Atopic dermatitis is a chronic, non-contagious inflammatory skin condition caused by atopy—a genetic predisposition to produce excess IgE antibodies that triggers allergic responses. The condition follows a self-perpetuating vicious cycle where intense itching leads to scratching, causing skin barrier breakdown that allows allergens to enter and trigger further inflammation. Management follows a step-up approach: emollients as baseline, low-potency topical corticosteroids for mild cases, topical calcineurin inhibitors (TCIs) for moderate disease to avoid steroid atrophy, and systemic treatments or biologics like dupilumab for severe cases. A critical red flag is when an adult presents with a new chronic rash without childhood eczema history, as this could indicate cutaneous T-cell lymphoma (mycosis fungoides), which must be ruled out before prescribing steroids.
Webinar 245 - Atopic Dermatitis, by Dr C H AsraniAñadido:
[music] [music] >> Good evening, friends.
So, today let's talk on a very common condition atopic dermatitis.
Why we should learn to treat it?
Number one, it's a virtually lifelong condition.
And the treatment is very simple.
It's just a diagnosis and we have to learn talking to patients well.
So, what is the basis of atopic dermatitis? It's a mechanism called atopy.
What is atopy? Atopy is a genetic predisposition to produce excess IgE.
We all know IgE is an antibody in the body that the body produces in response to insult to skin.
In these patients, there is a genetic tendency to produce a lot of IgE in response to common allergens which other people may not respond.
This causes a group of allergic conditions like asthma, eczema, and allergic rhinitis.
And collectively this is called allergic march. We will see what is allergic march.
Because a patient having any one of these is likely to have the other two also subsequently.
It affects approximately 80% patients, not of common population, but those with a family history of allergic disease.
Management of symptom is very easy via lifestyle management and medications, largely topical.
Atopic dermatitis, as the name suggests, inflammation of the skin due to the atopy or atopic tendency in the patient.
It's a chronic, non-contagious condition.
Remember, patients are little panicky. Doctor, will he or she spread to others? No, it is not contagious.
Causing itchy, inflamed, and dry skin.
There is itch. There is inflammation.
And the itch starts from dry skin.
Typically starts in childhood, but can affect all ages.
Going ahead, we'll see if it occurs first time in 50 plus, then it could be something else.
It involves periodic flare-ups. You may treat a flare-up, which may get controlled, and after few months or years, patient may get another flare-up.
Driven by genetics.
How the immune system responses to surrounding allergens and environmental triggers.
If the patient who's taking 2 L of water suddenly is exposed to 45° plus temperature and does not increase the water intake or reduces the water intake, the skin will turn dry, and there may be a flare-up.
It's not just dry skin, but it's a much deeper disease with genetic predisposition.
I mentioned atopic or allergic march.
It describes the typical sequential progression. It's a sequential progression.
It always follows a sequence of allergic problems as we mentioned.
Eczema, allergic rhinitis, and asthma.
Starts with atopic dermatitis in infancy.
An infant also can get atopic dermatitis, which may be initially called as milk eczema.
Then there are food allergies followed by asthma and allergic rhinitis.
Please remember one thing.
Asthma and allergic rhinitis are one and the same disease with different spectrum.
ARI A guidelines, asthma, allergic rhinitis, and its impact on asthma.
These are the international guidelines.
If you search them on the internet, you will get to know that both are related.
If a patient of allergic rhinitis is not taking regular treatment, you can warn them that this may go on to become asthma.
This progression represents what is known as allergic march through different conditions, skin to gut, that is food allergies and lungs due to asthma.
Due to shared genetic and immune pathway.
Immunity is affecting the whole body and person genetically has a predisposition to get allergic conditions.
Now there is a hypothesis.
There is a protein called filaggrin.
Filaggrin protein is deficient in patients who have allergic tendencies.
Primarily caused by FLG gene mutation.
Causes a weak skin barrier. So these people who are having tendency for atopic dermatitis or allergic march, their skin is thin.
It causes dry, itchy skin.
Xerosis is the medical term for dry skin.
Higher risk of atopic dermatitis.
And when it gets worse, ichthyosis vulgaris.
Which is a common hereditary skin disorder.
Characterized by excessively dry, thick, and scaly skin.
You see something like this.
Think of ichthyosis vulgaris, which is again genetic.
This defect of filaggrin protein deficiency increases the entry of allergens through the skin barrier.
And once they enter the skin, they cause the immune response.
And cause eczema or other allergies.
Skin pH changes.
Moisture goes down. Skin becomes dry.
Leading to breaking of skin and inflammation.
And this filaggrin protein deficiency is associated with asthma and other allergic disorders like allergic rhinitis and eczema.
The vicious cycle.
Atopic dermatitis is a self-perpetuating chronic cycle of intense itching. Now, we know itching and scratching is a vicious cycle, but atopic dermatitis vicious cycle is something much more.
Itching leads to patient scratching because it is said that you can hide love, you can hide hatred, you can't hide itching.
Itching leads to scratching.
Scratching intensely because see, scratching is pleasurable. People use nails, people use combs, they break the skin.
Skin barrier breakdown.
That damaged skin allows various allergens from our environment to enter the skin and then trigger an immune response.
Cytokines, IL-31 or IL-33.
We do not remember this, but just remember itching, scratching, skin barrier breakdown, allergen entry, and inflammation.
>> [gasps] [cough] >> That cause more itching.
And with scratching, further damage, inflammation, and maybe secondary infection.
Look at this vicious cycle diagrammatically shown.
There is intense itching.
Leads to scratching.
Leads to skin damage, epidermis disruption.
This causes genetic due to genetic defect.
loss of function mutation of filaggrin, trans epidermal water loss because of skin dehydration, changes in pH and dehydration.
This leads to allergen going under the dermis, which is a protective barrier.
And this leads to inflammation, and inflammation leads to more itching.
This is the vicious cycle of atopic dermatitis.
Diagnostic pearls, primarily affects children in 35 to 60% of cases starting within first 1 year of life.
And 85% by 5 years. So, any late onset suspected atopic dermatitis is to be seen with a pinch of salt.
While many cases improve with age, like you know, we say people who get wheezing or asthma tendency in childhood, if you manage them well, and make sure it goes away by 10, then they may come out without asthma.
A significant number of elders, adults, and elderly individuals over 9% over 65 still have atopic dermatitis.
The severity and the body side changes happen over time.
In infants, it is more on the face, then it goes to the flexural surfaces in adults and grown-up children.
Infants, 0 to 2 years, frequently presents on the face, almost 95% I'll be showing you pictures.
Scalp and extensor surfaces like psoriasis, but psoriasis is different, atopic dermatitis is different.
2 to 11 year children shifts from extensor to flexural involvement elbow creases, knee creases neck and chronic eczematous lesions between 2 and 11 years.
Adolescent and adults about 12 years typically affects hands almost 75% flexural creases and neck or around the eyes.
Look at this.
This shows elbow crease.
This shows just above the wrist.
These three are children.
Infants and this shows behind the knees, the flexures crease of the knees.
What are red flags in atopic dermatitis?
When you should get worried?
When an adult presents with a new chronic rash for which there is no etiology especially without a history of childhood eczema it is crucial to consider it could be anything other than atopic dermatitis.
And please before you prescribe a steroid cream, think.
Because the commonest possibility is cutaneous T-cell lymphoma.
Particularly the subtype of mycosis fungoides.
It's a red flag differential diagnosis because it's a great imitator of eczema.
We don't want to miss a cutaneous T-cell lymphoma.
This is how this will appear. Now, just understand all of us will first pick up a pen and write a steroid cream for this.
But ask if he has never had in childhood and now it is chronic, he's come to you with a history of over 6 weeks or 3 months, then maybe refer This may be a Hodgkin's of the skin.
Mycosis fungoides most common form of cutaneous T-cell lymphoma rare type of blood cancer where T lymphocytes turn malignant and affect the skin.
Typically causes itches, extreme itching, persistent rash, big patches or plaques like psoriasis.
And maybe tumors often misdiagnosed as eczema or psoriasis.
While chronic, many patients even with cutaneous T-cell lymphoma have a normal life expectancy with early stage skin-directed treatment. There are treatments available now if diagnosed early.
Sorry, repeat slide.
It's a slow-growing non-Hodgkin lymphoma.
Primarily originates in skin-homing T-cells. The T-cells T lymphocytes we know are a major part of our immune system.
There are certain T-cells which focus on skin and that is where they start.
Red, scaly, itchy patches often on the trunk, buttocks, or wrists.
May progress to plaques or tumors, hence confused with psoriasis.
Often advances through three stages, patch initially, plaque later, and tumor subsequently.
More common in men than women, and typically affects people over 20.
This is first is a patch phase.
Second is a plaque phase.
And third is a tumor phase.
Patchy dry skin.
Irregularly shaped plaques.
And raised tumors.
These changes are expected with mycosis fungoides.
Step-up approaches of management.
Baseline is emollients.
Never give steroids directly.
Ointments, creams, solutions, because the affected part should be soaked and sealed to prevent the entry of allergens through broken skin.
If it is mild, then you give low potency topical corticosteroids, hydrocortisone, 1 or 2.5% for face and folds.
On face, do not apply very strong steroids because it can cause hypopigmentation.
Moderate disease, mild or high topical corticosteroid or TCI, that is calcineurin inhibitors.
Pimecrolimus or tacrolimus ointment to avoid steroid atrophy.
Long-term steroid causes topical steroid causes the skin atrophy. To avoid that, this can be used, but I would recommend if you're not used to using these, better to talk to a dermatologist first.
When it is severe, there are systemic treatments or nowadays there advantage of biologic for everything, especially autoimmune problems.
When to refer for dupilumab or JAK inhibitors?
TCIs, topical calcineurin inhibitors, the tacrolimus.
They work by inhibiting the synthesis of pro-inflammatory cytokines, what we discussed IL-31 and IL-33, which reduces inflammation and relieves itching.
Available as tacrolimus 0.03 or 1% ointment.
Generally used for moderate to severe atopic dermatitis or pimecrolimus 1 1% used to mild to moderate atopic dermatitis.
Commonly used in India is tacrolimus.
Ideal for face, neck, and skin folds because it will avoid steroid atrophy as well as hyperpigmentation.
Used twice weekly for maintenance to prevent relapses.
Relapses means flare-ups.
The most common adverse effects of using TCIs are burning or stinging sensation where you apply.
Usually resolves after a few days of therapy.
FDA has given a black box warning in US that there's a theoretical malignant risk, but various long-term studies have not established a direct cause-effect relationship of TCIs and malignancy.
Not to be used under 2 years of age.
Topical corticosteroids potency to location and severity.
Low potency as we mentioned hydrocortisone.
Use on face, eyelids, groin, and axilla.
Areas which have thin skin.
Medium potency triamcinolone acetonide 0.1% or mometasone 0.1%.
Use on trunk and limbs in adults.
You may use short burst for children.
High or ultra-high potency clobetasol propionate 0.05% or betamethasone dipropionate.
Use on palms, soles, and thick lichenified plaques.
Never use clobetasol or Betnovate on the face.
Rule of two for dosing.
Twice daily is standard.
Evidence suggests that more frequent application does not increase efficacy.
So, people tell patients, "Don't apply too often. Just because it itches, don't apply steroid cream."
But, it increases side effect.
Then, you taper down to after 2 weeks and flare control, step down to either lower potency or once a day.
Or a steroid-free agent like TCI.
When to refer?
Failure of standard therapy after 2 to 4 weeks of appropriate strength topical steroid.
Please confirm that patient has been applying that.
Frequent flaring, patient is getting Frequent flare-ups despite remission.
Disease recurs immediately upon stopping then you should refer.
Significant quality of life impact, patient's life is impacted.
Chronic sleep loss because of itching, discomfort missing school or work or psychological impact.
Atypical presentation, if the diagnosis is in doubt as we discussed, maybe is it lymphoma?
Or it is contact dermatitis and not atopic dermatitis requires patch testing of whatever is suspicious to give contact dermatitis.
Complications, recurrent secondary infection or suspected eczema herpeticum.
Herpes, we know is a dreaded disease, should be diagnosed and treated as soon as possible.
At times in eczema, you may get herpetic involvement.
Severe, rapidly spreading infection of the skin caused by herpes simplex virus, HSV-1 or HSV-2 in patients who have pre-existing atopic dermatitis.
How does it differ? Normally, herpes infection affects one nerve, so it you always get it on one side of the body.
Never bilaterally but eczema herpeticum will occur bilaterally.
Characterized by clustered itchy, punched-out blisters or sores, often with fever and malaise, acting as a dermatological emergency.
This needs to be diagnosed and treated ASAP with acyclovir or similar.
Prompt antiviral treatment, acyclovir or famciclovir or whatever, essential to avoid complications like vision loss, bacterial infection or encephalitis.
This is how it appears.
So, this is don't get misled that because it is bilateral, it can't be herpes.
How much ointment to apply?
There is a fingerprint unit, a practical way to tell patients how much cream to use.
One FTU from tip of the index finger to the first interphalangeal joint, that much cream will be enough for surface area of two palms.
There is a steroid phobia. People on their own may use steroid creams, but they will ask you, "Is it steroid? Is it side effect?"
Address this head-on. Tell them that without steroid, this has no treatment.
Explain that under-treatment leads to chronic inflammation, which is much difficult to treat than initial flare-up.
Bleach baths, mention dilute bleach baths as a valid evidence-based medical to reduce bacterial load in recurrent infected patients.
This is actually homemade bleach, which is put in huge tubs of water. I'm not giving details because in India getting a tub in the bathroom is a very rarity.
Treatment failure. If the treatment fails, the reason is not wrong drug. It is under medication.
Patients are often too scared to use steroids for a long time.
And many times we doctors are also scared to advise steroids for a long time.
We have to treat the flare very aggressively.
It's like, you know, you put the fire out then make sure it doesn't ignite again.
Then focus on the skin barrier to keep it out.
After steroids don't work and when you refer, the dermatologist may suggest ultraviolet therapy or biologics, dupilumab. It's a once in 2 weeks injection that has been a game-changer in atopic dermatitis.
And there's another JAK inhibitor, upadacitinib.
This is an oral medication to control intense itching, but leave this to the dermatologist.
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Have a nice evening.
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