K15b Dermatitis Atopic
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Dermatitis Atopik, juga dikenal sebagai ekzema atopik, adalah suatu kondisi medis yang kronis yang ditandai dengan kulit yang kemerahan, kering, meradang dan gatal, biasanya pada lapisan dalam sendi (seperti siku dan lutut). Apabila kulit yang meradang memburuk, mungkin akan menjadi lecet atau terbentuk lepuhan. Kondisi ini dapat memburuk atau membaik seiring dengan waktu, kadang-kadang hilang ketika orang tersebut telah menjadi remaja. Namun, penyakit ini dapat kambuh beberapa waktu kemudian. Kebanyakan kasus untuk penyakit ini biasanya muncul sebelum usia 5 tahun dan terutama terjadi pada orang-orang yang tinggal di daerah perkotaan dan di iklim yang kelembabannya rendah. Penyebab untuk penyakit ini telah diidentifikasi, tetapi perlu diingat bahwa penyakit ini merupakan faktor keturunan. Sayangnya, penyakit ini tidak dapat disembuhkan, tapi dapat dikontrol melalui pemakaian obat-obatan dan menghindari alergen yang potensial. Komplikasi biasanya hanya terjadi apabila pemakaian obat-obatan tidak dilakukan dengan benar.
Transcript of K15b Dermatitis Atopic
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Chairiyah TanjungDepartment of Dermato-venereologyMedical Faculty, North Sumatera University
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Atopic dermatitis (AD) = Atopic eczemaA chronically relapsing skin diseaseOccurs most commonly during early infancy and childhoodFrequently associate with elevated serum IgE levelsA personal/family history of atopy(+)
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epidemiologyPrevalence 3x than 1960sIndustrialized countries > agricultural countriesFemale : male = 1,3:1 AD, associated with :- small family size- increased income and education- migration rural urban- use of antibiotic
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Etiology and PathogenesisHereditary(genetic)
Psychological effectAllergy (hypersensitivity)FoodaeroalergenCellularImmunity defectIrritantInfectionClimateXerosisDecreaseSkin barierDermatitis Atopic
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Genetic FactorStrong maternal influenceChromosome 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
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Immune Response in AD SkinKey cell types in AD skin :Langerhans cellsLymphocyte cellsEosinophilsMast cells
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Immunopatogenesis of DA
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Systemic Immune Abnormalities in ADIncreased synthesis of IgEIncreased specific IgE to multiple allergens, including foods, aeroallergens, microorganism, bacterial toxins, autoallergensIncreased expression of of CD23 (affinity IgE receptor) on B cells and monocytesIncreased basophil histamine release
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Systemic Immune Abnormalities in ADImpaired delayed-type hypersensitivity responseEosinophiliaIncreased secretion of IL-4, IL-5 dan IL-13 by Th2 cellsDecreased secretion of IFN- by Th1 cellsIncreased soluble IL-2 receptor levelsElevated levels of monocyte CAMP-phosphodiesterase with increased IL-10 and prostaglandin E2
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Skin barrierDermatitis atopic skin
Epidermal lipid TEWL Skin capacitance Soap &detergenDecrease skin barrier functionAllergen absorption Microbial colonization Treshold of pruritus
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Environment factorFood infant and children :milk and eggs adult :seafood and nutsAeroallergens : dust mites,animal danders,molds,pollens.Temperature &humidityIntens perspirationEmotional stressor
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CLINICAL FINDINGSinfantile phase (0-2 years)
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Childhood phase(2-12 years)
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Adolescent phase(12-18 years)
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diagnosisDiagnostic criteria of AD : SomeThe 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
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Major criteriaPruritusTypical morphology &distribution :facial & ekstensorInvolvement during infancy &early childhood flexuralFlexural dermatitis in adultChronic or Chronically relapsing dermatitisPersonal or family histrory of atopy
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Minor CriteriaXerosisSkin infectionHand/foot dermatitisIchthyosis/palmar hyperlinearity/keratosis piliarisPityriasis albaNipple eczemaWhite dermatografism&delayed blanched response
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Minor criteriaCheilitisInfra orbital foldAnterior subcapsular catarractsOrbirtal darkeningFacial pallorIchiness when sweating
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Minor criteriaPerifollicular accentuationFood hypersensitivityDuration of AD influecenced by environment and phychis factorsImmediate skin test reactivityElevated serum IgEEarly age of AD
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Xerosis
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Keratosis piliaris
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Hiperlinear palmaris and dennei morgan
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White dermographism & pitriasis alba
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Skin infection
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Differential diagnosisSeborrhoic dermatitisContact dermatitisNumular dermatitisScabiesIchthyosisPsoriasis Dermatitis herpetiformisSezary syndromeLeterrer-Siwe disease
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In infantWiskott-Aldrich syndromeHyper- Ig E syndrome
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General skin care measureEducationAppropriate skin hydration & use of emolient skin barier repair measureAvoidance of irritansIdentification & treatment of complication bacterial, viral of fungal infectionTreatment of psychosocial aspect of diseaseAntipruritic intervention
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Treatment Topical therapySystemic therapy
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Topical therapyCutaneus hydrationTopical glucocorticoidTopical calcineurine inhibitor ( tacrolimus & pimocrolimus)Tar preparationTopical anti histamin : not recommended except : doxepine cream 5%
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Systemic therapySystemic glucocorticoidAnti histaminInfection agentInterferoneCycloporinePhototherapy (UVB, UVA+UVB,PUVA)
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Prognosis Many factor correlate with AD difficult to predict prognosisThe predictive factors correlate with a poor prognosis of AD :Widespread AD in childhoodAssociated allergenic rhinitis & asthmaFamily history of AD in parents or siblingEarly age at onset of ADBeing an only childrenVery high serum IgE levels
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30-35% infatile AD asthma / hay feverOften develop non specific irritant hand dermatitis
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