PEDBASE.org - The Pediatric Database - Detailed information of ATOPIC DERMATITIS (ECZEMA)

ATOPIC DERMATITIS (ECZEMA)

DEFINITION:

An inflammatory disorder of the skin initiated by an IgE-mediated hypersensitivity.

EPIDEMIOLOGY:

incidence: 2-5% of children
age of onset:
- 80% of patients present by 1 year of age (rare before 2 months)
- 90% " 5 "
risk factors:
- 67% have a positive family history of atopy (asthma, hayfever, urticaria)
associations:
- an allergic triad
  - 50-80% of patients with atopic dermatitis will go on to develop asthma and/or allergic rhinitis, i.e., atopic dermatitis may be the forerunner for the development of other allergic diseases

PATHOGENESIS:

1. Allergy

1. Background

allergy is the manifestation of a hypersensitive reaction to the presentation of an allergen due to the propensity of the affected individual to develop a sustained IgE response following antigenic stimulation
the distinguishing feature of the allergic individual is the propensity to develop a sustained IgE response - there are several types of allergies based upon where the hypersensitive reaction occurs:

Surface-Allergy

Nasal Mucosa-Allergic Rhinitis
Skin-Hives (Urticaria), Atopic Dermatitis
Respiratory Tract-Allergic Asthma
Systemic-Anaphylaxis

2. Allergens

allergens are compounds capable of inducing human IgE antibody formation ("sensitization")

3. IgE

IgE is a Homocytotropic Antibody: an antibody capable of interacting with target cells such that these cells release mediators on contact with specific antigens
the IgE receptor consists of an externally located alpha chain that binds the IgE and is noncovalently associated with a beta chain and two gamma chains
there are two categories of IgE receptors dependent upon the type of cells targetted and the type of mediators re-leased from these cells:

1. Type 1

target cells - mast cells, basophils
affinity - high affinity for IgE
mediators - histamine, ECF-A, leukotrienes, bradykinins, prostaglandins, PAF, anaphylatoxins

2. Type 2

target cells - lymphocytes, platelets, eosino-phils, monocytes-macrophages
affinity - low affinity for IgE
mediators - chemotaxic factors, IgE binding factors (T cells), mitogens (B cells), inflammatory mediators

2. Atopic Dermatitis

1. Background

an allergy specific to the skin in susceptible individuals

2. Allergens

1. Internal

eczema triggered from ingested allergens

1. Foods

milk, eggs, fish, peanuts, wheat, soybean, corn

2. Beverages

3. Medications

2. External

eczema triggered by direct contact of the allergen with the skin (contact dermatitis)
location of rash may help to identify the offending allergen
may be worse in the winter (dryness, wool, tight-fit-ting clothes) or summer (moisture)

1. Cosmetics

applied lotions, ointments, soaps
cosmetics worn by caregiver

2. Fabrics

bedding, car seats, changing pads, clothing (on patient or caregiver)
detergents, soaps, softeners used to wash the above

3. Allergens

housedust mites, moulds, pet dander, pollens
cigarette smoke, wood smoke

3. IgE

within the dermis of the skin a Type 2 homocytotropic antibody response occurs
target cells
- lymphocytes, platelets, eosinophils, monocytes-macrophages, Langerhan cells
mediator responses
- intense pruritic, erythematous, maculopapular, warm, tender eruption
- begins at 4 hours post exposure with pruritis, peaks at 6-12 hours, and slowly resolves over
- 24-48 hours

CLINICAL FEATURES:

1. Background

Atopic Dermatitis typically occurs in 3 stages each with fairly distinctive features
the eczema may be called the "itch that rashes" because the first symptom is itchiness of the skin with the subsequent appearance of the rash which is made worse by further scratching ("itch-scratch-rash-itch-cycle")

2. Stage 1 - Initial Phase

1. Onset

birth to 2 years of age with a mean of 8 months

2. Rash

intense pruritis with scratching
diffuse erythematous flush
erythematous weeping patches (diaper area spared)
dry, red, scaly plaques

3. Distribution

cheek with spread to face, scalp, behind ears, neck
extensor surfaces of the extremities (arms, wrists, hands, legs) and the abdomen

4. Associated Symptoms

agitation - irritability
colic - urticaria

3. Stage 2 - Childhood Phase

1. Onset

2 to 12 years of age

2. Rash

intense pruritis with scratching
papules coalesce to form plaques
marked excoriation and lichenification (thickening)

3. Distribution

face (eyes, mouth), behind ears
flexural surfaces of the neck, antecubital and popliteal fossae, and wrists and ankles

4. Stage 3 - Adult Phase

1. Onset

greater than 12 years of age

2. Rash

diffuse, scaling, dried, lichenified, hyperpigmented

3. Distribution

whitish hue on forehead, upper eyelids (mask of atopic dermatitis)
flexural surfaces of the neck, antecubital and popliteal fossae
dorsal aspects of hands and feet

5. Signs

white dermographism
Morgan Fold - grooves below the lower eyelids
increased number of creases in the skin of the palm
sparcity of hair in the lateral portion of the eyebrow

6. Complications

1. Secondary Infections

1. Bacterial

streptococcal, staphylococcal

2. Viral

HSV (eczema herpeticum) - papilloma (warts)
molluscum contagiosum - vaccinia

2. Others

edema with lakes of serous fluid within the epidermis

INVESTIGATIONS:

1. Serum

elevated IgE (increased 5-10x over normal in 80% of patients)
eosinophilia

2. Allergy Tests

In Vivo - skin tests - immediate, delayed, patch skin test
In Vitro - Immunoassays - RAST, MAST, ELISA

MANAGEMENT:

1. Supportive

recognize that eczema is a chronic condition with periods of remission
during times of relapse may need reassurance and morale boosting
eczema tends to improve with age - see prognosis below
management is based on:
- avoidance
- reduce or eliminate itch
- medications

2. Avoidance

1. Internal Allergens

1. Foods

1. Elimination Diet

if patient is breastfeeding, try eliminating certain foods from the mother's diet
eliminate foods that the patient is eating and always one at a time
eliminate the suspected food for 4-7 days and observe for clearing of the skin
start with the most common eczema-causing foods
if difficult to identify triggering food, keep a diary and begin eliminating foods taken more than three times in one week
a food which does cause eczema, should be kept out of the diet for 4-6 months then reintroduced to see if the eczema returns

2. Medications

watch for reaction to anesthetics, antibiotics, anti-depressants, antiseptics, aspirin, birth control pill, laxatives, nose drops, tranquillizers, sleeping pills, vitamins

2. External Allergens

1. Cosmetics

change shampoo, conditioner, tint, dye, mousse, perm, nail polish, creams, makeup, deodorant, hair products, or aerosol products

2. Fabrics

change clothing, bedding, towels, laundry detergent, fabric softener, bleach
avoid strong irritant substances (soaps, detergents, bleach, fabric softeners)
avoid wool with cotten the least irritating
look for changes in cleansing agents ("new", "im-proved") or changes in water (soft vs hard, recent travel)
may wash clothes in a mild laundry soap (Ivory Snow) and double rinsing may remove residual soap - prewash all new clothing and bed linens

3. Others

avoid strong topical sensitizers (neomycin, anti-histamines, suphonamides)
avoid sudden changes or extremes of temperature and humidity (hot baths, saunas)
avoid sudden increase in physical activity or exercise
avoid sudden environmental changes at home/school/work
avoid irritants - cigarette smoke, wood smoke

3. Eliminate Itch

1. Moisturize Skin

1. Baths

aids in soothing & treating eczema by removing crust, softening skin, and decreasing secondary infections - bath 2-7 times per week using emollient unscented soap (White Dove of Petro-phyllic), mild cleansers (Cetaphil or Spectro Jel), or colloidal oatmeal but not regular soaps
prolonged cool baths of 30 minutes are most effective
may use certain shampoos if scalp is affected - coal-tar shampoo
may apply an unscented bath oil at the end of the bath and creams and lotions after bath (lanolin-based cream or an oil-in-water cream)
pat dry with towel
avoid hot baths, talc powder, bubble baths, bath salts

2. Skin Moisturizers

Vasoline, Glaxal base, and Nivea cream may decrease dry skin
apply when skin is wet (i.e., after a bath) to seal in the moisture
avoid moisturizers with urea and lactic acid

2. Local Dressings

Burrow's Solution (1:20) to affected areas

3. Antihistamines

Seldane (Terfenadine), Hismanal (Astemizole), Claritin (Loratodine), Reactine (Cetirizine)
may be helpful by sedating as well

4. Medications

1. Topical Steroids

1. 0.1% Hydrocortisone Acetate Cream

first line topical steroid therapy
apply to affected areas bid to qid
side effect includes thinning of skin in area of application

2. Mometasone Furoate (Elocom)

2nd line topical steroid therapy
apply to affected areas od

2. Antibiotics

for secondary bacterial infections - penicillins

5. Others

topical tar preparations
artificial UV light
antisuppressants
- Prednisone, Cyclophophamide, Azathioprine, Cyclosporin

6. Prognosis

1. Poor Prognosticators

generalized rash - other atopic manifestations
onset >2 years of age - prolonged extensor limb involve-
females ment

2. Long-Term

tends to improve with age
if onset in Stage 1, most are quiescent by 5 years of age, with 40% going into remission by 2-3 years of age - if onset in Stage 3, 50% of patient have lost eczema by age 21 and marked tendency towards lasting remission in the 4th and 5th decades

Pediatric Database - ATOPIC DERMATITIS (ECZEMA)

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