NurseCE4Less Podcast

Atopic Dermatitis: Contemporary Strategies for Durable Control - N593

NurseCE4Less Season 2026 Episode 7

Use Left/Right to seek, Home/End to jump to start or end. Hold shift to jump forward or backward.

0:00 | 23:39

This CE podcast summary provides a comprehensive examination of atopic dermatitis, outlining its biological origins and the heavy socioeconomic burden it places on patients. 

The authors emphasize that effective management relies on a layered treatment approach, starting with consistent moisturization and the identification of environmental triggers. This course details various pharmacological interventions, comparing traditional topical corticosteroids with modern biologic therapies and JAK inhibitors for more severe cases. Beyond standard treatments, the sources evaluate adjunctive options such as phototherapy, wet-wrap therapy, and the specific role of allergen immunotherapy. Clinical guidance is further supported by a pediatric case series demonstrating the successful use of targeted biologics in complex genetic syndromes. Ultimately, this resource serves as a guide for healthcare professionals to provide individualized care and achieve long-term disease control.

The NurseCE4Less Podcast delivers concise, engaging audio summaries of continuing education topics designed for busy Nurse professionals.

Each episode highlights key insights from accredited CE courses available on NurseCE4Less, covering essential clinical updates, emerging healthcare topics, and practical knowledge professionals can apply in their daily practice.

Whether you're staying current with licensure requirements or expanding your professional expertise, the NurseCE4Less Podcast makes it easy to learn on the go.

NurseCE4Less has helped over one million healthcare professionals meet their continuing education needs with affordable, accredited courses for over 20 years.  To receive CE credit for this course, visit www.NurseCE4Less.com.

SPEAKER_02

Welcome to the Nurse CE for Less Continuing Education Podcast. Each episode provides an engaging podcast style overview of individual continuing education courses to enhance your learning experience. These episodes utilize Notebook LM's Deep Dive AI audio to provide a podcast style conversation. To receive CE credit for this course, please visit NurseCE4Less.com. Use promo code podcast15 to receive 15% off an unlimited CE plan.

SPEAKER_03

Imagine treating a skin rash like a part-time job. I mean, literally clocking in 20 hours every single week.

SPEAKER_00

Yeah, it's exhausting just thinking about it.

SPEAKER_03

Right. You are applying these heavy ointments, you're wrapping limbs in wet bandages, uh washing specialized linens, and literally staying awake through the night just to physically stop a child from tearing their own skin open.

SPEAKER_00

Aaron Powell Exactly. And if you're listening to this right now, uh you or someone you love might be dealing with these exact, really frustrating realities.

SPEAKER_03

Aaron Powell You know better than anyone that atopic dermatitis is just not a scratch on the surface. So welcome to today's deep dive. We are taking a massive stack of clinical guidelines, contemporary research, and dermatological reviews to sort of uncover the hidden mechanics of this disease.

SPEAKER_00

Aaron Powell Because culturally we tend to view the skin as I don't know, merely a wrapper for the body. Like if the wrapper is dry, you just wet it.

SPEAKER_03

Right. Just put some lotion on it.

SPEAKER_00

Aaron Powell Yeah, a comforting, simplistic view. But stepping into the clinical reality of atopic dermatitis or AD, it forces a complete paradigm shift. I mean, we're looking at a systemic internal meltdown that just happens to manifest on the surface.

SPEAKER_03

Aaron Powell Which is exactly what we're going to show you today, why your skin interacts with your environment the way it does, and why medicine is moving totally away from that old dry skin narrative. But uh let's start with this bizarre global trend from the research.

SPEAKER_00

Oh, the prevalence rates.

SPEAKER_03

Yeah. Cases of AD are rising rapidly worldwide, but specifically in industrialized urban areas. Like, why is a skin condition tied to living in a modern city?

SPEAKER_00

Well, it points to this framework researchers call the hygiene hypothesis. In industrialized regions, you know, we spend the vast majority of our time indoors. We're breathing air-conditioned, filtered air. We are constantly sanitizing our hands, wiping down surfaces.

SPEAKER_03

And sanitizer everywhere.

SPEAKER_00

Exactly. But our immune systems are actually designed to be trained in infancy. They need to encounter soil, diverse environmental bacteria, a huge variety of natural microbes.

SPEAKER_03

Like you would get on a farm or something.

SPEAKER_00

Aaron Powell Right, in a rural environment. So without that early, messy training, the immune system essentially grows up bored and hyper-vigilant. It starts looking for threats that aren't actually there, which heavily skews the body toward allergic inflammatory responses.

SPEAKER_03

Aaron Powell Okay, let's unpack this. Because if the immune system is hypervigilant, what does that actually look like at the physical surface?

SPEAKER_00

Aaron Powell Well, down at the microscopic level, AD is driven by what we call a perfect storm. It's three interconnected failures.

SPEAKER_03

Aaron Powell Okay, what are they?

SPEAKER_00

You've got a physical barrier dysfunction, an immune dysregulation, and a microbiome imbalance. So if we look at the physical barrier first, your skin's outer layer is supposed to be an impenetrable shield. But in AD, there's a fundamental structural breakdown, mostly from genetics.

SPEAKER_03

And the sources mentioned a specific mutation, right? FLG.

SPEAKER_00

Yes, mutations in the FLG gene, which produces a protein called filigrin.

SPEAKER_03

Filigrin. Okay, what is its job? Because I never heard of that before.

SPEAKER_00

Aaron Powell It's the ultimate structural binding agent. Its primary job is to bind keratin fibers together to give skin cells their tough shape. And as those cells mature and reach the surface, the filigrin breaks down into natural moisturizing factors.

SPEAKER_03

Wait, turns into moisturizer.

SPEAKER_00

Essentially, yeah. Amino acids that literally grab onto water and hold it inside the skin tissue. But when that gene is mutated or when chronic inflammation basically turns the gene off, the skin loses its architecture. Water evaporates rapidly, leaving the tissue incredibly dry.

SPEAKER_03

And gaps open up, right? Like I was thinking about this. Think of the skin as a brick wall. The skin cells are the bricks, and the filigrin is the mortar holding everything tight.

SPEAKER_00

That's a great way to picture it.

SPEAKER_03

So when the mortar crumbles, the wall gets incredibly leaky. And it's a two-way street of disaster. The essential moisture leaks out, and environmental invaders like pollen, pet dander, pollutants, they slip right in through the cracks.

SPEAKER_00

Exactly. And when those invaders slip through that crumbled mortar, they immediately encounter the immune system's guards. In an AD patient, those guards are heavily biased toward what's called a TH2 dominant immune pathway.

SPEAKER_03

The hypervigilant ones from the hygiene hypothesis.

SPEAKER_00

Right. So instead of assessing the invader calmly, they panic. They flood the tissue with these chemical messenger molecules called cytokines. The heavy hitters here are interleukin 4 and intraleukin 13, which cause the redness and swelling, and crucially, intraleuin-31.

SPEAKER_03

Ah, IL-31, the source material called that the specific itch cytokine. That sounds like a really highly specialized chemical.

SPEAKER_00

It is incredibly specialized. And what's fascinating here is that it bypasses the normal inflammatory process. IL-31 directly binds to the sensory neurons embedded in the skin.

SPEAKER_03

Wait, really? It goes straight to the nerve.

SPEAKER_00

Straight to the nervous system. It wires an emergency signal directly to the brain saying you need to scratch this area immediately. It creates an intense, relentless itch that drives the classic itch-scratch cycle. And obviously, the more you scratch, the more the physical barrier you destroy.

SPEAKER_03

Aaron Powell So we have a leaky wall and we have a panicked immune system sending nervous system alarms. But you mentioned a third piece to this microscopic storm, the microbiome.

SPEAKER_00

Right, the microbiome.

SPEAKER_03

Our skin is covered in bacteria, which I mean is usually a good thing, right? We want a diverse rainforest of microbes. But the research says in AD that diversity just plummets.

SPEAKER_00

It drops off a cliff. The altered pH and the lack of natural antimicrobial peptides from that breaking barrier create a paradise for one specific bad actor, Staphylococcus aurais.

SPEAKER_01

Staph.

SPEAKER_00

Yeah, staph race. Yeah. The heavy bacteria die off, and staph heavily colonizes the skin. The real danger here is that it secretes specific toxins called superantigens.

SPEAKER_03

And those get through the leaky wall.

SPEAKER_00

Exactly. They penetrate the broken barrier and act as massive chemical accelerants. They force those TH2 immune cells to stay locked in the on position.

SPEAKER_03

That is a terrifying feedback loop. The barrier breaks, the immune system overreacts, bacteria multiply and dump toxins, which causes more inflammation, which destroys more filigrin mortar.

SPEAKER_00

And if we connect this to the bigger picture, the deeper issue is the systemic toll. This isn't just a local alarm going off on someone's arm. That persistent itch from IL 31 keeps the central nervous system in a constant state of arousal.

SPEAKER_03

Oh, because the brain is constantly receiving that signal.

SPEAKER_00

Right. We see severe sleep disruption in up to 80% of children with AD.

SPEAKER_03

80%.

SPEAKER_00

Up to 80%. They are spending their nights microawaking to scratch. And that chronic sleep deprivation leads to daytime fatigue, emotional dysregulation, profound anxiety. The psychological burden is just staggering.

SPEAKER_03

Yeah, we are definitely not talking about a scratch on the paint anymore. We are talking about the car's entire wiring system melting down. So the logical first step in fixing this isn't necessarily to attack the immune system, right?

SPEAKER_00

Yeah.

SPEAKER_03

We have to rebuild the wall, patch the mortar.

SPEAKER_00

Exactly. Prevent the leaks first.

SPEAKER_03

Which brings us to daily maintenance and moisturization. And I have to say, I was completely floored by this number in our source. For an adult with moderate to severe AD, the clinical recommendation is 250 to 500 grams of moisturizer every single week.

SPEAKER_00

It's a massive amount.

SPEAKER_03

That is a giant tub of cream used in its entirety every seven days.

SPEAKER_00

Aaron Powell Well, moisturizer in this clinical context isn't, you know, a cosmetic luxury just to make your skin feel soft. It's an active therapeutic intervention. You are literally providing artificial mortar for that broken brick wall. Right. The guidelines emphasize a highly specific technique called soak and seal. A patient bathes in lukewarm water to physically push hydration into the skin. But when they get out, they have a strict three-minute window to apply that heavy moisturizer.

SPEAKER_03

A three-minute race against the clock?

SPEAKER_00

Sure.

SPEAKER_03

Just to trap the bathwater?

SPEAKER_00

Yes, to physically lock that moisture inside the tissue before the ambient air evaporates it.

SPEAKER_03

Wow. And I'm guessing you can't just use any cheap watered-down lotion from the drugstore for this.

SPEAKER_00

Definitely not. A scientifically formulated AD moisturizer relies on three distinct mechanical elements. First, you have humectins like glycerin or hyaluronic acid, which actively draw water molecules from the deeper layers of skin up to the surface.

SPEAKER_03

Okay, humectins pull the water up.

SPEAKER_00

Right. Second, emollients like ceramides. These act as the spackle, physically filling in the microscopic gaps between the skin cells to repair the barrier. And third, occlusives like petrolatom, which create a heavy physical seal on top to lock everything in.

SPEAKER_03

So it's pulling water in, patching the holes, and sealing the top.

SPEAKER_00

Exactly. And ointments with a really high oil to water ratio work best for that occlusive seal, even if patients sometimes complain that they feel a bit greasy.

SPEAKER_03

And there's also a minefield of ingredients you have to actively avoid putting on that fragile wall, right? Like alcohols, which just evaporate water and burn.

SPEAKER_00

Oh, absolutely. Alcohols, fragrances, essential oils.

SPEAKER_03

Yeah. The essential oils thing is wild. You see natural lavender oil on a fancy lotion label, and you naturally think, oh, this must be healing. But for an AD patient, it's just a raw chemical irritant slipping directly through a compromised barrier.

SPEAKER_00

Because the skin barrier is wide open. Introducing known contact allergens like botanical fragrances directly into raw tissue will only provoke those hypervigilant TH2 guards even further.

SPEAKER_03

Okay, well, let me push back on this whole approach for a second. If my immune system is overreacting and causing all this systemic inflammation, shouldn't I just look at what I'm putting into my body?

SPEAKER_00

Ah, the diet question.

SPEAKER_03

Yeah. Because the very first piece of unsolicited advice anyone with a skin condition gets is oh, you need to cut out dairy or stop eating gluten. Does changing my diet fix the structural wall?

SPEAKER_00

No. And this is honestly one of the most pervasive, damaging myths in dermatology. The latest guidelines from the leading allergy and immunology academies emphatically debunk it. Routine elimination diets are absolutely not recommended for managing atopic dermatitis. No at all. Not unless the patient has a confirmed IgE-mediated food allergy.

SPEAKER_03

Wait, what does IgE mediated mean in plain English?

SPEAKER_00

It means the immune system produces a specific antibody, immunoglobulin E, that triggers an immediate systemic reaction when a specific food is eaten. We're talking about sudden hives, lip swelling, or anaphylaxis.

SPEAKER_03

So a traditional immediate allergic reaction.

SPEAKER_00

Right. If you do not have that specific immediate reaction, cutting out milk, wheat, or eggs is not going to clear up your eczema.

SPEAKER_03

So no guessing games, no starving yourself of bread for six months just to see if the skin clears up.

SPEAKER_00

Please don't. Doing that can actually be incredibly harmful. The research now clearly demonstrates that unnecessarily delaying a child's exposure to common allergenic foods can actually cause new food allergies to develop.

SPEAKER_03

Wait, really? By avoiding the food you create the allergy?

SPEAKER_00

Yes. Yeah. Because think about it, if an infant is kept away from peanuts, but peanut dust is in the household environment.

SPEAKER_03

Which it always is.

SPEAKER_00

Right. That dust settles onto their broken inflamed skin. So the immune system's very first encounter with the peanut protein is through a wound, surrounded by active alarm signals. The body registers the peanut as a dangerous invader and creates a lifelong allergy. Wow. So we must focus on repairing the skin barrier, not starving the patient of essential nutrients and driving caregivers crazy with impossible dietary restrictions.

SPEAKER_03

Patch the wall, don't restrict the food, that makes total sense. But uh patching the wall is preventative, it's daily maintenance. What do you do when a localized fire has already broken out? Because when someone is in the middle of a massive, agonizing flare, a tub of moisturizer isn't going to cut it.

SPEAKER_00

No, it won't. You have to move from prevention to active flare control. And for 60 years, the backbone of acute flare control has been topical corticosteroids or TCS.

SPEAKER_03

The steroid cream?

SPEAKER_00

Right. They're applied directly to the active lesions, and they work by broadly suppressing the inflammatory pathways at that specific site. They range from class one, which are incredibly potent, super high strength steroids, all the way down to class seven, which includes low potency over-the-counter options like hydrocortisone.

SPEAKER_03

But the source outlines some pretty serious risks here. Like you can't just slather a high potency steroid on your eyelids or the inside of your elbows for months at a time, right?

SPEAKER_00

No, you absolutely cannot. The primary risk of overusing topical steroids is skin atrophy, which is a permanent thinning of the skin tissue and the development of straya, deep stretch marks.

SPEAKER_03

Because it stops the cells from growing.

SPEAKER_00

Exactly. The steroid halts the inflammation, but it also halts the normal cellular turnover required to keep the skin thick and resilient. And if they're abused over massive areas of the body, they can even be absorbed into the bloodstream and disrupt the body's natural adrenal glands.

SPEAKER_02

Yikes.

SPEAKER_00

So the clinical mandate is strict. Use the lowest effective potency for the shortest duration necessary to put the fire out.

SPEAKER_03

But if the skin on the face or the neck is too delicate for steroids, how do you stop the inflammation without thinning the skin?

SPEAKER_00

Well, this is where steroid sparing agents come into play. The first class is topical calcinerin inhibitors, or TCIs. These medications penetrate the cell and bind to a specific protein, which prevents the activation of NFAT.

SPEAKER_03

NFAT.

SPEAKER_00

Yeah, NFAT is essentially a cellular switch that tells the cell to produce inflammatory cytokines.

SPEAKER_03

Uh-huh.

SPEAKER_00

By blocking that switch, the inflammation stops, but the cellular turnover isn't affected at all, meaning zero risk of skin thinning.

SPEAKER_02

Oh, that's clever.

SPEAKER_00

And another newer option is PDE4 inhibitors. These work by blocking an enzyme that normally breaks down a calming molecule called CMP. So by blocking the enzyme, CMP levels rise inside the cell, which actively dials down the inflammatory response.

SPEAKER_03

Aaron Powell Okay, I love that. So think of the inflammation like a stereo blasting at maximum volume, right? The steroids take a sledgehammer to the stereo. It definitely stops the noise, but it damages the equipment. Right. The TCIs unplug the speaker wire, and the PDE4 inhibitors just reach over and smoothly turn the volume knob down.

SPEAKER_00

Aaron Ross Powell That is a brilliant way to visualize it. And you know, for flares that are so severe they don't respond to any of those standard topicals, clinicians will turn to wet wrap therapy.

SPEAKER_03

Oh, I read this section. It sounds intense. Like you apply the steroid medication, then you tightly wrap the skin in a layer of warm, damp cotton or gauze, and then you put a dry layer over that. You're basically marinating the skin.

SPEAKER_02

You really are.

SPEAKER_03

You force the hydration in, you force the medicine to penetrate deeper, and you create this physical cage so the patient literally cannot scratch their own skin in their sleep.

SPEAKER_00

Aaron Powell It is intensive and it's usually performed for only a few days under medical supervision, but it rapidly breaks that maddening itch-scratch cycle and forces the localized ecosystem to just calm down.

SPEAKER_03

Okay, but here's where I really need you to explain something because it sounds completely unhinged. The clinical guidelines mention bleach baths.

SPEAKER_00

Uh yes.

SPEAKER_03

Taking a child with raw, broken, agonizingly inflamed skin and putting them into a tub of bleach. How is that not chemical warfare on their already compromised burial?

SPEAKER_00

Aaron Powell I know it sounds horrifying until you look at the actual math. We are not pouring pure concentrated bleach over a patient. The guidelines recommend a highly dilute.0005% sodium hypochlorite solution. Okay, what does that mean in practical terms? In practical terms, that is about a quarter cup of regular household bleach mixed into a standard 40-gallon bathtub full of water. The concentration is practically identical to a municipal swimming pool.

SPEAKER_03

Oh. Okay, pool water. That sounds much less terrifying, but why do it at all?

SPEAKER_00

Think back to our discussion about the microbiome. Remember the staphylococcus aureus bacteria that colonizes the skin and secretes toxins?

SPEAKER_03

Right. The staph.

SPEAKER_00

The dilute bleach acts as a highly targeted, broad-spectrum antiseptic strike against that specific bacteria. It reduces the microbial load on the skin.

SPEAKER_03

Why not just give them antibiotics?

SPEAKER_00

Aaron Powell Because the guidelines explicitly warn against routine oral antibiotics. They breed antibiotic resistance and wipe out the healthy gut bacteria without actually curing the eczema. So the bleach bath is just a safe topical maintenance strategy to keep the staph aureus from overrunning the wall.

SPEAKER_03

Okay, so topicals, wet wraps, and pool water to put out local fires. But what if the entire forest is burning from the inside out? Like for the most severe refractory cases, creams and baths aren't going to reach the core of the problem.

SPEAKER_00

No, they won't.

SPEAKER_03

If those TH2 immune commanders are stationed deep inside the body, constantly sending out attack orders, we have to change the internal weather of the entire system.

SPEAKER_00

Which brings us to the modern era of systemic therapies. And this has completely revolutionized dermatology. Historically, severe cases were treated with blunt immunosuppressants like oral steroids or cyclosporine.

SPEAKER_03

The sledgehammer approach again?

SPEAKER_00

Exactly. These drugs carpet bomb the entire immune system. They shut everything down, which leaves the patient vulnerable to serious infections, kidney toxicity, and massive rebound flares the literal moment the drug is stopped. Today, though, the focus is entirely on targeted therapies, biologics, and JK inhibitors.

SPEAKER_03

Let's start with biologics, like dupalumab. These are subcutaneous injections, and instead of carpet bombing, they act more like a molecular sniper fire.

SPEAKER_00

That's exactly what they are.

SPEAKER_03

They are engineered antibodies that selectively hunt down and block just the IL-4 and IL-13 cytokines. They take out the specific messengers ordering the attack without shutting down the rest of the immune system. And they are incredibly safe, requiring no root turn lab monitoring, but they come with a staggering price tag of$30,000 to$40,000 a year.

SPEAKER_00

Yeah, the cost is an immense barrier, but the clinical outcomes justify it for severe cases. To understand just how transformative this targeted approach is, the source highlighted a case series involving pediatric patients with a rare genetic disorder called hyper-IgE syndrome.

SPEAKER_03

Right, I saw that. These kids have genetic mutations that give them severe early onset eczema, massive allergic responses, and recurrent life-threatening pneumonias. Like their immune systems are just completely unbalanced.

SPEAKER_00

Their immune profile is so heavily skewed toward the TH2 allergic pathway that they literally lack the proper defenses in other areas to fight off basic bacteria. So researchers administered dupalumab to block the IL-4 and IL-13 signals.

SPEAKER_02

And what happened?

SPEAKER_00

Over several years, not only did their severe skin lesions achieve near complete clearance, but their massive recurrent infections. The pneumonias, the severe ear infections, they dropped drastically.

SPEAKER_02

Wait, really?

SPEAKER_00

Yes. By chemically balancing the TH2 scale, they restored enough overall immune function to allow the body to properly fight off external infections again.

SPEAKER_03

So a drug designed to stop eczema actually helped their immune system stop getting pneumonia just because it brought the entire systemic weather pattern back into equilibrium. That is remarkable.

SPEAKER_00

It's life-changing.

SPEAKER_03

But biologics aren't the only option. We also have JK inhibitors like upadacetinib. These are oral pills that work inside the cell to block multiple cytokine signals simultaneously. But I was looking at the safety profiles in the source, and I'm a bit confused. Biologics seem incredibly safe. Meanwhile, the FDA mandates boxed warnings on J-Kane inhibitors for severe cardiovascular events, thrombosis, and even malignancies.

SPEAKER_00

Yes, the black box warnings.

SPEAKER_03

So if biologics are so safe, why would a doctor ever prescribe a drug with a black box warning?

SPEAKER_00

It really comes down to the clinical mechanism and the agonizing reality of pruritus, the severe unrelenting itch. What's fascinating here is that biologics are large proteins. They take weeks, sometimes months to build up in the system and reach their maximum efficacy. But JK inhibitors block the Janus kinese enzymes inside the cell. Those enzymes transmit the itch signals, but they also transmit signals that regulate blood clotting and heart function. That broader blocking effect is exactly why those cardiovascular warnings exist.

SPEAKER_03

So they carry a higher risk because they are blocking pathways that do multiple jobs in the body.

SPEAKER_00

Exactly. But the trade-off is unparalleled speed. Because they are small molecules taken orally, JK inhibitors can shut down severe maddening paritis in literally two to three days.

SPEAKER_03

Wow. Days instead of months.

SPEAKER_00

Yes. If you have a patient who hasn't slept in a week, who is suicidal from the relentless sensation of their skin crawling, they simply cannot wait a month for a biologic to kick in. The choice is a highly calculated, shared decision between doctor and patient, balancing the immediate catastrophic distress of the disease against the specific cardiovascular risk factors of that individual.

SPEAKER_03

That makes total sense when you frame it like that. Well, we have covered a staggering amount of ground today. We started at the microscopic crumbling mortar of the filigrin gene. We watched the invaders slip in, setting off the TH2 immune alarm and that specialized IL-31 itch cytokine.

SPEAKER_00

We mapped out the race to patch the wall with a three-minute soak and seal moisturization technique.

SPEAKER_03

Right. And we totally dismantled the myth that cutting out dairy will fix a genetic skin defect.

SPEAKER_00

We also explored how to put out active fires with topical steroids and steroid sparing agents, and how dilute bleach bath strategically targets staphoresis.

SPEAKER_03

Pool water. And finally, we saw how medical science is shifting the internal weather with targeted biologics and rapid acting JA inhibitors. It is an entirely new era of personalized medicine. Before we wrap up, I just keep thinking about our very first point, the hygiene hypothesis, the idea that our sanitized indoor lives are causing our immune systems to misfire in the first place.

SPEAKER_00

It raises a profound philosophical question for the future of medicine, doesn't it? I mean, we just analyzed incredible$30,000 immune-blocking drugs. But if the root cause of this global rise in atopic dermatitis is our hyperclean environment, the ultimate preventative cure might not be found in a pharmacy. Right. What if the future involves deliberately rewilding our living spaces, exposing infants to dirt, to diverse environmental bacteria, and to farm-like environments right from birth to properly train their immune systems? We could theoretically stop the atopic march before the filigrin wall ever breaks.

SPEAKER_03

Rewilding our homes to save our skin? Now there's a thought to chew on. So the next time you look at a patch of dry skin, remember you are looking at the check engine light for a beautifully intricate, deeply complex immune system. And maybe next time you are tempted to aggressively sanitize everything your child touches, you might want to think about their filigrin. Let them get a little dirty. We will see you next time on the Deep Dive.

SPEAKER_01

Thank you for listening to the Nurse CE4 Less Continuing Education Podcast. To receive CE credit for this course and many others, please visit nursece.com. That's NurseCE, the number fourless.com. Use promo code Podcast15 to receive 15% off an unlimited CE plan. NurseCE4 Less, quality education at an affordable price.