Chairiyah Tanjung

Department of Dermato-venereology
Medical Faculty, North Sumatera University

Atopic dermatitis (AD) = Atopic eczema

o A chronically relapsing skin disease
o Occurs most commonly during early infancy and
childhood
o Frequently associate with elevated serum IgE
levels
o A personal/family history of atopy(+)

epidemiology
Prevalence 3x than 1960s
Industrialized countries > agricultural countries
Female : male = 1,3:1
AD, associated with :

- small family size

- increased income and education
- migration rural urban
- use of antibiotic

Etiology and Pathogenesis

Hereditary
(genetic)

Food
aeroalerge
n

Allergy (hypersensitivity)

Cellular
Immunity
defect

Dermatitis Atopic
Irritant
Infectio
n
Climate

Xerosis
Decrease
Skin barier
Psychological effect

Genetic Factor
Strong maternal influence
Chromosome 5q31-33, contains a clustered family

of functionally related cytokine genes :

- IL-3, IL-4, IL-5, IL-13
expressed
- GM-CSF
by Th2 cell
- Differences in transciptional activity of the IL-4
gene influence AD predisposition
- A significant association between a specific
polymorphism in the mast cell chymase gene and
AD

Immune Response in AD Skin

Key cell types in AD skin :
Langerhans cells
Lymphocyte cells
Eosinophils
Mast cells

Immunopatogenesis of DA

Systemic Immune Abnormalities

in
AD

Increased synthesis of IgE

Increased specific IgE to multiple allergens,
including foods, aeroallergens, microorganism,
bacterial toxins, autoallergens
Increased expression of of CD23 (affinity IgE
receptor) on B cells and monocytes
Increased basophil histamine release

Systemic Immune Abnormalities

in
AD

Impaired delayed-type hypersensitivity response

Eosinophilia
Increased secretion of IL-4, IL-5 dan IL-13 by Th2
cells
Decreased secretion of IFN- by Th1 cells
Increased soluble IL-2 receptor levels
Elevated levels of monocyte CAMPphosphodiesterase with increased IL-10 and
prostaglandin E2

Skin barrier
Dermatitis atopic skin
Epidermal lipid
Epidermal lipid
TEWL
TEWL
Skin capacitance
Skin capacitance

Soap &
detergen

Decrease
Decreaseskin
skinbarrier
barrierfunction
function

Allergen
Allergenabsorption
absorption
Microbial
Microbialcolonization
colonization
Treshold
Tresholdof
ofpruritus
pruritus

Environment factor
Food infant and children :milk and eggs

adult :seafood and nuts

Aeroallergens : dust mites,animal
danders,molds,pollens.
Temperature &humidity
Intens perspiration
Emotional stressor

CLINICAL FINDINGS
infantile phase (0-2 years)

Childhood phase(2-12
years)

Adolescent phase(12-18
years)

diagnosis
Diagnostic criteria of AD : Some
The UK working partys :proposed alternative

system,the criteria of Hanifin &Rajka (1994)

Diagnose of AD:
-Three or more of the major criteria
-three or more of the minor criteria

Major criteria
Pruritus
Typical morphology &distribution :facial &

ekstensor
Involvement during infancy &early childhood
flexural
Flexural dermatitis in adult
Chronic or Chronically relapsing dermatitis
Personal or family histrory of atopy

Minor Criteria
Xerosis
Skin infection
Hand/foot dermatitis
Ichthyosis/palmar hyperlinearity/keratosis

piliaris
Pityriasis alba
Nipple eczema
White dermatografism&delayed blanched
response

Minor criteria
Cheilitis
Infra orbital fold
Anterior subcapsular catarracts
Orbirtal darkening
Facial pallor
Ichiness when sweating

Minor criteria
Perifollicular accentuation
Food hypersensitivity
Duration of AD influecenced by environment

and phychis factors

Immediate skin test reactivity
Elevated serum IgE
Early age of AD

Xerosis

Keratosis piliaris

Hiperlinear palmaris and

dennei morgan

White dermographism &

pitriasis alba

Skin infection

Differential diagnosis
1.
2.
3.
4.
5.
6.
7.
8.
9.

Seborrhoic dermatitis
Contact dermatitis
Numular dermatitis
Scabies
Ichthyosis
Psoriasis
Dermatitis herpetiformis
Sezary syndrome
Leterrer-Siwe disease

In infant
1. Wiskott-Aldrich syndrome
2. Hyper- Ig E syndrome

General skin care

measure
Education
Appropriate skin hydration & use of emolient

skin barier repair measure

Avoidance of irritans
Identification & treatment of complication
bacterial, viral of fungal infection
Treatment of psychosocial aspect of disease
Antipruritic intervention

Treatment
1. Topical therapy
2. Systemic therapy

Topical therapy
1. Cutaneus hydration
2. Topical glucocorticoid
3. Topical calcineurine inhibitor ( tacrolimus &

pimocrolimus)
4. Tar preparation
5. Topical anti histamin : not recommended
except : doxepine cream 5%

Systemic therapy
1. Systemic glucocorticoid
2. Anti histamin
3. Infection agent
4. Interferone
5. Cycloporine
6. Phototherapy (UVB, UVA+UVB,PUVA)

Prognosis
Many factor correlate with AD difficult

1.
2.
3.
4.
5.
6.

to predict prognosis
The predictive factors correlate with a
poor prognosis of AD :
Widespread AD in childhood
Associated allergenic rhinitis & asthma
Family history of AD in parents or sibling
Early age at onset of AD
Being an only children
Very high serum IgE levels

30-35% infatile AD asthma / hay fever

Often develop non specific irritant hand

dermatitis