Eczema Dr. Majdy Naim. Majdy Naim Eczema 20102 Eczematous Diseases Contact Dermatitis Atopic...

Eczema

Dr. Majdy Naim

Majdy Naim Eczema 2010 2

Eczematous Diseases

Contact Dermatitis

Atopic Dermatitis

Seborrheic Dermatitis

Dyshidrotic Dermatitis

Nummular Dermatitis

Stasis Dermatitis


Contact Dermatitis

A pruritic, epidermal and dermal inflamatory reaction caused or aggravated by items in contact with the skin.


Contact Dermatitis

Irritant contact dermatitis Allergic contact dermatitis Phototoxic photoallegic contact dermatitis


Irritant Contact dermatitis

Acute chronic


Irritant Contact Dermatitis

It is the most common injury of the skin Irritant Responses include:

Wheals erythema Blistering Erosions Hyperkeratosis or thickening of the skin Pustules and skin dryness


Factors that determine the response (Irritant Dermatitis) Individual factors Time of exposure Region of the skin exposed


Acute dermatitis from turpentine


Cement ulcerations


Acute bullous contact dermatitis from a scabicide


Weak- ICD

Prolonged contact Multiple exposure In skin that too wet or too dry Bleaches, cleansers, detergents, plants,

soaps, solvents, weak acids, weak alkalis


W-napkin dermatitis


Napkin dermatitis under the plastic part of the diaper


ICD in a mechanic – caused by oil


Irritant dermatitis due to licking


Common agents that produce irritant contact dermatitis Water Cleansers Alkalis Acids Oils Organic solvents Oxidants Plants Animal substances


Most commonly located in the hands, forearms, face and legs


Diagnosis:

History

Examination

Laboratory investigations: patch testing


Differential diagnosis:

Atopic eczema

Discoid eczema

Allergic contact dermatitis

Fungal infection


Treatment:

- Removal of the offending contact

- Restore a protective lipid layer

- Topical steroid may be necessary


Allergic contact dermatitis It is a form of cell-mediated, antigen-

antibody immune reaction. Sensitization phase (1 week or longer) Elicitation phase (follows)

affect few workers; many skin sensitizers are also irritants

(chromates, nickel salts, and epoxy resin hardeners)

cross-sensitivity


Allergic Contact Dermatitis

Presentation: erythematous and edematous or vesicular skin in the pattern of contact

Mechanism: cell-mediated immune response to antigens (contact allergens)


Contact Allergens

poison ivy, poison oak Nickel sulfate Rubber Formaldehyde and related preservatives Para-phenylenediamine Fragrance Neomycin


Poison Ivy/Oak Dermatitis

Presentation: acute pruritic dermatitis with linear grouping of vesicles

Confirmation: history of exposure


Nickel Dermatitis

Presentation: areas in contact with jewelry or metal clothing fasteners

Confirmation: skin patch testing


Nickel dermatitis from brassiere clasps


Nickel dermatitis from spectacle frames


Rubber Dermatitis

Presentation: sites of exposure to… shoes (adhesive), elastic in clothing, surgical gloves, etc.

Confirmation: patch test to accelerators and antioxidants


Chromate dermatitis from leather in work shoes


Allergic contact dermatitis from thiuram in latex gloves


Allergic contact dermatitis from fragrance in a cosmetic


Allergic contact dermatitis from gluein sticking plaster


Allergic contact dermatitis from plants in the compositae


Allergic contact dermatitis from toluenesulfonyl urea in nail varnish


Allergic contact dermatitis caused by garlic


Allergic contact stomatitis caused by the mercury in amalgam dental fillings in a mercury-sensitive

person


Phototoxic contact dermatitis

Striped and bullous dermatitis of the legs after exposure to plant juices on a sunny day


Bullous dermatitis caused by squeezing lime on a sunny day


Diagnosis:

History

Examination

Laboratory investigations: patch testing


A positive patch test to the perfume-mixture

Identification of Contact Allergens

Patch Testing

Finn Chamber

Majdy Naim Eczema 2010 49Patch Test


Atopic Dermatitis


What is the Cause? nobody has identified a single “cause” atopic dermatitis is a genetic disorder atopic children or their relatives may also

have asthma allergic rhinoconjunctivitis food allergies urticaria


Atopic Dermatitis


Environmental Suspects???

urbanization outdoor pollution indoor pollution/insulated homes fewer infections/infestations changes in food processing

NOBODY KNOWS FOR SURE


Pathophysiology

specific gene abnormality not yet identified

may be more than one disease down regulation of TH1 lymphocytes (TH1

cells activate IFN- which inhibits IgE synthesis)

upregulation of TH2 lymphocytes (TH2 cells activate IL-4 which inhibits IFN-)


Is it a Food Allergy?

no conclusive evidence that eczema is “a food allergy”

atopic children have a higher incidence of urticaria or anaphylaxis to peanuts, eggs, fish, milk

certain foods cause contact irritation and erythema eg. tomato sauce


What about milk?

breast-feeding does not protect against atopic dermatitis

“allergen-free” diets in lactating women can compromise nutrition of the baby and mother

Effect of cow’s milk formula or soy formula in infants with eczema difficult to evaluate


What about Allergy Testing? negative tests may be helpful 80% of atopic children have positive prick and

RAST tests often leads to unnecessary food and lifestyle

restrictions with consequences for child’s emotional and nutritional well-being

parents must be told that positive tests are < 20% predictive of clinical allergy


Eczema – Psychological Issues

How does it affect sleep? How does it impact on the patient’s

behavior and family life? Is the patint’s diet or lifestyle restricted? Are there psychosocial factors that cause

anxiety eg. At home, at school


Atopic Dermatitis

There is no “cure” Eczema can be

controlled 60% of children

“outgrow” eczema by 11 years of age

Treatment better than searching for the “cause”


Treatment

Skin care and emollients Treatment of infection Topical anti-inflammatory agents

STEROIDS NEW NON-STEROID TOPICAL

IMMUNOMODULATORS Antihistamines


Is the eczema infected? most cases of eczema are colonized by Staphylococcus

Aureus - staphylococcal superantigens may play a pathogenetic role

consider antistaphylococcal antibiotic therapy in all cases of weeping, crusted or very excoriated eczema

also consider STREPTOCOCCUS, HERPES SIMPLEX


Treatment

Antibiotics, topical steroids, baths and emollients are safe and effective therapy


Eczema Checklist 1

do parents have a basic understanding of the disease

what have they been told by other health care professionals, pharmacists, naturopaths, family and friends

do they have realistic expectations


Eczema – Checklist 2

is skin care adequate Baths and emollients

is topical therapy optimal Topical

steroids/steroid-free agents

is the eczema infected Antibiotics oral/topical


Eczema Checklist 3

Are other measures necessary? Wet wraps Higher potency topical steroids for short

periods Phototherapy Psychological evaluation/counselling for

child, parents, parent/child interaction Cyclosporin, Azathioprine


Quality of Life


Atopic Dermatitis

Aim of treatment is to improve the child’s quality of life and that of the family


“Patients aren’t as concerned about how much you know until they know how much you care”

“Compassion without competence is dangerous”

Seborrheic dermatitis

Dr. Majdy Naim

Seborrheic dermatitis

a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk

In addition to sebum, this dermatitis is linked to Malassezia, immunologic abnormalities, and activation of complement

70Majdy Naim Eczema 2010

Commonly aggravated by changes in humidity, changes in seasons, trauma (eg, scratching), or emotional stress.

The severity varies from mild dandruff to exfoliative erythroderma.


Pathophysiology

normal levels of Malassezia but an abnormal immune response


Age

The usual onset occurs with puberty. It peaks at age 40 years and is less severe,

but present, among older people. In infants, it occurs as cradle cap or,

uncommonly, as a flexural eruption or erythroderma.


Frequency :3-5 %, dandruff 15-20% Race: Seborrheic dermatitis occurs in

persons of all races. Sex: The condition is slightly worse in males

than in females.


Scalp appearance varies from mild, patchy scaling to widespread, thick, adherent crusts

Skin lesions manifest as greasy scaling over red, inflamed skin

Distribution follows the oily and hair-bearing areas of the head and the neck, such as the scalp, the forehead, the eyebrows, the lash line, the nasolabial folds, the beard, and postauricular skin.


Treatment

Topical corticosteroids Dandruff responds to more frequent

shampooing Selenium sulfide (2.5%), ketoconazole, and

ciclopirox shampoos may help by reducing Malassezia yeast scalp reservoirs



Thank you for your attention!

Eczema Dr. Majdy Naim. Majdy Naim Eczema 20102 Eczematous Diseases Contact Dermatitis Atopic...

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