Dermatitis Atopic Presentation (Prof.harijono)

7/28/2019 Dermatitis Atopic Presentation (Prof.harijono)

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Prof. Dr. H. Harijono KS, dr. SpKK

Bag.Ilmu Kesehatan Kulit & KelaminFak.Kedokteran UNS / RSUD Dr.Moewardi

Surakarta


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A chronically relapsing skin disorder that arisesmost commonly during early infancy, childhood

or adolescence

Frequently associated with elevated Serum IgE

levels and/or asthma (Leung, et al, 1997).

Unknown etiology and its pathogenesis is still

obscure (Hanifin;1992 ; Marren et al, 1994)

Characterized by chronic skin inflammation

impact on quality of life.

ATOPIC DERMATITIS


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Infants < 2 yr usually present w/:

Signs of inflammation usually develop during the 3rd mth of life

Commonly presents w/ red, scaling, dry areas

- Usually found on the facial cheeks & or chin

- Lip licking may result in scaling, oozing & crusting on the lips& perioral skin, eventually leading to secondary infections

- Perioral & perinasal sparing can be characteristic & may

present w/ no lesions in these areas

Continued scratching or washing will create scaling, oozing, red

plaques on cheeks

- Infant may be restless or agitated during sleep

A small number of infants may present w/ generalized eruptions

- Papules, redness, scaling & lichenification

- Diaper area is usually not affected

SIGNS & SYMPTOMS


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SIGNS & SYMPTOMS

Children 2-12 yr Usually Present w/:

Inflammation in the flexural areas (eg neck, wrists, ankles,antecubital fossae)

Rash may be contained to one or two areas

May progress to involve more areas eg neck, antecubital &

popliteal fossae, wrist & ankles

Papules that quickly change to plaques then lichenified when

scratched

Constant scratching may lead to areas of hypo- or

hyperpigmentation

12 yr-Adult Usually Present w/:

Resurgence of inflammation that recurs near puberty onset Unusual for adults w/ no history of dermatitis in earlier years, to

present new onset dermatitis

Pattern of inflammation is the same as in a child 2-12 yr

Hand dermatitis may be present in the adult due to exposure to

irritating chemicals


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Childhood Type Adult Type


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PATHOGENESIS

Immunologic. mechanisme involved in path.is of AD

In AD skin lesion : - CD4+ T cells (mainly), CD8+ (lesser),

Epid. LC and dendritic cells

T cells play prominent role:

- induction hyper IgE, Eosin. survival,

- induce KC apoptosis formation of ezcema

- apoptosis of activated T cells prevented by

cytokines and EMC

Role of cytokines : important in DA as mediators of

inflammation (Th2 cytokines for acute phase and Th1 for

chronic lesions of AD.


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Triger factors of AD: - including irritants, foods,

aeroallergens, and infection

S. aureus play an important role in path.is AD, not only

as trigger but having disease-sustaining effects

produce potent toxins as super antigen for AD

Interactions between IgE-bearing APC, T cells, MC

degran., KC, Eo and combination of immediate and CMI

response skin lesions


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PATHOGENESIS


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Based on patient history & physical exam

Investigate exacerbating factors

- eg Aeroallergens, foods, irritating chemicals, emotional stress

Hanifin & Rajka criteria for diagnosis (1980)

3 of the Following Major Symptoms Must be Present:

Pruritus

Dermatitis which is chronic or relapsing

Personal or family history of atopic disease

- Asthma, allergic rhinitis, atopic dermatitis

Typical morphology & distribution:

- Facial & extensor involvement in infants & children

- Flexural lichenification in older children & adults

DIAGNOSIS


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Xerosis

Early age of onset

Nonspecific dermatitis of handor foot

Ichthyosis

Palmar hyperlinearity

Keratosis pilaris

Nipple eczema

Facial pallor or facial erythema

DIAGNOSIS

3 of the Following Minor Symptoms Must be Present:

Pityriasis alba

Cheilitis

KeratoconusRecurrent conjunctivitis

Orbital darkening

Infraorbital folds affected

Positive type I hypersensitivity

skin test

Elevated serum IgE level


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Pityriasis Alba


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Atopic Dermatitis Treatment

in Pediatric patients

An important aspect a trusting relationshipw/ the family inform to the patients parent that the aim of tx is :

- to control pruritus & eczematous lesions, but- cure is not possible

I. EDUCATION OF THE FAMILY :

-explain the multifactorial etiology of AD-each case of AD has to be considered individually.-should listen and understand the familys

expectations of the tx


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II. GENERAL ADVICE :

- The life of child with AD should be as normal as

posible.AD : itchmost distressing symptomlack of

sleep

- Reduce factors that could increase the itch :

* hot and sweaty condition

* sport activities, but should not be arbitrarilyprohibited, eg. swimming : use emollient before,

rinse off completely and reapply afterward )* dryness and irritation of the skin(synthetics/wool clothes, etc)


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- Potential allergens should be identified & avoid :

eg. * avoid food allergen,

*use of dust mite-proof casings on pillowsand mattresses,

* removal of bedroom carpetting & decreasingindoor humidity level,

* household pets should be avoided


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III. CONVENTIONAL TREATMENT

In pediatric patiens, tx is same as w/ adult

however, some special aspect :

1. TOPICAL CORTICOSTEROID :

-choose a good potency level (low to medium),

begin w/ weaker steroids

- location of eczema is important eg. the face,diaper area must be carefully

-tx regimen is not standartized, once-per-day appl.is sufficient and not more than 10 days (number

of tubes should be evaluated each visit)


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2. INFECTIONS- 2nd infection, esp. Bact.: frequent- HSV inf. are special complic. of chilldhood AD

eczema herpeticum (EH)- Infections can delay response to topical steroid-smallpox vaccination is contraindicated

3. EMOLLIENTS

- easy in small child/infant but older childr mayrebel against it use less greasy

4. ANTIHISTAMINES

- non-sedating AH are ussually little benefit- sedating AH more ussefull,- the best tx for itching : cure quickly the relapse

w/ topical tx and reduce condition that enhancedryness and irritation of the skin.


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5. PSYCHOLOGICAL MANAGEMENT

- emotional stress -/--> AD, but may influence inflamand immune mechanism exacerbate the illness:

* pruritus and scratching disturb sleep,

* difficult chronic topic. tx anxiety of themother & parenting distress

* psychologic. problem for the child and familyQuality of life (QOL)

- when convent. tx fail in severe AD, a psychologicalapproach may be considered for the QOL of the

whole fam., w/ sometimes beneficial effect


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7. HOSPITALIZATION

-some childr fairing poorly at home become

quickly better when hospitalized, because:1.topic. steroid tx had not been applied as priscribed

2. hospital pediatr environment, psychologicalapproach, tx application are different

3. sec. infect delayed response time to steroid tx

Important to observe the child hospitalized for

several days before changing the tx and considersecond-line tx.


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IV. 2ND-LINE TX in REFRACTORY

PEDIATRIC AD.

A. DIET-The role of food HS in the path.is of AD has beendebated and dietary management is still contr.

versial.-food allergy AD : 5-30 %, very small cases(Atherton, et al)

-most frequent: eggs, milk, peanut, soy flour and fish

-avoidance diets in AD not recommended becausecan be dangerous, esp for long periode weight loss,growth retardation, malnutrition w/

hypoalbuminemia or richets


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- cow milk-based formula not seem to increase riskof atopic disease

-breast feeding had no protective effect inchildhood AD (Nakamura, et al)

B. PHOTOTHERAPY:

-only for > 10 years

-narrow-band UV better than PUVA

C. IMMUNOSUPPRESSIVE TREATMENTS:

-oral cyclosporine : severe recalcitrans cases chld ADdose = 5 mg/kg/day

very good efficacy, but frequent relapse after

reducing dose


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Immunosupressive tx:

- Local cyclosporine poor efficacy- Der. macrolide antibiotics = Tacrolimus (FK 506):

* early 1990 (Fujisawa) for prevent of allograftrejection following liver transpl.

* inhibit histamin release, IL-2,IL3,4,5 & IFN-gammafrom T cell

- Macolactam der. from ascomysine = Pimecrolimus:

* inhibit degran of MC* supress product of TNF


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Atopic

Dermatitis

Treatment Plan


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TREATMENT - PHARMACOTHERAPHY

Corticosteroids (Topical)* Ointments

* Creams

* Lotions

* Solutions

Antihistamines

Corticosteroids

Immunosuppressants (Oral)

* Ciclosporin

* Azathioprine


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CORTICOSTEROIDS (TOPICAL)

Low-Moderate Potency

Drug Available Strength Dosage

Hydrocortisone 1-2.5% cream, ointApply bid-

tid

Betmethasone

valerate

0.025-0.05% creamApply bid-

tid

etc


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CORTICOSTEROIDS (TOPICAL)


Clobetasol

propionate

0.05% cream, oint,

scalp application

Apply

once-

bid

Diflucortolone

valerete 0.3% fatty oint Apply bid

etc


Desonide 0.05% creamApply bid-

tid

Desoximetasone 0.025% cream Apply bid

etc

Very High Potency

High Potency


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PENGGUNAANpd WANITA HAMIL DAN BAYI

Belum ada bukti steroid menginduksi

foetal abnormalitas Penggunaan pd wanita hamil harus

dipertimbangkan manfaat dan resikonya

Tidak dianjurkan untuk neonatus dan bayi :untuk penggunaan jangka panjang


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PERHATIAN

Penggunaan pd wajah perlu diperhatikan.

Jika ada indikasi infeksi jamur atau

bakteri maka perlu ditambahkanregimen

pengobatan tersebut


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Studi Perbandingan antara Steroid Topikal Kuat

dan Sedang

Terapi dengansteroid sedang

Terapi dengan

steroid kuat

Perbandingan 2 lesi

psoriasis yg diberi steroid

topikal sedang dan kuatselama 14 hari, 2 kali sehari

Respons yg baik didapatkan

pd terapi dengan steroid

topikal kuat


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TOPICAL CORTICOSTEROID INDICATION

VERY RESPONSIVEAtopic dermatitis Numuler dermatisis

Contact dermatitis PsoriasisSeborhoic dermatitis

LESS RESPONSIVELupus eritematosus Likhen planusPalmoplantar psoriasis Urticaria papulosa

RESISTANCEDyshidrosis Prurigo nodularisKeloid Granuloma anulare


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Allergic contact Dermatitis

(cause by nickel)

Seborhoic Dermatitis


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Perioral Dermatitis Neurodermatitis


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Numular Dermatitis Psoriasis


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Chronic Discoid LE


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Dermatitis Atopic Presentation (Prof.harijono)

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