Atopic Dermatitis: Immunology and management Dr Amal Kokandi (MBBCh, DDSc, MD)

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Transcript of Atopic Dermatitis: Immunology and management Dr Amal Kokandi (MBBCh, DDSc, MD)

Atopic Dermatitis: Immunology and management

Dr Amal Kokandi

(MBBCh, DDSc, MD)

ECZEMA

Synonymous with dermatitis Large proportion of skin disease in

developed world 10% of population at any one time 40% of population at some time

Features of eczema

Itchy Erythematous Dry Flaky Oedematous Crusted Vesicles lichenified

Diagnosis

Clinical No specific laboratory test Family history of atopy is helpful Criteria for research studies: Hanifin &

Rajka (1980), United Kingdom Party Criteria (1994)

Severity

Clinical: Extent, sleep disturbance, Itching, Quality of life.– ADASI (diagramatic), SASSAD, SIS (intensity

scoring), etc Biophysical methods:

– Eosinophils– IgE (80%)– Immunological markers (sIL-2R, ECP, sCD23,

sICAM-1, sELAM-1, sVCAM-1, E selectin, MBP…..)

Atopic eczema

Endogenous Atopic i.e asthma, hay fever 5% of population 10-15% of all children affected at some

time

Exacerbating factors

Detergents Infection Teething Stress Cat and dog fur ???? House dust mite ???? Food allergen

Clinical features

Itchy erythematous scaly patches Flexures of knees and elbows Neck Face in infants Exaggerated skin markings Lichenification Nail – pitted ridged

complications

Bacterial infection Viral infections – warts, molluscum,

herpes Keratoconjunctivitis Retarded growth

Pathogenesis

Not fully understood Genetics Environmental factors: Irritants,

aeroallergens, seasonal, hormonal and stress Microbial organisms (Staph Aureus,

Malassezia, skin fungi.) and superantigens Modified skin barrier function Deficiency in innate immune system and toll

like receptors Specific immunity (biphasic Th1 & Th2)

Genetics of atopic eczema

77% & 15% concordance in mono- & dizygotic twins.

significant linkage on chromosomes 1q21, 3q21 , 3q24-22 , 3p26-24 &17q25

polymorphisms in genes important for epidermal differentiation, inflammation (IL-4, IL-12, Fillagrin….)

investigations

Clinical ??IgE ??RAST

Prognosis

Most grow out of it! 15% may come back – often very mildly

Treatment

Patient education Emollients Avoid triggering factors: irritants especially

soap Topical steroids Treat infections Sedating antihistamines Second line agents: Calcineurin inhibitors, UV

therapy and systemic therapy Immunotherapy: Desensitization

creams

Cosmetically more acceptable Water based Contain preservatives Soap substitutes

ointments

Oil based Don’t contain preservative Feel greasy Good for hydrating

Topical steroids potency (European)

Mild – “hydrocortisone” Moderate – “eumovate” Potent – “betnovate” Very potent – “dermovate”

Topical steroid potency (American)

Class1 (superpotent) Class2 (potent) Class3 (potent) Class4 (midstrength) Class5 (midstrength) Class6 (mild) Class7 (least potent)

FTU

Finger tip unit Helps to give estimation of topical

steroid amount used To avoid over and under use of steroid

FTU

2 FTU = nearly 1 gram Enough for twice size of adult hand

– A hand and fingers (front and back) = 1FTU– A foot (all over) + 2FTU– Front of chest and abdomen = 7FTU– Back and buttocks = 7FTU– Face and neck = 2.5 FTU– An entire arm and hand = 4 FTU– An entire leg and foot = 8 FTU

Finger tip unit

Face Intertriginous areas Children Effect of occlusion infections and combination formulas

(with antibiotics and antifungals)

Special considerations

Topical steroid side effects

Perioral dermatitis and rosacea Tachyphylaxis & steroid addiction Infections (tinea incognito, herpes

simplex, pityriasis versicolor, scabies……)

Adrenal suppression Glucoma and cataract Angina bullosa purpura (hard palate)

Topical steroid side effects

Telangiectasia, purpura, epidermal, dermal and subcutaneous atrophy, striae, psuedoscars……

Folliculitis Allergic reactions Hypopigmentation Hypertrichosis Delayed wound healing Alteration in skin elasticity & mechanical

properties tinea incognito