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Expanding on Atopic Dermatitis Triggers and Comorbidities, and Advancements


Mark Lebwohl, MD, discusses the rapid expansion of therapeutic options, including targeted drugs like JAK inhibitors and IL-13 treatments for atopic dermatitis, paralleling the progress seen in psoriasis treatment over the last decade.

This Dermatology Times Expert Perspectives series delves into the multifaceted landscape of atopic dermatitis (AD) care and treatment. Through interviews with 4 leading dermatologists, this series explores key benchmarks, emerging trends, personalized medicine approaches, long-term safety considerations, and the integration of novel therapies in the management of AD. Each episode provides valuable insights into navigating the heterogeneity of AD presentations, selecting appropriate treatment plans tailored to individual patient needs, and incorporating the latest guidelines from the American Academy of Dermatology (AAD). From discussing the nuances of patient education and shared decision-making to addressing the intersection of comorbidities with AD management, this series equips dermatology clinicians with the knowledge and strategies necessary to optimize patient outcomes and enhance the quality of care.

In this episode, Mark Lebwohl, MD, dean for clinical therapeutics at the Icahn School of Medicine at Mount Sinai in New York, New York, discusses the rapid expansion of therapeutic options, including targeted drugs like JAK inhibitors and IL-13 treatments for atopic dermatitis, paralleling the progress seen in psoriasis treatment over the last decade.

Episode Transcript

Lebwohl: So there are a number of very specific triggers for AD. For example, a patient who comes in and tells you that they're bathing 3 times a day, you know that that's excessive, and that will be exacerbating their AD. So something as simple as reducing the frequency of bathing using gentle soap substitutes and using moisturizers might be adequate for those patients. Patients will often tell you that they get worse during the wintertime because cold dry air and steam heat dry out their skin. Again, reducing bathing and using more moisturizers may be helpful to those patients. Other patients will tell you that they get worse after exercise or in the summertime because sweat is a factor. Something as simple as air conditioning may help those patients. So identifying the factors that trigger AD in particular patients should have a direct effect on the treatments that you suggest.
Comorbidities may have a direct effect on the treatments that you select for patients. So for example, if a patient happens to have asthma as well, we have treatments such as dupilumab (Dupixent), which effectively treat both the AD and the asthma. There are other comorbidities such as osteoporosis, for example, that have been reported in patients with AD. So that gives you yet another reason to avoid the use of systemic steroids in those patients. And there are a whole host of other comorbidities that impact the disease. If patients have complications of other treatments, for example, striae because of excessive use of topical steroids. Then, we finally have, non-steroids that we can go to that are very effective for the topical therapy of AD without having the risk of stretch marks or cutaneous atrophy. So, again, many of the comorbidities have to be considered when you are picking the best treatment for a patient with AD.
There are many new diverse treatments that are highly effective for AD, regardless of severity. So for example, we have new topical therapies that are non-steroids, ones already on the market recently introduced ruxolitinib (Opzelura) cream. There are 2 additional ones tapinarof (Vtama) cream and roflumilast (Zoryve) cream that are on the way. They've completed their early phase trials. So in the realm of topical therapy, we have a lot of breakthroughs. In the realm of systemic therapy, we also have a lot of breakthroughs. There are also additional therapies on the horizon for chronic hand dermatitis, which is a form of AD delgocitinib cream, which hopefully will be available in the United States sometime soon. We also have many new top systemic therapies for AD. We've had dupilumab for a number of years already. Coming hopefully soon, we'll be lebrikizumab (Ebglyss). We already have tralokinumab (Adbry). These block IL-13, so they're a little bit more targeted than dupilumab and comparably effective. We have JAK inhibitors that have been introduced specifically, upadacitinib (Rinvoq) and abrocitinib (Cibinqo), which are already approved for AD. Several others certainly have been studied for AD.
So our therapeutic armamentarium for the disease has grown very quickly and looks like it will continue to grow. There are a number of additional anti IL-13 drugs on the horizon. Also drugs that target OX40 antibodies, which appear to be promising for AD. So I think we're going to experience in AD what we have experienced in the last decade for psoriasis where we have an explosion of new, better, safer treatments that help our patients live better lives.

Transcript edited for clarity

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