New Therapies, Immunologic Insights in Atopic Dermatitis: Lawrence Eichenfield, MD

How are dermatologists redefining atopic dermatitis care amid a wave of novel therapies and lingering immunologic mysteries? Lawrence Eichenfield, MD, professor of dermatology and pediatrics at the University of California San Diego and chief of pediatric dermatology at Rady Children's Hospital San Diego, breaks down strategies on monoclonal antibodies, Janus kinase (JAK) inhibitors, and topical nonsteroidal therapies.

This transcript was lightly edited; captions were auto-generated.

Transcript

With the rapid expansion of monoclonal antibodies, oral JAK inhibitors, and topical nonsteroidal therapies, how do you approach treatment selection in clinical practice?

In real life, I'm trying to assess the patient and family, if it's a kid, or even adults, and sort of what's been the historical journey, what's the life impact of the disease, and then what's been the experience with topicals? We have new nonsteroidal topicals. And for patients who aren't coming in with incredibly high body surface areas, [you can] just tell this is a systemic candidate, it's still highly appropriate. There are going to be patients who don't need systemics because of our newer nonsteroids being put in residence at care.

Then we have now a panoply, so to speak, of systemic options, other than under [age] 12 for severe atopic dermatitis. I think moving to that quickly when families understand the risk-benefit and the relative safety of our products over 12, there's also a question of speed of response and the degree of response. And a lot of patients, were sort of patients who've been on systemics and come back, decide, “Are we in good enough shape that we want to stay, or [do] we want to try to change our systemic either to another biologic or to move to oral JAK?” Those are really active in space.

The punch line is long-term disease control. My spiel to my families is that I want minimal rash, minimal itch, [and] minimal sleep disturbance; they sort of get that. And then we figure out, is that topicals alone? Is that systemic alone? Is that systemic with topical tune-ups? All of those have active patients on regimens like that, but successfully.

As our understanding of the pathogenesis of atopic dermatitis and pruritus continues to evolve, which emerging mechanisms or pipeline therapies do you believe will most meaningfully change how we manage patients in the next few years?

I will say that it's really interesting with atopic dermatitis. We have our experience with our biologics, and then experience with our JAK inhibitors, and then newer biologics, and then the pipeline coming in. To me, I'm driven by what’s the core clinical response to patients, but it's really interesting to think about what’s happening immunologically. If I put a patient on dupilumab, for instance, for 3 years and take them off, and they end up having just 1% to 3% body surface area managed with a topical, there seems to have been some immunologic reboot. And is that going to be different with an IL-[interleukin] 4/13 as compared to an IL-13 blocker or an IL-31 blocker. It's too early, really, to see that

There's differences in IgE [immunoglobulin E] responses. If I look at EASI [Eczema Area and Severity Index] scores in a patient on a JAK, it could have some of the best EASI score changes. But the IgE doesn't go down with a JAK inhibitor; it goes down with dupilumab. Does that matter in the overall course of the disease over time? For OX40 and OX40 ligand, we consider a sort of upstream; it may sort of block more of T-cell expansion. Is that good or bad in different populations, including teens or kids as compared to adults? We don't know that. These [are] core immunologic questions, and while that's intriguing, the translation of how it may impact the life experience of eczema over time, with and without therapy, [and] how it impacts how long therapy will be, those are still totally open questions.