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    Atopic Dermatitis

    By

    Dr saad I. almohize

    ATOPIC DERMATITIS

    BY

    DR SAAD I ALMOHIZEA

    OCTOBER 2004

    SFH

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    ATOPIC DERMATITIS

    Atopy?

    Prevalence is 10% in children and 1% in the adultpopulation

    Rising AD may be more common among Caucasian and

    Chinese persons, but it affects all races.

    Sex: The male-to-female ratio is 1:1.4.

    Age: In 85% of cases, AD occurs in the first year oflife, and in 95% of cases, it occurs before age 5years.

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    criteria

    Major

    1.pruritus 2.typical morhology and distribution

    3.chronicity

    4.family history of atopy

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    Minor criteria

    Xerosis

    Icthyosis/hyperlinear

    palms/keratosis p.

    IgE reactivity

    Elevated IgE level

    Early onset

    Skin infection

    Chelitis

    Nipple eczema

    Recurrent conjuctivitis

    Keratoconus

    Dennie morgan fold

    Anterior c. cataract

    Orbital darkening

    Facial erythema

    Pityriasis alba

    Food hypersensitivity

    White dermatographism

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    SKIN INFECTIONS

    STAPH AURIOUS:

    1.folliculitis

    2.impetigo

    HSV

    SMALL POX

    TRICHOPHYTON RUBRUM MALASSEZIA FURFUR

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    PHYSICAL

    Infancy

    xerosis, often spares the diaper area.

    folds (antecubital and popliteal fossae). The

    appearance is erythematous with exudativepatches. Over a few weeks, lesions localize to thecheeks and forehead and extensors of the lowerlegs but may occur on any location on the body.

    The scalp is dry and flaky.

    Lichenification is not seen often in infancy.

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    PHYSICAL

    Childhood

    Xerosis often is generalized.

    Lesions are eczematous and exudative. Often,

    pallor of the face is noted, with erythema andcrusting around the eyes.

    Flexuralcreases most often are affected, includingthe antecubital and popliteal fossae and buttock-thigh crease.

    Excoriations and crusting are common

    LESS WEEPY

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    PHYSICAL

    Adulthood

    Lesions become more diffuse with anunderlying background of erythema. The face

    commonly is involved. Dryness is prominent.

    Lichenification is present.

    A brown ring around the neck is typical butnot always present

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    Causes

    chromosome 11q13 or 5q31.

    colonization by S aureus.

    AD flares in extremes of climate. Heat is poorly

    tolerated, as is extreme cold. A dry atmosphereincreases dry skin. Sun exposure improves lesions,but sweating increases pruritus.

    The role of food ??

    role for aeroallergens and house dust mites??.

    autoallergens

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    Pathophysiology

    IL4 /IL5/ IL10are all increased

    Laboratory findings suggest an abnormality of Thelper 2 (TH2) cells resulting in increasedproduction of interleukin 4 (IL-4) and increased IgE.The excess IL-4 causes decreased interferon glevels. Cells may react with environmental antigensto produce increased levels of IgE.

    Serum histamine is increased

    stratum corneum abnormalities of lipid (particularlyceramide production).

    abnormality of prostaglandin metabolism

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    Differential diagnosis

    Contact dermatitis

    Ataxia-telangiectasia syndromeHistiocytosis X

    Lichen simplex chronicusPhotosensitivity rashesPsoriasisWiskott-Aldrich syndromeSeborrheic dermatitis

    Mycosis fungoides

    scabies

    Ichthyosis vulgaris

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    workup

    Laboratory testing is seldom necessary.

    Allergy testing is of little value.

    Radioallergosorbent assay is of little value.

    Food challenge/elimination diet Perform CBC for thrombocytopenia to exclude

    Wiskott-Aldrich syndrome.

    T-cell markers to exclude immunodeficiency

    Scraping to exclude tinea corporis Histologic Findings: Biopsy shows an acute,

    subacute, or chronic dermatitis, but no specificfindings are demonstrated.

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    treatment

    Moisturization

    Topical steroids

    UV light: UV-A, UV-B, NBUVB

    Antihistamines:

    Ketotifen

    Oil of evening primrose

    Antibiotics (cloxacillin or cephalexin) Ascomycin

    Tacrolimus (topical FK506)

    methotrexate and cyclosporine

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