Atopic Dermatitis

Dr. Maged El-Batawi, MD.

Professor of Dermatology
Cairo University
2004
 What is atopic dermatitis?
A chronic relapsing, intensely pruritic dermatitis,
with a characteristic distribution pattern, in
an atopic individual.
 What is atopy?
An inherited tendency to develop a
hypersensitivity response (i.e. allergy) to
certain environmental stimuli (i.e. allergens),
in presence of a characteristic immunologic
profile.

A = no, topos = place

Atopos = ‘out of place’ or ‘strange’
 Atopic Disorders
Asthma
Allergic rhinitis (hay fever)
Atopic dermatitis
Allergic gastroenteritis
Allergic conjunctivitis
 Aetiology
Genetic predisposition, inherited
tendency
Immunologic profile
Environmental triggers (allergens)
Pathogenesis
Immunologic Profile in Atopy

Elevated total serum IgE (RIST)

Elevated serum allergen-specific IgE
(RAST)
Frequent positive prick tests to many
environmental allergens
Eiosinophilia; blood and tissue, MBP
Immunologic Profile in Atopy (cont…)
Biphasic Th1/Th2 reversal response:
– Th2 predominance in acute and subacute lesions
(early phases)
Elevated IL-4, IL-5 and IL-13
Relative anergy for eliciting allergic contact dermatitis ( ↓
Th1)
Increased susceptibility to viral and fungual infections ( ↓
Th1)
– Th1 responses predominate in chronic lesions (late
phase)
Elevated Interferon-γ
Reversal of DTH suppression
Environmental Trigger Factors
Inhalants Microbial agents
– Dust mites – Staph. aureus (superantigen)
– Animal furs, dander – Candida
– Pollens Climate
– Extremes of temperature
Ingestants
– Dryness
– Cow’s milk
Emotional stress
– Nuts; peanuts, …
– Eggs
Contactants
– Wool fibers
– Lipid solvents;
soaps, detergents
– Chlorine in
swimming pools
 Pathogenesis
High PDE activity → ↓ cAMP
→ hyperreleasibility of mast cells
FcεRI gene abnormality
– Carriage of FcεRI on:
Mast cells → immediate reaction
Langerhans cells → late phase reaction
Neuropeptide abnormality
– Abnormal vascular responses
– Intense pruritus
 Clinical Phases
Infantile phase
Childhood phase
Adolescent and adulthood phase
 Infantile phase

– 2 months to 2 years
– Face, extensors
– Acute oozing lesions
– Subacute crusted lesions
 Childhood phase

– 4 to 10 years
– Less acute lesions
– More dry subacute and lichenified lesions
– Flexors
 Adolescent and Adult phase

– Early teens to early twenties

– Dry lichenified hyperpigmented plaques
– Flexors
Infantile Eczema
Infantile Eczema
Infantile Eczema
Childhood phase
Childhood phase
Childhood phase
Lichenification
Lichenification
Adulthood AD
Adulthood AD
 Other Presentations of AD
– Nummular dermatitis
– Eyelid dermatitis
– Ear dermatitis; post-auricular fissures
– Cheilitis
– Nipple dermatitis
– Facial dermatitis
– Hand dermatitis
– Juvenile plantar dermatosis
Nummular dermatitis
Nummular dermatitis
Eyelid dermatitis
Ear lobe dermatitis
Simple Cheilitis
Angular cheilitis
Nipple dermatitis
Facial dermatitis
Hand dermatitis
Juvenile plantar dermatosis
 Associated Features

Skin conditions
Atopic stigmata
Eye
 Associated Features (1)
Cutaneous
– Xerosis
– Ichthyosis
– Pityriasis alba
– Keratosis pilaris
– Reticulate pigmentation of the neck (dirty neck)
– Keratosis punctata palmaris et plantaris
– Chapping of the digits (pulpitis sicca)
– Periorbital milia
– White dermographism
– Cholinergic urticaria
– Infections; Staph. aureus, HSV (eczema herpeticum)
Pupitis sicca
Staph. Infected AD
Eczema Herpeticum
Eczema Herpeticum
Eczema Herpeticum
Eczema Herpeticum
 Associated features (2)
Atopic stigmata:
Low hairline
Perinasal pallor (headlight sign)
Darkening of orbital skin (allergic shiners)
Hertoghe’s sign (thinning of outer eyebrows)
Dennie-Morgan fold
Anterior Neck fold
Hyperlinearity of the palms
Palmar hyperlinearity
Hertoghe’s sign
Denne-Morgan lines
 Associated Features (3)
Eye complications
– Cataract
– Keratoconus
– Atopic keratoconjunctivitis
 Diagnosis
Clinical criteria
– Major; Pruritus, Dermatitis, Atopy history
– Minor
Hypersensitivity to environmental factors…
Dry skin
Dermatitis in specific areas…
Associated
– Dermatologic conditions…
– Stigmata
– Eye conditions
IgE; (RIST, RAST)
 Investigations
– Skin prick test
– Total IgE (RIST)
– Specific IgE (RAST)
– Eosinophilia; blood, lesions
– Th2 cytokine profile; IL-4, IL-5, IL-13
– Reduced Th1 response; interferon-γ, DTH to
contact allergens
Skin Prick Test
 Treatment
General
– Avoid any possible environmental trigger factors:
cow’s milk, nuts, eggs, …
extremes of temperature and humidity, hot water showers
over bathing, swimming pools, harsh soaps and detergents
wools, non-absorbent or tight clothes
emotional stress, anxiety
– Wear absorbent comfortable clothes (cotton)
– Avoid dryness of the skin, use emollients
– Elimination diets (doubtful benefit)
– Breast feeding
 Treatment
Topical
– Wet compresses for oozing lesions:
Aluminum acetate 5% (Burow’s solution) 20-30 minutes,
4-6 times daily
– Topical corticosteroids (problems!)
– Hydrating agents for dry skin:
10% urea in hydrophilic cream
Eucerin cream
– Tar preparations
– Macrolide immunomodulators:
Tacrolimus 0.3% ointment
Ascomycin macrolactam derivatives (Pimecrolimus 1%)
 Treatment
Systemic
– Antihistamines
Sedating; hydroxyzine, doxepin, …
– Antistaphylococcal antibiotics
Penicillins, cephalosporins, erythromycin, …
– Systemic corticosteroids
Side effects!
Only for acute flare-ups
– Phototherapy; PUVA, UVB
– Cyclosporine
Side effects!
Expensive
– Interferon-γ; Th1 promoter
– Papaverine; PDE inhibitor
– Evening Primrose oil; γ-linolenic acid, PG modulator