This is a really important topic because so many times when people develop a new problem with their HS, some practitioners or offices are quick to refer them out. A good example is an abscess. One of these cysts turns into an abscess, it’s actively draining. I believe most people are comfortable with doing an incision and drainage. But many times people and clinicians are underutilizing intralesional injections. This is a quick procedure that can provide a lot of relief and less scarring for the patient. Obviously, there are limitations to that. But for some of the bigger areas that are more involved and resistant to I&Ding [incision and drainage] or intralesional injections, doing a deroofing procedure can provide a lot of benefit for patients. This is a way to keep the patient in your practice, have good continuity of care, and treat them effectively without referring them to a general surgeon. There are lots of resources available for that procedure, but that is something that I encourage everyone to get better at doing because it really provides a lot of relief for those patients with HS.

Ask your patients about HS. There is definitely a knowledge gap for practitioners across all specialties. And many times patients are not forthcoming with having this disease. And so when you’re seeing someone who comes in for acne, or you’re seeing someone who comes in and you’re draining an abscess, have the conversation and ask them, “Do you have these anywhere else? How many cysts have you had in your life?” Oftentimes, that opens up a good conversation, and patients will be more forthcoming with having this disease. Also, for the patients who have HS, talk to them about the benefit of early treatment. We’ve discussed this here, but a lot of people feel that biologic treatment is only necessary when they have severe disease or stage III Hurley disease, and that is not the case. Early intervention in this window of opportunity can provide people with an improved quality of life, less surgery, less sequelae from this disease, so that is really important. And also, develop a good multidisciplinary team. People in the medical community—some have very strong personalities. And it may take a little bit of time to find a group of individuals you trust to refer. Whether it’s a psychiatrist or a surgeon or whoever you’re working with for these patients, making sure that you’re on the same page about what it takes to truly treat this disease effectively is so important. And the last is to make sure you’re going to tell your patients that you’re going to follow them closely, you’re going to be seeing them frequently, you’re going to make sure that their medications are working for them. If they develop a hot spot or a draining abscess, make sure that you tell them that you’ll get them in quickly to manage this to prevent them from going to ERs [emergency rooms] and urgent care facilities. And just having polypharmacy, because so many times these patients are being bounced around. So just let them know that you care and that you’ll be there with them throughout this journey.

An expert in dermatological conditions discusses office-based procedures that can benefit patients with HS and shares clinical pearls for the management of the disorder.

Clinical Pearls for the Management of HS

Andrew Baker PA-C, MBA

Panelist introductions for an editorial program titled: Embracing New Therapies in Schizophrenia Management

Embracing New Therapies in Schizophrenia Management: Introductions

On September 26, 2024, the US Food and Drug Administration (FDA) approved 

 (Cobenfy), backed by evidence in phase 3 EMERGENT trials. The approval marks the start of a new era in the management of 

, as the agent, formerly known as KarXT, marks the first new pharmacological approach to treating schizophrenia since the 1970s.

Xanomeline and tropism chloride capsules act as a dual M1/M4 muscarinic acetylcholine receptor agonist in the central nervous system. Unlike previous schizophrenia treatments, this drug does not directly regulate the dopamine receptor—only indirectly modulates. 

To commemorate and offer perspective on what this approval means for the healthcare community, 

 hosted a Special Report where leading subject matter experts discussed the approval of xanomeline and tropism chloride capsule for schizophrenia. In this opening segment, moderator Sam Clark, MD, PhD, introduces panelists Rishi Kakar, MD, lead investigator of the EMERGENT trials, and Andrew J. Cutler, MD. The remainder of this panel discussion, which can be found below, focused not only on the approval of xanomeline and tropism chloride capsules but also on the latest updates and the most pressing unmet needs in schizophrenia management.

Mechanism of Action of Xanomeline and Trospium Chloride Capsules

Applying EMERGENT Trial Results to Real-World Clinical Practice for Schizophrenia

Balancing the Benefits and Risks of Xanomeline and Trospium Chloride Capsules

Unmet Needs, Future Research in Schizophrenia and Muscarinic Agonists

(Moderator) is a former practicing psychiatrist and is the founder and chief executive officer of Terran Biosciences.

is a clinical associate professor in the Department of Psychiatry and Behavioral Sciences at SUNY Upstate Medical University and the chief medical officer of the Neuroscience Education Institute.

is a psychiatrist based out of southern Florida as well as the medical director and chief scientific officer of Segal Trials. Kakar served as the principal investigator on the pivotal EMERGENT trials.

Relevant disclosures for Cutler include Karuna, Bristol Myers Squibb, and 

. Relevant disclosures for Kakar include Karuna, Bristol Myers Squibb, and others. Relevant disclosures for Clark include Terran Biosciences.

The FDA's approval of xanomeline and tropism chloride capsules (Cobenfy) on September 26, 2024, introduces a novel pharmacological approach to schizophrenia treatment, the first since the 1970s. This dual M1/M4 muscarinic acetylcholine receptor agonist indirectly modulates dopamine receptors, differing from traditional treatments. A Special Report by HCPLive Psychiatry featured experts discussing the drug's approval, its mechanism, and its application in clinical practice. The panel also addressed unmet needs and future research directions in schizophrenia management, highlighting the significance of this advancement.

In part 1 of 5, panel moderator gives an overview of the Special Report focusing on the approval of Xanomeline and tropism chloride capsules for schizophrenia.

Andrew Cutler, MD

Devrey Martin is a Master’s Student in Forensic Psychology at the University of Denver with interests in the overlap of forensic psychology with health psychology and neuropsychology. During her first year, Devrey has been involved in traumatic brain injury research and writing for an advocacy newsletter. She aims to provide forensic evaluations and assessments while advocating for prison reform.

Devrey Martin, BS

managing cases of high-risk PDR and DME, exploring new therapies and synergistic combinations with anti-VEGF and steroids for longer-lasting responses.

Managing Patients With High-Risk PDR and DME

This is a video synopsis of a discussion involving Ehsan Rahimy, MD, a retina specialist at the Palo Alto Medical Foundation and adjunct faculty at Stanford University School of Medicine. Dr. Rahimy addresses the management of a patient with high-risk proliferative diabetic retinopathy (PDR) and diabetic macular edema (DME) who has shown limited response to anti-vascular endothelial growth factor (anti-VEGF) therapy.

He discusses the need for a flexible treatment approach and mentions the possibility of switching to different agents such as aflibercept or faricimab based on the patient's response. Dr. Rahimy emphasizes the importance of close monitoring and quick adjustments in treatment, including the consideration of adding steroid therapy like Ozurdex (dexamethasone implant) for cases exhibiting signs of inflammation on optical coherence tomography (OCT).

Dr. Rahimy highlights the significance of phenotypic markers in determining treatment strategies, suggesting the use of wide-field fluorescein angiography (FA) to assess vascular leakage and guide therapy decisions. He also discusses the potential role of longer-term steroid options like a fluocinolone implant for patients with a good response to initial steroid treatment.

Furthermore, Dr. Rahimy emphasizes the importance of integrating panretinal photocoagulation (PRP) laser therapy for patients with high-risk PDR, particularly those who may be non-compliant with office visits. He stresses the need for patient education regarding the intensive nature of treatment and the potential consequences of non-adherence, especially for patients at risk of significant vision loss.

In summary, Dr. Rahimy provides insights into a comprehensive and dynamic approach to managing complex cases of diabetic retinopathy, highlighting the importance of personalized treatment plans and proactive monitoring to optimize patient outcomes.

Video synopsis is AI-generated and reviewed by HCPLive® editorial staff.

Ehsan Rahimy, MD, outlines strategies for managing cases of high-risk PDR and DME, exploring new therapies and synergistic combinations with anti-VEGF and steroids for longer-lasting responses.

Ehsan Rahimy, MD

Eric Lawitz, MD, is the medical director of the Texas Liver Institute and a clinical professor of medicine at the University of Texas Health San Antonio.

Trivedi and Lawitz review long-term data from the phase 3 open-label ASSURE study and explain what they add to our understanding of seladelpar for PBC.

Insights from Long-Term ASSURE Data for Seladelpar

 treatment landscape has long been limited to just a handful of agents with limited efficacy, 2024 saw a major shift in PBC management with the addition of 2 new second-line therapies.

Seladelpar (Livdelzi), a proliferator-activated receptor (PPAR) delta agonist, was one of these recent additions to the PBC treatment armamentarium and was a major topic of discussion at 

The Liver Meeting 2024 from the American Association for the Study of Liver Diseases (AASLD)

Findings from a 2.5-year interim analysis of the ongoing open-label phase 3 ASSURE study were presented in a late-breaking abstract at the meeting and highlight seladelpar’s sustained efficacy and long-term safety for the treatment of PBC.

In this segment, which is the final installment of a 4-part series, experts Palak Trivedi, MD, PhD, and Eric Lawitz, MD, discuss the long-term ASSURE data and what they add to our understanding of seladelpar’s safety and efficacy for PBC.

Trivedi begins by emphasizing the significance of seladelpar’s long-term safety profile, calling attention to the lack of new treatment-emergent adverse events or concerning safety signals. While acknowledging the inherent limitations of safety extension studies without matched control groups, he describes how the ASSURE data provide confidence in the drug’s sustained biochemical response and tolerability, additionally advocating for real-world studies to validate these findings and establish whether seladelpar improves transplant-free survival over time beyond its biochemical markers.

Similar to Trivedi, Lawitz highlights the importance of long-term follow-up in chronic therapies. He notes that the ASSURE data not only confirm the stability of seladelpar’s safety profile but also reveal a potential increase in efficacy with extended treatment. He notes the consistent durability and lack of unexpected toxicities offer clinicians greater confidence in prescribing seladelpar for prolonged use.

: associate professor and honorary consultant hepatologist and clinical research director for industry engagement at the University of Birmingham

: medical director of the Texas Liver Institute and a clinical professor of medicine at the University of Texas Health San Antonio

Relevant disclosures for Trivedi include Bristol Myers Squibb, Gilead, Intercept, CymbaBay, and others. Relevant disclosures for Lawitz include 89Bio, Boehringer Ingelheim, Merck, Novo Nordisk, Sagimet Biosciences, AstraZeneca, Bristol Myers-Squibb, Cymabay, Eli Lilly, Gilead Sciences, GlaxoSmithKline, Intercept, Ipsen, Madrigal, Novartis, Regeneron, Takeda, Terns, Viking Therapeutics, AbbVie, and others.

Brooks A. FDA Grants Accelerated Approval to Seladelpar (Livdelzi) for Primary Biliary Cholangitis. HCPLive. August 14, 2024. Accessed December 4, 2024. 

https://www.hcplive.com/view/fda-grants-accelerated-approval-to-seladelpar-livdelzi-for-primary-biliary-cholangitis

Brooks A. Seladelpar (Livdelzi) Demonstrates Long-Term Benefit for Primary Biliary Cholangitis. HCpLive. November 15, 2024. Accessed December 4, 2024. 

https://www.hcplive.com/view/seladelpar-livdelzi-demonstrates-long-term-benefit-primary-biliary-cholangitis

The treatment landscape for primary biliary cholangitis (PBC) has evolved with the introduction of new second-line therapies, including seladelpar, a PPAR delta agonist. At The Liver Meeting 2024, findings from the ASSURE study highlighted seladelpar's sustained efficacy and long-term safety. Experts Palak Trivedi and Eric Lawitz emphasized the drug's stable safety profile and potential increased efficacy over time. They advocated for real-world studies to further validate these findings and assess seladelpar's impact on transplant-free survival beyond biochemical markers.

Eric Lawitz, MD

Topicals are the mainstay of treatment for patients with plaque psoriasis (PsO) of any disease severity.

 Since 1997, corticosteroids, retinoids, and vitamin D analogues have been the only active ingredients used in topical therapies for PsO; new formulations introduced since then have featured changes in the vehicle components or in combinations of active ingredients. Many of these formulations have limitations on duration of use and body areas on which they can be applied due to the potential for certain adverse effects (AEs). Patients may need to use multiple different topical agents at a time, which increases the likelihood of medication misuse and nonadherence. The 2022 approvals of the tapinarof cream, 1% (VTAMA®; Dermavant Sciences) (an aryl hydrocarbon receptor agonist) and roflumilast cream, 0.3% (Zoryve®; Arcutis Biotherapeutics), (a phosphodiesterase-4 [PDE4] inhibitor) for treatment of plaque PsO has provided 2 new options for safe, effective, and well-tolerated steroid-free topical therapies with the potential to simplify management for patients.

As an aryl hydrocarbon receptor agonist, tapinarof uses a novel mechanism of action to downregulate expression of T helper type 17 cytokines that drive inflammation in PsO, normalize skin barrier function, and increase antioxidant activity.

 In the pivotal phase 3 PSOARING 1 (NCT03956355) and PSOARING 2 (NCT03983980) trials, researchers found that a Physician’s Global Assessment (PGA) score of 0 or 1 with a 2-grade reduction was achieved by a considerably greater proportion of groups given once-daily tapinarof compared with the respective vehicle groups at 12 weeks (PSOARING 1: 35.4% vs 6.0%; adjusted difference, 29.4 percentage points; relative rate, 5.8; 95% CI, 2.9-11.6; 

 < .001; PSOARING 2: 40.2% vs 6.3%; adjusted difference, 33.9 percentage points; relative rate, 6.1; 95% CI, 3.3-11.4; 

 Among 312 patients who achieved PGA 0 at least once during the vehicle-controlled and/or the open label extension period, the median time to relapse (defined as PGA 2 or greater) was an unprecedented 4 months. Additionally, patients treated with tapinarof, 1%, cream who had a Peak Pruritus Numerical Rating Scale (PP-NRS) score of at least 4 points at baseline experienced at least a 4-point reduction as early as 2 weeks, which continued to increase to 60.7% and 56.9% by 12 weeks, compared to just 43.2% and 29.6% of patients in the vehicle groups, demonstrating rapid and robust itch reduction.

In the 40-week, open-label safety study (PSOARING 3), participants continued the tapinarof cream until they had complete skin clearance, after which the patients held application of the cream. The duration to symptom recurrence was measured, and a durable remittive effect was observed. On average, the median remittive duration was approximately 4 months, and some remained symptom-free for up to 8 to 9 months. In addition, the trial results showed a durable response out to 52 weeks without evidence of tachyphylaxis.

Overall, tapinarof demonstrated good local tolerability. In the PSOARING 1 and PSOARING 2 trials, respectively, contact dermatitis was experienced by 5% and 5.8% of the patients who received tapinarof vs 0.6% and no patients who received the vehicle; one of these cases in PSOARING 2 was a severe adverse event. Folliculitis was reported in 23.5% and 17.8% in the tapinarof-treated groups vs 1.2% and 0.6% in the vehicle groups. Most cases of folliculitis were mild to moderate with only 1 grade 3 event that was reported during the PSOARING 1 trial; therapy was discontinued due to folliculitis in 1.8% and 0.9% of patients.

Folliculitis presentation includes keratotic papules, pustules, and milia and varies among patients; it was generally limited to the site of application. In the authors’ experience, this appears to occur more frequently in hair-bearing areas. Treatments for folliculitis include temporary interruption of tapinarof, antibiotics, urea, retinoids, salicylic acid, or topical corticosteroids; however, many cases resolved even without any treatment. Educating patients about the potential for this AE and how it may be managed is important to ensure patient adherence.

Unlike other available PDE4 inhibitors, roflumilast has 3 major anchoring points that bind to the PDE4 enzyme, which drastically increases the potency (as assessed in vitro) compared with that of other PDE4 inhibitors. In the phase 3 DERMIS-1 (NCT04211363) and DERMIS-2 (NCT04211389) trials, considerably greater proportions of patients given roflumilast achieved the primary end point of Investigator’s Global Assessment (IGA) scale (clear or almost clear status and at least a 2-grade improvement from baseline) at 8 weeks compared to those given the vehicle (DERMIS-1: 42.4% vs 6.1%; difference, 39.6% [95% CI, 32.3-46.9]; DERMIS-2: 37.5% vs 6.9%; difference, 28.8% [95% CI, 20.8-36.9]).

 Additionally, significant improvements in IGA success with roflumilast were observed as early as 4 weeks after start of treatment (DERMIS-1: 20.6% vs 2.3%; difference, 19.3% [95% CI, 13.5-25.1]; 

 < .001; DERMIS-2: 19.1% vs 5.3%; difference, 13.5% [95% CI, 7.2-19.9]; 

Additional findings from the DERMIS-1 and -2 trials showed that roflumilast was also beneficial for patients with intertriginous psoriasis. Compared with use of the vehicle treatment, roflumilast treatment significantly improved intertriginous IGA scores at 6 weeks among patients having an intertriginous IGA score of 2 or more at baseline (DERMIS-1: 56.6% vs 22.2%; difference, 41.0% [95% CI, 20.1-61.8]; 

 = .005; DERMIS-2: 57.8% vs 13.8%; difference, 40.5% [95% CI, 18.7-62.2]; 

 = .004), leading to the inclusion of intertriginous psoriasis in the US prescribing label.

Regarding safety, nonsteroidal options have traditionally been associated with tolerability issues. Findings from the DERMIS-1 and -2 trials indicated that application site pain was infrequent, and nearly 99% of patients reported no signs of irritation at 4 and 8 weeks.

 Additionally, the rates of diarrhea and headache, which are commonly associated with oral PDE4 inhibitors, were low (diarrhea, 2.8%-3.5%; headache, 1.0%-3.8%) and mild or moderate in severity; no events involving diarrhea required interruption or discontinuation of treatment.

Given the difficult of treating intertriginous PsO, a topical nonsteroidal option that is effective, safe, and well tolerated when used in these areas is particularly valuable. The ability to use roflumilast, 0.3%, cream on multiple areas of the body, including difficult-to-treat areas like the elbows and sensitive areas like the skin folds, can simplify treatment options for appropriate patients.

Roflumilast has a trademarked drug delivery formulation (HydroARQ Technology™) that does not contain propylene glycol, a potential irritant and allergen, and includes a proprietary hydrophilic emulsifier (Crodafos™ CES) found in many other popular cosmeceuticals, resulting in an elegant cream that is well tolerated and compatible with most other skin care products.

 Educating patients about the formulation’s novel mechanism of action and the well-tolerated vehicle may provide reassurance in patients who have had a negative experience with previous PDE4 inhibitors or topical agents.

Use of roflumilast in a foam vehicle has also been studied for scalp and body PsO. In a phase 2b study (NCT04128007), use of this formulation yielded an achievement of scalp-IGA clear or almost clear and a 2-grade or more improvement from baseline to week 8 in 59.1% of patients vs 11.4% of those given vehicle, with significant effects observed as early as week 2.5 Roflumilast foam was also well tolerated; there was no evidence of irritation in 96% or more of patients based on investigator-rated tolerability and mild or no sensation in 94% or more on patient-rated tolerability.

 Due to the anionic nature of the Crodafos CES emulsifying wax, roflumilast foam is repulsed by the natural negative charge of the hair, allowing it to selectively target the scalp skin while avoiding the hair shaft. This is particularly advantageous for patients with tightly coiled hair who may be more susceptible to hair shaft breakage from harsh ingredients.

Incorporating Novel Topical Agents Into Clinical Practice

While topical corticosteroids will continue to be an important option in our topical armamentarium, novel nonsteroidal topicals such as tapinarof and roflumilast can address some of the limitations associated with topical corticosteroids. Furthermore, these agents could simplify the treatment regimen because of both their once-daily application versus the twice-daily frequency required by many other topical agents and their effectiveness, safety, and tolerability across a wide range of body areas. No direct comparative studies have been conducted between tapinarof or roflumilast, yet each of these agents has unique characteristics that should be considered when choosing treatment for a given patient.

Both of the pivotal studies were conducted as monotherapy, yet the product label allows for tapinarof and roflumilast to be used together with other therapeutic agents. Prescribing a topical corticosteroid in addition to tapinarof or roflumilast may benefit patients who want a more rapid response. Patients on a systemic treatment with residual disease may also benefit from adding tapinarof or roflumilast. Educating patients on the mechanism of action and setting specific expectations on the timeline for a therapeutic response is particularly important to improve treatment adherence.

Faculty presenters: Eingun James Song, MD, FAAD; and Kimberly Gutowsy Baker, MSN, FNP-C

. This article was reviewed, edited, and approved by Dr Song, Ms Gutowsy Baker, and Dr Stein Gold.

Lebwohl MG, Stein Gold L, Strober B, et al. Phase 3 trials of tapinarof cream for plaque psoriasis. 

. 2021;385(24):2219-2229. doi:10.1056/NEJMoa2103629

FDA approves Dermavant’s VTAMA (tapinarof) cream, 1% for the treatment of plaque psoriasis in adults: first topical novel chemical entity launched for psoriasis in the U.S. in 25 years. Press release. 

. Updated May 24, 2022. Accessed December 14, 2023. https://www.dermavant.com/u-s-fda-approves-our-novel-topical-treatment-for-adults-with-plaque-psoriasis/

FDA approves Arcutis’ ZORYVE (roflumilast) cream 0.3% for the treatment of plaque psoriasis in individuals age 12 and older. Press release. Arcutis Biotherapeutics. Updated July 29, 2022. Accessed December 14, 2023. https://www.arcutis.com/fda-approves-arcutis-zoryve-roflumilast-cream-0-3-for-the-treatment-of-plaque-psoriasis-in-individuals-age-12-and-older/

Lebwohl MG, Kircik LH, Moore AY, et al. Effect of roflumilast cream vs vehicle cream on chronic plaque psoriasis: the DERMIS-1 and DERMIS-2 randomized clinical trials. 

. 2022;328(11):1073-1084. doi:10.1001/jama.2022.15632

Strober B, Stein Gold L, Bissonnette R, et al. One-year safety and efficacy of tapinarof cream for the treatment of plaque psoriasis: Results from the PSOARING 3 trial. 

. 2022;87(4):800-806. doi:10.1016/j.jaad.2022.06.1171

Kircik LH, Alonso-Llamazares J, Bhatia N, et al. Once-daily roflumilast foam 0.3% for scalp and body psoriasis: a randomized, double-blind, vehicle-controlled phase IIb study. 

. 2023;189(4):392-399. doi:10.1093/bjd/ljad182

This publication was developed independently by MJH Life Sciences Global Medical Affairs. Support for the thought leaders meeting and the publication was provided by Arcutis Biotherapeutics, Inc; The Bristol Myers Squibb Company; Janssen Global Services, LLC; and UCB, Inc.

New Topical Agents for Treatment of Plaque Psoriasis

James Song, MD

John Salgo, MD

The last piece is about education. This is important because to make a good shared decision-making process with the patient, they have to be on the same page. There’s a huge amount of education that has to happen. Of course, we all have luxurious amounts of time. You guys usually have, what, 1 to 2 hours for a new visit? Maybe longer—it’s only a few patients a day. No. We’re crunched. You have crunched time, and you have so much to cover. Sometimes the visit has many factors: where have you been? What are you using currently? What are your hopes, your fears, concerns? Then you get derailed. All they want to talk about is food. What food should we avoid? If we mention that, it can derail the whole visit. You’re trying to get to the next step to figure out how to get their skin better, and they’re doing this.

That doesn’t take into account the paperwork that has to happen after: the insurance forms, the prior authorization, the patient support stuff—all these things. How do we do that? One thing that’s so important is to bring external resources. I’m obsessed with handouts. I’m the king of handouts. Every time I see anybody for anything, they’re going home with a handout, and it’s usually going to list my action plan: what to do when you’re flaring up and what to do when you’re better. That’s such a big deal for me because it’s cut a lot of calls. Not 100%, but many calls [are answering the questions], “Which do I do first? Do I put this 1 on and then this 1?” I put them in numeric order. “In the morning, you’re going to do 1, 2, and 3.” We can really bring them through that.

The other piece that’s important is utilizing some of the national organizations that have patient support resources. I’m very conflicted because I’m a board member of the National Eczema Association. I don’t get paid any money. In fact, I donate a lot every year. I love the National Eczema Association. They’re a nonprofit organization that does a lot of patient advocacy support and education. I try to have my patients go to their website , to get signed up, to learn a little more about it. It’s nice when it doesn’t have to come directly from us. Sometimes they have a rapport with us, they understand us, but it’s nice to hear someone else’s voice, to get another opinion. That can help and give them some of the tools that can help them ask the good questions at the next visit, because I don’t like to be pushy. 

On the first visit, sometimes I say, “Here are some options. I want you to think about this. Here’s some homework for you to read. Let’s talk, either by phone”—if they’re from out of state or from far away—“or when I see you in a few weeks, we’ll make our decisions at that point.” How do you guys feel about the education burden that we have?

I agree. All of our patients are—if they haven’t already before they come to the visit—going to Google and Facebook to crowdsource and ask for advice from trusted friends and family members beyond their trusted allergist or dermatologist. Beyond the sheet that has all those important, point-by-point instructions, there needs to be a trusted links list. Something like the [National] Eczema Association and our national societies, which have great patient handouts. Let them kind of go down the rabbit hole online in a safe place, in a place they’re going to get good information.

Giving links and trusted sources are really helpful. But I also find that having that patient back with a short turnaround time is important. We’re all busy, but in patients with atopic dermatitis, we give them homework, we give them food for thought, but they need to come back shortly thereafter with questions fresh in mind. [Once they’re] able to move the ball along the field, get closer to that touchdown, get closer to that goal line, we can make management decisions incrementally. It’s OK to make management decisions incrementally for these patients. If you do that, they’ll follow you along that pathway.

I was going to make 1 quick [point]. We’ve alluded to the food thing. There may be some listeners [wondering], “Why are they laughing about the food? Why aren’t they talking about that?” I can speak a little for Dr Jain because I just attended 1 of his amazing lectures about food allergy and atopic dermatitis. The point—and the way I say it to my patients—is that I wish the food were the cause. When food is the cause, it’s easy. Arguably, you don’t actually have atopic dermatitis. You have an eczematous food reaction—you’re done, you don’t need us, you don’t need any of this. But for many patients, food may be playing some role. It might be inflammatory. They may have some food triggers. Of course, there’s a huge concurrence of real food allergies that are IgE mediated.

It’s a complex, messy thing, but it’s often not where the money is to get the skin better. There’s this tension because the patients want to focus on the diet, “How can I fix my diet to get better?” [We say], “I don’t know.” Even if you did a super-severe, extreme diet—we’ve all had patients with literal malnutrition because they’ve been so stringent on their diet, and their eczema is still terrible. It’s trying to redirect, not because we’re trying to push drugs on somebody, but because we’re trying to help them. Some of the patients and families have done this for years. I’ll just sit there and say, “You would’ve found it without me. You’ve cut everything out. You’re feeding the child rocks and water, but his eczema is still bad. I don’t think it’s food. I want it to be too, but can we work on other things?”

One of the little tools in my toolbox that I’ll share—this is a pretty universal thing; we all feel the pain of this is that I often say to families who are fixated on it, “When the skin is super inflamed, like now, when it’s a mess, it’s similar to when you get up on the wrong side of the bed.” You’re in a bad mood. No matter what anybody says to you, you’re going, “Grr.” Somebody says, “Good morning,” and you’re, “Grr.” But when you get up and you’re in a good mood, even if someone says, “You’re a jerk,” you say, “Have a great day.” It rolls off you.

It’s very difficult to evaluate what’s triggering your skin when it’s a mess, so I say, “Let’s get it better.” Let’s spend a little time cleaning things up. If there are still triggers, we can then see with much clearer eyes If they had an aha moment when they ate—fill in the blanks—dairy, gluten, strawberries, whatever it may be. That definitely made it worse. But right now, we can’t even see that. I put that there not because we don’t take it seriously. We do, but it could take up all the time. Sometimes that’s all people want to talk about. We have to redirect, because I want to get people better. Do you guys agree with that? Not to derail it too much, but it’s so important.

Absolutely. When we talk about what works and what helps patients get buy-in, we take for granted that we understand this pathology of atopic dermatitis, but they don’t. You just spoke about this with regard to their focus on foods or other things, what mindset they come in with. We need to take a step back and teach them that this is a disease where there’s barrier dysfunction, helping them understand that we’re learning that this is true not only of atopic dermatitis but also other type 2 inflammatory diseases, whether it’s asthma, allergic rhinitis, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis.

We know that there are these similarities with this barrier dysfunction, and that barrier dysfunction leads to this inflammation. That’s how you develop food allergies. It happens first there. We need to help them understand this so that they get the focus away from some things that they have preconceptions about, and then we can educate them about the options to manage that and help restore that function to help their skin better. That’s hugely helpful. When this comes from reputable sources like the National Eczema Association, the AAD [American Academy of Dermatology], our societies in allergy, getting that same message repeatedly helps.

We did some survey on patients’ perceptions about bathing. You hear these patients coming in, saying that they’ve been told 15 things about what they should do with bathing, and they’re just confused. So to have some science to back this up gives us credibility, and that allows for the buy-in that ultimately leads to success in skin improvement.

Educating patients about their disease course is very important at the outset. It’s important to set expectations, and there’s no more important way for me to do that than to tell them this is not something you’re doing. It’s not your fault. It’s a genetic skin condition, and it’s a condition that waxes and wanes over time. There are going to be periods when you forget that you have eczema. There are going to be periods when it’s very flared. Our job is to control those flares so that you’re not having flares very often and when you do have flares, to not be concerned about treating them at the first sign of trouble.

One way to do that is to talk about the use of steroids and how to properly use them so that they’re not afraid to use them. Another way is to use nonsteroidal medications that might promote less fear within the patient or the parents so that they use them at the first sign of trouble. I always say that it’s like a little fire that’s burning. The sooner you put it out, the better off you’ll be—but you have to completely put it out. If you use your medication for a few days and then there are still some embers there, it will come right back. It’s important to set those expectations.

A third thing that’s very important to talk about is avoiding systemic steroids. Very commonly, patients come to the office with chronic waxing-and-waning flares. It’s a vicious cycle, and it’s usually triggered by the use of systemic steroids, either injectable or oral prednisone or Medrol dose packs. What happens is the patient’s skin rebounds once they come off their systemic steroids. It’s important to educate parents, patients, and providers that using systemic steroids should be a bridge to some other therapy and should not in and of itself be the plan to treat someone’s atopic dermatitis. In the long term, they have adverse effects. In the short term, they’re going to create a rebound that’s only going to continue their waxing-and-waning flare cycle.

Shared insight on the best ways to educate patients on their atopic dermatitis and explain the nuances of available therapies.

Educating Patients on Atopic Dermatitis and Inflammation 

Marc Serota, MD

Reynold Panettieri, Jr, MD, Robert Wood Johnson Medical School 

 You touched on the brand-new drug anifrolumab. It’s another breakthrough in lupus, developed for SLE [systemic lupus erythematosus]. In the mid-1990s, they found that interferons were highly expressed in SLE, and particularly in the pathogenesis…

 Maybe so. But the trials had showed efficacy in both high and low responders, but maybe we’ll get there later.

 Yeah, it’s interesting. But it means you need to inhibit it a little—that’s all, right? There’s only so much you can get with interferon-alpha blocker probably.

 But it’s so new, we don’t know yet, right?

 Right. But that drug was developed out of genome-wide studies and that showed multiple SNPs, or single-nucleotide polymorphisms, in genes that encoded for the expression of interferon alpha. It’s this idea of rational drug design that’s being applied to SLE, that had been applied to other rheumatic diseases. We’re finally here, where we’re going to be at the breakthrough with new therapies.

 I’m very curious because it’s been approved in the United States for a number of months. Are you now—I mean 

 in the plural, so rheumatologists practicing in the United States—gaining experience with anifrolumab? Is it available?

 We are. It’s becoming available in the community setting. Most academic centers are getting it on their formulary. I have patients on the medication, and I’m doing a clinical trial incorporating that medication with Joan Merrill. We’re starting pick up, and it’s still too early to know how important this may be in the treatment of lupus and when it should be employed in SLE. As you know, the study showed an effect that was fairly rapid, so that there was a divergence of the treatment curves at 2 or 3 months, from what I recall. There was a particular improvement in skin disease with lupus. This might be an agent that 1 may try for rapid amelioration of skin manifestation of lupus.

 Interesting. There are also data that in the skin, interferon is upregulated. If you do a molecular analysis, you can see that.

 That stands to reason. But I’m also still intrigued by how lupus may be several pathophysiologies. In some people you have the high interferon signature or the low interferon signature, going back to belimumab you have patients for whom B-cell activity is very high, and they have all these other antibodies. Other patients might have lupus, but they may have only antinuclear antibodies and not the other ones. There could be a difference also. It might be that in the future, which is what I hope, we’ll do these analyses, immunological analyses, and it will tell us this patient should be treated with anifrolumab, this patient should be treated with belimumab, this patient will do best with a conventional therapy. That’s also possible. We might be able to start doing it that way. We’re not there yet by a long shot, but I want it for the future.

 Right, and there may be cycles of therapy. They may want to treat patients with anti-interferon therapy followed by B-cell therapy or combinations, particularly if there’s severe disease, and we’ll learn how to use them in combination to get our patients better. But it’s an exciting breakthrough.

 Interesting. I was involved in a combination trial with—I don’t know if you knew about this—the combination of belimumab with rituximab. That’s quite strange because rituximab is not approved for lupus. It’s used off-label, but it’s not approved. Then there’s a trial. There were several trials where these were combined with the idea that you could get some sort of a synergy. It’s a very interesting scientific concept, and it could work. The patients in the trials did well, but it was not so clear that the combination gave an added benefit. That’s still a little unclear. Some parameters said they did, but others said that it was the same. It will be very interesting to see it.

 You showed this data in an abstract at the American College of Rheumatology, am I right?

 I was a coauthor, so there were others who showed it.

 Right. After 52 weeks, though, you had stopped therapy, so of course lupus will flare. One wondered why these were not continued.

The rationale for using a newer monoclonal antibody therapy, anifrolumab, to manage patients with systemic lupus erythematosus.

Authors