Tim Smith joined the MJH Life Sciences team in 2022 and is currently an associate editor for HCPLive. He is also the executive producer of two podcasts: Skin of Color Savvy and The Medical Sisterhood. Previously, he was the producer of the Lungcast podcast. He graduated from UC Berkeley and worked in multimedia journalism as a staff writer prior to joining MJH. You can contact him at tsmith@mjhlifesciences.com.

 research and care: the lack of universally accepted definitions for several key treatment outcomes, such as low disease activity (LDA), very low disease activity (vLDA), and disease remission.

Atopic dermatitis, often referred to as atopic eczema, is a relapsing inflammatory skin disease with clinical manifestations known to be both variable and dependent on patient’s age.

 It is also 1 of the most common skin disorders around the world.

This new statement regarding disease definitions for key outcomes in atopic dermatitis was authored by such investigators as Joseph Merola, MD, MMSc, of the Department of Dermatology and Department of Medicine at UT Southwestern Medical Center and O’Donnell School of Public Health in Dallas. Merola et al noted that, although recent advances in targeted medications have led to higher levels of disease control being more attainable, variability in the ways outcomes are defined has complicated clinical trial comparisons.

It has also made regulatory decision-making and treatment goal-setting difficult. In order to address this concern, the team of investigators with the International Eczema Council set out to determine what will become the standardized, consensus-driven definitions to be applied across both research and clinical practice around the world.

“This modified Delphi initiative establishes a globally endorsed, expert-derived framework defining LDA, vLDA, on-drug complete control, and off-drug remission in [atopic dermatitis],” Merola and coauthors wrote.

The initiative was led by a steering committee from the International Eczema Council, which began by conducting a focused systematic literature review. Using PubMed, the group identified relevant studies published between 2004 and 2024 that examined clinician-reported and patient-reported outcomes, disease activity measures, and pruritus severity in patients with atopic dermatitis.

The quality of evidence was evaluated using established criteria from the Oxford Centre for Evidence-Based Medicine. These findings informed the development of key conceptual domains that would guide a structured consensus-building process. In order to ensure agreement among the team’s set of experts, Merola et al employed a modified Delphi method consisting of 3 sequential survey rounds. They conducted their development of this statement in the period between January - July 2025.

Those who took part included a set of members currently involved with the International Eczema Council who also had recognized expertise in atopic dermatitis. Across the 3 rounds, those involved as panelists looked over the proposed definitions, providing various levels of feedback and refining the thresholds for disease activity measures. The process incorporated a set of predefined criteria to determine the levels of agreement, with 70% consensus at minimum being required for the adoption of a definition.

There were 151 experts in total who were invited to take part, with varying response rates across rounds. Those taking part represented a broad global distribution, including Europe, North America, Asia-Pacific, Latin America, and areas around Africa and the Middle East. The expert panel was made up primarily of clinician-researchers and practicing clinicians, in addition to a smaller proportion of researchers and individuals representing patient perspectives or advocacy groups.

One of the key outcomes of panel’s process was strong support for a modular framework that distinguishes between clinician-assessed signs and patient-reported symptoms as separate but complementary elements related to disease control. This approach allows for more nuanced categorization of remission, including distinctions between improvement in patients’ visible disease and relief of symptoms such as itch.

Overall, Merola and colleagues noted the final consensus definitions laid out specific thresholds using commonly utilized clinical tools. Low disease activity was defined by the panelists as moderate but controlled disease, based on validated global assessment scores or limited atopic dermatitis extent combined with manageable levels of itch. Very low disease activity reflected minimal or near-clear skin alongside little to no itch.

The team of experts also defined “on-drug complete control,” describing individuals who attain full disease clearance and resolution of symptoms while continuing medication use for a sustained timeframe. In contrast, “off-drug remission” was defined by the panelists as the maintenance of such outcomes for an extended time period following the discontinuation of a treatment.

Overall, the consensus statement was described by Merola and colleagues as representing 1 of the first globally coordinated attempts to standardize treatment outcome definitions in the atopic dermatitis space. Through the establishment of clinically meaningful and clear benchmarks, the team’s framework is designed to allow for improvement of consistency across clinical trials, support regulatory assessment of novel treatments, and facilitate long-term comparative research. Ultimately, the set of definitions may also allow for guidance in a more structured, treat-to-target approach in clinical practice.

Merola JF, Childs BA, Bartley BR, et al. International Eczema Council Definitions of Low Disease Activity and Remission in Atopic Dermatitis: A Consensus Statement. JAMA Dermatol. Published online April 15, 2026. 

Jeskey J, Kurien C, Hostoffer R, et al. Atopic Dermatitis: A Review of Diagnosis and Treatment. J Pediatr Pharmacol Ther. 2024 Dec;29(6):587-603. 

. Epub 2024 Dec 9. PMID: 39659858; PMCID: PMC11627575.

Articles

A globally endorsed consensus statement from the International Eczema Council establishes standardized definitions for low disease activity, very low disease activity, on-drug complete control, and off-drug remission in atopic dermatitis. A steering committee conducted a 2004–2024 literature review, graded evidence per Oxford criteria, and used a three-round modified Delphi process (January–July 2025) requiring ≥70% agreement. The framework is modular, separating clinician-assessed signs from patient-reported symptoms, and sets thresholds using common validated instruments to support trial comparability, regulatory evaluation, and treat-to-target care.

The International Eczema Council set out to create a set of consensus-based definitions of remission, LDA, and vLDA in atopic dermatitis.

Atopic Dermatitis

Atopic Dermatitis condition center page, audiences can find a variety of coverage mediums for medical news and updates, including articles, video interviews, podcasts, and breaking news on dermatitis research, treatment, and drug development.

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International Eczema Council Releases Definitions of Remission, Low Disease Activity

Linda Stein Gold, MD, is a dermatologist at Henry Ford Health. 

Eingun James Song, MD, is the director of clinical research for Frontier Dermatology. 

IL-17 Inhibition and Long-Term Outcomes in Psoriasis

In this episode, ‘IL-17 Inhibition and Long-Term Outcomes in Psoriasis,’ the panelists provide a deeper exploration of IL-17–targeted therapies in psoriasis, focusing on the biological rationale behind different mechanisms of action and how these translate into clinical outcomes. The faculty explored the distinction between selective IL-17A inhibition and dual inhibition of IL-17A and IL-17F, highlighting the evolving understanding of the IL-17 cytokine family and its role in driving inflammation. While IL-17A has historically been considered the primary therapeutic target, emerging insights suggest that IL-17F may also play a significant role due to its higher abundance in psoriatic lesions, raising the possibility that broader pathway inhibition may offer additional clinical benefit.

The faculty examined the complexities of interpreting long-term efficacy data across therapies. While individual clinical trials demonstrate sustained responses over multiple years, they emphasized that differences in study design, patient populations, and statistical methodologies make cross-trial comparisons challenging. Factors such as responder enrichment, rescue criteria, and analytic approaches can significantly influence reported outcomes, underscoring the need for careful interpretation of long-term extension data.

Additionally, the panelists explore the role of real-world evidence as a complementary perspective to clinical trial findings. Although real-world data may introduce variability, it can provide valuable insights into treatment durability and performance in broader patient populations. They also highlight both the benefits and limitations of evaluating therapies aimed at achieving sustained remission in psoriasis.

The next episode in this series, ‘Rapid Response in Psoriasis Treatment,’ the panelists examine the role of rapid treatment response in psoriasis and how speed of efficacy influences treatment decisions and patient satisfaction. It highlights differences within IL-17 inhibitors and the ability to achieve both rapid and sustained disease control without compromising outcomes.

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Expert panel weighs IL‑17 vs IL‑23 biologics for psoriasis, highlighting fast onset, durability, and why switching within class may work.

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Professor of Medicine and Renal Division Chief at the University of Pennsylvania Perelman School of Medicine

April 28th, 2026, was the American Kidney Fund’s third annual APOL1-Mediated Kidney Disease (AMKD) Awareness Day, which urges clinicians to identify high-risk patients of African ancestry with unexplained kidney failure.

More than a decade after the discovery of APOL1 risk variants, translation into clinical care has been slower than many anticipated, with the field reaching an important milestone with the first proof-of-concept data for APOL1-targeted therapies.

As these treatments advance and longstanding questions around risk prediction, screening, and access remain unresolved, the focus is shifting toward how to translate this progress into equitable, real-world care.

In this Q&A, Kirk Campbell, MD, a nephrologist at Penn Medicine, discusses the evolving clinical landscape of APOL1-mediated kidney disease, the challenges that have slowed progress, and what must change to ensure emerging advances reach the patients most at risk.

HCPLive: We’ve known about APOL1’s role in kidney disease for over a decade. Why has translation into clinical practice been so slow and what has that delay meant for patients?

Campbell: It is a long time, but the fact that it took 13 years from the discovery of APOL1 kidney disease genetic association to the first proof-of-concept APOL1 inhibitor efficacy report should be celebrated. At the same time, the many uncertainties around disease pathogenesis have slowed translation in several ways. There are still no approved APOL1-specific therapies, no consensus on population screening, limited ability to predict who among carriers will progress and unresolved questions about “second hits,”

For patients carrying APOL1 high-risk variants, what does “risk” translate to in terms of real-world monitoring and follow-up today?

Approximately 14% of African Americans have the APOl1 high risk genotype. These two APOL1 risk variants confer roughly a 15%–20% lifetime chance of kidney disease, while also emphasizing that about 80% of people with two risk variants do not develop kidney disease

: With AMPLITUDE now in Phase 3 and Maze Therapeutics advancing a Phase 2 program, if one of these therapies succeeds, what needs to happen to ensure equitable access, particularly for patients with the highest genetic risk?

Campbell: Equitable access would require more than drug approval. It would require payer coverage for APOL1 testing, genetic counseling, urine albumin testing, nephrology referral, and the medication itself. It would also require that eligibility be based on genotype and clinical phenotype, not crude racial categories. Otherwise, we risk repeating the same inequities: patients with better insurance and academic-center access get tested and treated, while safety-net, rural, and historically underserved remain underdiagnosed. The highest-burden regions cannot be an afterthought. KDIGO notes that APOL1 kidney disease disproportionately affects communities with limited health-care and research infrastructure, and the report calls for community engagement, education, and clinical-trial participation strategies involving trusted community partners

: There’s ongoing debate about how to frame APOL1 risk, as a biological story, a population genetics story, or one rooted in structural inequities. Where do you land on that, and has your thinking evolved?

I would not choose only one frame. APOL1 is a biological mechanism, a population-genetics story, and a health-equity story at the same time. The biology matters because APOL1 variants can injure kidney cells and are now targetable. The population-genetics story matters because G1 and G2 variants are enriched in people with West and Central African ancestry and likely rose in frequency because of protection against certain trypanosomal infections. But the structural inequity story is just as important. Genetics may help explain susceptibility; it does not explain who gets screened, who has a primary care relationship, who sees a nephrologist early, who gets a transplant evaluation, who is offered genetic counseling, or who can afford a precision medicine.

: The KDIGO conference on APOL1 was held in Accra, Ghana. What does it mean for the field to be having these conversations on the African continent, and does that reflect a meaningful shift toward meeting patients where they are?

Campbell: It matters a lot. West Africa is central to our understanding of APOL1 kidney disease. KDIGO reports very high frequencies of APOL1 high-risk genotypes in West African populations, including up to 37% in Central Ghana and 50% in Southeastern Nigeria, and estimates that more than 100 million people in Sub-Saharan Africa may have two APOL1 high-risk alleles.

Holding the conference in Accra signals that the field is beginning to locate the conversation closer to the populations most affected, rather than treating African populations only as a source of retrospective genetic insight.

: If you had to leave clinicians with one practical implication about APOL1 today, what should it be?

Campbell: APOL1 testing is worth considering when the result can change follow-up, trial eligibility, transplant donor counseling, or future targeted-treatment decisions. But the test should come with counseling, and it should never replace a full kidney-disease workup. KDIGO explicitly says APOL1 testing can guide risk stratification and follow-up, but should not preclude diagnostic evaluation, including biopsy when clinically indicated.

APOL1-Mediated Kidney Disease (AMKD) awareness efforts underscore the lag between discovery of APOL1 risk variants and meaningful clinical translation, despite emerging proof-of-concept inhibitor data and late-stage trials. About 14% of African Americans carry a high-risk genotype, translating to an estimated 15%–20% lifetime kidney-disease risk, while most carriers never progress, highlighting persistent gaps in prediction and “second hit” biology. Equitable implementation will require coverage for testing, counseling, monitoring, referrals, and therapy, plus genotype-driven—not race-based—eligibility and stronger community-engaged infrastructure.

Campbell answers questions about the current research and clinical landscape of APOL1-mediated kidney disease. 

Nephrology

The HCPLive nephrology page is a resource for medical news and expert insights on kidney disease. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments in nephrology, and more.

APOL1 Reaches Turning Point While Clinical, Equity Challenges Persist, With Kirk Campbell, MD

Comparing Biologic Classes and Durability in Psoriasis

This episode, titled ‘Comparing Biologic Classes and Durability in Psoriasis,’ features panelists discussing how different biologic classes compare in achieving and sustaining remission in psoriasis, with a focus on both speed and durability of response. The faculty discussed how treatment paradigms have evolved as head-to-head clinical trial data have emerged, allowing for more direct comparisons between classes such as IL-17 and IL-23 inhibitors. Historically, IL-17 inhibitors have been associated with rapid onset of action, while IL-23 inhibitors have demonstrated durable long-term responses.

The expert faculty highlight that not all agents within a biological class perform identically. Differences in efficacy and durability within the same class have become more apparent through direct comparisons, prompting clinicians to reconsider traditional approaches to treatment sequencing. Rather than automatically switching to a different class when a patient has an inadequate response, there may be value in selecting another agent within the same class.

They emphasize the growing importance of nuanced, evidence-based decision-making in psoriasis care. With an expanding array of therapeutic options, clinicians must consider not only class-level characteristics but also individual drug performance. Ultimately, the discussion reinforces that both achieving and maintaining disease control along with personalized treatment strategies are essential for optimizing long-term outcomes.

In the next episode, ‘IL-17 Inhibition and Long-Term Outcomes in Psoriasis,’ the panelists explore the mechanistic differences within IL-17 inhibition and their implications for treatment outcomes in psoriasis. It also highlights the challenges of interpreting long-term clinical trial and real-world data when evaluating sustained disease control.

Christopher G. Bunick, MD, PhD, is an associate professor of dermatology at Yale University School of Medicine.

In a recent review on emerging therapies for 

, Christopher G. Bunick, MD, PhD, and colleagues highlighted a notable limitation in the treatment landscape: many of those treated with existing monospecific biologics do not achieve optimal or sustained disease control.

, Bunick emphasized that although currently available medications targeting individual pathways have led to improved outcomes, they often fail to fully impact the breadth of inflammation and symptom burden.

 In response, Bunick and colleagues outlined a rapidly expanding pipeline of bispecific and trispecific antibodies designed to simultaneously target multiple inflammatory and neuroimmune pathways.

In this new Q&A segment of his interview with 

, he touched on these emerging therapies being developed to address both immune-driven inflammation and itch signaling concurrently, noting several key points about his team’s findings and their significance:

Based on the early clinical data your team reviewed, what signals would you say are most encouraging in terms of efficacy, itch control, and durability of response?

For me, last year at EADV, we saw our first glimpse of what the multi-targeted biologics could achieve. What I refer to there is an early phase 1 study from galvokimig. Now this is a molecule that's targeting IL-13 with a tralokinumab-like epitope, but also has the ability to target like by bimekizumab, IL-17 A and F. And what this answered for us was a couple of things. Number one, it asked the question, ‘Can tackling some of the cytokines historically associated with psoriasis improve atopic dermatitis?’

We know from a number of molecular studies that there is overlap between psoriasis and atopic dermatitis in terms of some of the molecular drivers; some of the transcriptomic analyses show the overlap between these diseases. Therefore, it actually makes a lot of sense that inhibiting some of the cytokines that go both ways and that can be involved in psoriasis and can be involved in atopic dermatitis, hitting the breadth of those cytokines, it sort of makes sense.

We really didn't have that masterful proof, in my opinion, until we saw galvokimig, the ability of a biologic to achieve that. We saw in this phase 1 study…this was IV galvokimig, not the final product that's ultimately going to end up in atopic dermatitis patients, but this phase 1 study was IV galvokimig. What it did show was that at Week 12, about 47% of patients achieved EASI 90, which is an incredibly high and fast response for that level of response. That really signaled to me that there's now a connection between the underlying scientific data saying that the atopic dermatitis and psoriasis patients can overlap in some of their molecular drivers.

We know this also from the fact that there are a number of atopic dermatitis patients who kind of have this immune phenotype, switching between atopic dermatitis and psoriasis. We know this happens, and certainly, there are also other examples, such as the flare of the head and neck atopic dermatitis, which may be largely IL-22 driven. We see these things in the clinic every day: the psoriasiform type shift in our atopic dermatitis patients, the head and neck atopic dermatitis. The reality is that galvokimig showed that this can, in fact, really push the levels of what a biologic can achieve.

In addition to galvokimig, we also have tilrekimig. This is a tri-specific antibody that targets the cytokines IL-4, IL-13, and TSLP. Some data was just released around the AAD 2026, which showed that this drug, in its phase 2 studies, actually met its endpoint in achieving EASI 75 response. It is now moving onto phase 3. One of the drugs where we saw an effect that we didn't want to see was one of the tri-specifics being developed by Johnson & Johnson, which showed that it didn't hit the efficacy bar that they were looking for in order to advance the program. One of the tri-specific agents in development has already been discontinued. This was targeting IL-4 receptor alpha and IL-31.

While we've had a couple of very positive responses from galvokimig and tilrekimig in some of the early phase 1 and phase 2 data, galvokimig and tilrekimig represent two really good phase 1 and phase 2 responses that give us clues that this multi-target approach is going to work from a biologic perspective and for atopic dermatitis. We also have another bi-specific antibody developed by J&J targeting the IL-4 receptor alpha and IL-31 cytokines that did not hit the efficacy bar that the company was looking for, and they have discontinued further development of that program.

This goes to show that in developing the bi- and tri-specific antibodies for atopic dermatitis, it is not as simple as just mixing and matching. There's a lot of science that goes into trying to develop a bi- or tri-specific that is much more complicated than developing a mono-targeted biologic. Then again, how you target these agents, the sizes of the molecules, the tissue penetration of these molecules, all matter, and they can all differ. I do think that these complexities in both pharmacodynamics and pharmacokinetics of these drugs are very important to pay attention to, and it's not a given just because we see a good itch response from nemolizumab versus dupilumab or any of the other biologics. The reality is, just mixing and matching isn't necessarily guaranteed to work.

We've seen some successes. We've already seen a failure, and it's going to be really interesting to see over the coming months to years, how this entire landscape plays out. I do believe very strongly, regardless of whether a drug succeeds to the very end and gets clinical approval, or whether that drug ultimately doesn't meet that new efficacy threshold and doesn't make it into FDA approval and into the patients and into the clinics. The reality is that we are going to learn a lot about the disease itself. We're going to learn so much about the pathophysiology of atopic dermatitis, how to manipulate different cytokine and receptor pathways underlying atopic dermatitis, as well as other th two driven diseases. I think that that is also one of the major benefits of the program that we're seeing in the multi-targeted biologics, [which is] how we're going to learn about other diseases. This is because the reality is, these multi-targeted biologics aren't going to stay combined to atopic dermatitis. They're going to be expanded into other diseases, particularly they're already being explored in hidradenitis suppurativa.

Looking ahead, how do you envision these multi-specific biologics fitting into the current treatment landscape, especially compared with Janus-kinase (JAK) inhibitors and existing biologic options?

Well, right now, when we think about the drugs for atopic dermatitis that have the best chance of hitting an optimal target or a minimal disease activity state for our patients, the reality is the JAK inhibitors, upadacitinib and abrocitinib, and all the network meta-analyses and head-to-head clinical trials that have occurred, that the JAK inhibitors have set the response bar in terms of EASI 90 and EASI 100 in terms of composite EASI 90, and Itch 01. In reality, the JAK inhibitors have raised that ceiling because of their ability to target multiple cytokines driving the atopic dermatitis. That is what they do. They can hit IL-4, IL-13, and IL-31. They can also hit IL-22, TSLP, and interferon gamma. All of that is what underlies the success that we've seen with JAK inhibitors in not only raising how well they treat the skin disease of atopic dermatitis, but how they reduce very quickly the itch burden that our patients feel. That is really what the multi-targeted biologics are trying to accomplish.

They're trying to match or exceed what the JAK inhibitors have been able to do, and that is having greater skin control, greater itch relief, and all the patient-reported outcomes. Can we ultimately improve these patients to the point where the quality of life, from a biologic standpoint, really continues to improve and grow? That is why half-life extension is so important. Because part of that narrative in terms of patient convenience and patient comfort, comes from the fact that if you're going to have to take an injection, it is difficult]. A lot of patients, when they have to take an injection, the injection fatigue can be real. The reality is, if you're taking it every 3 months or every 6 months, it's a lot different than needing to take an injection every 2 weeks.

For any additional information, view Bunick’s interview segment posted above.

Bunick has reported receiving consultant fees or serving as an investigator for AbbVie, Incyte, LEO Pharma and Pfizer.

Amid-Toby G, Alani O, Bunick CG. Bispecific and trispecific antibodies in atopic dermatitis: a review of the emerging clinical pipeline. Front. Drug Discov. 6:1766021. 

Bunick C. Bispecific and Trispecific Antibodies in Atopic Dermatitis, With Christopher Bunick, MD, PhD. HCPLive. April 24, 2026. Accessed April 28, 2026. 

https://www.hcplive.com/view/bispecific-trispecific-antibodies-atopic-dermatitis-christopher-bunick-md-phd

Multi-specific antibodies are being advanced to overcome suboptimal depth and durability seen with many monospecific biologics in atopic dermatitis, aiming to co-modulate inflammatory and pruritic circuitry. Early clinical signals suggest that broadened cytokine coverage can drive rapid, high-level responses, while setbacks underscore that target pairing and molecular engineering are nontrivial. JAK inhibitors currently define the efficacy ceiling through pleiotropic pathway inhibition and rapid itch reduction, setting a benchmark these biologics must meet or exceed. Longer half-lives and less frequent dosing may improve adherence and patient experience.

This Q&A interview highlights emerging therapies for atopic dermatitis, featuring Christopher G. Bunick, MD, PhD of Yale Medicine.

Positive Signals for Bispecific and Trispecific Antibodies in Atopic Dermatitis, With Christopher Bunick, MD, PhD

Tatyana Kushner, MD, is an associate professor of medicine in the division of gastroenterology and hepatology at Weill Cornell Medicine.

Brelovitug met the primary endpoint for virologic response and ALT normalization in the phase 2b portion of the AZURE-1 trial.

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New Phase 2b AZURE-1 Data Signal Progress in Chronic Hepatitis D Treatment, With Tatyana Kushner, MD

Martina J. Porter, MD, is a dermatologist at Beth Israel Deaconess Medical Center.

54-week STOP-HS safety data for the JAK1-selective inhibitor povorcitinib showed no dose-dependent safety signal and few laboratory abnormalities.

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Contextualizing JAK Safety With Povorcitinib in HS, With Martina Porter, MD

Endocrinology experts compare pediatric and adult growth hormone deficiency—causes, testing, MRI use, and transition care tips to improve outcomes.

Recognizing Growth Hormone Deficiency — Symptoms, Presentation, and Quality of Life

Experts compare pediatric vs adult growth hormone deficiency—causes, testing, MRI use, and why retesting matters during transition to adult care.

Unraveling Growth Hormone Deficiency — Etiology and Prevalence

Baba Inusa, MBBS, is a Consultant Paediatrician in the School of Life Course & Population Sciences at King's College London.

Study investigator Inusa explains the gap in sickle cell disease findings from SWAP, a multinational survey. 

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Increased Sickle Cell Pain Burden in Sub-Saharan Africa Despite Younger Patients

Diana Isaacs, PharmD, is an endocrine clinical pharmacist, director of Education and Training in Diabetes Technology, and codirector of Endocrine Disorders in Pregnancy at the Cleveland Clinic.

Isaacs covers the range of AID devices currently available and approved for T2D, providing suggestions for implementation and continuous glycated hemoglobin monitoring.

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Andrea Cipriani, MD, PhD, from the University of Oxford.

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Victoria Johnson joined MJH Life Sciences in 2020 and has written for NeurologyLive, CGTLive, and is now an assistant managing editor for HCPLive and RheumatologyLive. She doesn’t have enough time for her numerous hobbies. You can reach her at vjohnson@mjhlifesciences.com.

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International Eczema Council Releases Definitions of Remission, Low Disease Activity

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APOL1 Reaches Turning Point While Clinical, Equity Challenges Persist, With Kirk Campbell, MD

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