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7/30/2019 Atopic Dermatitis (1)

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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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