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At EADV 2025, dermatologist Peter Lio, MD, a clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine and founding director of the Chicago Integrative Eczema Center, delivered a forward-looking perspective on managing atopic dermatitis, emphasizing the patient journey from daily moisturization to advanced therapies. In this exclusive Q&A, he unpacks practical strategies for pediatric care, the role of patient and caregiver preferences, and how new biologics, JAK inhibitors, and non-steroidal topicals are reshaping treatment. Lio also addresses gaps that remain, from rapid itch relief to access and affordability, while underscoring why foundational skin care still matters in an era of expanding systemic options.

Q&A

Optimizing patient journey: from daily moisturization to hydrotherapy

DT: How do you prioritize different hydration strategies—daily moisturizers, emollients, and bath practices—in pediatric AD care?

Lio: Daily moisturization is the foundation for almost everyone. It is a safe, low-cost, and very effective way to strengthen and protect the skin barrier. I like folks to apply moisturizer liberally at least once on dry skin and after bathing (‘soak-and-seal’). Wet-wrap therapy is really important for tougher flares. As for bathing, I like daily bathing for most and I really do prefer a gentle, oil-based cleanser.

DT: How do you integrate patient or caregiver preferences into a daily skin care routine without compromising efficacy?

Lio: I feel strongly that we need to work together to find the products and a routine they can actually do: cosmetically elegant is very subjective, so they have to like it and want to use it. I am a huge fan of eczema action plans because I find that when families help design the regimen, adherence and outcomes improve.

Navigating remaining gaps and new goals in AD management

DT: What are the most significant unmet needs in current pediatric AD management?

Lio: We have a lot! Rapid itch relief for sleep, long-term remittive control with fewer flares, options that don’t sting on sensitive areas, safe data down to the youngest ages, and—crucially—access and affordability are all key issues. With all of the great systemics, there can be this unfortunate (and incorrect) conclusion that we don’t need topical agents any more, but nothing could be further from the truth.

DT: How do you incorporate new therapies, like JAK inhibitors or biologics, into the treatment paradigm?

Lio: I’m an early adopter, in part because I have so many patients with unmet needs. I try to base care on severity and impact. For mild to moderate disease not controlled with moisturizers and low- to mid-potency steroids/TCIs, I lean on non-steroidal topicals like JAK or PDE-4 inhibitors for flare control and maintenance. For moderate to severe or quality-of-life-limiting disease, I escalate to targeted biologics (e.g., IL-13 or IL-31 pathway agents) while keeping a strong skin care routine at the core. I also am open to integrative approaches and try to incorporate them when patients and families are amenable.

Food allergies, nutrition, and atopic dermatitis

DT: When do you recommend formal allergy testing for children with AD?

Lio: This is always very tough, and many of my patients–most of them even–have already had testing. But, personally, I try to only test when the history suggests an immediate-type reaction (hives/vomiting within minutes to hours) or when severe, persistent AD isn’t improving despite optimal skin care and there’s a clear dietary link. Broad screening panels tend to have a lot of false positives and can cause all sorts of confusion and unnecessary food avoidance.

DT: Are there patient subgroups who may benefit most from dietary interventions, and how do you identify them?

Lio: Those with proven IgE-mediated food allergy need allergist-guided plans. That part is clear. Otherwise, elimination diets offer at best modest benefit and potential nutritional risk as well as the more recent understanding that avoiding some foods can actually make food allergy happen. Dr. Ruchi Gupta puts it beautifully: “Through the skin allergies begin, through the diet they stay quiet.” In the meantime, I try to focus on general healthy patterns, vitamin D supplement, and probiotics.

DT: With so many recent approvals spanning a variety of MoAs, to what degree are additional new therapeutics options needed in the AD landscape?

Lio: Even with IL-13 and IL-31 pathway biologics and new non-steroidal topicals, there’s room for therapies that act more quickly, are better tolerated, and deliver durable remission with fewer visits and lower out-of-pocket costs. Choice matters in a heterogeneous disease like AD and I’d say we still have a long way to go to meet the needs of all my patients.

DT: In June we saw a focused update on AD guidelines in JAAD, how important is this proactivity in terms of encouraging uptake of emerging therapies?

Lio: I think this is actually important. Clear, frequently updated guidance accelerates appropriate adoption and gives clinicians confidence to individualize care. This is all the more important because of the rapid rate of change right now in AD.

DT: What newer therapies would you say have the most potential but are currently being underutilized?

Lio: I think that while the systemic agents get lots of attention (and reasonably so), I want to call out the newer non-steroidal topicals for maintenance on sensitive areas and for steroid-sparing strategies. I honestly think that well formulated topicals have the potential to touch–literally and figuratively–far more patients than the biologics and systemic agents in general, so they warrant more attention than they are currently receiving.

A new clinical trial has revealed encouraging results for a muscle-targeting therapy aimed at improving motor function in children and adolescents with spinal muscular atrophy, according to a study published in The Lancet Neurology. 

Spinal muscular atrophy (SMA) is a rare genetic disorder that affects motor neurons – nerve cells in the spinal cord responsible for controlling voluntary muscle movement. Caused by mutations in the SMN1 gene, SMA leads to progressive muscle wasting and weakness, and can severely impact mobility, breathing and swallowing. 

SMA is one of the most common genetic conditions affecting children, with an estimated 1 in every 6,000 to 10,000 babies born worldwide with the condition. 

While current treatments help slow disease progression and improve motor milestones, they do not fully restore muscle strength or function. Even mild improvements in motor function, however, can significantly improve a child’s quality of life, said co-author Nancy Kuntz, MD, Medical Director, Mazza Foundation Neuromuscular Program at Ann & Robert H. Lurie Children’s Hospital of Chicago and Professor of Pediatrics at Northwestern University Feinberg School of Medicine.

Gene replacement therapy has been very effective for SMA. But this and other motor neuron targeted therapies are not cures. There’s been a real flurry of activity trying to figure out ways of getting the treatment started earlier so that there are fewer motor neurons lost. Inclusion of SMA in the Newborn Screening in the US has been a great improvement. However, SMA patients, particularly those beginning treatment when symptomatic, have weakness as compared to peers and over time can experience some loss of function.” 

Nancy Kuntz, MD, Medical Director, Mazza Foundation Neuromuscular Program, Ann & Robert H. Lurie Children’s Hospital of Chicago

The current trial, conducted across 48 hospitals in Europe and the U.S., evaluated the safety and efficacy of the new drug in 188 patients aged 2 to 21 years with non-ambulatory type 2 or type 3 SMA. All participants were already receiving standard-of-care treatments prior to the trial. 

The drug, apitegromab, is designed to inhibit myostatin activation, a biological process that limits muscle growth. By targeting this pathway, investigators hoped to enhance muscle strength and function in SMA patients, who typically experience progressive muscle weakness. 

Among children aged 2 to 12, those treated with the drug showed a statistically significant improvement in motor scores, compared to those receiving a placebo. 

“All of these individuals could sit or walk, but they did not have normal mobility,” Kuntz said. “While improvements seen on the drug were not something that would be the difference between being bedridden and walking, the changes led to functional independence. Being able to facilitate some kind of movement so patients can interact with their environment is incredibly meaningful and allows them to be a little bit more independent, have more dignity and improve their quality of life.” 

Although the results were encouraging, more work is needed to ensure patients have access to therapies that delay progression of the disease, Kuntz said. 

“The therapy is a bit of a challenge for individuals to undergo long-term because it requires intravenous administration once every month,” Kuntz said. “There are other types of myostatin inhibition that have been developed with subcutaneous injection, which is under the control of the individual themselves at home. Apitegromab is being developed for subcutaneous administration, but it will take several years to get that to be commercially available.” 

Moving forward, Kuntz and her collaborators will continue to study new treatments for SMA, with the goal of halting motor function loss in children, she said. 

The study was funded by Scholar Rock, the biotechnology company developing apitegromab. 

A new research paper was published in Volume 17, Issue 8 of Aging-US on August 9, 2025, titled “The myokine FGF21 associates with enhanced survival in ALS and mitigates stress-induced cytotoxicity.”

In this study, led by first author Abhishek Guha and corresponding author Peter H. King from the University of Alabama at Birmingham and the Birmingham Veterans Affairs Medical Center, researchers discovered that a hormone called FGF21, which is released by muscles, is elevated in people with amyotrophic lateral sclerosis (ALS) and may play a protective role. These findings are especially relevant because ALS is a fatal and currently incurable neurodegenerative disease.

Amyotrophic lateral sclerosis is an age-related and progressive condition that affects the nerve cells responsible for muscle control. While some treatments can slow the disease, there is still a need to understand why ALS progresses at different rates in different individuals.

“In a prior muscle miRNA sequencing investigation, we identified altered FGF pathways in ALS muscle, leading us to investigate FGF21.”

The research team analyzed muscle biopsies, spinal cord tissue, and blood samples from ALS patients and found that FGF21 levels were significantly elevated. This increase was particularly evident in atrophied muscle fibers-those that had shrunk due to nerve loss-and in the surrounding tissue. Importantly, patients with higher plasma levels of FGF21 showed slower loss of function and longer survival, with some living more than six years after diagnosis.

Using animal models and cultured cells, the researchers demonstrated that FGF21 levels rise even in the early, symptom-free stages of ALS. The hormone appeared to protect both muscle and motor neurons from stress-related damage. When added to stressed cells, FGF21 improved cell survival and reduced markers of cell death. In human muscle cells, FGF21 also supported the formation of new muscle fibers, a process known as myogenesis.

Blood tests revealed that patients with higher levels of FGF21 not only experienced slower disease progression but also tended to have a higher body mass index (BMI), a factor previously associated with longer survival in ALS. This suggests that FGF21 may reflect a patient’s ability to counteract ALS through natural protective mechanisms. It could also serve as a biomarker to monitor disease severity and potentially guide treatment decisions.

The study also investigated how FGF21 communicates with cells. It found that the hormone’s activity depends on a protein called β-Klotho, which was also altered in ALS-affected tissues. These changes were especially noticeable in motor neurons and muscle cells under stress, further highlighting FGF21’s role in the body’s response to damage.

While the study does not show that FGF21 can be used as a treatment, it highlights the hormone as a promising target for future research, clinical trials, and strategies to slow ALS progression by leveraging the body’s natural protective systems.