Chapter 12: Contact Dermatitis – Drug Treatment & Care

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Welcome back to the Deep Dive.

Today we are really getting into the skin of things.

Literally.

Exactly.

We're cracking open the advanced pharmacotherapeutics of dermatitis.

It's a huge area dealing with chronic inflammation, hypersensitivity.

It's complex.

It really is.

And we're focusing on two big ones today.

Contact dermatitis, or CD, and atopic dermatitis, AD eczema, as most people know it.

Right.

And our goal here isn't just to list drugs.

We want to dig into why these conditions are different at a fundamental level.

Because that pathophysiology, that's what drives the whole treatment approach.

It dictates the stepwise therapy we use.

So we'll be breaking down the diagnosis, the treatment steps, and those key differences in applying the medications.

Let's start with the basics then.

Setting the stage.

Okay.

Contact dermatitis, CD, that's the one triggered by something touching the skin, right?

A substance exposure.

Correct.

And it causes either an allergic reaction or just a direct irritant reaction.

It's incredibly common.

It counts for something like nearly 6 million clinic visits a year.

Big occupational health issue too.

And you mentioned two types.

Yeah, we split CD into irritant contact dermatitis, ICD, which is the bulk of occupational cases.

Maybe 80%.

That's a direct toxic hit to the skin.

Like a strong chemical.

Exactly.

And then there's allergic contact dermatitis, ACD.

That's the immune system, specifically T cells overreacting.

Think poison ivy, nickel allergy,

that kind of thing.

Affects about 20 % of adults.

Got it.

ICD is direct damage.

ACD is an immune response.

Now, atopic dermatitis, AD eczema.

That's different.

Very different.

AD is chronic.

It's itchy, intensely itchy.

That's pruritus and inflammatory.

It tends to stick around.

Yeah.

Not just a one -off reaction.

And it affects a lot of people.

Significant numbers.

Around 12 % of children, maybe 7 % of adults.

It's often a lifelong condition you manage, not cure.

That distinction, acute reaction versus this chronic inflammatory state, that seems critical for treatment.

Absolutely fundamental.

If you understand the why, the mechanism, the how of treatment just falls into place.

Okay, let's dive into those mechanisms then.

ICD, the irritant type, sounds like the simplest.

It is, relatively speaking.

The irritant hits the skin and the skin cells themselves, the keratinocytes, they just, well, react badly.

They directly release pro -inflammatory cytokines.

Like a direct alarm signal.

Pretty much.

And that immediately messes up the skin barrier, that crucial water protein lipid matrix.

It's like a chemical burn disrupting the structure right away.

Okay, so ICD is a direct physical or chemical insult, but ACD, the allergic type, that's sneakier.

Much sneakier.

It needs that set -up phase.

It's T -cell mediated, remember.

So first, exposure sensitization.

The allergen gets picked up by specialized immune cells in the skin, Langerhans cells.

They travel to the lymph nodes and basically teach specific T -cells to recognize this allergen.

They create memory cells.

So the body's now primed.

Exactly.

Then comes phase two, elicitation.

Next time that allergen touches the skin, those memory T -cells are recruited super fast to the site and bam, inflation.

It's a delayed reaction, but the body's ready for war, so to speak.

Right, and AD eczema, that's even more complex.

Not just about external triggers, is it?

Not at all.

AD is, well, it's complicated.

There's a strong genetic component.

We often see mutations in a gene called filigrin.

Filigrin.

What does that do?

It's absolutely essential for building a healthy skin barrier.

Think of your skin like a brick wall.

Filigrin is like the mortar holding the bricks together.

If that filigrin gene is faulty, the mortar is weak.

The skin barrier is leaky, loses too much water leading to that characteristic dry skin or xerosis, and it lets irritants and allergens penetrate much more easily.

So the structure itself is compromised from the start.

Precisely.

And that leaky barrier, combined with environmental factors and immune system dysregulation, that's the complex norm of AD.

Okay, that foundational difference is clear.

Now, how do we spot them clinically?

What are the telltale signs?

For contact dermatitis, you often see distinct patterns.

Acute looks like redness, maybe little blisters, sometimes oozing.

Bessy.

Can be.

Yeah.

Then subacute is more crusting and scaling,

and chronic exposure leads to thickened, leathery skin.

We call that leakinification.

And if you suspect it's the allergic kind, ACD.

Patch testing.

That's the gold standard.

Apply potential allergens under patches,

wait 48 to 72 hours, and see what reacts.

Okay.

And for AD, eczema.

What are the key features?

Three main things.

Itch, pruritus, the eczema rash itself, and that underlying dry skin xerosis.

Location is also a big clue.

Where does it typically show up?

In babies and young kids, often face, scalp, maybe the outside of elbows and knees extensor surfaces.

But in older kids and adults, it classically moves to the flexural areas.

The creases.

Like behind the knees, inside the elbows.

Exactly.

Those flexural spots are very typical for adult AD.

Regardless of the type, though, the treatment goals seem similar.

Fix the barrier, calm the inflammation, stop the itch.

Those are the pillars, yes.

Restore, treat, control.

So obviously, avoiding the trigger in CD is the best plan.

Use gloves, change soaks, whatever it takes.

Prevention is always number one if you know the cost.

But when that fails, or for AD where avoidance isn't really the whole picture, what's the first step drug -wise?

Well, even before drugs.

Especially for AD patients with that known barrier defect, you absolutely have to start with non -pharmacologic stuff.

The cornerstone is aggressive moisturizing.

Liberal, frequent use of moisturizers.

Absolutely critical.

It's foundational for managing AD long -term, and it helps soothe the skin in CD too.

And we're not just talking any old hand lotion here, are we?

No, definitely not.

We need products designed to repair that barrier.

They need emollients to soften the skin.

Occlusive agents like petrolatum to physically block water from evaporating.

Create a seal.

Yep.

And humectants like glycerin or urea to actually draw water into the skin and hold it there.

You're actively trying to compensate for that weak mortar.

Makes sense.

And does the type of product like cream versus ointment matter?

Oh, hugely.

The delivery vehicle is key.

Ointments being greasy and lipid -based generally provide the best absorption and protection.

Gels are similar.

Better barrier.

Right.

Creams are less greasy, more cosmetically acceptable maybe, but often less effective for really dry skin.

Solutions are good for hairy areas, like the scalp.

And you mentioned something about occlusion -enhancing penetration.

Yes.

This is a really important point for topical corticosteroids or TCSs.

Covering the treated area, say with plastic wrap or a vinyl glove, can boost the penetration of that steroid by 10 times, even up to 100 times.

Wow.

Okay.

So that's a powerful tool, but needs careful use.

Very careful.

But extremely useful for thick, stubborn patches.

So let's talk about those TCSs, topical corticosteroids.

They seem like the go -to for calming down localized inflammation.

They are the workhorse, absolutely.

First line for localized CDE and for knocking down those acute AD flares.

How do they actually work?

What's the mechanism?

They act broadly on immune cells, right there in the skin.

They suppress the release of those inflammatory cytokines we talked about, interfere with how antigens are processed.

Basically, they dial down the local immune response and reduce inflammation.

Okay.

But the big challenge I always hear about is choosing the right one, the potency issue.

That's probably the single most important clinical decision with TCSs.

They're classified by potency, ranging from class 7, very low, up to class 1.

Super potent.

And there are strict rules about where you can use which potency, right?

Absolutely non -negotiable rules.

Low potency, think hydrocortisone 1%, that's what you must use on sensitive skin areas.

Face, eyelids, groin, underarms, skin folds.

Why?

What's the risk?

Skin atrophy.

Thinning of the skin.

It's often permanent.

You can also get stretch marks, striae, easy bruising, purpura, tiny blood vessels,

chaliejectasias, or even trigger a type of acne called steroid rosacea.

Okay.

So low potency for sensitive areas.

Where do the stronger ones go?

Medium to high potency steroids are reserved for thicker skin.

The torso, arms, legs.

The super potent ones are really just for very thick, light -genified plaques, often on palms or soles, and usually for short durations.

Duration is another key factor, isn't it, to minimize side effects.

Definitely.

For CD, you want the shortest course possible that clears the rash.

For AD flares, you treat daily until the flare resolves, but then critically, you often shift to maintenance.

Maintenance?

Yeah, applying the TCS maybe just once or twice a week to the previously affected areas can help prevent flares from coming back.

It's proactive.

And what about systemic risks?

Can using too much topical steroid cause problems elsewhere in the body?

It's much less likely than with oral steroids, but yes, especially with high potency agents used over large areas or under occlusion for a long time, you can get systemic absorption.

The main concern is suppressing the body's own steroid production, HPA -axis suppression.

Right.

So use the lowest effective potency for the shortest time needed.

That's the mantra.

Okay, this brings us to, I think, a really interesting area, especially for chronic AD.

What happens when you need long -term treatment, especially on sensitive spots like the face, but you want to avoid those steroid side effects, the steroid sparing options?

This is where the topical calcineurin inhibitors, the TCIs, come in.

Big step forward for managing AD.

TCIs.

Okay, what are they and how do they work differently?

They are amino suppressants, but they work differently than steroids.

They specifically inhibit an enzyme called calcineurin, which is needed for T cells to get activated and release those inflammatory cytokines.

So they stop the inflammation signal further upstream.

Kind of.

They block T cell activation without directly causing that skin thinning, the atrophy that we worry about with steroids.

That's their major advantage.

Makes sense.

Less inflammation, no atrophy risk.

So when do you use them?

Second line.

Typically second line for AD, yes.

They're indicated for patients usually over age two who can't tolerate TCSs, haven't responded well, or crucially need treatment on those sensitive areas like the face, eyelids, neck, where long -term steroid use is just too risky.

Which drugs are we talking about here?

Two main ones.

Tecrollin assortment comes in 0 .03 % and 0 .1 % strengths, and pamirallin is 1 % cream.

How are they used, similar to steroids?

Applied twice daily during flares.

And like with steroids, there's evidence that using them proactively, maybe two or three times a week on areas prone to flares, can help keep the skin clear longer.

Okay.

Now if you had to give one critical, practical tip differentiating TCI application from TCS application, what would it be?

Yes.

Absolutely crucial.

Do not use TCI's with occlusive dressings.

No plastic wrap, no vinyl gloves over the top.

Why not?

We just said occlusion boosts TCS penetration.

It does.

But because TCI's are immunosuppressants,

significantly increasing their absorption into the system via occlusion isn't recommended.

There are theoretical concerns about systemic immunosuppression and potentially increased risk of skin infections or even malignancy, though rare.

Patients using TCI's should also be advised to limit sun exposure.

Got it.

No occlusion with TCI's, that's a key takeaway.

Any other major side effects?

The most common thing people notice, especially initially, is some burning or itching right after application.

Often gets better with continued use, though.

Okay.

So TCI's are a major steroid sparing option for AD.

Are there others?

Yes.

There's chrysabrol, a topical ointment, a PDE4 inhibitor.

PDE4.

How does that work?

It inhibits the phosphodiesterase 4 enzyme inside inflammatory cells.

This increases levels of something called cyclic AMP, which then helps to calm down the inflammation cascade.

It's approved for mild to moderate AD.

Another tool in the toolbox?

What if topicals just aren't cutting it?

Then phototherapy, using specific wavelengths of UV light, can be an option for AD, usually after TCS's and TCI's have been tried.

And what about good old antihistamines for the itching?

Here's an important distinction.

Oral antihistamines, especially the sedating ones like diphenhydramine or hydroxazine, can be helpful for the intense itch associated with contact dermatitis, partly because they help you sleep through it.

Makes sense.

Knock you out so you don't scratch.

Pretty much.

But importantly, topical antihistamines are generally not recommended for either condition.

And oral ones aren't considered a primary treatment for the itch of atopic dermatitis itself.

The itch in AD is more complex than just histamine release.

Interesting.

Okay, so we've covered topicals.

What happens when the dermatitis is really severe, widespread, or just not responding?

When do you have to escalate to systemic therapy?

That's reserved for refractory cases.

Definitely.

For severe, widespread contact dermatitis that isn't manageable with topicals, the first systemic option is usually oral corticosteroids.

Pred -dysone is the common one.

The big guns.

Same mechanism as topical steroids, just body -wide.

Essentially, yes.

Broad suppression of inflammation, reducing cytokine release, decreasing capillary permeability.

The works.

But the risks are higher systemically, right?

Dosing must be careful.

Absolutely.

Typical starting dose is around one milligram per kilogram per day.

Usually taken all in the morning.

But the taper is critical.

Tapering off slowly.

Yes.

Especially for things like severe poison ivy.

If you give too short a course,

say less than two, maybe even three weeks, you run a very high risk of rebound dermatitis.

The rash comes back with a vengeance when you stop the steroid.

Exactly.

You need to taper off slowly to allow the body's own system to kick back in to fully extinguish the inflammation.

And there are definite situations where you just can't use oral steroids.

Oh yes.

Contra indicated if someone has a systemic fungal infection, you shouldn't give them with live vaccines.

And you need extreme caution in patients with conditions like TB,

uncontrolled hypertension, diabetes, osteoporosis.

The list of potential side effects is long.

Right.

Okay, so that's for refractory CD.

What about really severe, stubborn AD that doesn't respond even to potent topicals or phototherapy?

Then we move into the realm of potent systemic immunosuppressants.

This is usually managed by specialists, dermatologists, or allergists.

What kind of agents are we talking about?

Options include cyclosporine, which inhibits T -cells but carries risks like kidney problems and high blood pressure.

Others are azithoprine, methotrexate, and mycophenolimophil.

These all have significant potential side effects and require careful monitoring.

And you mentioned methotrexate specifically earlier?

Yes.

Critical point.

Methotrexate is an absolute contraindication in pregnancy.

It's teratogenic, must be avoided in anyone who could become pregnant, and isn't using reliable contraception.

Really important safety note.

Okay, let's quickly touch on special populations, pediatrics.

Kids have that higher body surface area to weight ratio, meaning they absorb topical drugs more readily per pound.

So rule number one,

use the least potent TCS that will work.

And the TCIs?

Tacrolimus 0 .03 % and primocrolimus 1 % are approved for kids aged two and older.

The higher strength tacrolimus 0 .1 % is usually for 16 and up.

Makes sense.

What about older adults, geriatrics?

Their skin is often already thin and fragile, sometimes from sun damage or just age, so that risk of TCS -induced atrophy is even more of a concern.

You have to be extra cautious with potency and duration.

And you mentioned their rash might look different.

Yeah, sometimes in older adults, especially with AD, the presentation can be less weepy or blistery, maybe more just dry, scaly, itchy patches.

A bit atypical sometimes.

Good to keep in mind.

Okay, let's try to synthesize this.

Can you walk us through the treatment hierarchy again first for contact dermatitis?

Sure.

For city D.

Step one is prevention, avoidance, plus maybe low -potency TCS for localized spots and oral antihistamines if needed for severe itch.

Step two.

If needed, increase the potency of the TCS, but always being mindful of location, avoiding face fold, etc.

Step three.

For severe widespread cases, consider oral corticosteroids, remembering that crucial long taper.

Got it.

Avoid topical steroid, low, then maybe higher, oral steroid.

Now for atopic dermatitis, where maintenance is key.

Right.

AD is different.

Step one is the foundation.

Non -pharmacologic measures intense moisturizing,

maybe wet wrap string flares, plus appropriate potency TCS for the flares themselves.

Moisturize, moisturize, moisturize.

Always.

Step two involves bringing in those steroid sparing options if needed.

TCI's are often the go -to here, especially for sensitive sites or long -term use.

Crisabrol or phototherapy are other options in this tier.

Okay, TCI, Crisabrol, phototherapy.

And step three, only for truly refractory severe AD, is that escalation to systemic immunosuppressants like cyclosporine or the others under specialist care.

That lays it out clearly.

Now, all of this depends heavily on the patient actually doing it right.

Patient education must be huge.

Absolutely critical.

You could prescribe the perfect drug, but if they don't use it correctly or are afraid to use it, it won't work.

What are the non -negotiable teaching points?

Okay, three things.

One, reinforce avoidant strategies for CD and for everyone.

Emphasize gentle, fragrance -free cleansers, lukewarm baths, patting dry.

Basics first.

Two, teach them to apply topical meds, especially moisturizers and corticosteroids, to damp skin, like right after bathing.

This dramatically increases absorption and effectiveness, traps the moisture in.

Apply to damp skin.

Got it.

Three,

clarify the occlusion rules.

Explain how to use occlusion safely with TCS if recommended.

Plastic wrap, vinyl gloves, et cetera.

But drill home that occlusion is absolutely contraindicated with TCI's and address steroid fears head on.

Explain that low -potency TCS used correctly on the right areas is safe and necessary to control the inflammation.

Compliance depends on their understanding and trust.

Fantastic.

That really covers the practical application and the roadmap for managing these common but often challenging conditions.

We've hit the key differences, ICD, ACD, AD, and the roles of TCSs, TCI's, and when to escalate.

You know, what's really fascinating, stepping back, is that while we have these quite potent drugs, especially for AD,

the real challenge isn't just treating the flare,

it's achieving that long -term control.

The maintenance phase.

Exactly.

And often, the foundation of that successful long -term management isn't the fancy prescription drug but the consistent, daily, liberal use of those simple, inexpensive emollients to keep that skin barrier as healthy as possible.

That's what reduces flare frequency in the first place.

A brilliant reminder that sometimes the most basic intervention is the most impactful one.

Well, thank you so much for walking us through this complex topic today.

This has been incredibly insightful.

My pleasure.

Always good to break these down.

And thank you, our listeners, for joining us for this deep dive into dermatitis pharmacotherapeutics.

We hope this detailed exploration helps you in your practice and studies.