ATOPIC DERMATITIS

HIS 2 / K-24

Allergy – Immunology Division

Departement of Child health
Faculty of Medicine
Sumatera Utara University/H Adam Malik Hospital
Medan
Mahasiswa mengerti tentang:
 Definisi
 Etiology
 Patofisiologi/patogenesis
 Gambaran klinis
 Diagnosis
 Tatalaksana
Introduction

 Atopic Dermatitis (AD)

Chronic relapsing inflammatory skin disease
characterized: - intense itching
- dry skin
- inflammation
- exudation
Introduction…
Sinonim: Eczema
Incidence and Prevalence
- 10% - 20% children
- Most of them before 5 yo
- 1 % -3% adult

 Significant impaction quality of life

- affecting sleep
- school performance
- social interactions
- self-esteem
Etiology of atopic dermatitis
 Genetics:
Family history of AD
Loss of function mutation in filaggrin
 Environment;
infection, hygiene, climate
 Food antigen
 Aeroalergen : House dust mite
 Pathogenesis of AD
A dysfunctional skin barrier can trigger allergic
sensitisation1,2
Environmental
modifiers
Defective (hygiene hypothesis and
skin geographical lifestyle)1
barrier2

Allergy
Genetic Atopic sensitisation1,2
predisposition1,3 dermatitis Systemic Th2
response1,2

Environmental
risk factors4

Diagram has been independently created by GSK

1. Dharmage SC et al. Allergy 2013;69:17–27; 2. Agarwal RA and Woodfolk JA Curr Allergy Asthma Rep. 2014;14:433;
3. Margolis DJ et al. J Allergy Clin Immunol. 2012;130(4): 912–917; 4. Kantor R and Silverberg J Exp rev Clin Immunol. 2017;13:http://dx.doi.org/10.1080/1744666X.2016.1212660;

6
 ……… Atopic Dermatitis

Genetic
Atopic dermatitis can occur in
predisposition1, three phases6
2

Filaggrin mutations are present

in around 48% of patients with
severe atopic dermatitis3 Atopic
dermatitis

Infantile Childhood Adult

(0 to 2 years) (2 years (puberty to
Environmental
to puberty) adulthood)
risk factors4

Clinical studies suggest that there is a high

prevalence of proven food allergies (30–40%) in
children with moderate to severe atopic
dermatitis5
1. Margolis DJ et al. J Allergy Clin Immunol. 2012;130(4): 912–917; 2. Böhme M et al. J Allergy Clin Immunol. 2012;129:1153–5;
3. Mohiuddin MS et al. J Allergy Clin Immunol: In Practice 2013;1:534-6; 4. Kantor R and Silverberg J Exp rev Clin Immunol. 2017;13:http://dx.doi.org/10.1080/1744666X.2016.1212660; 5. Gray CL and Levin ME
Current Allergy & Clinical Immunology 2014;27:82–6; 6. Salazar-Espinosa JF Int J Med Students 2014; 2:119–124.
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^NMF: Natural Moisturizing Factor,
 Clinical manifestation

 Usually begins in infancy

 49-75%: present by 6months of age (usually within the
2-3 first months of life
 Acute lession : erythema and scalling
Tiny erythematous vesicle may rupture
and weeping,oozing
 Sub acute lession: mild scalling and lichenification,
minimal skin erythema
 Chronic lession : thickened, elevated plaques of
scalling skin, hyperpigmentation or
hypopigmentation
Clinical Manifestations…
16
DIAGNOSTIC CRITERIA OF ATOPIC DERMATITIS

Hanifin & Rajka, 1980

Major Diagnostic Criteria : ≥ 3

 Pruritus
 Typical morphology and distribution
 flexural lichenification in adult
 facial and extensor involvement in infant and children
 Personal and family history of atopy
 Chronic and chronically relapsing course

AND 20
DIAGNOSTIC CRITERIA OF AD
(Hanifin & Rajka, 1980)

Minor Diagnostic Criteria : ≥ 3

 Xerosis
 Ichthyosis/palmar hyperlinearity/keratosis pilaris
 Immediate (type I) skin test reactivity
 Elevated serum IgE
 Early age of onset dermatitis
 Tendency toward cutaneous infections
 Tendency toward nonspecific hand & foot dermatitis
21
DIAGNOSTIC CRITERIA OF AD
(Hanifin & Rajka, 1980)

Minor diagnostic criteria…

Nipple eczema
Cheilitis
Recurrent conjunctivitis
Denni-Morgan infraorbital fold
Keratoconus
Anterior subcapsular cataract
Orbital darkening
Facial pallor/facial erythema
22
 DIAGNOSTIC CRITERIA OF AD
(Hanifin & Rajka, 1980)

 Minor diagnostic criteria:….

 Pityriasis alba
 Sweating itch
 Intolerance to wool and lipid solventPerifollicular
accentuation
 Food hypersensitivity
 Course influenced by environmental/emotional factors
 White dermagraphism/delayed blanchKeratoconus

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History taking :Should take detailed clinical and drug
histories that include questions about:

 time of onset, pattern and severity of the atopic

eczema
 response to previous and current treatments
 possible trigger factors (irritant and allergic)
 the impact of the atopic eczema on children and
their parents or carers
 dietary history including any dietary manipulation
growth and development
 personal and family history of atopic diseases.
Laboratory studies

 Complete blood count

 Imunoglobulin E serum level
 Skin Prick test, Pacth test,
 Uji provokasi
Differential Diagnosis
 Scabies
 Seborrhoeic Dermatitis
 Contac dermatitis
 Photosensitivity dermatitis
 Immune deficiency dideases
 Infection
Complication
 Skin infection:
- Staphylococcus aureus
 Funggal skin infection:
-Malassezia furfur
-wart
-Moloscum conntagiosum
 Viral infection
-Herpes
Management
 Atopic dermatitis
 Managing atopic eczema:

What improvements are needed?

 Ideally, a cure
 The next best alternative is a treatment that
is safe and effective and adds a significant
dimension to existing therapies
Simplified,stepwise algorithm for the treatment AD
 Five Pillars of Atopic Dermatitis
(Asia- Pasific 2012)
a. Education and empowerment of patients and
caregiver(s)
b. Avoidance and modification of environmental
trigger factors
c. Rebuilding and maintenance of optimal
barrier function
d. Clearance of inflammatory skin disorders
e. Control and elimination of itch- cratch-cycle
Rubel D, Thirumoorthy T, Soebaryo RW et al. Consensus guidelines for the management of
atopic dermatitis : An Asia-Pasific perspective . J of Dermatol 2013; 40:160-171.
 Education
 Educate patients and family members about:

The chronic nature of atopic dermatitis

Exacerbating factors
Apropiate treatment options
Patient support organization
 Potential AD triggers
Food allergen

Cows milk, eggs, peanut, tree nut, soy, wheat, fish shellfish, etc
Food processed of any above

Direct contact
- Toiletries containing alcohol ,astringents or fragrances
- Harsh detergents/soaps
- Abrasiveclothing(wool or synthetics)

Physiologic^ /emotional stressor *

^Infections(especially from S.aureus, viruses, fungi,etc)
Overheating/sweating
*Psychological stress
 Skin care
Regular Bath :
Once or twice daily
Warm water
Short time (10-15 minute)
Gentle cleanser : free preservative and parfume

Emolient and moisturizer;

Backbone of AD therapy
 Regular emollient therapy is an important pillar in the
management strategy of AD
 Applied 2 to 3 times daily or as frequently
 Emollients should be used during active disease flares
in conjunction with topical anti-inflammatory agents,
and also as maintenance therapy.
 Apply before and after swimming or bathing while the
skin is still moist (within 5 min).
 Patients should be advised to: cleanse with a non-
irritant cleanser, moisturize all over and medicate active
areas of eczema.
Characteristics of the main emollients
Product Action
1st generation Vaseline, paraffin oil, fatty
emolients alcohols, hydrophilic polymers
(collagen, ac. hyaluronic acid, Hygroscopic and occlusive
chitosan, polysaccharides gelling)

Glycerol, sorbitol, substitutes

2nd-generation NMF (Natural Moisturizing
emollients Factor) derivatives of pyrrolidone Restoring hydration and
carboxylic acid, urea (5–10 %), barrier function
lactic acid, ammonium lactate

Physiological lipids: ceramides,

3rd-generation cholesterol, polyunsaturated fatty
emollients acids Barrier repair therapy
Topical corticosteroid (TCS)

 TCS the first choice drug for AD

 Anti inflammatory effect
 Dose standardized:
Finger tip unit (FTU)

Choice of TCS depends on the strength and

vehicle preparation
  Choice of TCS formulation according to
the phase and location of AD

Gali et al, Italian journal of Pediatrics.2016:42;26

Topical corticosteroid…

 TCS are effective and safe when used

appropriately and under adequate supervision.
 During maintenance treatment, TCS can be
applied to “hot spots” twice per week (e.g. weekend
therapy).
 TCS should be used until skin flares are under
control (i.e. up to 14 days or longer).
 TCS can be applied to areas of broken skin
 For the face and flexura, flare be control with moderate
potency TCS for 5-7 days----- switch
to mild potency TCS and/or topical calcineurin
inhibitors (TCI).
 TCS are not contraindicated in the presence of infection
but the infection should be treated.
 The choice of potency, frequency and duration of use of
TCS should be based on clinical judgment according to the
location, severity and chronicity of the eczema, and the age
of the patient.
 Commonly used topical corticosteroid

Rubel D et al journal of Dermatology; 40:161-71

Topical calcineurin inhibitor (TCI)
 Pimecrolimus : 1% cream
 Tacrolimus : 0,03% ointment

 Non steroidal topical immunomodulator

Decreasing the inflammatory cytokine transcription in activated
Tcells

 TCI : considered as second-line therapy for the shortterm and

intermittent treatment of AD in cases where TCS therapy is
contraindicated.
 Do not use TCI under occlusion as this may enhance percutaneous
absorption and increase risk of immunosuppression.

 TCI may be used in the long-term treatment of patients with chronic

AD where adverse effects from TCS may develop from their chronic
use.
Wet Dressing
 Wet dressings are an indispensable component of
management of severe flares of eczema (despite
contradictory results in the published work).
 Whole-body wet dressings with TCS should be
used until clinical improvement is noted, although
this can be difficult to apply, particularly in hot
weather. Follow up is advised.
 Close monitoring on a case-by-case basis for
infection is critical while using wet dressings.
 Wet dressings should be at least used with caution
in the presence of infection.
 Anti histamin
 Reduce pruritus due to histamine
mediator
 Recent research results suggest that
nonsedative antihistamines have varying
effectiveness to treat pruritus in AD.
 Sedating antihistamin may be used short
term, under supervision.
 Nonsedative antihistamines are useful when
administered when other atopy conditions,
such as allergic rhinitis or bronchial
asthma

D Rubel et al. j of Dermatol 2013;40:160

Systemic teraphy

Systemic corticosteroid

 Rarely used in chronic AD.

 Dramatic results followed with severe rebound.
 Good for acute exacerbation with tapering off
dose.
 Follow with topical corticosteroid and emollient.
 If no response, switch to other alternative drugs.
Antimicrobials therapy
 Secondary infection should be suspected in patients
with moderate to severe eczema who have weeping
dermatitis, folliculitis and overt clinical signs of
infection, or who are not responding to first-line
topical therapy.
 Topical antibiotic therapy may be appropriate for
localized areas of infection.
 Systemic antibiotics that are active against
staphylococcus for 1 week should be used according
to clinical response.
Akdis CA, dkk. J Allergy Clin Immunol. 2006;118:152-69.
Immunomodulator systemic therapy

 Phototherapy
 Cyclosporine
 Azathioprine
 Mycophenolate

Refracter AD
Take home message

 Atopic dermatitis ; chronic, relapsing inflamatory skin

desease.
 result from complex interaction of genetic, epidermis,
environment and immunologic reaction
 Management : education, reducing sign and symptoms,
preventing and decreasing degree and frequency of flare,
 Triger avoidance
 Moisturizer is backbone therapy, TCS is first choice
 Antimicrobial therapy is given if there is secondary
infection
Thank you