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DEFINITION:
Atopic Eczema or atopic dermatitis is an itchy, chronic or
chronically relapsing inflammatory skin condition.
 WHAT IS ATOPY?

’ Atopy is a personal or familial tendency

to produce IgE antibodies in response to
low doses of allergens and to develop
typical symptoms of asthma,
rhinoconjunctivitis or
eczema/dermatitis
• ATOPIC MARCH:

• Progression within an individual from AE

to other atopic diseases including allergic
rhinitis, food allergy and asthma .
AGE OF ONSET
Presents in infancy (less than 2 years
of age)
GENDER

Slight higher prevelance in females.

AE can be described in two forms:

1. Extrinsic eczema.
2. Intrinsic eczema.
EXTRINSIC ECZEMA

High levels of IgE (>200 ku/l).

Intrinsic Eczema

normal levels of IgE.

GENETICS
• Genes Il4,IL13 and PI SPINKS are
responsible but fillagrin is an important gene
in its pathogenesis.

• Expressed within EDC on 1q21 which have

skin barrier protiens like loricrin,involucrin,
s100.
• Asthma and allergies are also ass: with FLG mutations.

• Tight junction proteins claudin1 and 23 in low levels in

AE skin.

• Coal tar application up regulates FLG expression.

• Lipid dysfunction in skin can also cause loss in natural

moisturizing factor which causes skin barrier
dysfunction.
KERATINOCYTES  STRATUM CORNEUM

Profillagrin • dephosphorylation

Cleavage
of • matriptase

profillagrin

Free • (-)of
fillagrin LEKT
monomers 1
ENVIRONMENTAL FACTORS.
IMMUNODYSFUNCTION:
T REGS:
T REGS

• These are to counter-balance pro-

inflammatory environment.

• T regs suppress immune cells.

• Glucocorticoids increase T-reg

population.

• Fox-p3-T-regs (Tr1) is found in lesional

AE.
ROLE OF IG-E IN ATOPIC ECZEMA
• igE is produced by plasma cella in lungs and
skin.
• it may be induced by staph aureus antigens.
FOOD ALLERGY
• Urticarial reactions secondary to food arising in an
individual with AE inevitably lead to a deterioration
in AE following increased inflammatory mediator
release and scratching, therefore food allergen
avoidance can be beneficial if not ’curative’. Allergic
responses to milk, egg, wheat, soy, peanut and fish
account for 85% of reactions in this group
• >90% food allergies arise within 2 hrs involving resp.
and GI tracts.
• Positive skin prick test >3 mm or serum‐specific IgE
0.35 kU/L are sensitive and specific for diagnosing
type 1 allergic reactions to egg.
INFECTIONS
• Innate immunity is compromised in AE, as
demonstrated by reductions in keratinocyte‐derived
antimicrobial peptides (cathelicidin LL‐37, β‐
defensin 2 and β‐defensin 3) , neutrophil
chemoattractant IL‐8 and inducible nitric oxide
synthetase which mediates pathogen death through
release of NO.
• Most (>90%) individuals with AE have S. aureus
identifiable on skin swabs
• Others develop erythema
Herpeticum.
• igA production is also reduced in sweat and tears of
AE patients  staph. Production on skin.
HANFIN & RAJKA’S DIAGNOSTIC CRITERIA OF
AE
In order to qualify as a case of atopic dermatitis (eczema) with the UK diagnostic
criteria, the child must have:
• An itchy skin condition (or parental report
of scratching or rubbing of child)

Plus three or more of the following:

1  Onset below age of 2 years (not used if child is under 4 years)
2  History of skin crease involvement.
3  History of a generally dry skin
4  Personal history of other atopic disease (or history of any atopic
disease in a first‐degree relative in children under 4 years)
5  Visible flexural dermatitis.
CLINICAL FEATURES

• Itching
• Macular erythema
• Papules or papulovesicles
• Eczematous areas with crusting
• Lichenification and excoriation
• Hyper‐ or hypopigmentation
• Dryness of the skin
• Secondary infection
The rash is characterized by erythema,
itchy papules/papulovesicles which may
become excoriated and lichenified, and
typically has a flexural distribution.
Pallor of skin after stroking

White dermographism
CLINICAL FEATURES OF AE
The clinical features presentation varies with age.

Infantile phase
Childhood phase
Adult phase
 INFANTILE PHASE
• (2month to 24 months)
• The lesions most frequently
• start on the face.

• The napkin area is spared.

• When the child begins to crawl,

extensor aspect of the knees and elbows
• The lesions consist of erythema.
• The papules are intensely itchy, and may become
exudative and crusted as a result of rubbing.

• Secondary infection and lymphadenopathy.

 CHILDHOOD PHASE
• From 18 to 24 months onwards.
• elbows and kness.
• Erythema, crusting, excoriation, hyper‐ and hypopigmentation,
and lichenification of neck (atopic dirty neck), wrists and ankles.
ATOPIC DIRTY NECK
 ADULT PHASE (12 Y AND OLDER)
• Lichenification of flexures and hands.

• Involves nipples in young women & vermilion border of lips.

• Face, upper arms and back.

• Photosensitivity positive.
PRURITIS
• The sensation to itch central to AE.

• TSLP is a key itch mediator. Il 31 also causes itch.

• Ciclosporin for rapid itch resolution.

• Histamine is the best known pruritogen

• Sweating also induces itch due to altered

inflammatory responses to Ach.
CLASSIFICATION OF SEVERITY

Skin/physical assesment

Clear: Normal skin, no evidence of active atopic eczema

Mild: Areas of dry skin, infrequent itching (with or without
small areas of redness)
Moderate: Areas of dry skin, frequent itching, redness
(with or without excoriation and localized skin
thickening)
Severe: Widespread areas of dry skin, incessant itching,
redness (with or without excoriation, extensive skin
thickening, bleeding, oozing, cracking and alteration of
pigmentation
Impact on quality of life and psychosocial well being

None: No impact on quality of life

Mild: Little impact on everyday activities, sleep and psychosocial

well‐being

Moderate: Moderate impact on everyday activities and psychosocial

well‐being, frequently disturbed sleep

Severe: Severe limitation of everyday activities and psychosocial

functioning, nightly loss of sleep
 COMPLICATIONS AND CO-MORBIDITIES
Psychosocial aspects
• Growth delay: due to severely affected child treated with steroids.
• Secondary bacterial infections
• Viral infections (erythema herpeticum)
• Ocular manifestations like Dennie- Morgan fold, conjunctival
irritation.
• Cataracts, rectinal detachments are observed.
• Lymphomas
• Cartilagenous pseudocyst in external
• ear.
• Allergic rhinitis and asthma.
• Dryness (xerosis): icthyosis vulgaris
and KP are associated.
ERYTHEMA HERPETICUM
• Herpes simplex virus (HSV) poses an increased risk
for individuals with AE and superficial dissemination
on the skin known as ’Kaposi varicelliform eruption’
or eczema herpeticum. Constitutinal symptoms +ve.

• Rapid detioration of
Eczema. Papulovesicle
Eruption. Ddx.
Impetigo, chickenpox.
Associated conditions

• There is psychological morbidity like life-time

scratching,sleep loss and stigma of visible skin disease.

• Associated with attention deficit hyperactivity syndrome.

• Costly to manage 338 dollars per year per individual which

is increased 2.5 fold with risk of other atopic co morbidities.

• Spink5 and LEKT1 in netherton syndrome also ass: with

AE.

• 30% icthyosis vulgaris patients with AE.

Food allergy: abdominal symptoms.

Alopecia areata

Contact urticaria usually on hands in slaughter house

workers d/t latex sensitivity.
ATOPIC HAND DERMATITIS
• More than 50% of patients with active AE

• A patchy, somewhat vesicular and lichenified eczema

is a common manifestation of AE in childhood.

• The nails are often involved, resulting in coarse

pitting and ridging.

• diffuse, chronic lichenified eczema in extensive AE.

• Involvement of the feet is also common.

 DIFFERENTIAL DIAGNOSIS OF AE
Seborrhic dermatitis: it usually presents earlier than AE.
Clinically indistinguishable.
Allergic contact dermatitis: greater chance of ACD in AE
patients.
Lip-lick chelitis: moist or fissured eczema around mouth
• Common in children
• hyperpigmented in darker individuals
• Lip-licking, chapping, dribbling and thumb-sucking.
• Contact-sensitivity like tooth-paste.
scabies
DIFFERENTIAL DIAGNOSIS HAVING AE LIKE
RASH
• Hyper‐IgE syndrome
• Hypereosinophilic syndrome
• Agammaglobulinaemia
• Anhidrotic ectodermal dysplasia
• Ataxia telangiectasia
• Netherton syndrome (ichthyosis, bamboo hairs)
• Phenylketonuria
• Wiskott–Aldrich syndrome (infections and
thrombocytopenia)
INVESTIGATIONS
• Serum IgE
• Prick test
• Gold-standard is double-blind placebo controlled
food-challenge.
• Atopic patch test for aeroallergens and food-allergy
in late phase.
• Immunoglobulins, WBCs, plaltelets, HiV screening.
• Bacterial swabs
• Tznack smear, PCR
• The APT consists of a petrolatum preparation of
protein allergens applied in 12‐mm diameter
Finn chambers for 48 h to non‐abraded, non‐
tape‐stripped skin of the upper back for 48 h.
The test is read at 48 and 72 h assessing
erythema as well as number and distribution
pattern of the papules according to the EFTAD
guidelines.

• There is a 15‐ min immediate weal and flare due

to histamine release from skin mast cells. A late‐
phase response comprising erythema and a
deeper edematous reaction occurs between 6 and
24 h, and there is a delayed response at 48 h.
APT
 • Raised Wbcs,
Skin biopsy eosinophils
• Raised IgE
Skin • On scratchin
scratch/prick shows allergen
test
• To detect
Total & specific
environmental
IgE allergens
MANAGEMENT
 MANAGEMENT
• Moisturise your skin atleast twice a day (emolients, creams and
lotions).
• Identify and avoid triggers that worsen the condition (sweat,
pollens, obesity, detergents and soaps)
• Take shorter baths or showers (for 10-15 minutes with warmer
water other than hot water).
• Take a bleach bath ( diluted bleach in water for 10 minutes to
avoid superbacterial infections)
• Use mild soaps
• Dry yourself after bath (gently pat your skin)
TREATMENT
 1ST LINE
• Emollients (sodium lauryl sulphate should be avoided)
• (alpha hydroxyacid is made up of glycolic acid8 percent +
• Lactic acid 12 %+ urea6%)
• Vanicream, eucream, vaseline
• Urea creams
• Oils
• Apply emollients once a day after bathing and whenever skin feels
dry
 TOPICAL STEROIDS
• Hydrocortisone 1-2.5% applied to all skin
• Safe and used for months if not misused.
• Use intermittently on thin areas
• Stronger potency steroids used in non-facial and genital areas
ORAL THERAPY
• Oral corticosteroids (0.5 mg/kg)
• H1-receptor antagonists (hydroxyzine, promethazine
or trimeprazine) HS useful in nocturnal itch.
• Oral flucloxacillin or erythromycin for secodary
bacterial infections.
 2ND LINE
• Topical immunosuppressants and topical calcineurin inhibitors
like tacrolimus (adults 0.1% children 0.03%) and pimecrolimus.
• Used when continuous use of topical steroids are not useful and
not advisable
• Phototherapy: UV light can be an effective treatment
• Combined UVA & UVB therapy is more useful than single UVA or
UVA therapy
• Also helpful in reducing bacerial infections.
 WET WRAP TECHNIQUE
Two layers of absorbent tubular bandage are applied to the skin. The
inner layer is presoaked in warm water and the outer layer is dry. A
generous quantity of a low‐potency topical corticosteroid is applied to the
skin before the dressings. The dressings can be used overnight or changed
every 12 h. This regimen can be used in hospital or for short‐term out‐
patient treatment. Close supervision should be maintained because
suppression of the hypothalamopituitary axis can occur when topical
steroids are employed.
Regimens using emollient only under the wet dressings have become
popular but are somewhat less effective. Localized areas of severe
lichenification can be treated with occlusive colloid dressings or paste
banding that is left on for several days.
 3RD LINE
systemic treatments:

• Anti-histamines for itching

• Linoleic acid and linoleic gamma for pruritis
• Macrolide and cephalosporin for bacterial infections.
• Acyclovir of herpeticum eczema.
ADVANCED THERAPIES

Cyclosporin

Methotrexate

Biologics (anti-IgE i.e

Azathiprione
Omalizumab)
• Ciclosporin: highly effective in adults and children.
• Initial dose 2.5-3.5 mg/kg/day with maximal daily dose of 5
mg/kg/day.

• Reduction in 55% patients in 6-8 weeks.

• Regular monitoring of renal function and blood pressure.

• Azathiprine: dosage depends on thiopurine methyltranferase

(TPMT) activity in RBCs.
• Those with high TPMT activity 1-3mg/kg/day
• Low TPMT activity 0.5-1 mg/kg/day.
• Regular blood monitoring as it can cause neutropenias.
• Methotrexate : 10 mg/week following a 5 mg test dose and
increasing by 2.5 mg weekly to max 25 mg/week.

• Maximum effect in 10 weeks.

• Mycophenolate mofetil: failed to respond on azathioprine or

methotrexate.
• Forth line agent
• 2 g/day
• Side effects: GI disturbance, lukopenia lymphopenia and
anemia.

• Alitretinoin (9-cis retinoic acid) for hand eczema

Biologics (anti-IgE i.e omalizumab)
• Rituximab
• Duplimab ( fully human monoclonal antibody)

• Topical phosphodiesterase inhibitors and are under

work.
IMMUNODYSFUNCTION
Primary immonudeficiencies:

Wiskott-Aldrich Syndrome:
• X-linked
• Clinical triad of micro thrombocytopenia, eczema
and recurrent infections.
• Eczema is d/t abnormal T-cell response.
• Eczema appears in first month.
• Fulfills rajka’s criteria.
HYPER IG-E (JOB) SYNDROME
• Characterised by recurrent abscesses, recurrent
pnemonica with pneumatocoele, eczematous
dermatitis and raised Ig-E levels.

• AD, AR

• Skeletal, connective tissue and dentition.

• Th-17 deficiency, Il-17 high (FLG down-regulation ->

skin barrier dysfunction).
Coarse faces, a prominent
forehead, a broad nasal bridge,
and a bulbous nose.
OMENN SYNDROME
• AR DO, form of severe combined immunodeficiency
DO.

• Erytheroderma, desquamation alopecia, chronic

diarrhea, lymphadenopathy, hepatosplenomegaly,
failure to thrive.

• Virtual absence of B-cells and presence of autoreative

T-cells.

• Elevated IL 4, IL 5, Ig-E, eosinophils.

OMENN SYNDROME. UNIQUE DERMATITIS
RESEMBLING ECZEMA BUT LATER
PANCHYDERMIA.
IPEX SYNDROME
• Immunodysregulatory polyendocrinopathy,
enteropathy, x-linked syndrome.

• Early onset ID DM, severe watery diarrhea often

with failure to thrive, spontaneous dermatitis, food
allergies and hyper igE.

• Males only

• fOXP3 mutations