4. IDI_011115

Date of Birth : Surabaya, August 4th 1967Occupation : Head of Dermatology Venereology Study Programme

Faculty of Medicine, Airlangga UniversityDr Soetomo Teaching Hospital

EDUCATION :1992 : Medical Doctor, School of Medicine, Airlangga University2001 : Dermato Venereologist, School of Medicine, Airlangga University2007 : Doctoral Programme, Airlangga University 2008 : Consultant of Dermato Venereology2013 : FINSDV2014 : FAADVAWARD: The Best Presenter Award, 8th Asian Dermatological Congress, Seoul, South

Korea, 2008. The 1st Model Lecturer Airlangga University (Dosen Berprestasi I Universitas

Airlangga), 2012 Scholarship Award, 23rd World Congress of Dermatology, Vancouver, 2015JOB EXPERIENCES : Consultant of The Department of Dermatovenereology Faculty of Medicine, Airlangga

University Dr.Soetomo Teaching Hospital, Surabaya, Indonesia Secretary of Planning & Development Board, Airlangga University Researcher in Institute of Tropical Disease, Airlangga University. Peer Review Risbin Iptekdok. Ministry of Health Republic of Indonesia Secretary of Ethical Committee & HTA Dr Soetomo Hospital

Dr. Cita RS Prakoeswa, dr,SpKK(K), FINSDV, FAADVDr. Cita RS Prakoeswa, dr,SpKK(K), FINSDV, FAADV

Cita Rosita Sigit PrakoeswaDepartment of Dermato Venereology Dr Soetomo Hospital

Faculty of Medicine, Airlangga University, Surabaya

Pathophysiology Atopic Dermatitis

Clinical Manifestation DiagnosisManagement

Pruritic, chronic, recurrent inflammatory skin disease

Affects : 5-20% of children & 1-3% adults Approximately 80% of cases 5 years

of age

Spergel et al. JCI 1998Spergel et al. JCI 19986

AD resolved in 35.1% of children

43% developed asthma

45% developed allergic rhinitis

Risk of developing asthma

higher in children with a FH of eczemaBarnetson RS, Rogers M. Childhood atopic eczema.

BMJ 2002; 324: 1376Gustafsson D, Sjoberg O, Foucard T. Development of allergies and asthma in infants and young children with atopic dermatitisa prospective follow-up to7 years of age. Allergy 2000;55:2405.

Genetic

GeneticSusceptibility

Susceptibility

Immune

Immune

Dysfu

nction

Dysfu

nction

Epide

rmal

Epide

rmal

Barri

er

Barri

erDy

sfunc

tion

Dysfu

nctio

n

Environmental

EnvironmentalFactorsFactors

Inside-OUT Hypothesis

impaired skin barrier function is a

consequence ofinflammatory

phenotype of patient

Outside-IN Hypothesis

intrinsic defect in skinbarrier is

responsible forinflammation

Zhanglei Mu, et al, 2014. Molecular Biology of Atopic Dermatitis. Clinic Rev Allerg Immunol

Journal of Investigative Dermatology (2009) 129, 18921908

William Criteria

Skin symptomps in flexural regions & neck (cheeks in children < 10 years)

Asthma / allergic rhinitis (or atopic diseases in close relatives in children < 4 years)

Dry skin during the last years Visible eczema in flexural areas (or on cheeks and/or

forehead in chlidren < 4 years) Eczema starting before age 2

Diagnosis : Itchy skin + at least 3 of the additional features

Itchy skin

Genetic predisposition(e.g. Filaggrine null mutation)

Genetic predisposition(e.g. Filaggrine null mutation)

Childhood Eczema

Childhood Eczema

Defective skin barrier

Defective skin barrier

Allergen entryAllergen entry

Epicutaneous sensitization

Epicutaneous sensitization

Th2 memory cell migrate to nasal & bronchial lymphoid tissue

Th2 memory cell migrate to nasal & bronchial lymphoid tissue

Sensitized airway & airway inflammation

Sensitized airway & airway inflammation

Asthma and / or Allergic Rhinitis

Asthma and / or Allergic RhinitisEnvironme

ntalrisk factors(e.g. infection, sensitization)

Environmentalrisk factors(e.g. infection, sensitization)

Trauma, microbial entry

Trauma, microbial entry

Overexpression of TLSPOverexpression of TLSP

Allergen re-exposure

Environmental modifiers of atopic march (e.g. daycare, animal

exposure)

Environmental modifiers of atopic march (e.g. daycare, animal

exposure)

1. Dharmage SC, Lowe AJ, Matheson MC, Burgess JA, Allen KJ, Abramson MJ. Atopic dermatitis and the atopic march revisited. Allergy 2014; 69: 1727.

2. Burgess JA, Lowe AJ, Matheson MC, Varigos G, Abramson MJ, Dharmage SC. Does eczema lead to asthma? J Asthma 2009;46:429436.

AD can be effectively managed Individualized approach is based on:

age severity distribution of lesions family history medication history disruption of the patients familys quality of life

Focus of treatment of an acute flare of AD: symptomatic relief control of pruritus rapid control of cutaneous inflammation reverse xerotic skin changes.

Focus of treatment between flares of AD : Promote maintenance of SC (epidermal) barrier integrity & function.

Approach of treatment regular incorporation of proper skin care prevent at least some of the endogenous & exogenous

triggers that can induce flares of AD

Prevention of Complications Infections, Fissures, Erythroderma

Control of Symptoms and Signs Non-progression

Reduction of Extent and Severity Clearance of Lesions

Return to normal structure and function Prevention and Reduction of relapses

Maintenance phase Improvement of Quality of Life17-24/11/13 APAD roadshow 19

1. Education & empowerment of patients & caregivers

2. Avoidance & modification of environmental trigger factors

3. Rebuilding & maintenance of optimal barrier function

4. Clearance of inflammation of Eczema5. Control and elimination of itch-scratch-cycle

Thirumoorthy T, 2012 personal communication17-24/11/13 20

Clearly explain AD pathogenesis and treatment

Establish and review short- and long-term goals of therapy

Structured education program can improve children/parent coping behaviour1

Verbal and written information

1Kupfer J, et al. J Psychosom Res 2010;68:353-8.17-24/11/13 APAD roadshow 22

APAD roadshow24

Concept:

*Outside in

*Inside out

Proksch & Brasch. Role of Skin permeability in Contact Dermatitis . In Johanson etalContact dermatitis 5thed. Springer, 2011, pp 121-36

17-24/11/13

25APAD roadshow

Cornified material of keratinosit - keratohyalin - fillagrin

Str. corneum

Intercellular lipidsceramides fatty acids cholesterols

17-24/11/13

1. Predisposing Factors Personal/Family history of atopy

2. Precipitating (initiating) Factors

3. Perpetuating factors

17-24/11/13 APAD roadshow26

2. PRECIPITATING FACTORS: Climate change

Low Humidity (travel). Air-conditioning Heat Humidity Sweat

Irritans Soap, detergents, solvents, wool, dust, grass, sand, swimming pool, hot showers, medicaments, cosmetics

Allergens Nickel, Fragrance - Plaster, Medicaments

Injury to Skin Arthropod bites - Physical injury

Illness Chicken pox - Viral infections

Stress syndrome Psychogenic pruritus Impaired repair mechanisms17-24/11/13 27

3. PERPETUATING FACTORS:

Itch-Scratch Cycle Damaged keratinocytes release of cytokines Psychogenic pruritus Skin picking syndrome

Medicaments Excess washing ALL THE PRECIPITATING FACTORS

17-24/11/13 APAD roadshow 28

Inflammation

Barrier Function

Low Barrier

High Avoidance

High Barrier

Minimal Avoidance17-24/11/13 APAD roadshow 29

First-line therapy Emollients retain the skins barrier function (keep water in & irritants/pathogens out) to prevent painful cracking Frequent and continuous use is recommended even in the absence of symptoms

.Proksch & Brasch. Role of Skin permeability in Contact Dermatitis . In Johanson etalContact dermatitis 5thed. Springer, 2011, pp 121-36


APAD roadshow 32

Occlusive Lipid film

Humectants Attracts water

Emollients

17-24/11/13

Emollients:Consensus Recommendations

using greasy emollients for dryskin and more creamy textures for red,

inflamed eczema17-24/11/13 APAD roadshow 33

Propylene glycol easily irritating in

Topical Corticosteroids (TCS) Topical Calcineurin Inhibitors (TCI) Systemic Immune modulators

Systemic steroids Oral Cyclosporine Azathioprine, Methotrexate

Narrowband UVB Phototherapy17-24/11/13 APAD roadshow

Emolient

37

plus

the volume of a ribbon of cream or ointment the length of the distal phalanx of an adults index finger expressed from a tube

with a 5 mm diameter nozzle.

Katayama I, Kohno Y, Akiyama K et al. Allergology International. 2011;60:205-220

Veien KN. Atopic Dermatitis 2005 pp 89-90, Leo casebook

-FTU= 0.5/0.4 g for a male/female

-Infants and children 1/3 1/4 of

the adult amount

APAD roadshow

Veien KN. Atopic Dermatitis 2005 pp 87, Leo casebook17-24/11/13 42

*Skin with scratch wounds, acute inflamed eczema with oozing or chronic eczema with fissures


topical antiseptics (e.g triclosan,benzalkonium chloride,chlorhexidine) have limited role in AD management and may

aggravate AD


48

Box 1 - Rapid Improvement1-2 weeksAM. Topical

SteroidsPM. Topical

Steroids

Box 2 Consolidation of Improvement 1- 2 weeksAM.AM. Topical Topical

Steroids Steroids (TCS)(TCS)

PM.PM. Topical Topical Calcineurin Calcineurin Inhibitors Inhibitors (TCI)(TCI)

Box 3 Box 3 Rebuilding Rebuilding Barrier Barrier 4weeks4weeksAM.AM. TCITCIPM.PM. TCITCI

Box 4 - MaintenanceAM. Moisturiz

erPM. Moisturiz

erSevere Relapse

Moderate Relapse

Mild Relapse

RELAPSEMoisturizer

T.Thirumoorthy. Atopic Dermatitis. Expert Forum, Jakarta-Indonesia. 22 Juni 2014

49Danby S; Duff GW & Cork MJ; 2010; Academic Unit of Dermatology Research, The University of Sheffield

Initial assessment: history, extent, severity

Emollients, education

Acute control of itch & inflammationTopical corticosteroid

Topical calcineurin inhibitor

Adjunctive therapyAvoidance of trigger

factorsBacterial infections: oral and/or topical

antibioticViral infections: antiviral therapyPsychological interventions

Antihistamines

Disease remission(no sign

or symptom)

Maintenance therapyLocal recurrence: topical calcineurin inhibitor

Long term maintenance: topical calcineurin inhibitorIntermittent use of topical corticosteroid

Severe refractory disease:Phototherapy

Potent topical steroidsSystemic immunosupressant, methotrexate

Oral steroidsPsychotherapeutic

Other treatmentMycophenolate

mofetilTopical doxepin

Future treatment:Recombinant IFN-Leukotriene inhibitor

PDE inhibitorBiologic agents

Endogenous Immune response dysregulation

Environmental Injurious Factors

ECZEMA

Itch-ScratchBarrier Dysfunction


Anti-inflammatory agents OCS/TCS -OCI/TCI

Antihistamines Hyposedative antihistamines in day Sedative antihistamines ??

Emollients is a MUST !! Environmental control

allokinesis Behavioral control

psychogenic


+

Atopic Dermatitis Pathogenesis: Multifactorial 5 Pillars Atopic Dermatitis Management:1.Education & empowerment of patients

& caregivers2.Avoidance & modification of

environmental trigger factors3.Rebuilding & maintenance of optimal

barrier function4.Clearance of inflammation of Eczema5.Control and elimination of itch-scratch-

cycle

Dr. Cita RS Prakoeswa, dr,SpKK(K), FINSDV, FAADVPowerPoint PresentationOutlineWhat is Atopic Dermatitis?Slide 5Slide 6AD can evelop in very early childhood, yet resolution may occur as an infant agesSlide 8AD Pathogenesis MULTIFACTORIALInside out vs. Outside inImmunological Pathway in Atopic DermatitisDefective Epidermal Barrier in Atopic DermatitisDiagnosis Atopic DermatitisComprehensive Management of Atopic DermatitisSlide 15Slide 16Comprehensive Management of Atopic DermatitisSlide 18Slide 19Slide 20Slide 21Patient EducationRecurrency Prevention StrategiesSkin BarrierBarrier functionExplaining the Etiologic Factors in AD for the Education of Patient and Caregivers using the 3 P modelSlide 27Slide 28Avoid / Modify Aggravating FactorsSlide 30Slide 31Slide 32Emollients: Consensus RecommendationsSlide 34Types of emollientSlide 36Clear the Inflammation of Eczema & Restore the barrierMedical managementClasification of Topical Corticosteroid based on formulationThe fingertip unit (FTU) has been used as a method of determining the amount of TCS to applySlide 41Slide 42TCS: Consensus RecommendationsTCIs: Consensus RecommendationsAntihistamines: Consensus RecommendationsAntimicrobials: Consensus RecommendationsSystemic Agents: Consensus RecommendationsSlide 48Terapi proaktif dan reaktifSlide 50Slide 51Itch Scratch cycleEczema Breaking the Itch- Scratch cycleTake Home Message

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4. IDI_011115