Atopic Dermatitis

DERMATOLOGY
ATOPIC DERMATITIS
PRESENTED BY ABDALLH FAIZ GHULAM
OBJECTIVES
1)To know the epidemiology and pathogenesis of the disease
2)To define the course and clinical features of the disease
3)To know the diagnosis and management of the disease
EPIDEMIOLOGY
Age of Onset → First 2 months of life and by the first years in 60% of
patients(so usually start in early infancy). 30% are seen for the first time
by age 5, and only 10% develop AD between 6 and 20 years of age .
Part of atopic triad: AD (often first manifestation), allergic rhinitis, and
asthma
Gender Slightly more common in males than females.
Eliciting Factors Inhalants Specific aeroal- lergens, especially dust
mites and pollens, have been shown to cause exacerbations of AD.
Infections S. aureus is almost always present in severe cases ,Exotoxins of
Staphylococcus aureus may act as superantigens and stimulate activation
of T cells and macrophages.
Foods Subset of infants and children have flares of AD with eggs, milk,
peanuts, soybeans, fish, and wheat.
Autoallergens Sera of patients with AD contain IgE antibodies directed at
human proteins.
1
PATHOGENESIS
- Complex interaction of epidermal barrier dysfunction, immune

dysregulation, and environment (Barrier dysfunction causes
transepidermal water
loss and xerosis, allowing penetration of allergens)
- Genetic factors are important
■ Twin studies (monozygotic > dizygotic concordance)
and family history (high probability that one or both parents are atopic)
■ Genes encoding epidermal proteins (e.g., FLG and SPINK)
CLINICAL FEATURES
An acute, subacute, or chronic relapsing skin disorder

Diagnostic criteria →
Essential: pruritus
Plus ≥ three of the following:
• ○ History of xerosis
• ○ Personal history of allergic rhinitis or asthma
• ○ Onset <2 yo
• ○ History of skin crease involvement (antecubital,
popliteal, ankle, neck, and periorbital)

• ○ Visible flexural dermatitis
Acute form: erythema, edema, vesicles, oozing, and crusting

Subacute and chronic forms: lichenification, papules, nodules, and
excoriations
Distribution Predilection for the flexures, front and sides of the neck,
eyelids, forehead, face, wrists, and dorsa of the feet and hands .
Generalized in severe disease (see figure 1and figure 4)
Pruritus
■ Worse in evening
■ Triggers: wool clothing, sweat, and stress
2
Figure (1)
Special Features Related to Age
Infantile AD The lesions present as red skin, tiny vesicles on “puffy”
surface. Scaling, exudation with wet crusts and cracks (fissures). Skin
lesions seem to be a reaction to itching and rubbing. Favors face, scalp
and extensor surfaces.(see figure 2)
Childhood-type AD The lesions are papular, lichenified plaques,

erosions, crusts, especially on the antecubital and popliteal fossae(favors
Flexures), the neck and face (see figure 3); may be generalized.
■ Children have ↑incidence of: pityriasis alba , lichen spinulosis,
dyshidrotic eczema, and juvenile plantar dermatosis.
Adult-type AD There is a similar distribution, mostly flexural but also face

and neck(see figure 5), with lichenification and exoriations being the
most conspicuous symptoms . May be generalized.
Special Forms of AD
Hand Dermatitis Aggravated by wetting and washing with detergents,
harsh soaps, and disinfectants; leads to ICD in the atopic. Clinically
indistinguishable from “normal” ICD (see figure 6)
3
Figure (2) Picture of AD infantile type
Figure (3) Picture of AD childhood type
COMPLICATIONS
▪ Infectious Secondary infection with S. aureus and herpes simplex

virus (eczema herpeticum)
▪ Ocular Rarely keratoconus, cataracts and keratoconjunctivitis with

secondary herpetic infection and corneal ulcers.
4
DIAGNOSIS
History in infancy, clinical findings (typical distribution sites,

morphology of lesions, white dermatographism)
LABORATORY EXAMINATIONS
-Bacterial Culture almost 90% of patients with severe AD are

secondarily colonized/infected.
-Viral Culture Rule out herpes simplex virus (HSV) infection in crusted
lesions (eczema herpeticum)
-Blood Studies Increased IgE in serum, eosinophilia.
-Dermatopathology Various degrees of acan- thosis with rare
intraepidermal intercellular edema (spongiosis).
-Consider testing for food hypersensitivity (eggs, milk, peanuts, soy,
and wheat) in children with severe/ refractory AD and reliable history of
immediate reaction, or worsening dermatitis after ingestion of specific
food. (10-15% of severe AD cases have coexistent food allergies)
COURSE AND PROGNOSIS
Untreated involved sites persist for months or years. Spontaneous, more

or less complete remission during childhood occurs in >40% with
occasional, more severe recurrences during adolescence, Generally AD
tends to clear in most children by puberty .In many patients, the disease
persists for 15–20 years, but is less severe. From 30 to 50% of patients
develop asthma and/or hay fever. If disease persists beyond childhood it
tends to be chronic, Adult onset AD often runs a severe course, S. aureus
infection leads to extensive erosions and crusting, and herpes simplex
infection to eczema herpeticum, which may be life-threatening.
5
Figure (4) Predilection sites of atopic dermatitis.
MANAGEMENT
▪ Education of the patient to avoid rubbing and scratching is most

important. Topical antipruritic (menthol/camphor) lotions are helpful
in controlling the pruritus.
▪ Avoid irritants: overheating, wool, sweating, saliva, harsh soaps,
fabric softeners, bubble baths, and smoke.
▪ Treatment ladder that ranges from topical treatments (steroids, and
calcineurin inhibitors) to light therapy (nbUVB > bbUVB, UVA1, and
PUVA) to systemic meds (systemic corticosteroids, cyclosporine,
azathioprine, MMF, and MTX) depending on severity . (note that
systemic corticosteroid should be avoided except in rare instances in
adults for only short courses (rescue treatment) in severe cases).
▪ Topical corticosteroids are mainstay
▪ Sedative antihistamines as adjunctive treatment for itch
▪ Treat secondary infections
▪ Primary prevention via breastfeeding or formulas w/
hydrolyzed milk products for the first 4 to 6 months of life is protective
in high risk AD patients .
6
▪ If true IgE-mediated allergy → practice avoidance or undergo
allergen-specific immunotherapy through allergist
Figure (5) Lichenification in adult type AD
Figure (6) Hand AD
Sources: -FITZPATRICK’S COLOR ATLAS AND SYNOPSIS OF CLINICAL DERMATOLOGY

-Review of Dermatology
-https://emedicine.medscape.com/article/1049085-overview

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DERMATOLOGY

- Complex interaction of epidermal barrier dysfunction, immune

An acute, subacute, or chronic relapsing skin disorder

• ○ Personal history of allergic rhinitis or asthma

• ○ History of skin crease involvement (antecubital,

popliteal, ankle, neck, and periorbital)

Acute form: erythema, edema, vesicles, oozing, and crusting

Childhood-type AD The lesions are papular, lichenified plaques,

Adult-type AD There is a similar distribution, mostly flexural but also face

Figure (3) Picture of AD childhood type

▪ Infectious Secondary infection with S. aureus and herpes simplex

▪ Ocular Rarely keratoconus, cataracts and keratoconjunctivitis with

History in infancy, clinical findings (typical distribution sites,

-Bacterial Culture almost 90% of patients with severe AD are

COURSE AND PROGNOSIS

Untreated involved sites persist for months or years. Spontaneous, more

▪ Education of the patient to avoid rubbing and scratching is most

Figure (5) Lichenification in adult type AD

Figure (6) Hand AD

Sources: -FITZPATRICK’S COLOR ATLAS AND SYNOPSIS OF CLINICAL DERMATOLOGY

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