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Efi.

Gelerstein 2011

Topic 6. Atopic dermatitis Atopy: familial predisposition to the development of allergic asthma, conjunctivitis, rhinitis, and atopic dermatitis. Atopic dermatitis: In the best tradition of a circular definition, atopic dermatitis is the dermatitis that develops in individuals with atopy. It usually appears in infancy, is chronic and intensely pruritic with varying clinical patterns at different stages of life. Pathogenesis of AD Genetic Environmental Skin barrier defect Immunological factors Pathogenetic factors in AD 1. Non-immunological changes (Intrinsic AD) sebum production asteatosis, biochemical changes Disturbancies in vegetative nerves - Abnormal reactions of the blood vessels white dermographisms - sensitivity to acetylcholin 2. Immunological changes (Extrinsic AD) Disturbed cellular immunity - activity of Th2 cells - activity of Th1 cells acitivity non-specific immunity - activity of monocytes - chemotaxis and phagocytosis of neutrophils Disturbance of humoral immunity IgE production General features: 1. Chronically relapsing disease that occurs most commonly during early infancy and childhood. Associated with abnormalities in skin barrier function and allergen sensitization There is no single distinguishing feature of AD or a diagnostic lab test 2. Commonly associated with: Personal of family history of atopy (allergic rhinitis, asthma, atopic dermatitis) Xerosis (abnormal skin dryness) or skin barrier dysfunction IgE reactivity. 3. Genetic basis influenced by environmental factors with alternation in immunologic responses in T cell, antigens processing, inflammatory cytokines, host defense proteins, allergen sensitivity and infection.

Efi. Gelerstein 2011

Epidemiology: A major public health worldwide problem Prevalence: children (10-20%) in the USA. Adults (1-3%) Female : male - 1.3:1.0 Environmental factors are critical in determining disease expression Associated with western life style Etiology and Pathogenesis: (skin barrier defect) : Highly pruritic inflammatory skin disease that results from complex interactions b/t genetic susceptibility genes defective skin barrier, defects in the innate immune system and heightened immunologic responses to allergens and microbial antigens. There appear to be two rather different ways to reach the same disease state: Extrinsic atopic dermatitis syndrome (EADS): (80%) - total serum IgE. - Polyvalent type I sensitization (children against foods, adults against pollens and house dust). - CD4 cells dominate infiltrate. Intrinsic atopic dermatitis syndrome (IADS): (20%) - No immunologic changes as in EADS. - CD8 cells dominate infiltrate. skin barrier function: - Down-regulation of cornified envelope genes (filaggrin and loricrin) - ceramide levels - levels of endogenous proteolytic enzymes - Enhanced trans-epidermal water loss Presentation: Major features of: 1. Pruritus (itching) 2. Eczematous dermatitis (acute, subacute, or chronic) with typical morphology and age-specific patters 3. Facial and extensor involvement in infancy and young children 4. Flexural eczema/lichenification in children and adults Other common findings: 1. Dryness 2. Dennie-morgan folds (accentuated lines or grooves below the margin of lower eyelid) 3. Lateral thinning of the eyebrows (Hertoghe sign). 4. Allergic shiners (darkening beneath the eyes) 5. Facial pallor 6. Pityriasis alba (pale patches) 7. Lichenification (thickening and hardening of the skin)

Efi. Gelerstein 2011

Provocation factors: Irritants, type I allergens, pseudo-allergens (citrus fruits; other foods or food additives), bacterial super antigens, hormones, increased sweating, dry air, emotional stress. Special investigations: 1. Prick testing with common food and inhalant allergens. 2. Allergen-specific IgE determinations. 3. Atopy patches testing. Common aeroallergens are applied and interpret as in a routine patch test. Differential diagnosis: 1. Contact dermatitis (allergic and irritant) 2. Seborrheic dermatitis 3. Scabies 4. Psoriasis 5. Ichthyosis vulgaris fine scales on the trunk and extremities 6. Keratosis pilaris common, skin condition that looks like small goose bumps (dead skin cells) 7. Dermatophytosis Therapy: 1. Identification of provocative factors 2. Treatment of dry skin 3. Anti-inflammatory/immunosuppressive Elimination of provocative factors Irritative factors Aerogene allergy Food allergy Contact allergy (including steroid contact allergy) Treatment of dry skin Oil bath Neutral basis crmes Lipobase, Lipobase Repair Carbamide Excipial U-hydrolotio, U-LipolotioAsf Local immunosuppressive treatment Corticosteroids (Elocom, Cutivate, etc) Calcineurin inhibitors (Protopic, Elidel) Phototherapy Topical corticosteroids Creme: inflammed, weeping skin Ointment: dry skin Lotiont: scalp Intermittent treatment

Efi. Gelerstein 2011

Frequent side effects of topical corticosteroids Skin atrophy Striae Telangiectasia Perioral dermatitis Acne Purpura Hypertrichosis (excessive hair growth) Phototherapy of atopic dermatitis Acute, severe: High-dose UVA1. Chronic, mild: 311 nm UVB Systemic treatment Antihistamine (loratadine, cetirizine) reduce itching Antibiotics, antiviral drugs only in case of super infections Systemic immunosuppressive treatment: cyclosporine, corticosteroids

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