Observing BSA Changes and Inflammation Resolution

EP: 1.Exploring Long-Term Data and Combination Therapies

EP: 2.Rethinking Itch Severity in Atopic Dermatitis

EP: 3.Understanding Long-Term Safety, Efficacy, and Demographic Variances in Ruxolitinib Trials

EP: 4.Measuring Sleep Impact

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EP: 5.Observing BSA Changes and Inflammation Resolution

EP: 6.Assessing Quality of Life and AAD Research Considerations

EP: 7.Comparing the Landscape of Topicals

EP: 8.Utilizing Multidisciplinary Solutions for Itch

EP: 9.Pediatric Potency: Ruxolitinib vs Triamcinolone

EP: 10.Remaining Research Gaps and Bright Future in AD

EP: 11.Revealing Ruxolitinib’s Potential in Pediatric AD Treatment

This news content has been independently developed and is not endorsed by the American Academy of Dermatology.

In this Dermatology Times Expert Perspectives series, 5 experts delve into the multifaceted aspects of pediatric atopic dermatitis care including demographic variances to long-term safety and efficacy, comparative analyses, key takeaways from recent research, personalized approaches, and future research directions. Discover clinical insights into the role of ruxolitinib (Opzelura) in addressing critical challenges and enhancing patient outcomes.

In this episode, Alan Irvine, MD, DSc, dermatologist at Trinity College Dublin in Dublin, Ireland, offers an understanding of BSA changes and anti-inflammatory effects of ruxolitinib in the latest research presented.

Dermatology Times Interview With Alan Irvine, MD, DSc

Dermatology Times: How does ruxolitinib impact the change in body surface area affected by atopic dermatitis over time? Are there notable trends or patterns in terms of rapid improvement, stabilization, or potential fluctuations in response to treatment?

Irvine: I have a big practice and research interest in AD. What we saw with topical ruxolitinib in the age group between 2 and 11 years or 2 to under 12 years, is that we saw within the first 2 weeks there was a mean average body surface area (BSA) dropped from about 60% at study entry to down into the low teens, 10% to 11%, after 2 weeks of treatment. Then on continuous treatment, up to 4 weeks and then intermittent treatment after 4 weeks, it pretty much remained at 10% or less with the with the ruxolitinib used initially in a continuous way, and then on an as needed basis in the next 4 weeks. And then in long-term extension, it was used on an as needed basis and again, maintain those responses in BSA.

Dermatology Times: Considering the inflammatory nature of atopic dermatitis, can you elaborate on how ruxolitinib addresses skin inflammation in pediatric patients? Are there specific markers or indicators of inflammation that significantly improve with treatment, and how does this contribute to the overall management of the condition?

Irvine: So ruxolitinib is a JAK inhibitor and many of the key inflammatory pathways signal through JAK stat pathways. So, a small molecule that penetrates the skin well and works very quickly. It's switching off that signaling, but also switches off comes off again quite quickly too. So it's a very short half life molecule and it does look like you do need intermittent treatment with it. So it's a treatment that works very rapidly, very rapid itch relief within the same day or even within hours. In some studies, it kicks that inflammation very rapidly as well, as we've seen with BSA within 2 weeks, a very dramatic increase in it. So topical JAK inhibitors, they're super fast on drugs, they switch off things really quickly. And then they need a little bit of maintenance to continue to maintain just the nature of the drug. That's the way it'll work.

In clinical practice in the office, nobody will be talking about markers because it's just about the clinical responses in a child, in this case we're talking 2 to 11 year olds. Are they getting better? Are they less itchy? Is their quality of life improving? Are they sleeping well? Are they sleeping thoroughly through the night? So in the office, we talk about those as measures of success or not. When you look at biomarker studies, the biomarkers that are associated with type 2 inflammation do respond. Skin Barrier markers, which are associated with underlying inflammation, damaging the skin barrier, they also respond in a in a positive way. So we see markers that change in the direction that we want that show that the disease has been modified in the time under treatment. So it's very positive, but in average office conversation, it probably doesn't arise too much. It's just good to know the mechanism of why things work.

Transcript edited for clarity