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Article

Peter Lio, MD: The Latest Perspectives on Pathophysiology and Treatment of Eczema

Key Takeaways

  • Eczema involves complex pathophysiology, including barrier dysfunction, inflammation, immune overactivity, and microbiome disruption, influenced by environmental factors like pollutants.
  • Eczema is a spectrum disease with overlapping morphologies, requiring dermatologists to consider diverse presentations and tailor treatments accordingly.
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Lio addresses one of the NEA's Eczema Awareness Month weekly themes, "What is eczema?"

The National Eczema Association (NEA) is highlighting the lived experience of eczema with weekly themes throughout October as part of Eczema Awareness Month. Each week sheds light on different aspects of the disease.

Dermatology Times recently spoke with Peter Lio, MD, a clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine in Chicago, Illinois, and the founding director of the Chicago Integrative Eczema Center.

Lio discussed the NEA's theme: "What is eczema?", delving into evolving understandings of pathophysiology and exploring the future of treatments for eczema.

Peter Lio, MD
Peter Lio, MD | Image Credit: © Integrative Dermatology Symposium

Q&A

Q: What is the latest understanding of the complex pathophysiology of eczema, and how has it evolved over time?

A: The plot keeps getting thicker and thicker, and we're learning more and more about this. I would say that our understanding in the past 10 years is more than everything leading up to it in the history of like modern medicine. We've learned so much more about it. I think we understand, first of all, that there are several pathogenic pillars or aspects of disease. We understand there's a barrier problem, there's an inflammation issue, the immune system is overactive. There's an itch portion, which is the nerves and central nervous system, and a neuro-behavioral piece. There's also a microbiome story that we have to talk about.

We have these different stories, maybe even 5, depending on how you count it: barrier, inflammation, itch, behavior, this mind-body connection, and then the microbiome. We understand that they all play off each other, and you can kind of make them fall like dominoes. If one starts to fall, the others follow. The biggest understanding is that thinking it was all genetics, was barking up largely the wrong tree. There are many patients who have susceptibilities, being it definitely runs in families, and there's no doubt.

But the biggest changes that we now understand: There are some environmental factors that seem to be damaging our barriers. There's an author. His last name Akdis; he's unbelievable, and he has written a lot about this, what's called the epithelial barrier hypothesis, that things in the environment are damaging our skin, gut, and lungs, and in so doing, it's opening the door for all of these allergic diseases, which are happening at a crazy rate. One of the big breakthroughs, I think, happened in the wake of the California and the Canadian wildfires. People who were exposed to the wildfire smoke developed eczema at a higher rate. In fact, many adults who never had eczema before developed it. One of the chemicals in there we think can do it is something called isocyanates. These seem to actually damage the microbiome in the barrier. This has cracked the story wide open. We also understand that staph bacteria is playing a direct role, as well.

It turns out there's a lot of external things. We've often blamed the patient. We thought it's food, and it's them, and it's actually, "Wow; it's all these external things." It's pollutants and detergents and microplastics and, of course, staph bacteria. All these things are actually damaging us from the outside, and I think that maybe it's an important way to look at it, because if we keep looking inward, but it's actually coming from outside of the house, then we need to change our tactic here. It's not just the things we can control. Sometimes it's stuff in our air, in our water, and in our environment.

Q: How should dermatologists approach cases where patients present with atypical or overlapping eczema types?

A: I would argue that that is actually probably more common than not. In fact, we see so many people have multiple morphologies at the same time, and I think it is helpful to see it as a spectrum disease. In fact, we wrote a paper a couple of years ago calling it the atopic dermatitis spectrum, that they really are all part of this family. You can see it change, not only in time, of course, across individuals, but across time. But even at the same time, just different body areas, you can have multiple morphologies.

I do think that the treatment principles are very similar. Now, while different areas might require specialized approaches, face and neck, eyelids, hands, feet; there are some specialized areas, but I think the overall approach is the same. We want to be gentle. We start simple. We escalate as needed, but we really do want to try to get patients better, because I firmly believe that if we break the vicious cycle, many patients actually can enter into a phase of remission, because now they have a virtuous cycle. Instead of being all in trouble, all those factors are improved, so they actually are much more resilient and stable, and that's really what we're going for.

Q: What are some of the key clinical signs that dermatologists should look for in identifying different types of eczema in diverse populations?

A: I think we know that this is a worldwide condition, and it affects patients everywhere. In fact, we think that patients with darker skin types are more likely to have eczema and may be more likely to be severe. The insult to the injury is that they may be underdiagnosed and have less access to medical care, particularly in the US. We know that things are not perfectly balanced for everybody. It's not entirely fair; there are a lot of different inequities that are there, so this makes it very challenging.

We have to make sure we're paying attention to each patient as an individual. We have to make sure we understand that in darker skin, it can be harder to appreciate redness. It can be harder to appreciate dryness. It can be harder to appreciate the disease extent and severity. There's a risk, a real risk, a measurable risk, of underdiagnosing patients and under-rating them as being severe. We can misdiagnose their severity, as well.

In terms of morphologies, there can be some changes, as well. We know darker skin tends to show more lichenification, more pigmentary change, and often tends towards more follicular patterns. Again, you have to be tuned into that. Most people, I think, if they've studied and worked with a range of skin, they're okay with it. But some clinicians are less comfortable outside of a more narrow spectrum. It's good to be aware because, again, patients are everywhere, and it's so common that it's almost unavoidable that you're going to see patients from all walks of life with eczema. It really doesn't discriminate very much at all. It picks on everybody, so we have to be careful of that, as well. Then I think the treatment approaches, again, are very similar regardless of your skin tone, regardless of the location. We have a similar approach overall. The specifics can be a little different, knowing that again, on sensitive skin areas we want to be careful. We also want to be particularly tuned into pigmentary problems. The darker your skin, the more likely you are to notice pigmentary issues and for that to be an issue, so we have to make sure we're addressing that, as well.

Q: Have you encountered any specific cases where eczema’s appearance masked or mimicked other dermatological conditions?

A: Yes, and this is a huge problem, particularly in my line of work, because of a lot of resistant cases, tough cases that don't seem to be responding. The thing we always have to ask ourselves is, "Why didn't you respond to any of the basic treatments? Why is this so tough? Is it because it's really, really, really bad eczema, or is it something else altogether?" I've had, over the years, several cases where they've been seen by multiple derms, and I think that they have scabies because they have little burrows in the genital area or between their fingers, and I scraped them, and they have scabies mites on their skins, then you end up with this very bizarre situation where the patient says, "Has it been scabies all along, or is this just a secondary thing?" And sometimes, I don't know. Sometimes, it may be to just a secondary thing. If you have bad eczema, you still could get scabies.

Contact dermatitis is another very common thing, and of course, that can develop over time, and patients are often very surprised by it. They'll say, "Well, I've used this cleanser my whole life," or, "I've used this moisturizer for years," but at some point your body just decided it didn't like it anymore, so now it's making you worse. It's actually causing an allergic reaction.

Contact dermatitis is huge, and it looks just like eczema a lot of times. Sometimes, it's more obvious, but sometimes it's not. We have to do testing, like patch testing. There's all this confusion about testing. Sometimes patients confuse it for testing. They say, "Oh, I already had that. They told me I'm allergic to rabbit hair and mold." And it's like, "Well, that's a different kind of testing that is looking for urticarial responses. We're trying to look for an eczematous response, a T-cell mediated response." There's just so many pieces to that, and then even things like cutaneous T-cell lymphoma can masquerade, and we have to really stay alert for these things, because, again, they're not all mutually exclusive, either. We have people with overlapping conditions, and that makes our job really, really tough.

Q: What are the key considerations in tailoring treatments for different types of eczema, especially for refractory or chronic cases?

A: I think the most important things are, really, a shared decision-making process. I like to present a very broad landscape to the patient. I like them involved in that decision-making, in part, because a.) I really do feel like they should be comfortable and have a role in it, but b.) I think if the patient's excited about a treatment, they're much more likely to use it, and much more likely to get better from it. If they're kind of grudging and not really interested in it, I don't think it's going to be as likely to help. I want them to have this sense of it. I want them to also be empowered and feel like we're not at the end of our rope; it's not the last thing, and it's not this or nothing, because it's very rarely the case.

Even for my patients, I almost always have a couple of tricks up my sleeve, or a couple of new things to offer, and that's really important. Shared decision-making with the patient, really being open to the landscape of possibilities, always going back to the beginning. How many times have I talked to a patient that haven't even used something pretty basic, and everybody kind of skipped over that? We can go back to the basics, and honestly, I'm not ashamed. I write a lot about it. I'll pull a paper and say, "Let me show you a recent paper I wrote that talks about some of the new treatments, or some of the approaches, and what strikes you, and how do you think about it?" And I think that's really empowering for the right patient who's interested in getting directly involved. That's powerful.

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