more and more just how important it is. So I think having an antibiotic that doesn't disturb it as much is a huge advancement for our patients, because our patients don't stay on an antibiotic for a week or ten days. They're on it sometimes for months at a time. Right. So I think having. But, Gary, even with those short courses, there's data with these antibiotics that destroy the microbiome. Yeah. Those completely. Bacteria persist for months to years. 100%. I agree with you. But for us, it's even more important because our patients. Down for so long. Exactly. So I think using something that's more specific is very important. I always counsel my patients to make sure that they're taken in live bacterial cultures at the same time. So whether they're taking a probiotic or they're eating a food that's rich in bacterial cultures, usually it's a fermented food. Those are things that we can do just to preserve the patient's general health, because like you said, sometimes it takes a very long time for the gut microbiome to recover. And sometimes we now have evidence that sometimes it never recovers. So we want to keep our patients healthy, not just their skin beautiful and clear, but healthy overall. And I think that's just another thing that we can add to our. Even if you're not fully convinced, if you can avoid the problem in the first place, why wouldn't you? But you said, scratching the itch. We don't have time to go through all of this. But itching has really gotten a lot of attention, and we have agents that are now approved or in development for paragonagularis, more coming with atopic dermatitis, but we'll have to put that off to a future. Sounds great discussion. So we want to thank Bristol Myers Squibb for supporting this particular podcast. And Dr. Goldenberg, as usual, you are elucidating to our colleagues. Thank you so much for having me. I appreciate it. Thank you for listening to this episode of Derms and Conditions. If you have any questions, please email us at podcast@dermsquared.com that's podcast at D-E-R-M-S-Q-U-A-R-E D.com podcast@dermsquared.com and now a message from our advertiser, bristolmeyersquib sotic two to kravacitanib. It's showtime. To learn more, visit www.sotiktuhcp.com, spelled www dot so tyktu hcp.com, or visit us at the Bristolmeyersquib booth.

In episode 61 of Derms and Conditions, our host, James Q. Del Rosso, DO, presents a self-made episode where he clarifies key points on many therapies relevant to everyday clinical practice. First, he discusses topical alpha-agonist therapy for persistent facial erythema (PFE) of rosacea. Long-term data shows that daily use of either topical oxymetazoline or brimonidine appears to “reset” (lower) the baseline level of PFE in patients with rosacea.

In episode 61 of Derms and Conditions, our host, James Q. Del Rosso, DO, presents a self-made episode where he clarifies key points on many therapies relevant to everyday clinical practice. First, he discusses topical alpha-agonist therapy for persistent facial erythema (PFE) of rosacea. Long-term data shows that daily use of either topical oxymetazoline or brimonidine appears to “reset” (lower) the baseline level of PFE in patients with rosacea.Next, he talks about subantibiotic dosing of doxycycline and how its anti-inflammatory properties, including support of the dermal matrix, can be used for the treatment of rosacea. He notes that studies have demonstrated reduced antibiotic selection pressure with decreased emergence of antibiotic-resistant bacterial strains with this therapeutic approach. Additionally, monotherapy with subantibiotic dose doxycycline used as maintenance treatment has been shown to be effective in reducing relapse of papulopustular rosacea (PPR), an approach that is appealing to those patients who do not prefer or are not compliant with topical therapy. Dr Del Rosso then mentions sarecycline, a narrow-spectrum tetracycline FDA approved for the treatment of acne in patients &gt;9 years of age, which has also been shown in a large pilot study to be effective for PPR. Microbiological data demonstrates that the narrow antibiotic spectrum of sarecycline spares activity against many strains of bacteria, especially gram-negative organisms that inhabit the GI tract.He then transitions to hidradenitis suppurativa (HS) and the welcome emergence of IL-17 inhibitors for HS, which are very effective based on study results to date. Dr Del Rosso stresses the importance of early consideration of biologic therapies (such as anti-IL agents) for HS, as this disease progresses below the skin surface with eventual development of sinus tracts and scarring. If we wait until we “see” these consequences, it is too late as they have already occurred. FDA approvals and published guidelines typically depend on visibly seeing the clinical manifestation before a specific therapy is recommended, which is not early enough in many cases.He finishes with a discussion on dupilumab for the treatment of atopic dermatitis, which is often remarkably effective but at times may be limited by partial efficacy or side effects such as conjunctivitis and facial erythema. Dr Del Rosso discusses practical use of JAK inhibitors such as abrocitinib and upadacitinib for AD in dupilumab “nonresponders” and also case reports with tralokinumab, a monoclonal antibody targeting IL-13. Tune in to this episode to learn more!

Once Is Not Enough: Round 2 on Therapeutic Insights

You're listening to the Derms and Conditions podcast. So I'm Dr. Jim Dolasso, a dermatologist in Las Vegas, Nevada. And one of my wishes is that all of you find the Derms and Condition podcast that we've been doing. Now, we're into our third season, a third year, that you're finding them beneficial, and that's really important to me and to the team that puts them together. So we hope that they have been, we hear that they are, and we hope that that continues today. I'm going to be bringing you an episode where I'm flying solo periodically. I do that after hearing a lot of information from different people at meetings, reading, talking to people on these podcasts. A lot of things come to mind, and I really want to focus on some therapies that I think there's some information that's important that you may or may not be familiar with. And one of these is the use of alpha agonists. Topical alpha agonists. We have two. We have topical bromonidine and topical oximetazoline. There are some differences between the two of them in terms of the subalpha receptors that they interact with, but the bottom line is they're designed to reduce the persistent facial erythema that's due to the dilated vasculature, right. Not related specifically to the redness from papules and pustules. But there's an important aspect to the use of alpha agonists, which are applied each day and over a period of time. Usually, they'll kick in within an hour to a couple of hours, and you'll have the decrease in the persistent facial erythema that will usually go for a good 1012 hours or longer, but then it comes back and you have to apply the medication the next day. Both of these agents were studied being applied once a day. An important factor that really wasn't a primary endpoint, but was something that was observed over a year's use with either agent, topical vermontidine, or topical oximetazzoline, and the solutions that are designed for use on the skin. The solution of the cream designed for use on the skin is that if you look at the baseline erythema, that diffuse persistent facial erythema in the very beginning, before the start of the study, and you look at it on the last day, after 52 weeks, the baseline before they treated on that last day, overall, the magnitude, the severity of that baseline erythema goes down across the group that's treated in the study. So there's some sense that you're resetting with the continued use of the topical alpha agonists every day and that vasoconstriction that you're allowing to occur with their use, that you reset the baseline of the amount of erythema they have each morning when they wake up before they utilize the medication. And that's a very important concept because hopefully we're resetting or we're having influence on the disease progression because a lot of people will use these agents. Prn only when I'm going out and I don't want to look as red, but I think it's really important if you're really trying to treat all the different manifestations of rosacea, that component of it, to utilize an alpha agonist every day and hopefully see over time that that baseline redness diminishes. Another area that I think is important to differentiate when we talk about antibiotic use and we hear about antibiotic stewardship and antibiotic resistance, and to some dermatologists it's like, I don't really know that it's something that I see or that I'm that concerned with. Others understand it when we have a patient use a topical antibiotic or a systemic, usually we're using an oral antibiotic, you're going to have a selection of agents of bacteria that are responsive because they're more sensitive to that antibiotic. So ones that are less sensitive are going to emerge and you have selection pressure leading to the emergence of resistant strains. And then you can have some other mechanisms whereby continued exposure can select out some resistant organisms. So there are two concepts that have been discussed. One is anti inflammatory dose doxycycline was what it was initially called, but now we call it sub antibiotic dose doxycycline, which is FDA approved for papules and puffels of rosacea. And initially it was a 20 milligram twice a day of an immediate release doxycycline and then eventually the modified release to 40 milligrams once a day became FDA approved specifically for rosacea, papules and pustules of rosacea. Keeping in mind that this therapy was initially developed, the original brand product was called periostat because it was for periodontal disease. We know that when you give tetracyclines and certainly with doxycycline, you have some antiinflammatory effects that are unrelated to their antibiotic effect. And one of those effects is to inhibit collagen breakdown. And that was noted in the gum tissue, the gingiva of individuals. And it was developed to try to assist in preventing breakdown of collagen of the gingiva. Right. And that's where it started. And then noticed by some individuals that people that had rosacea, papules and pustules, that improved. So this therapy eventually got into dermatology. So now, looking at the sub antibiotic dosing, there were a variety of studies done out of stony Brook by Dr. Gollop, where he looked at several different analyses to look at the anti inflammatory effects and found a breakpoint with doxycycline that he wasn't able to find effectively with the other tetracyclines. Right. And there's a dose below which you're not getting what's felt to be significant antibiotic activity. It's not necessarily zero, but you don't see the progressive emergence of several different, in this case, doxycycline resistant strains, but you do see the antiinflammatory effect being sustained. And that has been proven for papillopustular rosacea, with particularly that 40 milligram modified release doxycycline. Studies that were done over a prolonged period of time showed that there was no what was believed to be relevant or any significant emergence of resistant bacteria. Right. That were tested in the mouth, tested in the GI tract, tested in the vaginal flora, on the skin. So that's where the idea of giving something that can help reduce papules and pustules of rosacea and get around selection of resistant bacteria came to light. And I still think that is very important. And there is data on long term treatment, of utilizing only that particular therapy to try to maintain control of papillopusteurization without a topical agent. Now, that sounds like heresy, but there are some people that do better with taking one capsule a day, for example, than necessarily utilizing a topical agent regularly. So you do have that option, and I think you can feel comfortable that you are obviating the emergence of resistant bacteria to a significant degree. Now, there's also a concept, and there's a lot of data to support that, quite frankly, several references. There's also the concept of narrow spectrum tetracyclines with the development of saracycline. And that's really the only new agent that we've had come to light was FDA approved on a weight based dosing with saracycline, oral saracycline patients with acne vulgaris down to the age of nine. Right, nine years of age. And looking at it from a microbiologic perspective, it's narrow spectrum as compared to doxycycline and minocycline, which are approved as antibiotics for the treatment of a variety of different infections. Right. And so these are agents that have a broad spectrum of antibiotic activity. They're certainly used for acne and sometimes for rosacea outside of the FDA approved minocycline, which is an extended release minocycline, or the sub antibiotic dose doxycycline. Other than that, they are grandparented in for acne. They never receive formal approval based on large scale studies and phase three studies, but they're so widespread in their use and they're accepted as a standard care. But when you give someone immediate release doxycycline at an antibiotic dose, which is typically thought of as more than 50 milligrams a day, or minocycline in a formulation that's not one of the extended release formulations, you are going to get emergence of resistant bacteria. And it's not necessarily selective. It doesn't spare a lot of gram negatives or gram positives. It's very broad spectrum. Saracycline is narrow spectrum. It's still antibiotic, but its activity is primarily against gram positive organisms. So that would be the c acnes, which used to be p acnes that were targeting in acne. Because it's only approved for acne, it's not approved as an antibiotic. It was only evaluated for acne, just like extended release minocycline was. Right. But it spares gram negatives significantly. And that's based on mic evaluations and some other studies that were done looking at microbiologic profiles, where if you give serocycline, it spares gram negatives, it spares also several different anaerobes. Right. And so the GI tract microbiome is felt to be spared with saracycline, at least based on the mics, which is something that's important because we don't want to disturb any microbiome, especially the GI tract. Now, there are data with other antibiotics like quinolones, extended activity, penicillins, minocycline, et cetera, where when you give these antibiotics and you get resistant organisms in the GI tract, they can persist after the antibiotic is stopped, even azithromycin. This has been shown in some compartments. You have those resistant organisms persisting for several months to even years. So that's the basis of saracycline being a narrow spectrum tetracycline agent. So that is a differentiating feature and something to consider though we do need more data, we do need longitudinal data. The other thing I want to discuss is hydratinitis separativa is a disease that, for years, when I saw it, except when there were milder cases that tended not to seemingly be progressing and becoming more severe. And I can control them with intralesional triumphsinolone injection and chronic antibiotic therapy, et cetera. When patients came in and they had any significant disease, it was heartbreaking. And the struggle was, I was having difficulty really helping these people. They're in pain. They get scarred down in areas. It's in the axilla, it's in the groin. Sometimes it's on below the breasts. Right. And it could even be more diffuse, and it's very, very difficult to treat. It was heartbreaking, and a lot of times I felt like I really wasn't helping patients very much with the advent of anti tnf agents, like we've had out of limumab, but now we have anti IL 17 agents that are knocking at the door for approval, FDA approval, that, based on the data, to me, look very significantly effective for hydratinitis separativa. But my concern is with any of these agents, that we get FDA approval and we understand their use overall. They're very, very safe. They have some considerations. They are expensive treatments. They clearly are so much better than anything we've had before in really improving the disease and significantly suppressing the disease. Now, my concern is the way guidelines are written, and if you look with hydratinitis, when they're talking about Hurley stages, Hurley stage two of the three stages, you're already seeing scar formation, and with hydratinitis, you're looking at the skin. It could look normal at the surface, or you may see some older lesions that have resolved, some pigmentation, et cetera. You don't know what's going on under the surface until the volcano erupts. And at that point, it's likely too late. They already have some scar formation and some sinus tract formation, and you can certainly see that in some cases, especially if they've had the disease over a period of time. My concern is that guidelines, typically for diseases, typically wait until you see the problem before you initiate the patient. When you have a disease like hydratinitis suprativa, that causes sinus tracts and scarring, I don't want to wait till I see that problem, because the horse is already out of the barn and running way in the distance away from when you can close that door. So I think we're going to have to pay a lot of attention, especially as more agents come along, like we have with the anti IL 17s. Right. That we really need to be looking at initiating therapy earlier so we can look at suppressing the disease to get it under control and sustaining the control of the disease, much like we're doing now with biologics for psoriasis and even atopic dermatitis. We're not only treating that peak of the roller coaster ride, we're treating that disease that's really there every day. It may be what lies beneath or what is less active, but it's something that they have every day of their life. So we're not only controlling flares, we're actually treating the disease itself. My concern is still a lot of these patients are going to get the therapy too late because the guidelines are going to be written in that way, or the FDA approved prescribing information is going to be written that way, and there's going to be pushback on earlier prescribing. So that is a concern I have, I think especially hedridinitis, because it does scar, it does lead to a lot of pain, does lead to sinus tracts. Early treatment is even more important, I think, with that particular disease. So I do want to end with a discussion of a topic that we hear a lot about. We hear a lot about atopic dermatitis, for example. And if patients are not adequately controlled with topical therapies, prescription topical therapies, or previously used agents that they may have used even if they were some of the older immunosuppressive agents, like cyclosporin, methotrexate or corticosteroids, intermittently, that it's time to think about utilizing a monoclonal antibody. Right. One of the ones we have, like topiliumab, now we have trollachinumab, leprechiziamab is knocking on the door, or one of the Janus kinase inhibitors that we have, like abracitinib or upaticitinib. Right? And here we have agents that really have dramatically improved the quality of life of these patients that have very severe itching, extensive disease. Been on that roller coaster, that frustrating roller coaster, getting to the point of utilizing too much systemic corticosteroid or just can't use enough topical corticosteroid. Right. Because of limitations on how long you can prescribe it over to wide body surface areas. Even newer non steroidal agents that we have going to be limited to some extent by the body surface area that they can cover. Right. So now we're going to these systemic agents. But we often hear about with depiliumab because it's been around for six years, right. And we've had it. And it significantly helps many of the patients approve down to six months of age. Right. So it has a tremendously successful track record of success and overall very good safety. But we do have some patients that occasionally may have problems with it. Maybe they get some form of diffuse erythema or the red face that we do see some cases of that that become difficult or conjunctivitis that isn't mild or doesn't diminish with time or is difficult to adequately control, fortunately uncommon. But we see these situations, cutaneous eruptions or they're just not responding adequately based on the clinician or the patient's complaint about the symptoms that they have, moving them on to something else. And that's where the Janus kinase inhibitors have really become a part of the conversation. Now, they can certainly be used, those agents can be used in patients that didn't necessarily previously utilize a biologic, that's based on individual assessment and discussion with the patient of the benefits of those drugs, working very fast, having what looks like the highest efficacy data, with the higher doses of those agents especially. So they certainly have a definitive place and they do shut down itching very, very rapidly and successfully. There are data with both upaticitinib and abracitinib that in patients that had been treated with depiliumab, that if they have had an incomplete response or some other difficulty and they're switched to one of the Janus kinase inhibitors, that they'll get an incremental improvement in their response. So there's certainly data to support that. However, what's not talked about is if you have a patient, let's say that's using depiliumab and one of those situations comes up, can you switch that patient now to trallicinumab? Now trallicinumab is an anti IL 13, where dupiliumab is anti Il four and antio 13. And that does seem to correlate with some differences, maybe sometimes the efficacy, but even sometimes some of the reactions that patients may have right now, anti IL 13 is certainly effective in atopic dermatitis. And we now have a collection of case reports that appearing in the literature in patients that for whatever reason depiliumab was no longer being used, or some cases where they develop problematic conjunctivitis, where when they were switched to trallicinumab, they were successfully treated in terms of efficacy and did not have the conjunctivitis that they had with depiliumab. Now trallicinumab, in the studies there can be conjunctivitis, but it's not necessarily going to be those same patients. There are a collection of case reports that show that. So that gives us another option that we need to look at more. Even if they started in trolicinumab and they didn't have an adequate response, switching them, or if they got conjunctivitis, switching them to depiliumab, and I've not seen cases of that reported, but that may be a potential option or the option of Janus kinase inhibitors. So my take home point is we really have to have an open mind because we're going to run into patients that have a variety of different scenarios with any of these drugs, and we have other options that may be very helpful and successful in these patients. So stay tuned. We really have to look at this in more detail and hopefully get more studies and even good case report selections and reports that help us. There was even one patient that had difficulty with depiliumab with some erytheminous eruption was changed to upaticitinib, and they had difficulty with cutaneous eruption, and they responded to trolley kinumab. One case, an n of one. But we have to have an open mind in going in all these different directions. So I hope that helps you in thinking about some of the therapies that we use. And I hope you continue to tune in to derms and conditions because I will have my usual sequence of tremendous speakers. You're not just going to be stuck with Jim Delrasso, thank you very much. Thank you for listening to this episode of Derms and Conditions. If you have any questions, please email us at podcast@dermsquared.com that's podcast at D-E-R-M-S-Q-U-A-R-E D.com. Podcast@dermsquared.com you it.

In episode 60 of Derms and Conditions, our host, James Q. Del Rosso, DO, sits down with Cheri Frey, MD, the residency program director of dermatology at Howard University. The 2 discuss how to address skin care with patients and key products that should be incorporated into a skin care routine for specific skin types and populations.

In episode 60 of Derms and Conditions, our host, James Q. Del Rosso, DO, sits down with Cheri Frey, MD, the residency program director of dermatology at Howard University. The 2 discuss how to address skin care with patients and key products that should be incorporated into a skin care routine for specific skin types and populations.Dr Del Rosso begins by asking Dr Frey about her approach to advising the general patient on their skin care. She notes that interest in skin care has grown tremendously, and dermatologists are rightfully being increasingly viewed as the foremost skin care experts. She recommends that dermatologists embrace and directly incorporate skin care into management recommendations for patients and should also consider offering products to patients directly in the office for efficiency and convenience. She also stresses the importance of validating the patient’s concerns by confirming that their dermatologist is the appropriate person to consult.Next, Dr Del Rosso delves deeper into Dr Frey’s more specific recommendations for skin care. She notes that while it is difficult to generalize, data supports typical concerns that are more prevalent in certain populations, such as hyperpigmentation with darker skin tones. She recommends incorporating toners with salicylic acid and glycolic acid into acne treatment routines to tackle pigmentation. Additionally, she acknowledges that patients reluctant to discontinue using an unessential type of skin care product that may not be optimal for their skin should instead be switched to a better alternative to maintain the patient-physician relationship.They then switch topics to discuss skin care tips for dry skin. Dr Frey mentions that African American patients should use moisturizers rich in ceramides, as their skin is likely to be more deficient in this lipid based on current evidence. She emphasizes the need for open discussion and education about these skin care trends with patients. Dr Del Rosso finishes by asking about some common helpful ingredients. Dr Frey notes that ascorbic acid has beneficial antioxidant properties. She also favors niacinamide 3-5% for its antioxidant activity and recommends having glycolic acid in moisturizers specifically for concerns with dyschromia. Tune in to this episode to learn more! &nbsp;

Cheri Frey, MD

A Closer Look at How to Address Skin Care With Your Patients

In Episode 59 of Derms and Conditions, our host, James Q. Del Rosso, DO, continues his conversation with Christopher Bunick, MD, PhD, an associate professor of dermatology at Yale University School of Medicine who performs specialized research on novel treatments and therapies.&nbsp;

In Episode 59 of Derms and Conditions, our host, James Q. Del Rosso, DO, continues his conversation with Christopher Bunick, MD, PhD, an associate professor of dermatology at Yale University School of Medicine who performs specialized research on novel treatments and therapies. After discussing sarecycline for acne in part 1, the 2 switch gears to monoclonal antibodies (MAbs) and Janus kinase (JAK) inhibitors.Dr Bunick begins by discussing dupilumab, an IL-4 and IL-13 blocker with significant clinical efficacy and a favorable safety profile in treating atopic dermatitis (AD). He states that in a network meta-analysis, upadacitinib and abrocitinib were shown to be more effective at treating AD than dupilumab, but dupilumab was shown to be more efficacious than tralokinumab and lebrikizumab. Both agree that despite the similarity of many of the MAbs on cursory review, especially with the capability to inhibit IL-13, each agent needs to be evaluated independently due to structural, pharmacologic, and pharmacodynamic differences. They noted case reports where tralokinumab was effective and well tolerated in treating patients with inadequate response or problematic conjunctivitis with dupilumab. &nbsp;Next, they discuss IL-13 signaling in more detail, which is increased and more persistent in tissues compared to IL-4. However, Dr Bunick explains that IL-4 has more potent signaling, so IL-13 isn’t necessarily more clinically relevant. He notes that more research is required to further understand the structure-function mechanisms of cytokines within cells. He then mentions the noncanonical receptor, also called the decoy receptor, for IL-13, which may explain some differences in drugs that inhibit IL-13.Dr Del Rosso then addresses a very important recent publication by Dr Bunick and colleagues that evaluated adverse effects of special interest (AESI) of conventional immunosuppressive drugs as compared to 2 oral JAK inhibitors, upadacitinib and abrocitinib, used for AD. While the study population that used conventional immunosuppressives addressed a patient population beyond AD affected by more comorbidities, Dr Bunick notes that the risk of AESI also exists for these agents and is not limited to only JAK inhibitors. Dr Del Rosso agreed that many risk factors can contribute to AEs and not all the focus should be placed on JAK inhibitors. Tune in to this episode to learn important details about understanding and using monoclonal antibodies and JAK inhibitors!&nbsp;

Christopher Bunick, MD, PhD

Improving Our Understanding of How Drugs Work: Clarifying Questions with Monoclonal Antibodies and JAK Inhibitors

In episode 58 of Derms and Conditions, our host, Dr James Q. Del Rosso, presents a self-made episode where he discusses some clarifications regarding commonly misunderstood therapies in dermatology.&nbsp;

In episode 58 of Derms and Conditions, our host, Dr James Q. Del Rosso, presents a self-made episode where he discusses some clarifications regarding commonly misunderstood therapies in dermatology. Dr Del Rosso begins by discussing the use of benzoyl peroxide (BPO) for papulopustular rosacea and notes that many providers are hesitant to use this treatment given the perceived irritant effects. He notes that the microencapsulated BPO 5% cream (FDA approved EPSOLAY®), specifically formulated to allow for the slow release of the drug in the skin, is the only formulation proven to be efficacious, safe, and tolerable in rosacea. He summarizes a 12-week study of patients with moderate to severe papulopustular rosacea in which 25% of patients were clear or almost clear at 4 weeks with total inflammation reduced by 70% at 12 weeks. In addition, he notes that the tolerability was favorable with no differences noted between the active and vehicle groups.Next, Dr Del Rosso discusses clascoterone 1% cream, FDA approved for twice daily use for acne in patients aged 12 years and older with no limitations on duration of use. He explains findings from a recently published study that show even with the maximum use of clascoterone, 4 to 6 times greater than the normal 1-gram dose, there were no clinically significant hyperkalemia readings, adverse events, or EKG changes in any participant in the control or experimental groups. Given its topical use, negligible systemic absorption especially when used as recommended, and the findings of this study, Dr Del Rosso agrees that clinicians should be reassured about the lack of risk of hyperkalemia with clascoterone use.Lastly, Dr Del Rosso switches focus to Janus kinase (JAK) inhibitors and biologics. He discusses where the boxed warnings for JAK inhibitors originated and why they are not as concerning overall with oral JAK inhibitors used for dermatologic indications in younger populations who exhibit fewer comorbidities and/or concomitant therapies. In addition, he notes that the risk of several side effects of special interest, such as lymphopenia, malignancy, and thromboembolic events are quite low. He also emphasizes that not all monoclonal antibodies with similar modes of action exhibit the same pharmacologic and therapeutic profiles. In a selected case where a patient with AD has an inadequate response or adverse event such as persistent conjunctivitis caused by dupilumab (which inhibits IL-13 and IL-4), case reports have shown that changing to another monoclonal antibody that inhibits IL-13 (ie, tralokinumab) can exhibit relevant efficacy without associated conjunctivitis. Ultimately, it is good for clinicians to have options and &nbsp;as much data as possible to differentiate their use. He concludes that although certain drugs are part of the same category or class, they all have differences in pharmacokinetics, and the benefits and differences of each drug must be understood to optimize treatment selection for individual patients. Tune in to this episode to learn all the valuable clinical pearls surrounding many commonly confused therapies!&nbsp;

Removing the Confusion Surrounding Some Commonly Used Therapies

You're listening to the Derms and Conditions podcast. Well, I'm Dr. Jim del Rosso and I'm bringing you a self made episode of Derms and Conditions Podcast, which I really hope you're enjoying. The series that we put together. We're now on our third season, and I thought it was important to discuss what I think are some misunderstood therapies, or therapies that are easily confused based on a lot of the information that's out there. So I'm picking a few selected areas that I'll bring to light from my perspective, areas that I've done work on, clinical research, studies, advising, consulting, a lot of data evaluation that will hopefully be relevant to you clinically. And the first area I want to talk about is the area of benzoil peroxide used to treat Rosacea, specifically patients that have papules and pustules that have Rosacea. This is very confusing, and not a week goes by that I don't get questioned about this from a clinician in dermatology, whether it be a dermatologist, physician assistant, nurse practitioner, or even other individuals from companies. Benzel peroxide for Rosacea benzel peroxide is going to be too irritating and they know about it for acne, but they just can't wrap their head around it with Rosacea even if they've seen some of the data. I think it's really important here to emphasize that the studies that were done with benzoil peroxide for rosacea specifically used encapsulated benzoil peroxide, what's also been called microencapsulated benzoil peroxide that is a specific formulation of benzoil peroxide. And there only one branded formulation of benzoyl peroxide incorporated of 5%. For rosacea, there is benzoyl peroxide microencapsulated along with microencapsulated tretinoin that is FDA approved for acne vulgaris, a combination formulation. The microencapsulation separates those active ingredients in the formulation and allows the benzoil peroxide and the tretinoin to be applied together in the same single formulation. Right first time that's been done that it could be done in the same vehicle because benzo peroxide had always degraded tretinoin and they were applied separately and couldn't be put in the same formulation. But the benzel peroxide 5% encapsulated in the cream formulation was specifically evaluated for patients that had moderate to severe rosacea with papules and pustules and the average number of the range I should say of papules and pustules in the actively treated patients in the two studies, and in the vehicle. Patients that had the same vehicle but without the encapsulated 5% benzel peroxide was anywhere from 26 to 30 lesions. So these patients had a pretty robust number of papules and pushules at baseline, and they were treated over a twelve week period with one Staley application of the active versus the vehicle in a double blind, placebo controlled, or vehicle controlled fashion randomized study, just the way it needs to be done to get approval by the FDA. Important to recognize that this is the only formulation that's been evaluated to show efficacy, safety and very importantly, tolerability for rosacea. So if you're going to think about utilizing benzoil peroxide for rosacea, regardless of whether it's over the counter or prescription, this is the only formulation you should utilize, or you should anticipate that you will get irritation from benzoil peroxide in many cases because it's being immediately released and not in the slow release that you get from the encapsulation. So the encapsulation is a special technique used in the manufacturer with a silicon dioxide shell that creates a shell that encapsulates the benzoil peroxide, that has some small micro channels that allows the benzoil peroxide to be released slowly. So you're not getting that quick dump into the skin, but with the slow release over time, you get the therapeutic effect and there's data to show how that actually happens. Right. So let's move on to what we can expect from encapsulated benzoil peroxide. Importantly, that the patient gets this specific brand formulation, not because we're promoting it for one particular company, but because it's the only one that the studies have actually been done that shows that you can get this benefit and where the efficacy was actually evaluated. But I think what's really important that we learned is that there is a very fast onset of clinical effect. Right. You see about 25% of the patients getting to clear, almost clear by four weeks of use, with the encapsulated 5% benzoil peroxide cream applied once a day. So that's impressive. We also see that by the end of twelve weeks, there's a 70% reduction in inflammatory lesions. Right. We don't have head to head, but that's very impressive and probably the highest number that we've seen in any particular study. Keeping in mind that we have 26 to 30 papules and pustules at baseline which is a robust number of baseline lesions. Also about 40% inflammatory lesion reduction. That's papules and postules. By week two, which was also a very impressive quick onset, the tolerability was very favorable. It was just about the same in the active group as the vehicle group when you're looking at local tolerability reactions. So, yes, it's possible you may get some stinging, some erythema, but not much different than the vehicle that does not have the encapsulated bencible peroxide. So this data is out there, it's available, and the drug is FDA approved under the brand name of Epsila. So if you don't believe Jim Dolaso, look at it for yourself, and I think you will find this to be a very helpful topical formulation for patients with papillopustular rosacea. We have several others. We obviously have metronidosol, azalaic acid. We have brands and generics. Of those. We have brand generic topical ivomectin. All of these have been very helpful for papillopustrial lesions of rosacea, minocycline foam, 1.5% foam. All of these FDA approved. This is a new agent, but I would encourage you not to get stuck on. It's benzol peroxide. It's not benzoyl peroxide, it's encapsulated benzo peroxide. So now I want to move on to another agent. It's topical clascodone. It's a 1% cream FDA approved twice a day for patients twelve years of age and older with acne vulgaris. Right. Male or female, doesn't matter the severity, the site, and no limitations on duration of use. It was studied on the face and also in long term extension on the trunk. A couple of caveats. There was a recent article published by Hannah Peterson and also with Leon Kursick and April Armstrong in the Journal of Drugs and Dermatology, which is a review on the efficacy safety mechanism of action of this particular agent, hot off the press in June of 2023. There's a lot of other publications that are out there, but this is a very good one. Also in the Journal of Clinical and Aesthetic Dermatology this month, there is a review where I was the lead author, but we also had Lindestine gold, Diane Tibetot and Nick Squateri, these other physicians that assisted on the hyperkalemia data with topical quescoderone. Right. And this does show, first of all, hyperkalemia. It was looked at because of issues that surrounded spironalactone. Right. And these drugs are structurally different. Right. But because spironalactone can cause hyperkalemia as an oral agent, with clascodorone being topically applied and having negligible systemic exposure, quite frankly, if you use it as recommended, approximately 1 gram twice a day to acne vulgaris in patients twelve years of age and older. Right. You have really, based on maximum use data, negligible concern about systemic exposure and issues such as clinically relevant hyperkalemia. But that being said, in the patients that were evaluated in twelve years of age and older in maximum use, which was four to six times the amount that you would typically use, there was no evidence that there was any clinically relevant. Meaning alert signals with hyperkalemia in the active versus the vehicle control group. And that is good news. The drug is FDA approved, twelve years of age and older. The bottom line was looking at exposure response analysis, looking at the levels of hyperkalemia. Hyperkalemia not meaning that it was high, that there was an alert, that there was an adverse event, because there were no EKG changes, no adverse events, or no alert levels that led to discontinuation in any of the patients, whether they be the vehicle, meaning they weren't exposed to the closcoderone or the closcoderone group. Importantly, these were just levels that may have been slightly above the limit of normal. So that could certainly happen in anyone, and it certainly happened in almost the same number of patients treated with vehicle as in the active. The denominator was a higher number in the active versus the vehicle because the randomization was two to one. But the bottom line is evaluated through phase two. And after that point, there was no recommendation by the FDA to evaluate in phase three or post marketing surveillance, and no laboratory monitoring recommendations in the product monograph. So I think you can feel comfortable with that. And the publication is available in the Journal of Clinical Anesthetic Dermatology. If you search it in Pubmed under my name, you can download an individual pDF of the article for use by yourself for review. If you want to look at it further. The next area I want to discuss is one that I've talked a lot about and many other people have talked about, and I think it can get somewhat confusing, and it has to do with monitoring guidelines with Janus kinase inhibitors. And I'm going to specifically focus on the drugs abracitinib and upaticitinib for atopic dermatitis. They're available orally. The package inserts recommend that you start with the lower dose and then step up to the higher dose if the patient does not get an adequate response within an appropriate amount of time to evaluate that patient. It's a little bit different in how it's written with each of the package inserts. But when we look at the box warnings, we have to recognize that some of the statements, a lot of what's in the box warning, and you've likely heard this from many people, is based on another Janus kinase inhibitor, which inhibits januskinase one, two and three. Abrasitinib and upaticitinib are primarily Janus kinase one, and they can have some Janus kinase two. Right inhibition. But the important thing being that tophacitinib, which is one that a lot of the statements are based on, looked at a comparison in a population of patients that were over the age of 60 that often had rheumatoid arthritis and other indicated comorbid diseases and were not just the atopic dermis population. So they had comorbidities that can predispose them to some of those adverse events of special interest, like tuberculosis, venous thromboembolism, arterial thromboembolism, major cardiovascular events, serious infections, et cetera. And in that population of patients, compared to tumor necrosis factor alpha inhibitors that are used in many of those patients that also be receiving methotrexate, many of these patients are receiving other therapies. It was higher with the tofacitinib that got transferred over to the other oral Janus kinase inhibitors. But looking at those only in the population of atopic dermatitis patients with upaticitinib and abracitinib, the age average is younger and the associated comorbidities are significantly less. But it doesn't mean that patients were not included that had comorbidities. For example, in the upatacitinib studies, they did include patients that were smokers, right? About 30% were smokers, about 20% were chronic smokers, 10% were past smokers. About 20% of the female population were utilizing oral contraceptives. And there were some patients that may have had some of the other comorbidities. But they did certainly exclude patients that had certain significant comorbidities from the study based on the inclusion criteria of those studies. But nevertheless, when we look at those population of patients, we have to factor in what is the risk of these adverse events of special interest and those we think about with Janus kinase inhibitors in this specific population. When we're talking to our patients that we believe need either abrasit, nib or eupatocitinib for the aratopic dermatitis based on the severity of the disease, based on whether or not they've had difficulties or not adequate response with previous treatments, including other systemic therapies, corticosteroids, classic immunosuppressives like cyclosporin and methotrexate, and even biologic agents like dupliumab, betrala, kenyumab. Right. We know that these monoclonal antibodies are very effective, and many patients are not going to need to think about utilizing another therapy. But in some of them, these oral Janus kinase inhibitors are certainly something that can provide them additional benefit if they need a better response, if they're not responding as well as they like, have difficulty sleeping, their disease has progressed or gotten worse. Whatever the case may be, your judgment as a clinician and the patient's interest is to look at another therapy. So we know that with upaticitinib and abracitinib, that switching to them in patients that had previously used the piliumab can get incremental benefit. Right. But also you have to factor in the blood monitoring that's required and the potential safety risks to discuss with the patient so you have a proper risk benefit. Discussion, joint decision making, which to me is always implicit, but is commonly talked about now, and making sure there's a full discussion on what they can anticipate in terms of benefit, certainly the benefit is there. So, for example, I'm going to use upatacitinib, for example, because I have that there's actually data on this drug going out to five years. There's longer data than one year also with abracitinib, and there's collections of data with both that support what I'm saying right now. But, for example, if you look at the one year data with upaticitinib, looking at 30 milligrams a day, which is the higher dose, and if you had 100 patients treated for a year in this population of patients with atopic dermatitis that were in pivotal trials, you would have less than two cases of anemia, less than one case of lymphopenia, less than four cases of serious infections, less than six cases of herpes oster, less than one case of active tuberculosis, less than one case of malignancy in general, less than one case of mace, and less than one case of venous thromboembolism. That's if you treated 100 patients for one year. So, yes, these can occur, right. And these cases may or may not been related to the upatacitinib, but they occurred in patients that were receiving upatacitinib. So, yes, we could not guarantee that these adverse events are not going to happen. And we do need to follow the monitoring guidelines, both clinical patient assessments, history, understanding their medication history and their medical background, and updating it each time we see them and looking at the blood test monitoring, that is recommended. Right. And it's pretty well worked out. I just published on LinkedIn. You could look up under my name a slide that has my recommendations. Based on what's published and the package inserts that are out there, you're certainly welcome to use that. But as long as we're doing that, we're treating patients with systemic therapies that can help them significantly with their disease, that are changing the lives dramatically of patients that are suffering from a very significant disease. Itching, difficulty sleeping. Whatever the case may be, we all know it. We just don't want to harm our patients. Well, this is not much different than when we first learned how to use isotretinoin or. Okay, I'll pick a chronic disease. Atopic dermatitis, psoriasis with cyclosporin, methotrexate, mycophenylate, mafatil, hydroxychloroquine. Whatever drug had some associated testing that we had to do or blood testing. It was a learning curve then. It's a similar learning curve now. So I don't want to sound like I'm on a soapbox, but I do want to encourage you to take into account the realities of what the risks are and feel comfortable having those conversations with your patients. So I try to bring forward three areas that I think are important. I do want to end with another factor. Remember that the monoclonal antibodies are not all the same. You can get conjunctivitis with topiliumab. You can get it with the anti IL 13 agents. Traloquinumab is available now. Lebricizumab will likely be available coming up. But just because a patient has conjunctivitis with topiliumab doesn't mean they're going to have it. If you treat them with tralicanumab or you switch them with tralicinumab, which in some cases may be helpful in patients that had conjunctivitis where you had to take them off topiliumab or didn't respond for some other reason, there are case reports on this. So the bottom line here is, just because drugs are in the same chemical class, like antial 13, stramab and lebricizumab, or are very similar, like monoclonal antibodies to pilumab being il four and il 13, where tralokinumab and leprechizumab being anti l 13. We may make assumptions of similar activities or similar adverse events. We truly cannot do that because there are many differences between these drugs, where they bind, their pharmacokinetic profiles, their activities are different, even drugs within the same chemical class. So I think that's a take home point. Learn each agent, regardless, topical or oral, individually, what its merits are and what its risks are, and then I think you'll feel very comfortable utilizing them in your clinical practice to help a lot of our patients. I hope this is helpful to you. This is some of the things I've gleaned through my own reading, teaching, and through many of the people that I talk to on derms and petition derms and conditions podcasts. I've mispronounced my own show, but it's been a long day. But I hope this was helpful to you. Thank you. Thank you for listening to this episode of Derms and Conditions. If you have any questions, please email us at podcast@dermsquared.com that's podcast at D-E-R-M-S-Q-U-A-R-E D.com. Podcast@dermsquared.com.

In episode 57 of Derms and Conditions, our host, James Q. Del Rosso, DO, sits down with Christopher Bunick, MD, PHD, an associate professor of dermatology at Yale University School of Medicine who performs specialized dermatologic research utilizing x-ray crystallography and other novel techniques.&nbsp;

In episode 57 of Derms and Conditions, our host, James Q. Del Rosso, DO, sits down with Christopher Bunick, MD, PHD, an associate professor of dermatology at Yale University School of Medicine who performs specialized dermatologic research utilizing x-ray crystallography and other novel techniques. The 2 discuss research findings surrounding new information on properties that differentiate the activity of antibiotics, with specific data on how narrow spectrum activity with sarecycline differs from the broad-spectrum tetracyclines we use in dermatology. There are new data described by Dr Bunick and his team on how the unique molecular structure of sarecycline targets Cutibacterium acnes (C. acnes) through multiple mechanisms of action, making it less vulnerable to antibiotic resistance.&nbsp; Dr Del Rosso begins by introducing sarecycline, a major new antibiotic in dermatology, and has Dr Bunick discuss some of his research on the medication. Dr Bunick explains how the recent scientific findings on the biochemistry of sarecycline translate clinically and have allowed us to not only advance our understanding of sarecycline but also other tetracyclines, including minocycline and doxycycline. Drs Del Rosso and Bunick follow this up by agreeing on the importance of dermatologists having a strong understanding of tetracyclines given their prevalence and frequency of use in clinical practice. Next, they switch focus to C. acnes, and Dr Bunick discusses his new findings on the ribosomal structure of C. acnes through the use of cryo-electron microscopy and how tetracyclines interact with it. Dr Bunick’s research group found that sarecycline binds C. acnes at both the 30S ribosomal subunit and a new additional ribosomal binding site, which had not previously been discovered. In addition, Dr Bunick notes how these variations in the mechanism of action can explain why tetracycline antibiotics have different properties, such as side effect profiles, despite being in the same chemical class. Drs Bunick and Del Rosso further solidify this point by explaining how similar research has established differences between PDE4 inhibitors such as roflumilast. Finally, they discuss antibiotic resistance in acne and how clinicians can better select therapies. Dr Bunick explains that sarecycline has the lowest rate of antibiotic resistance amongst tetracyclines because it targets C. acnes through 2 ribosomal binding sites and has an mRNA interfering carbon side chain that no other tetracycline possesses. Overall, Drs Bunick and Del Rosso agree that there is substantial scientific evidence on the effectiveness of sarecycline that supports its use by clinicians. Tune in to this episode to learn more about the new developments on antibiotics being discovered at a molecular level in the treatment of acne!

Improving Our Understanding of How New and Established Drugs Work: Let's Start With Our Most Often Used Antibiotic Class

In Episode 56 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Marc Serota, MD, a dermatologist in private practice in Denver who is triple board certified in dermatology, allergy and immunology, and pediatrics and serves as an adjunct faculty at the University of Colorado. The 2 discuss teledermatology and how Dr Serota uses it to increase access to care and develop additional revenue streams.

In episode 56 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Marc Serota, MD, a dermatologist in private practice in Denver who is triple board certified in dermatology, allergy and immunology, and pediatrics and serves as an adjunct faculty at the University of Colorado. The 2 discuss teledermatology and how Dr Serota uses it to increase access to care and develop additional revenue streams. They begin by recounting how teledermatology became as widespread as it is and its evolution during the COVID-19 pandemic. Even though its use has slowed down as people have returned to in-person visits, Dr Serota shares his reasons that it will remain a valuable asset to clinicians for years to come.&nbsp; Next, Dr Del Rosso voices the concerns of many physicians regarding diagnostic limitations with telehealth and liability concerns if you do not do a full exam. Dr Serota points out that there has never been a successful malpractice lawsuit due to misdiagnosis in telehealth, and you can avoid problems by setting expectations and discussing limitations with the patient in advance. Finally, Dr Serota shares his tips and pitfalls for incorporating teledermatology into your practice. Whether you want to add in a few telehealth visits to your practice or completely transition to remote work, this episode is filled with pearls to help you get started.&nbsp; &nbsp;

Marc Serota, MD

Can Teledermatology Be a Win-Win for Patients and Clinicians? What You Need to Know Now

In Episode 55 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Guy Webster, MD, PhD, FAAD, a Clinical Professor of Dermatology at Jefferson Medical College. The two discuss new developments in the pathophysiology and management of acne as well as key pearls and pitfalls when using topicals, antibiotics, and isotretinoin.&nbsp;

In episode 55 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Guy Webster, MD, PhD, FAAD, a clinical professor of dermatology at Jefferson Medical College. The 2 discuss new developments in the pathophysiology and management of acne as well as key pearls and pitfalls when using topicals, antibiotics, and isotretinoin.Dr. Del Rosso begins by asking Dr. Webster about any major changes to acne dogma over the last few decades. Dr. Webster points out that while our knowledge is constantly evolving, our understanding of acne hasn’t changed as drastically as it has for diseases such as psoriasis. We know the 4 common pillars for acne pathophysiology, and we know the immune system is involved. The main mistake we have made is placing too much weight on newer data and ignoring older, equally robust data.Next, they switch focus to antibiotics and Dr. Del Rosso asks about their role in acne management. Dr. Webster finds topical antibiotics such as erythromycin and clindamycin ineffective as monotherapy due to drug resistance. However, benzoyl peroxide has not been shown to create resistance and therefore remains very effective. They also discuss oral antibiotics and some of the newer narrow-spectrum options like sarecycline.Dr. Del Rosso then asks Dr. Webster about a hypothetical but very common case of a patient with moderate acne and how he would approach treatment. Dr. Webster states that he disagrees with stepwise therapy and believes you should use your clinical experience to start with the right medication, right away. You should also identify what the patient’s goals are and recognize what they are willing to tolerate with regard to treatments. He notes that after about 4-6 weeks of treatment he can tell if a therapy is having a beneficial effect or if he needs to recommend a stronger option. Finally, they discuss isotretinoin and key considerations surrounding its usage. Tune in to this episode to learn more!&nbsp;

Guy Webster, MD, PhD, FAAD

The Right "Guy" For the Job to Bring Us Up to Date: Important Observations About Acne and Beyond

In Episode 54 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Raja Sivamani, MD, MS, AP, a board-certified dermatologist who practices at the Pacific Skin Institute and runs the Integrative Dermatology Symposium through LearnSkin.&nbsp;

In episode 54 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Raja Sivamani, MD, MS, AP, a board-certified dermatologist who practices at the Pacific Skin Institute and runs the Integrative Dermatology Symposium through LearnSkin. They discuss the concept of integrative dermatology, which involves uniting principles from pharmaceuticals, diet, nutrition, supplements, and probiotics to deliver holistic care. Dr. Del Rosso begins by asking how to learn more about the science and evidence behind specific supplements and diets. Dr. Sivamani advises starting with medical literature and evaluating publications with a search of PubMed or even Google. He suggests specific integrative medicine journals such as the Journal of Integrative Medicine and the Journal of Complementary and Integrative Medicine. However, he notes that even the Journal of the American Academy of Dermatology and British Journal of Dermatology will publish on nutrition and cosmeceuticals. Regarding social media posts or blogs, Dr Sivamani advises considering the source–is it a board-certified dermatologist or a local beauty educator? Next, Dr. Sivamani discusses how to counsel patients on the evidence behind making certain holistic changes using atopic dermatitis as an example. Even for his naturopathic patients, he is able to convince them to start a biologic or other systemic medication by discussing how to approach their symptoms from multiple facets. This can be particularly helpful for conditions such as acne where patients are often concerned with what they are eating. Tune in to this episode to learn more about integrative dermatology and how you can incorporate it into your practice. &nbsp;

Raja Sivamani, MD, MS, AP

Alternative Approaches: A Thoughtful Conversation on Integrative Dermatology

In Episode 53 of Derms and Conditions, our host James Q. Del Rosso, DO, continues his conversation with Matt Zirwas, MD, a dermatologist in Columbus, Ohio, and founder of the Bexley Dermatology Research Clinic. After reviewing localized eczematous dermatitis in part 1, they switch gears to discuss adults with scattered eczematous dermatitis in part 2. &nbsp;

In episode 53 of Derms and Conditions, our host James Q. Del Rosso, DO, continues his conversation with Matt Zirwas, MD, a dermatologist in Columbus, Ohio, and founder of the Bexley Dermatology Research Clinic. After reviewing localized eczematous dermatitis in part 1, they switch gears to discuss adults with scattered eczematous dermatitis in part 2. Dr. Zirwas shares several pearls for differentiating among atopic dermatitis, psoriasis, photosensitive dermatitis, CTCL, and contact dermatitis, and describes a new method for diagnosing scabies. &nbsp;He also discusses when to perform a biopsy and management approaches when the biopsy does not provide a clear answer. Dr. Zirwas then names several topical products with low allergenicity, including everything from cleansers and moisturizers to detergents and fabric softeners, that are beneficial to patients with sensitive skin. Dr. Del Rosso asks about disease-directed therapy and systemic treatment options, prompting Dr. Zirwas to dive into his medications of choice for each phenotype and patient population.This episode is full of pearls for a variety of eczematous and inflammatory dermatoses, so tune in to learn more!

Matt Zirwas, MD

Thinking Through Diagnostic Challenges in Patients with Eczema: Considerations and Pitfalls Part 2

In Episode 52 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Darrell Rigel, MD, MS, a Clinical Professor of Dermatology at the Mount Sinai Icahn School of Medicine and a world leader in research and patient care for melanoma and other skin cancers. The two discuss the current state of sunscreens and how to address the most common questions that patients have in the office.&nbsp; Patients often wonder if they need to use sunscreen when the UV index is low, if sunscreen is necessary for patients with darker skin tones, what the difference is between organic and inorganic sunscreens, and if sunscreen is safe for the environment. Dr. Del Rosso and Dr. Rigel answer all of these questions and many more, so tune in to this episode to learn how to counsel your patients and improve their sunscreen usage.&nbsp;

In Episode 52 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Darrell Rigel, MD, MS, a Clinical Professor of Dermatology at the Mount Sinai Icahn School of Medicine and a world leader in research and patient care for melanoma and other skin cancers. The two discuss the current state of sunscreens and how to address the most common questions that patients have in the office.Patients often wonder if they need to use sunscreen when the UV index is low, if sunscreen is necessary for patients with darker skin tones, what the difference is between organic and inorganic sunscreens, and if sunscreen is safe for the environment. Dr. Del Rosso and Dr. Rigel answer all of these questions and many more, so tune in to this episode to learn how to counsel your patients and improve their sunscreen usage.&nbsp;<div style="border:1px solid rgb(210, 62, 135);margin:15px 0;padding:20px;text-align:left;">Neutrogena is proud to sponsor this episode of Derms and Conditions - listen for the code at the end of the podcast to request a free full-size sunscreen. We also invite you to <a target="_blank" rel="noopener noreferrer" href="https://www.neutrogenamd.com/?action=sign-up&amp;utm_source=Fred&amp;utm_medium=email&amp;utm_campaign=DermsConditionsPodcast&amp;utm_content=sign_up">CLICK HERE</a> to register at <a target="_blank" rel="noopener noreferrer" href="https://www.neutrogenamd.com/?action=sign-up&amp;utm_source=Fred&amp;utm_medium=email&amp;utm_campaign=DermsConditionsPodcast&amp;utm_content=sign_up">NeutrogenaMD.com</a> for patient samples and educational resources.</div>

Darrell S. Rigel, MD, MS

Sunscreens 2023: Where Are We Now and What Else Can We Do?

In Episode 51 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Matt Zirwas, MD, a dermatologist in Columbus, Ohio and founder of the Bexley Dermatology Research Clinic. The two discuss how to approach a patient with an unspecified dermatitis.

In Episode 51 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Matt Zirwas, MD, a dermatologist in Columbus, Ohio and founder of the Bexley Dermatology Research Clinic. The two discuss how to approach a patient with an unspecified dermatitis.Dr. Zirwas begins by recounting his experiences with dermatitis unspecified, also known as non-atopic adult dermatitis, and how he became interested in treating this complex disease. Dr. Del Rosso asks how to differentiate between this disease and other similar diagnoses, prompting Dr. Zirwas to share his algorithm for recognizing the many types of eczema and contact dermatitis.Patients that receive this diagnosis often want to know what caused it and how it can be prevented. While the answer is not always clear, Dr. Zirwas provides his tips for counseling patients on possible triggers. This can include the food that they eat and its effect on the microbiome, as well as the many products they apply to their skin. Dr. Zirwas has plenty of suggestions for products with low allergenicity that these patients can try.Finally, the two discuss the role nickel plays in contact dermatitis and how to differentiate between atopic dermatitis, allergic contact dermatitis, and irritant contact dermatitis. This episode is full of pearls for one of the trickiest diagnoses in dermatology, so tune in to learn more!

Thinking Through Diagnostic Challenges in Patients with Eczema: Considerations and Pitfalls Part 1

In Episode 50 of Derms and Conditions, our host James Q. Del Rosso, DO, continues his conversation with Andrew Blauvelt, MD, MBA, a clinical trials investigator and former President and Owner of the Oregon Medical Research Center. Dr. Blauvelt has conducted almost 200 clinical trials on biologics and JAK inhibitors for the treatment of psoriasis and atopic dermatitis. While part one of this series focused on psoriasis, part two takes a deep dive into new therapies for atopic dermatitis.Dr. Blauvelt first discusses dupilumab and how this medication blazed the trail for the treatment of severe atopic dermatitis in patients with very limited options. Dr. Del Rosso clarifies the difference in mechanism of action between dupilumab and the newer drugs tralokinumab and lebrikizumab, and the two comment on how this impacts efficacy and safety. A common adverse effect seen with these drugs is eye related issues such as conjunctivitis and keratoconjunctivitis sicca, and they advise how to manage these conditions if they arise.Next, Dr. Del Rosso switches focus to the FDA-approved oral JAK inhibitors for atopic dermatitis, abrocitinib and upadacitinib. The biggest concern with JAK inhibitors has been their safety profile and black box warnings. However, Dr. Blauvelt discusses how these black box warnings came from a trial for tofacitinib to treat rheumatoid arthritis in a patient population featuring older patients with cardiac comorbidities that were taking prednisone and methotrexate concomitantly. This episode is full of clinical pearls for using the newest and most efficacious drugs for atopic dermatitis, so tune in to learn more!

In Episode 50 of Derms and Conditions, our host James Q. Del Rosso, DO, continues his conversation with Andrew Blauvelt, MD, MBA, a clinical trials investigator and former President and Owner of the Oregon Medical Research Center. Dr. Blauvelt has conducted almost 200 clinical trials on biologics and JAK inhibitors for the treatment of psoriasis and atopic dermatitis. While part one of this series focused on psoriasis, part two takes a deep dive into new therapies for atopic dermatitis.

 Andrew Blauvelt, MD, MBA

From the Research Center to the Clinic: Biologics and Other Systemic Therapies Part 2

You're listening to the Derms and Conditions podcast. Hello, I'm Jim Delrasso, and we have for a part two because part one was so fascinating. Dr. Andy Blaval, who is from Portland, Oregon. He's an investigator at Oregon Medical Research center in Portland. He was previously the owner and founder of this, but sold it recently. But he's still very active, and he's done a tremendous number of clinical trials. His main areas are psoriasis, atopic dermatitis, but certainly others, and has studied many biologic agents, systemic agents, primarily for psoriasis and atopic dermatitis. So, Andy, great to have you here. And the first conversation was fantastic. So I want to dive right into the second. What about atopic dermatitis? And the therapies that we have available now, we have monoclonal antibodies and Janus kinase inhibitors. Right. Jim, it's fascinating to me because we've had such an evolution in the psoriasis field and really not much happening at all in atopic dermatitis until recently. And so we had dupiliumab, also known as dupixant, approved several years ago now. And really, I consider that drug like a trailblazer. I mean, it was really an incredible advance. We had patients coming out of the woodwork, right, with such severe ad, and they just flowed into the trials. And Dupixent was just a godsend for so many people because those patients were stuck with cyclosporin, with methotrexate, phototherapy. It just really changed the field. It was interesting, Andy, you had the stepwise progression that happened in psoriasis, but it was a quick jump. We got spoiled in atopic dermatitis, right. We went from not having what you mentioned, which had a lot of problems and wasn't optimal of the systemics we had and just topicals to suddenly have this drug that was really, to use a modern term, a game changer. Right. Was a game changer, right. And people would say to me, well, oh, it's just like 2018 is just like 2004, when we started with embryo, and I said, absolutely not. I said, embryo is a good first step, but then we got so much better after that. Whereas dupixant, from the beginning, it was more like having a stellara. So for me, a really good drug from the beginning. And what we've seen is it's held up. It's really held up because it's been kind of tough to beat Dupixent in the last few years. So a bunch of people now kind of getting into it we have what I call dupy like drugs, and those there you have Tralo kinyumab, which is Adbre, which is a selective aisle 13 blocker. And then you have coming soon Lebri Kizumab, which is also a selective aisle 13 blocker that's probably going to be approved this summer, actually, 2023 summer. So those three are kind of working in similar ways. And then you have dupe four Nio 13. Right. Works in both types of receptors, one and two. Also, do you see any difference? What difference happens in terms of efficacy or safety when you're blocking I o four nio 13 versus just I o 13? Anything? Yeah, it's a really good question, Jim. And so back in the day, th one versus th two, and we only had kind of the two to talk about, il four was considered the prototypic th two cytokine. And so companies were trying to make il four blockers. And actually, way back when, there was an anti il four drug studied for eczema, and it didn't work. It actually didn't work and didn't go forward. But the whole Il four was kind of stuck with us and stuck with immunologists. And so when the makers of dupiliumab were working on that drug, they say, well, let's block Il four and aisle 13 another th two cytokine. And it worked. And really, what we think now, it's really the aisle 13 part of dupixent that works. It's really not much contribution to the aisle four blockade. And so that's why we're seeing now those selective aisle 13 blockers, because essentially we're getting comparable results as we get with duplimap. It sounds to me like, I hate to pick on Garfunkel, but it sounds sort of like Simon and Garfunkel. And I o four is Garfunkel, though he did have a couple of hits in there. Right? So he's showing up. It's important to have him there. But I o 13, I always thought of anti I o 13 as having more of a peripheral effect on skin as opposed to a central effect of some of the things that might happen in lymph nodes. But maybe I'm wrong about that. Actually, Jim, let me talk. Actually, there may be something to that because we see dupliumab approved for a number of other conditions. So it's approved for asthma and chronic rhinosinusitis with nasal polyposis, yasinophilic esophagitis. So these other sort of th two atopic manifestations we see dupab work in them, too. And so maybe in skin you only need 13 blockade, but sort of for asthma, maybe you do need that il four blockade because we don't have an asthma approval for those selective il 13 block. Right. And I believe trollchinumab was studied early on by another company, not the company that has it for asthma, and it didn't work that well, but it was a lower dose than what we're using now. So you still have a lot more to learn. And now we have the approval for. I almost said polyodoritis. No, dosa parigonularis. Excuse me, parigonodularis, even in patients that don't have any atopic background or atopic dermatitis. So diseases don't own the cytokines. Those cytokines can sneak up in other disease states, and I think we're learning that. But now we have Janus kinase inhibitors, so we have this array of monoclonal antibodies. We have two. Now we have dupixent and Adbre, as you mentioned, but we have Janus kinase inhibitors that are very effective for atopic dermatitis but carry some baggage that people get concerned about with safety. So can you walk me through that, how you decide on utilizing what agent and what you actually do? Monitoring. I don't get any baseline labs typically with dupixin, unless I'm expecting the patient may have something else going on. Do you get any baseline labs with dupixin or adbury? So you just asked a lot of things. Did. I'm excited, Andy. I can't help it. Okay, so I'm going to break that down a little bit. So first I'm going to say what are the commonalities between the biologics and the jacks? They both are linked to th two cytokines because those cytokines need to signal through the jax. And so they're both blocking Il four, IL 13, basically both types of drugs, and they're both getting at itch as well. So we know that the Il four receptor alpha is actually on neurons. It's on neurons. And so when we're using both types of drugs, the biologics and the jacks, we're actually blocking itch directly by blocking that neuron signaling. So it's really cool. And I think that's why we're seeing the prigonodularis incredible results is we're really blocking the itch rather than sort of getting at the disease. So that's really cool. And that's the link between these four drugs, the two biologics and the two jacks, is they all get at itch. Okay, so let's go to safety of the biologics. So we'll get rid of the biologics and talk about the jacks, adbri, and dupixent. 100% agree with you, Jim. They're very safe. There's really no blood test monitoring recommended with those drugs. The main issues are going to be conjunctivitis. Right. So eye disease, you get dry eye, you can get red eye, you can get swollen eyelids. I've kind of seen it all. Most of those patients are mild and manageable. And I always send to an ophthalmologist, by the way. But sometimes it's really bad, and you got to stop. You got to stop because the eyes get really bad. So I'd say for dermatologists, have an ophthalmologist in your back pocket, if you can, and send any dupixin adbree patients that have eye issues, send it to the ophthalmologist. Now, when I start those drugs, I often try to get patients just like we have atopic dermatitis patients moisturize their skin. I try to get them to use, like, an emollient for the eyes. There are several different products as a preventative. I don't know how well it works, but I haven't seen a lot of conjunctivitis with either of those two drugs to date. So I don't know how helpful that is. Do you do anything like that? Yeah, you're Lucky, Jim, because it's a pretty common side. You know anybody that has bad facial eczema or a history of allergic conjunctivitis where their eyes are runny a lot in the spring and fall, they're at risk for the dupey induced conjunctivitis in those patients. Definitely eyedrops. Just saline eyedrops is great. And then the main treatment for when it gets worse is just corticosteroid eyedrops that are used PRN. So not all the time, but sort of to knock down that inflammation. Right. What about the red face, that facial rash that we hear about? Well, I want to point out that conjunctivitis has been seen with both dupiliumab and trailicinumab. And in the PN trials, it was lower, but there was still some conjunctivitis. But some of those people, they did allow some people in that had mild atopic dermatitis. I don't know if they found only the conjunctivitis in the people with atopic background, I don't think they broke that down. But what about the transitioning now to Janus kinase inhibitors or switching to a Janus kinase inhibitor? We have abracitinib and we have eupatocytinib, Sabinco, and remvoke. Right. So can you walk us through that? All right, so both of these drugs are jack inhibitors, and they were both approved by the FDA for moderate to severe atopic dermatitis in January of 2022. So we have one year of FDA approval. And both of the drugs, what we're seeing is that is not a huge uptake, actually, in the dermatology community. And I think that the drug companies that make them are a little bit disappointed at the uptake. And for me, the elephant in the room, as you mentioned already, is the safety. Right. The safety of the Jax is kind of scaring, I think, a lot of dermatologists. It's the elephant in the room, because if you first will, first talk about efficacy, if you look at efficacy, they're terrific. They're actually, as a group, they're better than dupixin and Adbury, and it's one pill once a day and terrific efficacy, and it's fast. You see itch go away within a few days, and the drugs work fast. They're highly effective. So in terms of efficacy and quickness and working on itch, they're the best. But let me ask you a question right there, though, because if you look at how the trials were done, they used two different doses, but the FDA kind of tiptoed into it and set it up in the package inserts differently than how the trials were. Know, in the trials, a patient may have gotten one particular dose versus a higher dose. Right. They didn't start with one and then step up to the other. But the FDA, in the package inserts recommended with either one, whether it's Revoka, Sabinco, you start with the lower dose, and if they don't respond, go to the higher dose. Do you think that's really necessary from a safety standpoint? Because the higher doses work better, right. They definitely work better than the lower dose. It's a really good point. And thanks for catching me on that. I'm paying attention, Andy. I pay attention, but I'd still think they work better. So you have 15 milligrams and 30 milligrams of rinvoke, and you have 100 milligrams and 200 milligrams of sabinko. Okay, so you're right. In that, in the comparator head to head trials, they used the 30 of rinvoke and 200 of abro. So they used kind of the two higher doses and beat dupliumab. But if the 100 dose of Subinko and the 15 dose of rinvoke both work terrific as well. And so that is why the FDA has said, look, because of the safety issues, don't go to the high dose first. They say start at the low dose for both of those drugs and then only go to the high dose if you need it. And if you have good control on the high dose, go back down to the low dose to see if you can maintain control. But if you look at the safety data, is there you saving yourself potential adverse effects, the array of them, which we'll get into in a minute by going with the lower dose versus the higher dose, was there that much difference in adverse events in the two groups between the higher or lower doses of those two jacks? Yeah, you do see it. And actually you see it a little bit over time, but it's not a huge, it's not like a doubling. You don't see like a doubling of side effects with a double dose. You see an incremental increase. You see an incremental. Yeah, a little bit. And because of that, the FDA says, yeah, because you see a little bit more side effects with the higher doses. Let's try keep it on the low dose if you can. So let's get into, now you're deciding a patient, for whatever reason, is not responding as well as you would like with one of the monoclonal antibodies, or they got fatigue from it, they look tired of injections, whatever the reason is, or they just didn't respond that well, or they have really bad conjunctivitis and they can't get through that. So you're thinking about going to a jack inhibitor. What steps do you take, what monitoring do you do? And do you think there is a difference in the safety in the younger population that has fewer comorbidities, that were typically using them in atopic dermatitis versus patients that have used jacks for rheumatoid arthritis and other more severe disease, older patients with more comorbidities? A lot of question, but we're going to wrap it up with that. Okay, I'm going to take you step by step so doctors in private practice can understand jack safety. And Jim, I just got back from Hawaii Maui Durham meeting, and I spoke for 20 minutes on one topic on jack safety. So I gave a 20 minutes lecture, but I'm going to try to take it down to a few minutes to give you the highlights from that lecture. And so there are five boxed warnings for jack inhibitors. That's what everybody needs to know. And the five box warnings are cancer, heart attack and stroke, deep venous thrombosis, serious infections, serious infections and death. Okay, the bottom line is, and then the history, you have to know the history of where those boxed warnings came from, right? So they all came from rheumatoid arthritis studies in people with an average age of 62. There were 62 coming into the trial. They had to have heart disease to come into the trial. And 75% of the rheumatoid arthritis patients were on concomitant prednisone and methotrexate, and they were on a jack inhibitor called zeljans, which is a little more broad acting jack. So you have the creation of these five boxed warnings from trials done on another jack inhibitor in another population, and people who are old who, and people who are on prednisone at the same time. So that's where the safety warnings come from. And so I'm a little upset by it, because if you look at the safety data and the atopic dermatitis patients who are younger, right, the average age is in the 30s, they are not on prednisone or methotrexate, they're on monotherapy, they're on a newer type of jack that is more selective to jack one, and they don't have a lot of baseline heart disease risk. And so basically you have this whole different population with a different type of jack. And so what's happening in the ad data, three years now for both Sabinko and Rinvoc, is really only one of the five boxed warnings. Jim is really playing out for our ad patients, and that's serious infections. So we see a little bit of a signal. It's not huge, but there is a signal for serious infections. So jack inhibitors that we use in our eczema patients, yes, they can increase the risk of infection. It's not a huge thing, but we need to know that. And none of the other things are really statistically significant or above background levels. So even the venous thrombosis, the heart disease, cancer, basically none of that is playing out. So that's really good news, actually, for dermatologists. And I think they have to, I think, in my opinion, have to start to use Jax, because not only in ad, right, we've got jacks now in alopecia we got jacks in vitiligo. Jacks are coming for HS. And I really do think dermatologists need to get comfortable, really, with this class of drugs and kind of think of them as a possible infection signal and not worry as much as they should about all the other sort of warnings that are in the label. Well, think about it. Dermatology was, from so many years, a topical specialty. Occasionally, we would take out our prescription pad and write a systemic drug, tetracycline, toxicycline, minocycline. And when we had to learn about cyclosporin and even methotrexate, there was a learning curve for people there, too, because they're doing these blood tests for kidney problems or blood just. I think it's just going to take time. Andy, this has been fascinating. I want to thank you for joining us today, and I'm sure I'll be back to you in the future. And do me a favor. Say hello to your lovely wife, Molly, for me. She's a gem. Okay, Jim. Well, I really appreciate you asking me to do this and hopefully did some good with some folks out there that will help with patient care. That's the goal. Thank you. All right, take care. Thank you for listening to this episode of Derms and Conditions. If you have any questions or comments, please email us at podcasts at Fred Health. And most importantly, if you like this episode, subscribe to the Derms and Conditions podcast on Apple Podcasts or wherever you get your favorite shows. Thanks for joining us.

In Episode 49 of&nbsp;Derms and Conditions, James Q. Del Rosso, DO and Mark Lebwohl, MD discussed the pathophysiology of atopic dermatitis and the role of cytokines in its management.

Sponsor <img class="image_resized" style="width:16.6%;" src="https://d18uhdhjoz8by6.cloudfront.net/leo_08ae41f5c3.png" alt="LEO Pharma">In Episode 49 of Derms and Conditions, James Q. Del Rosso, DO and Mark Lebwohl, MD discussed the pathophysiology of atopic dermatitis and the role of cytokines in its management. Drs. Lebwohl and Del Rosso discussed how specific cytokines can be targeted for a safer treatment of atopic dermatitis. They emphasized that the targeted therapies for atopic dermatitis do not have any boxed warnings and the treatment of cytokines, specifically interleukin-4 (IL-4) and IL-13, can significantly improve itching and dermatitis. Dr. Lebwohl discussed the inhibiting of IL-13 to make atopic dermatitis better and that blocking IL-4 and IL-13 was highly effective for treating atopic dermatitis. In terms of utilizing less targeted therapies, Dr. Lebwohl stated that all the drugs they use work by knocking down IL-13 but with varying side effects. The use of old drugs such as methotrexate and cyclosporine has several side effects, and doctors need to be cautious about their usage. &nbsp;

Atopic Dermatitis: Connections Between Cytokine Inhibition and Clinical Outcomes

Leopharma is driving innovations toward a brighter future within medical dermatology, advancing research and development, and expanding medical education in dermatologic diseases to help better equip clinicians in making informed decisions for their patients. Learn more at Leo Pharma us. That's Leo Harma us and Conditions podcast. So welcome to Derms and conditions. We're here live at winter clinical Miami, and it's exciting to be here doing a live podcast. And I have with me a great friend and colleague and one of the co directors and founders of these meetings, and that's Dr. Mark Webwall. So, Mark, it's great to see you. You haven't aged a bit since this all started 22 years ago, but we've developed a lot of new concepts in treatment. So we talk about cytokines. What we're talking about today is atopic dermatitis and variety of different cytokines and chemical messengers that are involved in the pathophysiology of that disease. So, Mark, when you're with a patient, you're looking at a patient that has atopic dermatitis, regardless of the age or the severity or the duration of the disease. Do you think about specific cytokines in terms of managing the atopidermatitis in that patient? I dream about cytokines. So as you get older, the things you dream about gets narrower and narrower. But indeed, when I see a patient, the beauty that we learn from other diseases is that if you can target a specific cytokine, you end up with usually a safer treatment. And I think the testimony to that is that the targeted therapies for atopic dermatitis don't have any boxed warnings, and it's because they are very targeted. We know what we're blocking. We're not going to get in trouble. And we recognize, and we know that with targeting interleukin four, Il four and IL 13, that those cytokines are very operative in most patients, the majority of patients with atopic dermatitis. And so if you give something that inhibits Il four and IL 13, obviously those patients improve significantly with itching and their dermatitis. But we know that even just inhibition of IL 13 has significant change in those patients. Yeah, very clear that blocking IL 13 is what makes atopic dermatitis better. That is very straightforward. We got lucky when Il four, which was the anti Il four, was the first approved biologic for atopic dermatitis. I think nobody was thinking, or maybe they were already thinking about IL 13, because IL 13 and Il four share the alpha subunit of the Il four receptor. So if you target that, you're going to knock out both. And that was highly effective. We came to realize what Il four did and how it activated, and it's involved in lymph nodes and with some central components of atopic disease. But IL 13 is present in such high concentrations in active lesions and also non lesional skin in atopic patients. It just gets higher. It just appears higher where I O four is somewhat not found as reliably in skin the same way IL 13 is. But going beyond that, going one step further, you mentioned about immunosuppression, the lack of being an immunosuppressive treatment. Yeah. Actually, what you just said is quite important. The package inserts on the biologics for atopic dermatitis do not mention the word immunosuppression. It does not appear there. And, in fact, Emma Gutman in our department has done great work on this. She showed that in atopic skin, Il four is very elevated. When you treat that, when you block Il four, it doesn't lower it below normal. It lowers it down to a normal level. So that's why we're not seeing an increase in infections in patients treated with these drugs. You're turning the volume knob down. You're not shutting the switch off like you might with a corticosteroid therapy that blocks so many different pathways and shuts them down. So what I'd like to do is stop at this point and just read you a message from our sponsor, leopharma. Medical dermatology is fast growing, driven by the promise of new leading medicines. As such, leopharma focuses its resources on investing in medical dermatology, where there are significant unmet medical needs and a high burden of disease. Certainly, atopic dermatitis relates to all of that. So when do you consider utilizing less targeted therapies in patients with atopic dermatitis? Interesting question. So, for the drugs we use, whether they be biologics, jack inhibitors, cyclosporin, methotrexate, mycophenola, mophin, immunosuppressant, and for the record, I never use the old ones. They're not approved for atopic dermatitis. They were all we had until the first biologics came out. But they all work. And if you looked at how they work, they all actually knocked down IL 13. So they all work by a similar mechanism, but they certainly didn't do that alone. They had a lot of other effects. And, of course, when you use the older drugs, they have a million side effects, and those side effects are real. You use methotrexate. I tell my residents, I used to have a couple of hundred patients on methotrexate. I would periodically wake up at night because I was worried about what was going to happen. So here I'm using an off label drug that's not approved, and you end up wiping out somebody's bone marrow, and you're in trouble with psychosporin. We know that 100% of patients end up developing kidney damage if you stay on it long enough. And interestingly, one of the first patients I treated with the first biologic for atopic dermatitis had been on. He was a lawyer on cyclosporn for about eight years because basically he said he would rather be in kidney failure than have severe atopic dermatitis. That tells you about how his chart was as thick as a telephone book, an old telephone book, because he was signing all these disclosures. So he's now a devotee to the biologics because they're so targeted and so much safer. The jack inhibitors are safer than the old drugs, for sure. They do have boxed warnings. Those are the only targeted, non targeted therapies that I use for atopic dermatitis. Now, they are affect several cytokines. They're not just targeting. Correct. One or two specific cytokines. Right. And actually, if you look specifically, Jack one and Jack three inhibition blocks Il four and therefore also blocks IL 13. Those two jack inhibitors are quite effective for atopic dermatitis. Pretty much. I use them when patients fail the biologics. Why is that? The package insert says that you should use other systemic therapies first. And obviously, the only other systemic approved therapies we have are biologics and steroids, which I always avoid using. So let's talk a little bit about vaccinations and how you approach in adult patients. In children, obviously, there are some live vaccines, there's MMR. Is one of the considerations there where we were cautious about coadministration with live vaccines just because we don't have the data, not because we know anything is going to happen with any of these drugs. But how do you approach the vaccination story when you're treating patients with atopic dermatitis, let's say adults or adolescents? So there is some data that blockade of Il four does not interfere with vaccination. So the response you're looking for in a vaccination, unlike Jack inhibitors, where there's some data showing that they do suppress the response to vaccination with the biologics. That data does not exist. In fact, the data says the opposite. However, the package inserts all warn against live vaccines, and that is an issue. Certainly, this came out actually during the yellow fever epidemic in Brazil, where there were patients getting biologics for. I think it was during one of the clinical trials for biologics for atopic dermatitis. So there were 37 or 38 cases, and those patients actually did fine. The worry is, of course, you're suppressing some of the immune system. That's vaguely. And so maybe the vaccine will actually make you sick, and it didn't. And you're modulating in many cases, not necessarily suppressing per se, though I realize some people consider that to be semantics. Now, what about the subject of conjunctivitis? We know that with inhibition of Il four and IL 13, we saw conjunctivitis in patients that were receiving that form of inhibition, but also that about 25, 30% of the patients have allergic, have conjunctivitis related to being atopic. Right. And so that's part of the atopic diaphesis, but some exacerbated or first developed it while they were receiving that inhibition of therapy. What about with IL 13 inhibition versus Il four and IL 13 inhibition? So I'll give you my experience, and there is some data in the literature as well. So, first of all, in my experience and also in the literature, the patients with most severe periocular disease were the ones who got in trouble. And by and large, the conjunctivitis is transient. Even if you don't treat it, it goes away. The usual therapy for. And I must have hundreds of patients on biologics for atopic dermatitis, and I have two in whom I've had to stop the drugs, and I'll tell you their story after. But by and large, there's one study that reported that looked at the question of glaucoma from topical steroids, and you can get glaucoma from topical steroids. So it turns out that there are some topical steroids that do it a little bit less. The topical cyclosporin eyedrops would be ideal. The problem is they're irritating, and they don't work that well. And actually, I've never had one patient with conjunctivitis from any of the biologics for atopic terminus. I've never had one patient respond to topical cyclosporin eyedrops. So pretty much when we have to, we use topical steroids. If we can get away without it, we prefer to. We use a lot of eyedrops. And again, in my experience, topical eyelid ointments, rather than drops work better. And there are these high saline ophthalmic ointments that actually, I think, reduce inflammation and work the best. I know David Cohen has talked about when you're utilizing some of the liquids to not get the bottle that you use repeatedly because there's preservatives in there that are irritating, get the single units because you don't have the preservative. So benzalconium chloride or other preservatives can be irritating of the eyes in and of themselves. Right. Now, I told you I've had two patients who did not tolerate one of the biologics. We tried the other one. The data would suggest that just blocking IL 13 might cause a little less conjunctivitis. But I can tell you, in my two patients, they both got it when they switched from the Il four blockade to IL 13. So ultimately, those are two patients that had to move to jack inhibitors. So that's going to happen. And the literature certainly supports that. We're doctors. We have to help people in individual situations, and that's going to happen with any therapies, with all therapies that we have. So do you have any final comments, Mark? I mean, to me, my comment would be, we are very fortunate to have some great options now. Yeah, I have to say, I'm sure. Remember the days when you and I, although I avoided it and many of our colleagues, used systemic steroids because the patients were miserable. I used a ton of psychosporin and I worried about it all the time. But here we're using these dangerous drugs, and now suddenly we have drugs where you treat a patient with one injection, and within weeks they are profoundly better. Even within days, you see their itches reduced, they're oozing, and the examiner is changing on their skin. They literally go from something where you're miserable to you hardly notice it. You get about 80% of the benefit within the first four weeks. I agree. And it's all the treatments. It's the biologics, it's the jack inhibitors, and patients who, you felt awful for them. They went from looking awful to looking normal. I don't like buzphrases, but I have to say, game changer definitely applies. Yeah, no question. Definitely a game changer. So thanks, Mark. It's always a pleasure to be with you, and you give historic insights. Right. And so do I, to a significant extent. But I really appreciate your time thanks for having me. I do have a question for you. Sure. And we ask this do you prefer a Chicago deep dish pizza or a New York thin crust? I am embarrassed to say I love deep dish pizza. So you're more to the Chicago side. Even being a New Yorker, that's the first time I've heard that. See, it's good to have options, which is the point of what we're talking about today. Thanks a lot, Mark. Thanks, Jim. So every day, hour and minute, people around the world are suffering from skin conditions, often severe and chronic, impairing their quality of life. Our purpose at leopharma is to help advance the standard of care for the benefit of people with skin conditions, their families, and society through innovative treatment solutions. Thank you for listening to this episode of Derms and Conditions. If you have any questions or comments, please email us at. Podcasts at Fred Health and most importantly, if you like this episode, subscribe to the Derms and Conditions podcast on Apple Podcasts or wherever you get your favorite shows. Thanks for joining us.

In Episode 48 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Andrew Blauvelt, MD, MBA, a clinical trials investigator and former President and Owner of the Oregon Medical Research Center. Dr. Blauvelt has&nbsp;conducted almost 200 clinical trials on biologics and JAK inhibitors! In part 1 of this series, the two discuss the best way to learn about these new therapies for psoriasis.&nbsp;

In Episode 48 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Andrew Blauvelt, MD, MBA, a clinical trials investigator and former President and Owner of the Oregon Medical Research Center. Dr. Blauvelt has&nbsp;conducted almost 200 clinical trials on biologics and JAK inhibitors! In part 1 of this series, the two discuss the best way to learn about these new therapies for psoriasis.&nbsp; &nbsp; With&nbsp;11 biologic medications now available for psoriasis, Dr. Blauvelt recommends breaking them down into three categories based on mechanism: the original&nbsp;TNF blockers, the IL-17 blockers, and the IL-23 blockers.&nbsp;He suggests that dermatologists should have a go-to medication in each class and provides several tips on choosing the right class for the right patient based on efficacy, safety, and convenience.&nbsp; &nbsp; Next, Dr. Del Rosso asks about the role these agents can play in affecting cardiovascular events for which psoriasis is a known risk factor. Dr. Blauvelt shares his favorite class of biologics for slowing down atherosclerosis, and recommends the best class for other common comorbidities, such as IBD, hepatitis or HIV infection, and cancer. &nbsp; Finally, the two switch gears and discuss oral options for psoriasis and how deucravacitinib, recently approved by the FDA last September, fairs against other options. This episode is full of clinical pearls for managing your psoriasis patients with all the newest therapies, so tune in to learn more!&nbsp;

From the Research Center to the Clinic: Biologics and Other Systemic Therapies Part 1

In Episode 47 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO sits down with Alexandra K. Golant, MD to discuss advances in the management of atopic dermatitis.

In Episode 47 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO sits down with Alexandra K. Golant, MD to discuss advances in the management of atopic dermatitis. &nbsp; They begin by highlighting the landmark approval of dupilumab in 2017 and how it completely revolutionized treatment of the disease at a time when options were very limited. Now, with additional biologics and a few JAK inhibitors on the market, both discuss some tips for choosing between the drug classes based on patient characteristics. Importantly, they also discuss the black box warning for JAK inhibitors and how to counsel patients on what this means. Next, they review some nonsteroidal topical medications including roflumilast, ruxolitinib, and tapinarof and their tolerability and efficacy. Finally, Dr. Golant provides some of her favorite clinical pearls from her years of experience treating atopic dermatitis. Tune in to hear her take on the growing options for atopic dermatitis!

It Is a Better Time for People with Atopic Dermatitis: A "Power Duo" Sorts Through Some Very Effective Options

In Episode 46 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Joel L. Cohen, MD, founder of AboutSkin Dermatology in Denver, Colorado. The two discuss how Dr. Cohen incorporated laser procedures and cosmetics into his general medical dermatology practice.

In Episode 46 of Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Joel L. Cohen, MD, founder of AboutSkin Dermatology in Denver, Colorado. The two discuss how Dr. Cohen incorporated laser procedures and cosmetics into his general medical dermatology practice. Dr. Cohen takes us back to the beginning of how his dermatology career evolved to include integration of devices and cosmetic procedures. He strategically chose an IPL device as his first purchase so that he could treat a variety of conditions important to his patients. He then reviews additional pearls and pitfalls as he looked to expand into other devices. These practical tips range from how to choose a device based on versatility and consumables to how to counsel patients on what to expect throughout the treatment course. The use of devices and procedures in dermatology continues to evolve and expand in clinical applications. If you are looking to add any devices, such as lasers and lights, or cosmetic dermatology into your practice, you won’t want to miss this episode with a dermatologist who has extensive expertise and experience in this important area of dermatology.&nbsp;

An Open Dialogue on the Use of Devices in Dermatology

In Episode 45 of Derms and Conditions, our host James Q. Del Rosso, DO sits down with Mark Kaufmann, MD, President of the American Academy of Dermatology. &nbsp; The two begin by discussing the many benefits of AAD membership and what the AAD is currently doing to support its members. In an economy that has seen record levels of inflation, physicians have still had to face an 8.5% cut to Medicare reimbursements. Dr. Kaufmann explains how he is working to counteract these cuts, and how you can support this mission by reaching out to him directly to get involved or by donating to the SkinPAC.

In Episode 45 of Derms and Conditions, our host James Q. Del Rosso, DO sits down with Mark Kaufmann, MD, President of the American Academy of Dermatology. &nbsp; The two begin by discussing the many benefits of AAD membership and what the AAD is currently doing to support its members. In an economy that has seen record levels of inflation, physicians have still had to face an 8.5% cut to Medicare reimbursements. Dr. Kaufmann explains how he is working to counteract these cuts, and how you can support this mission by reaching out to him directly to get involved or by donating to the SkinPAC. Finally, Dr. Kaufmann shares some of his favorite initiatives that he has worked on and some exciting ideas for the future. You won’t want to miss learning about his fruitful tenure as AAD president and everything he has done for the specialty.&nbsp;

What can the AAD do for YOU?

You're listening to the Derms and Conditions podcast. So it's a pleasure to bring up here. We don't need to be over here because we're Mike separately. It's a pleasure to bring behind each other, like some presidential debate. Presidential debate. Not going to be debating the president. So this is actually a live podcast for derms and conditions with Mark Kaufman, who I've known for many years as a friend and a colleague. We work together on things that advance dermatology and cosmetic surgery with different activities, but he has really done a great job so far and is just a great guy and somebody that we can depend on at the American Academy of Dermatology. So let's get the discussion. Mark, you know, things are getting a little tight. Everything's more expensive. So when different requests come in for money, and one of those is AAD dues, I thought about maybe I can save some money and not necessarily be a member of the AAD or other organizations. So if I'm looking at that invoice from the EAD, why should I keep being an AAD member? What, in your mind, what Ead does classically and what you're doing now, moving into the future. So, first of all, thank you for having me here. It's a pleasure to be here. It's great to be at a meeting that it almost seems normal, like Covid never happened. And it's great to see friends and meet new people. So I'm really happy to be here. I think the question is a great one. What does the academy do for me? And I'll be very happy to try and give you a short, concise answer. There are four things that the academy does for its members. They relate to education. You all know there's going to be a big meeting in New Orleans in March, and we hope to see many of you there. We work on advocacy, and I'm going to touch on that a little more. We work on public relations, and I hope to touch on that, too. And we also advocate for research. So there are a lot of things, I don't know if you want me to go into any detail on any of them, pick one that you think is the most important in dermatology right now in terms of what we're facing as a specialty. So the most important now is by far the advocacy realm. We are currently in an election season. And what I think is really important for dermatologists to understand is that it is really important for us to be the best at what we do. And that's why you're here at this meeting to become the best and better at what you do. But at the same time, we also live in a world where politics actually can determine whether or not your life is going to be miserable or you're going to be able to practice the way that you want to, to be able to treat the patients with all the medications that you're hearing about without dealing with some of the hassles that you're hearing about. And more importantly, for the moment, we're also dealing with a reimbursement cris in medicine, not just in dermatology, but all physicians are faced at the moment with an eight and a half percent cut for next year on Medicare rates. And we're hopeful that we can mitigate that. But I am someone who came in and told people that I don't want mitigation, I want elimination. I want a raise for inflation. And unfortunately, the political realities is that we don't always get that chance. Our legislators, and we just had a legislative conference with 200 people where we went to the hill. But we're getting mixed messages. Some of them are saying that there's just other greater political concerns that they have that are not going to allow for them to get rid of all the cuts. So I would encourage everyone to give to Skinpac to also individually get involved. If you know anyone who's in Congress, or even if you don't know your congresspeople, find out the way to write letters, because the AAD is really working hard for this. But we can't do it alone. We need your help. So I hear often give to skinpac. Can you give some examples of how skinpac actually makes a difference for dermatology? So we give money to Skimpak or to the AaD to solve some of these issues or combat some of these issues. What's actually done in the trenches for the members? Sure. So the first thing I'll say is, in your question, you said you give money to Skimpac or AAD. It is different when you give money to Skimpac or you give money to AAD. AAD has a philanthropic arm within its 501. I know I'm getting a little technical, but in order to do advocacy on the Hill, we have a separate arm, and that separate arm is a different tax category. So just because, and this is a good point, just because you give money to AAD, none of that is going for advocacy in Washington. We actually can only use the money raised on the other arm, on the association arm. So that's why Skinpac donations are really important because it doesn't come from anywhere else. And what Skimpak lets you do is it doesn't buy votes. We can't go and tell someone, we need you to vote for this, and here's a donation. But it does get us facetime with the legislator. So it gets us meetings with people who we might not otherwise get. And at least you have to be at the table. And what Skimpak does, it gets us a seat at the table. So are there examples you could point out where we've had, even if they were small, wins, where wins actually happened for, you know, on the federal level, we also work a lot at the state level, and we work to get legislation through for shade structures, to eliminate tanning bed taxes or to limit the use of tanning beds. On a federal level, we are always advocating for issues that are important to dermatology. And the way that we can talk to the legislators about those issues is through the donations from SkinPAc. So if an individual out here know, like the movie network, right? Was it network? I'm mad as hell and I'm not going to take this anymore. And they want to get involved, what should they do? Should they send an email to you? Do they send an email to somebody specifically at the academy? If they want to have a voice on some particular issue, anyone who wants to get involved can write an email to me. President@aad.org if it's not me who's going to respond, I can get it to the right person who will respond to you. And we would love to have more people get involved. And really, everyone should get involved now because it really is a moment of crisis right now with reimbursement and we need all hands on deck. So find out who your congresspeople are. You're going to be getting emails from us, probably from Ama as well, to do a grassroots email to all of your legislators to try and get them to understand that in order for us to keep our doors open, we're going to need not just an elimination of these eight and a half percent cuts, but actually an adjustment upward for inflation. So if someone is contacting a legislator or whoever you're recommending that they contact, how are they not just perceived as, oh, this is just a doctor who, yeah, they've had cuts, but they're still making plenty of money. And why should I feel sorry for them or do anything to help? Any specific things we should say about what dermatologists do that makes a difference with these political individuals? Well, I would stress to them that many times in the past. For those of you old enough in the audience to remember the days of the SGR, the sustained growth factor, which we got eliminated, and remember, it was eliminated on an annual basis. In total, we never got a cut, but we were still getting cut because inflation took place and we were getting cut. That was like death by 1000 cuts, literally. But it was very slow. And we're very good at adapting and working harder and seeing more patients. And you can do that for a while, but at some point you run out of Runway. And the way you run out of Runway quicker is when inflation goes from zero to eight and a half or double digits, which it is, and then you just can't do it anymore. So I would say it's just a matter of math. We can't survive in an inflationary environment with any cuts, let alone the lack of an adjustment upward. So how do we get ahead of it? Let's say people get involved and we have some success, and we reduce some of those rate cuts, we're going to go through this cycle again. And so how do we stay ahead of it all the time rather than just reacting to it on a case by case basis? Any thoughts on that? I know it's difficult. Yeah, that's a tough question. I have my own thoughts. I think in general, I think physicians are weaker because we are specialty driven. In other words, skin pack is dermatology specific. And so every specialty has their own pack. And it's great because you can lobby for your interests, but at the same time, physicians as a group are all splintered. We're not unified. We don't have one PAC that goes to Washington and tell them the realities of economics that are facing us. And I think that actually hurts us. So I'm thinking that in the future, we may need almost a super pack of all the specialty packs in order to go to Washington the way that the hospitals and the nursing homes go to Washington. They go as one entity. They don't go as 30 different entities asking for tiny little things. They go as one entity. And they're only asking for one thing. They're asking for an adjustment for inflation. And you know what? They get it. The hospitals are adjusted for inflation. The nursing homes are adjusted for inflation. The physician fee schedule stays the same. So are different physician groups actually cannibalizing each other where you might have one group primary care or whatever, saying that the dermatologists are fine, but we need the help. So that doesn't sound like a unified voice, if that's what's actually happening. And honestly, I think that gets to the crux of the problem is that physicians have never been a unified group. And so it does make it more difficult, I think, to be able to advocate as physicians when we're all advocating for each other's specialties. So are there ways that maybe some of our patients would understand what we're saying, that you get the patients involved? Absolutely. So how do you do that without seeming self serving? It is difficult. I don't think it's worth telling a patient we're going to get cut. But on the other hand, it is worthwhile if your patient comes, if you have to drop off of certain insurances to have that discussion with a patient who says, how come you're not taking my insurance anymore? I think it's totally fair to say, hey, I'd love to see you, I'd love to take your insurance, but it's just not possible. If you want, you can contact some folks that might be able to change that so that we can get back on the insurance. So is the way they can go to a website or someplace where the academy would then let the patients know, or skinpac would let the patients know what they can do. I may be barking up the road that's not available at the moment, but maybe something we can look at. So what else? Right? It's been an awesome year. It really has. I've been representing the academy all over the country, all over the world. I've been to remarkable places, seen other dermatology societies of other countries and how they work. But probably the most magical trip I took was to a small town in northern Minnesota of Cross Lake, which was really the birthplace of camp discovery. For any of you who know what the program is, it's a program where we send kids with horrible skin disease who suffer from tremendous self esteem issues and think that they're alone in the world. And the academy, through a lot of donations, is able to send these kids for one week to a camp where they feel like they're normal and they're around kids who have similar diseases. And it was really interesting because I was going from one lecture and giving an academy update, and I was on my way to another meeting to talk about burnout. And I tell people on my way to go talk about burnout, I actually found the cure to burnout because we never take the journey with our patient, really. We see the patient, they may have horrible skin disease. We help them, we prescribe, and then they go back to live in their own world and we don't and to be able to go and to see them living in their world and really getting what they get out of camp Discovery was completely life changing for me. And that's why my main initiative of my presidency has been to try and expand the camp Discovery program, its capacity. And my goal, my stretch goal, is to make it so that every resident in the United States would be able to spend one week out of their three years at Camp Discovery. That would be fantastic. So that's the focus because it goes by fast, right? You have a whole list of things you want to do, and it's really hard to get to all of them. So, Mark, I want to thank you for the effort you put in. It's one year as president, but there's a lot of years building up to that year of hard work in addition to what you've done at the ruck along the way. Appreciate it because it's a lot of hours. I appreciate it. Thank you, Mark. Thank you, Jim. Appreciate it. Pleasure. Appreciate it. Thank you for listening to this episode of Derms and Conditions. If you have any questions or comments, please email us at podcasts at Fred Health and most importantly, if you like this episode, subscribe to the Derms and Conditions podcast on Apple Podcasts or wherever you get your favorite watching for joining us.

In Episode 44 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO sits down with April Armstrong, MD, MPH and David Cohen, MD, MPH, live at Winter Clinical Hawaii 2023 to discuss highlights from the meeting.

In Episode 44 of Derms and Conditions, our host James Q. Del Rosso, DO sits down with April Armstrong, MD, MPH and David Cohen, MD, MPH, live at Winter Clinical Hawaii 2023 to discuss highlights from the meeting.The trio reviews important tips from a variety of topics, ranging from contact dermatitis to psoriasis. Many lectures from this meeting focused on the new biologics and JAK inhibitors available to treat inflammatory conditions such as psoriasis and atopic dermatitis. The group unpacks important considerations for each of these medications and how to effectively use them to improve patient outcomes. Finally, they discuss deucravacitinib and its unique mechanism of action of TYK2 inhibition. Tune in to hear our KOLs recap some of the best clinical pearls from the meeting! <img style="height:auto;max-width:100%;" src="https://mcusercontent.com/5ceb5997cef08be00c9571c4f/images/bd289527-b8c1-02b5-36aa-26548c4f1ca1.png" alt="Live Episode Recording at WCH23"> FINANCIAL DISCLOSURES: JAMES DEL ROSSO, DO: CONSULTANT/ADVISOR Abbvie, Aclaris, Almirall, Amgen, Arcutis, Bausch Health (Ortho Dermatology), BioFrontera, BioPharmX, Bristol-Myers-Squibb, Cassiopea, Dermata, Dermavant, Encore, EPI Health, Evommune, Ferndale, Galderma, Incyte, JEM Health, Leo Pharma, La Roche Posay, Lilly (Dermira), MC2, Novan, Pfizer, Regeneron, Sanofi-Genzyme, SolGel, Sonoma (IntraDerm), Sun Pharma, Trevi, UCB, Verrica, Vyne (Foamix; Menlo) SPEAKER BUREAU Aclaris, Almirall, Amgen, Arcutis, Bausch Health (Ortho Dermatology), EPI Health, Ferndale, Galderma, Genentech, JEM Health, Leo Pharma, La Roche Posay, Lilly (Dermira), Pfizer, Regeneron, Sanofi-Genzyme, Sun Pharma, UCB, Verrica, Vyne (Foamix; Menlo) RESEARCH INVESTIGATOR Aclaris, Almirall, Amgen, Anaptys Bio, Arcutis, Athenex, Bausch Health (Ortho Dermatology), BioPharmX, Biorasi, Botanix, Brickell, Cara Therapeutics, Cassiopea, Dermavant, EPI Health, Ferndale, Galderma, Incyte, Leo Pharma, Lilly (Dermira), Novan, Pfizer, Ralexar, Regeneron, SolGel, Sun Pharma, UCB, Verrica, Vyne (Foamix; Menlo). DAVID COHEN, MD, MPH: Consultant and Honorarium: Ferndale Laboratories, Asana Medimetriks [past] Leo UCB Novartis Dermavant FSJ FIDE. (FIDE receives industry sponsorship from AbbVie, Almirall, Amgen, Arcutis, Bausch and Lomb, Bristol-Myers Squibb, Celgene Dermavant, Dermira, Janssen, Kyowa Hakko Kirin, LEO, Lilly, Novartis, Ortho Dermatologics, Pfizer, Sanofi Genzyme, Regeneron, Sun Pharma, UCB, Valeant) Cosmetic Ingredient Review (CIR) Stock or stock options: Dermira [past], Medimetriks [past], Brickell Biotech [past], Kadmon, Evommune, Timber Board of Directors: Kadmon, Timber, Evommune, Dermira-[Past] APRIL ARMSTRONG, MD, MPH: Research investigator and/or scientific advisor to AbbVie, Almirall, Arcutis, ASLAN, BI, BMS, EPI, Incyte, Leo, UCB, Janssen, Lilly, Nimbus, Novartis, Ortho Dermatologics, Sun, Dermavant, Dermira, Sanofi, Regeneron, Pfizer, and Modmed.

Highlights of Winter Clinical Hawaii 2023

You're listening to the Derms and Conditions podcast in our third season with Derms and Conditions podcast, which we're very proud of. And I know you're going to learn a lot today, so let's get started. I have April Armstrong and David Cohen back from by topular demand, and I have to tell you, you better be sharp today because I've been here for a week, and I've been using that shower gel, and it says that I am enriched by flaxseed extract, white tea, and vitamin e. So I am pumped up with this stuff. Where do we start? You're better than you've ever been because of that. Now, the question is, how is it applied? And we got into that during the meeting. A bit on application technique, of course. I think what we did get to talk a little bit about is things like contact dermatitis really do reflect what we do on a daily basis. And I did want to highlight that. Of course, if you don't have contact dermatitis, this is just of interest for those that have eczema or poorly controlled dermatitis, where you really have to stop and think what, from the outside might be provoking it just to draw the highlight back. For those that weren't at the lecture, the 2023 allergen of the year by the American Contact Dermatitis Society was lanolin. Right. And got a mixed response from the group. Right. Some, I think, thrilled with it and some maybe not so much. But remember, lanolin is going to bring on dermatitis in a pretty slow onset. It's not going to be one of these fiery, quick onset, like maybe hair dye or poison ivy. So I think those who have dermatitis on their lips, eyelids, groins, even before you go to the patch test, consider that lanolin may be an issue. Most of us use lanolin products very safely, not an issue for most of us. So I don't want there to be hyperbole or over exaggeration of the importance of it. But lanolin creeps in. And when you have a lanolin allergic patient, get rid of lanolin and amercol containing products. So, April, any thoughts on that or anything else that you uncovered that you found in the meeting? Yeah. Thank you for inviting an adult to this conversation. And now I'm going to shift. She's sassy, isn't she? I'm going to shift the focus from the method of application to maybe talking about some of the wonderful psoriasis tips that we learned from our colleagues. Dr. Lovewall, Dr. Bhutani, and so forth. We now know, for example, for topical therapies, non steroidal topical therapies, we're actually looking at longer term results. So, for example, at this very meeting, we have topical roflumalast being studied and shown that it can maintain its clear or almost clear results for a median of at least ten months. So that's helpful. And I think for topinorov, about half of the patients achieve BSA, 1% or less, which is a very stringent criteria for topicals and nevertheless, even for a nontopical therapy. So we're seeing non steroidal topical therapies with good efficacy and as well as tolerability with longer term results. So one of the double edged swords I think about with that is if we tell people that you can use this and you're going to have months that you're clear without using it, do we want to be cautious about patients stopping treatment and then going back to square one, or we might want them to be using things, continue to use these therapies, since they do have the absence of side effects that you would have with the corticosteroid. So how do you see you're going to integrate that into your patient recommendations? Yeah, I think that's a great question asked by an adult. I want to. You're getting there, actually. Studies have shown if you want to treat the patients to clear, and then you can essentially try to stop. And then in the study that we've seen is that they then start as soon as they find any disease activity, at least for topical roflumalast, my recommendation is that you treat the person continuously to clear and then perhaps use them on the weekends as a proactive therapy to decrease flares. Yeah, I'm a strong believer in proactive therapy. So, David, I'm picturing this Allergen of the year scenario, and have you ever had a time where you had an allergen of the year, and then you looked out the window of your office in New York and there were dermatologists picketing against the allergen of the year? Any challenges there? Now you get some feedback about it. Remember, I'm the messenger most of the time. And this is a group at the american contact Dermatitis Society coming up with this. But the idea is just to draw some attention to the various allergens. You look at the ingredient lists of all these products and you just wonder, what are the important ones? What are the ones I need to think about? When do I need to test for them? So I get some adverse feedback every now and again, and Lanolin provided some of that. If I could just dovetail onto the last remarks before on the topicals, as I kind of sat through winter clinical, which really spanned the entirety of my week, taking care of patients of dermatology. If I would reflect, I might say, if 2010 to 2020 was the decade for psoriasis, where everything changed, the paradigms changed, what is 2020 to 2020, 30 going to look like? And I think that's probably going to be the decade of atopic dermatitis. We heard more talks on hydratinitis uppertiva, and we keep hearing more and more about evolving therapies. Jocelyn Kirby discussed the use of sporanolactone and metformin. These are drugs that we have experience with. We're adding them on, but I might say alopecia, ariata, vitiligo. And this is sort of the wringer here. Will this decade be the decade of topicals coming back? Because how do we integrate these new topicals that are more effective than any prior topicals we had other than super potent topical steroids? Where will they fit in and how will we use them? And I don't think there's a clear answer on that, but I think they need to get integrated pretty strongly. I think the safety of them is just so important because it gives you, like, with super potent topical corticosteroids, you still always have that in the back of your head. Even if you're telling a patient, use this twice a week, what are they really doing? And you don't have this concern with the newer agents. But why don't we move on to some of the systemic treatments? I think it's really important. We have a lot of discussion about Janus kinase inhibitors, and I think we need to have an open mind on how to approach them and really understand the patient populations and their potential risks of potential problems. But the agents that we do have, like the monoclonal antibodies that we have for atopic dermatitis, are highly effective. And we don't want to necessarily be thinking, oh, they're going by the wayside now because of Janus kinase inhibitors, because that's not true either. So, April, where do you see this going? Yeah, I think when we're looking at, for example, for atopic dermatitis, we have, for example, dupilumab, well established. And we also have trailokinumab now showing the 3.5 year data showing very good efficacy and safety. And then we have lebrechizumab, which is il 13 inhibitor as well. That is probably likely to be approved this year, that adding to our armamentarium. So I would think that our choices are actually, there are quite a few of them. And I think patient selection is going to be key. When we think of our Jack kinase inhibitors, our understanding of the safety profile, we know it works very well in ad at the doses that we're looking at. And I think the safety profile is something we're continuously learning. And I think the good message in that is that when we look at ad populations, specifically some of the black box warnings that was put on these medications from other indications and other populations seem to are not as relevant to our patient population. That being said, I think a good monitoring would be helpful. And then Jim, you and Nick and I, we created this jack inhibitor handout which I think would be very helpful for our clinicians, which talks about the monitoring guidelines, but the clinical mean, that's such an important part of it. So taking the time to just find out the key things, you need to know what's going on with the patient. So David, I know you have a lot of challenges. You get a lot of patients referred to you that have been managed by other clinicians, very good clinicians, that have difficult to treat inflammatory dermatoses, psoriasis, atopic dermatitis, dermatitis nos. So what's your feeling about these different treatments that are coming along? Right? And that comment about dermatitis nos is not a flipping comment, right? Because I think when we look at plaque psoriasis, we understand the pathophysiology, at least as it stands now, pretty well. It's IL 23 th 17, it's got close linkages and when you flip on those links, you can really influence the disease. Very much the problem when you have a patient with dermatitis, you send a biopsy and it comes back spongiotic dermatitis with a list of at least five exematist disorders like atopic derm, numular allergic irritant contact, derm id reactions, spongiotic drug reactions. You wonder if the pathophysiology of all these are the same, and they may not be. And of course, I think our first line of defense now are drugs that came out that really had very clean safety profiles, right. Very easy to use. So dupilumab and trailokinumab I think are really good. Go to when you have a spongiotic dermatitis that you haven't really clearly demonstrated as allergic contact or it doesn't appear to be, and then the question will be, do you move from one biologic to the other. Right. So we have two now. There's going to probably be a third soon. And where do you pivot into jacks. Right. And I think some sooner than later and depends on the severity and the conditions involved. Their labels, those jack labels suggest that you'd fail a systemic therapy. That doesn't necessarily mean a biologic therapy. It could be cyclosporin, methotrexate, mycophenylate, and I dare say prednisone. Right. The guidelines of care don't suggest the use of prednisone for the long term management, but that's probably used more often. I agree. You mentioned. I agree. I think it's easy to be up on a stage and say, don't use prednisone for eczema. But I don't think there's anyone in the room who has not written systemic steroids for an exematus flare to get a bridge to some control. So I think that's the reasonable way to do it. And then when you pick your right patient, the ones that have the fewest comorbidities, that may put you at risk for some of those black box warnings. And I know we do talk about those black box warnings as being seen more commonly in other disorders. We saw it with tofacidinib at 20 milligrams a day in inflammatory bowel disease. But I would suggest that almost every black box warning has occurred in eczema trials. Right. In one way or the other, and many with comorbidities that might put them at risk. So younger patients, those with less mace event potential, I think they're good choices. The jacks are the most spectacularly speedy and effective drugs we have available to us. And it's just a risk benefit for each patient. Right. So we'll see how they play out in the total paradigm of what we use. But they're here and they're really valuable. One of the things that Linda and I did in a session this morning is try to get people out of the weeds of getting caught up on how to monitor. I think it's pretty straightforward, the monitoring recommendations, and really not a lot different than what we would be doing with cyclosporin or some of the other agents that we used and just keep an eye on it and follow through with it. April, what's your feeling? Because I get this question a lot, and I'm sure others do. What's your feeling about inhibiting tyrosine kinase two? And is lightning up on the monitoring really something that we should feel comfortable with, or what's your sense on that? Yeah, I think when we were thinking about tyrosine kinase two, tick two, most of the development in the oral realm in psoriasis right now is actually directed against tyrosine kinase two, and importantly to the allosteric domain to make it more, even more specific. And what we saw clinically, too, no black mox warning with the approved ducravacitnib, for example, as an oral therapy, is acknowledgment, I think, by the FDA, after evaluating the evidence, seeing that the safety profile of a very specific tick two inhibitor being different from the jack one, two or three inhibitor. So I think that's something that's important. And I think we now have more oral choices, not only for psoriasis, but also beginning for psoriatic arthritis as well. So I think those are some things to mention. I think orally, we also saw at this meeting, presentation of a premalass being studied in kids six years and above. So really oral therapies, we traditionally think of them mostly studying in adult population. I think that's another shift that we're going to see also newer oral therapies being studied in people. I believe Mark Lebwald talked about oral apromolastin treating some other less common diseases that we're not likely going to see FDA approval for because they're more rare, but always go to the literature to look for those sorts of things. But we have other disease states, right? We have lichen planus being looked at with topic aruxalitnib and even some of the oral tick two agents. Hydratinitis, I think, is one that I'd like to at least touch upon. And don't forget, bimikizumab, very likely coming for psoriasis, and good data on psoriatic arthritis and also evaluation inhibiting 17 a and f. And hopefully we'll have approval for that soon for psoriasis, with excellent data, as you know. But what about some of these other disease states in terms of how we visualize treating them, things like hydratinitis and alopecia, that we now have a lot of hope for patients that we were desperate before. Yeah. Any thoughts on those, David? Yeah, I think the evolution of the development of drugs for hydroadinitis is really going in the proper direction. Right. We're getting a better understanding of pathophysiology of the disease because of some of these drug development. And we heard a lot during this meeting about the Il 17s really evolving in this area. I think generally dermatologists have more comfort level going long on IL 17s as opposed to long on, say, tnfs, if you had that option. And I was really happy to hear about that. And again, not to belabor the point, but the utilization of topicals and some systemic drugs early in the course may be very valuable, because once you have the tracks and the scars down, there's not going to be much you can do with that with a systemic agent. Right. When we're looking at the patient from the surface, we're looking in the axilla, and we're seeing those inflamed abscesses and things. We're not necessarily seeing what's going on on the surface, but these things are forming, and then when they finally emerge, it's too late. And so that's where I think that's a disease that you really want to get systemic therapy going early. What about will end with alopecia ariata? Any thoughts about the use of Janus kinase inhibitors or other therapies there? Yeah, I think what we've seen so far, with our approval of barricitinib in alopecia ariata has really brought changes for our patients. And one thing that I think as a field that we are now struggling with, what about those who have had alopecia ariata for a very long time? Right. So we see efficacy, good efficacy, in patients who have had it for a number of years, but beyond, let's say beyond ten years, it's quite difficult. So I think we're still looking at those specific patient populations, but certainly, I think it has been a game changer for a lot of patients with alopecia ariata at the current time, you still need continued use to maintain the efficacy, which I think takes a little bit of education with our patients. But I think as a field, we're also looking at more difficult to treat scarring alopecia. So frontal fibrosis, alopecia, LPP with dutasteride, or any other therapies I think was mentioned were some of the pearls. And right around the corner, we have another agent riddle sit nib for alopecia, which is a Jack three tech, so it's a different kinase. So Oxfordy Ox 40 ligands are coming for atopic Derma. The learning is not going to stop, and it's very fascinating. And even lupus is being looked at with tick two and some other agents. So I think it's very exciting. So thanks, David. Thanks so much, Jim. We ask if people want anybody else, and they keep coming back to you. So it's always back by top of the man. Thank you very much. Turn into Derms and Conditions podcast. They come regularly by going to Apple Podcasts or wherever you get your favorite shows. Thank you. That's.

In Episode 43 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Bruce Strober, MD, PhD, a Clinical Professor of Dermatology at Yale University. The two discuss some of the newest advances in psoriasis management.They start with an overview of therapies with new mechanisms of action and discuss other medications that are in the pipeline. Dr. Strober then provides important tips for screening for psoriasis comorbidities. Since at least 1 in 5 patients will get significant psoriatic arthritis, and patients with moderate to severe psoriasis are at increased risk for cardiac events, Dr. Strober emphasizes that working with other specialists is critical to ensure comprehensive care.

In Episode 43 of&nbsp;Derms and Conditions, our host James Q. Del Rosso, DO, sits down with Bruce Strober, MD, PhD, a Clinical Professor of Dermatology at Yale University. The two discuss some of the newest advances in psoriasis management.They start with an overview of therapies with new mechanisms of action and discuss other medications that are in the pipeline. Dr. Strober then provides important tips for screening for psoriasis comorbidities. Since at least 1 in 5 patients will get significant psoriatic arthritis, and patients with moderate to severe psoriasis are at increased risk for cardiac events, Dr. Strober emphasizes that working with other specialists is critical to ensure comprehensive care.Finally, Dr. Strober reviews the many benefits of deucravacitinib (SOTYKTU), including its once-daily oral dosing, excellent safety profile, and lack of lab monitoring. He notes that deucravacitinib is very effective, even more so than methotrexate, and comparable to cyclosporine but without all of the side effects. He discusses the unique mechanism of action of TYK2 inhibition and how this targeted action limits the drug’s side effects and allows it to avoid the black box warning that other JAK inhibitors carry. Tune in to this episode to learn more about this new drug that Dr. Strober believes will revolutionize psoriasis management.&nbsp;

Improving Our Understanding of How Drugs Work: Clarifying Questions with Monoclonal Antibodies and JAK Inhibitors

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