Video
Pediatric Atopic Dermatitis: Pathophysiology, Prevalence, and Symptomology
Raj Chovatiya, MD, PhD; Brittany G. Craiglow, MD; and Peter A. Lio, MD, provide insight into pediatric atopic dermatitis, focusing their discussion on the pathophysiology, prevalence, and disease symptomology.
Raj Chovatiya, MD, PhD: Hello, and welcome to this HCPLive® Peer Exchange titled “Expert Perspectives in the Management of Pediatric Atopic Dermatitis.” I’m Dr Raj Chovatiya, and I’m an assistant professor of dermatology and the director for the Center of Eczema and Itch at the Northwestern University Feinberg School of Medicine in Chicago, Illinois. Joining me in this session are my esteemed colleagues. We have Dr Britt Craiglow, who practices at the Dermatology Physicians of Connecticut. She’s an adjunct associate professor at the Yale School Medicine in New Haven, Connecticut. And we have Dr Peter Lio, who practices at the Medical Dermatology Associates of Chicago. He is also a clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine in Chicago, Illinois. Welcome everybody and let’s jump on into it.
Today we’re talking about all things pediatric AD [atopic dermatitis]. We couldn’t have a better panel to talk about some of the aspects facing us in terms of pathophysiology, burden, and some of the exciting new evolutions in treatment. To start, I want to get a bit of an overview about the disease itself, how we diagnose this in our kids, and how this might be different compared with adults as well. The first question I’ll toss over to Dr Lio. Tell me a little bit about your feelings about pathophysiology of atopic dermatitis and how all this has evolved over time when we think about the disease. When I talk to my patients, I think about the barrier and the immune system. Maybe you can tell us more about how all that works together.
Peter A. Lio, MD: Thank you. It’s been such an interesting journey learning more about this disease, especially looking at ancient conceptions of atopic dermatitis and how this relatively modern disease still does have some roots that go far back, maybe as far back the Ebers Papyrus in ancient Egypt. A lot of interesting stories over the years. We’ve refined our understanding to encompass what I think of as the 5 pillars. What’s interesting about these 5 pillars is that they’re really part of a vicious cycle that can develop. You already mentioned 2 that are fundamental. The skin barrier, we know that it’s leaky, as I like to tell my patients. That impaired barrier that allows water to come out also allows allergens, irritants, and pathogens to get in. Then we have the inflammation aspect as well. That can be a primary cause. Some people just seem to be hypersensitive—the immune system going crazy—but it also can be secondary. When those allergens and irritants get in, the immune system very appropriately reacts to that.
There are a couple of other pillars worth pointing out. One is the microbiome. We’re learning more that the microbiome is not just a bystander. It’s not just a colonizer hanging around. It can be a primary driver, particularly Staphylococcus aureus bacteria. It can produce a bunch of toxins that can drive barrier damage and inflammation, which is pretty amazing. Then we have the nerve endings themselves. This is an exciting area, thinking about itch and not only the morphology of the nerve endings—that they can get more dendrites—but also the physiology of the nerve endings. Their threshold for itch drops down over time. We can see this sensitization or potentiation of these pathways in the entire nervous system through the DRG [dorsal root ganglion] and into the brain. Finally we have the neurobehavioral aspect. That’s the mind-body aspect of this disease. We know behavioral things like the itch-scratch cycle, anxiety, poor sleep, and all these can feed back in. Those 5 give us a good sense of all the aspects of this disease, at least from 1 take.
Raj Chovatiya, MD, PhD: I couldn’t have put it better. When you think about the disease, historically there was this concept that this is a childhood disease and it doesn’t happen much after. A lot of this has been turned on its head. Dr Craiglow, you can tell us a little about the typical age of onset? Why was this the predominant theory, and how has it changed? What are some of the presentations you’re looking for in terms of the disease in a pediatric population?
Brittany G. Craiglow, MD: In pediatric dermatology, atopic dermatitis is our bread and butter. Most patients with AD are going to have an onset in childhood, usually pretty early. The majority has onset before age 6 or so. That’s an important point. If you have someone coming in with what you think is onset atopic dermatitis, you want to make sure it’s AD and that you’re not missing a contact allergen, CTCL [cutaneous T-cell lymphoma], some other diagnoses that may be a mimicker.
But for AD in kids—it doesn’t look the same in everybody—it’s a pretty straightforward diagnosis. We think about the morphology and distribution evolving over time, where oftentimes infants come in and have those bright-red stoplight cheeks, and they have involvement primarily of extensor surfaces. That can change a little as they get older to more flexural involvement. We learn that AD is red, dry, oozy, and itchy, and it’s oftentimes, but it’s important to note that it can be clinically very heterogeneous. Especially in darker skin types, it may not have that classic appearance. We see sometimes this monomorphic follicle-based papules which are clinically not as dramatic but can be very itchy and uncomfortable.
Sometimes it’s more of a prurigo nodularis type of picture. If a patient is itchy and has skin lesions, you have to be thinking about AD. Especially in younger kids, oftentimes there’s a family history. They may also have food allergy, or they’re going to have that whole atopic picture, so it makes a diagnosis fairly straightforward. It’s not a 1-size-fits-all thing. It’s important to keep that in mind as we see patients, especially if they’re presenting with more of the less classic presentations.
Transcript Edited for Clarity
