INTRODUCTION

The word ‘eczema’ comes from the Greek for ‘boiling’ – a reference to
the tiny vesicles (bubbles) that are often seen in the early acute stages
of the disorder, but less often in its later chronic stages.

‘Dermatitis’ means inflammation of the skin and is therefore, strictly

speaking, a broader term than eczema

The terms eczema and dermatitis are used interchangeably, denoting a

polymorphic inflammatory reaction involving the epidermis and dermis
 Eczema: a working classification
• Exogenous (contact) factors
– Irritant
– Allergic
– Photodermatitis
• Other types of eczema
(endogenous)
– Atopic
– Seborrhoeic
– Discoid (nummular)
– Pompholyx
– Gravitational (venous, stasis)
– Asteatotic
– Neurodermatitis
– Ptyriasis alba
 ATOPIC DERMATITIS
The word ‘atopy’comes from the Greek (a-topos
meaning ‘without a place’)

It was introduced by Coca and Cooke in 1923 and refers

to the lack of a niche in the medical classifications

then in use for the grouping of asthma, hay fever and

eczema.
 DEFINITION
Atopic dermatitis is a difficult condition to define
because it lacks a diagnostic test and shows variable
clinical features.

Atopic dermatitis is an (( itchy, chronic, or chronically

relapsing, inflammatory skin condition)).

The rash is characterized by itchy papules (occasionally

vesicles in infants) which become excoriated and
lichenified, and typically have a flexural distribution.
 EPIDEMIOLOGY
Age of Onset First 2 months of life and by the first years in
60% of patients. 30% are seen for the first time by age 5, and
only 10% develop AD between 6 and 20 years of age. Rarely
AD has an adult onset.

Gender Slightly more common in males than females.

Prevalence Between 7 and 15% reported in population

studies in Scandinavia and Germany, Prevalence of AD has
been increasing since World War II.
 AETIOLOGY

The
inheritance

Exacerbating Eliciting
Factors Factors
 The inheritance

The inheritance pattern has not

been ascertained. However, in
one series, 60% of adults with AD
had children with AD. The
prevalence in children was higher
(81%)when both parents had AD.
 ELICITING FACTORS
• Inhalants Specific aeroallergens, especially dust mites
and pollens, have been shown to cause exacerbations
of AD.
• Microbial Agents Exotoxins of Staphylococcus aureus
may act as superantigens and stimulate activation of T
cells and macrophages.
• Autoallergens IgE antibodies directed at human
proteins, release of autoallergens from damaged tissue
trigger IgE or T cell responses, suggesting maintenance
of allergic inflammation by endogenous antigens.
• Foods Subset of infants and children have flares of AD
with eggs, milk, soybeans, fish, and wheat.
 Exacerbating Factors
• Skin Barrier Disruption: increase transepidermal
water loss by frequent bathing and hand washing
and dehydration
• Infections: S. aureus present in severe cases; rarely
fungus (dermatophytosis, candidiasis).
• Season: AD improves in summer, flares in winter.
• Clothing: Wool is an important trigger; wool
clothing or blankets (also wool clothing of parents)
• Emotional Stress: results from or an exacerbating
factor in flares of the disease.
 PATHOGENESIS

SKIN
BARRIER

ENVIRONM
IMMUNOL GENITIC ENAL
OGIC

PHARMAC
OLOGIC
 Genetics
The inheritance were recognized early, Higher
risk was associated with maternal rather than
paternal atopy.

The chromosomal regions 3q21 and 5q31 have

been linked to elevated serum IgE levels and AD.

“Loss-of-function” mutations in the gene

encoding filaggrin; underlie ichthyosis vulgaris,
accompanied by AD in half of cases.
 Skin Barrier Dysfunction
 xerosis is hallmarks of AD , which affects lesional and
nonlesional skin areas increasing transepidermal water
loss, favor the penetration of high-molecular-weight
structures such as allergens, bacteria, and viruses.
Several mechanisms have been postulated:

1) decrease in skin ceramides, serving as the major

water-retaining molecules in the extracellular space
2) alterations of the stratum corneum pH
3) overexpression of the chymotryptic enzyme (chymase)
4) defect in Filaggrin
 IMMUNOLGICAL
1) Elevated serum Ig E in majorty of case
type 1 hypersensetivity reaction
 2) Increase number of Th2 ???????
The hygiene hypothesis
Low birth weight
Maternal smoking
Early infection with with respiratory syncytial
virus
Vaccination against Bordetella pertussis
Early allergen contacts.
 CLINICAL FEATURES

Atopic dermatitis is an itchy, chronic, fluctuating

disease that is slightly more common in boys
than girls, with a range of clinical features.

The age of onset is between 2 and 6 months in

the majority of cases, but it may start at any age,
even before the age of 2 months in some cases.

The distribution of the eruption varies with age.

 Infantile phase
most frequently start on the face,
but may occur anywhere. Often,
the napkin area spared

The lesions consist of erythema

and discrete or confluent
oedematous papules. The
papules are intensely itchy, and
may become exudative and
crusted as a result of rubbing.
Secondary infection and
lymphadenopathy are common.
Childhood phase

The lesions are

papular, lichenified
plaques, erosions,
crusts, especially on
the antecubital and
popliteal, the neck
‘atopic dirty neck’
and face; may be
generalized
 Adult phase

There is a similar
distribution, mostly
flexural but also face
and neck, with
lichenification and
exoriations being the
most conspicuous
symptoms. May be
generalized.
 Associated Clinical Features
Pruritus
• the hallmark of AD.
• worse in the evening, by
sweating or wool clothing.
• The rubbing and scratching
exacerbate pathogenic
events >> the dermatitis.
Excoriations
• Scratching & rubbing can
produce lichenified plaques
and prurigo nodularis.
 Xerosis
 cardinal feature of AD (dry,
scaly skin in a generalized
distribution ( beyond areas
of active dermatitis).
 Xerosis seen in 80–98% of
AD patients.
 Impaired epidermal barrier
function decreased water
content in the stratum
corneum >>> easier entry
of irritants, promotes
pruritus and initiate an
inflammatory response.
Keratosis pilaris
• Excessive keratinization
leading to horny plugs
within hair follicle orifices.
• seen primarily on the lateral
aspects of the upper arms
and thighs and the cheeks
in children.
• A small rim of erythema
surrounds the involved hair
follicles.
Ichthyosis vulgaris

• Up to 50% of AD
patients have this
autosomal dominant
disorder
• characterized by
excessive scaling, which
spares the flexures
Dennie–Morgan lines
• symmetric, prominent fold
(single or double) beneath the
margin of the lower eyelid.
• originates in or near the inner
canthus and extends to one-half
to two-thirds of the lower lid .
• Periorbital edema and
lichenification or darkening
under the eyes (‘allergic shiners’)
may seen.
Palmoplantar hyperlinearity

• Increased prominence
of palmar and plantar
creases may be seen in
AD patients, particular
those with associated
ichthyosis vulgaris
Pityriasis alba
• Infants and children with
AD may have patches of
hypopigmentation with
fine scale, most commonly
on the face. Such lesions
are more noticeable in
darkly pigmented children
 Cheilitis
• Dry, crusty, ‘chapped’ lips
or fissuring of the
commisures (angular
cheilitis) is more
common in infants and
children with AD than in
adults
 Lichenification
• results from repeated
rubbing and scratching
• the skin becomes
thickened and leathery
with exaggerated skin
markings.
• Early dermatologists
called AD an ‘itch that
rashes’, referring to the
cutaneous changes that
result from chronic
rubbing and scratching.
Prurigo nodularis
• Multiple intensely
and pruritic nodules
occurring chiefly on
the extremities
(especially the
anterior surfaces of
the thighs and legs)
COMPLICATIONS
Secondary infection
with S. aureus

herpes simplex virus

(eczema herpeticum).
• keratoconus
• cataracts

Rarely •
•
Keratoconjunctivitis
with secondary
herpetic infection and
corneal ulcers.
 DIAGNOSIS

Diagnostic fatures of atopic dermatitis by

the American Academy of Dermatology
(AAD)
 Essential
features (must
present)

Important
features
(support)

Associated
features
(helpful, less
specific)
 Essential features (must present)

Pruritus

Eczematous changes
• Typical morphology and age-specific distribution patterns:
• Facial, neck and extensor involvement in infants and
children
• Current or prior flexural lesions in any age group
• Sparing of groin and axillary regions

Chronic or relapsing course

 Important features (support)

Early age of onset

Personal and/or family history of atopy

(IgE reactivity)

Xerosis
 Associated features (helpful, less specific)

Keratosis pilaris/ichthyosis vulgaris/palmar hyperlinearity

Atypical vascular responses

Perifollicular accentuation/lichenification/prurigo

Ocular/periorbital changes

Perioral/periauricular lesions
The UK refinement diagnostic
criteria for atopic dermatitis
 In order to qualify as a case of atopic dermatitis
with the UK diagnostic criteria, the child must have:

• An itchy skin • Plus three or more of the

following:
condition (or 1. Onset below age 2 years
2. History of skin crease
parental involvement
3. History of a generally dry
report of skin
4. Personal history of other
scratching or atopic disease
rubbing in a 5. Visible flexural dermatitis
(or dermatitis of
child) cheeks/forehead and outer
limbs in children under 4
years)
PATHOLOGY
‘Acute’AD. Spongiosis in
the epidermis
producing intra-
epidermal vesicles with
exocytosis of
lymphocytes
‘Chronic’AD. There is
less spongiosis, with
more irregular
epidermal hyperplasia.
 DIFFERENTIAL DIAGNOSIS

Early stages of
Nummular eczema dermatophytosis, mycosis
fungoides.
ICD ACD
 SEBORREHIC
PSORAIASIS
DERMATITS
TREATMENT
Primary Prevention
• Allergen avoidance during pregnancy, infancy, or
both. Such investigations have typically focused
on dietary allergens (particularly cow’s milk and
eggs) and dust mites.

• breastfeeding (which is thought to have

immunomodulatory effects) and the reduce
development AD but (especially in a family
history of atopy) to suggestion of a higher risk of
AD with a longer duration of breastfeeding.
Supportive Care
1) After the onset of AD, a reduction of trigger
factors
 2) Hydration
a specific Foaming detergents and soaps should be avoided.

The regular use of emollients protect against inflammation

provoked by irritants such as detergent, and increase the
benefit obtained from topical corticosteroid therapy.

Ceramide-rich emollients may lead to improvements in

childhood atopic dermatitis through barrier repair mechanism
 Management of acute AD
1) Wet dressings and topical
glucocorticoids; topical antibiotics
(mupirocin ointment)

2) Hydroxyzine, 10–100 mg
four times daily for pruritus.

3) Oral antibiotics (dicloxacillin,

erythromycin) to eliminate S. aureus and
treat MRSA according to sensitivity as
shown by culture.
Management of chronic AD

TOPICAL

SYSTEMIC

PHOTOTHERAPY

ADVANCED TTT
TOPICAL

Emollients

Topical steroids

topical calcineurin
inhibitors (TCIs)
Emollients
Individually adapted
emollients containing
urea (4% in children;
up to 10% in adults)
should be used to
support the skin
barrier function and
allow hydration of
the skin.
 Topical steroids
Principles of treatment with topical corticosteroids.

Use the weakest Review their use

steroid that controls regularly; check for
the eczema local and systemic
effectively side-effects

In primary care,
avoid using potent
Be wary of repeat
and very potent
steroids for children prescriptions
with atopic eczema
Topical calcineurin inhibitors (TCIs)

Tacrolimus and potently not effective

Pimecrolimus, suppress enough to
are gradually itching and suppress acute
flares but work
replacing inflammatio very well in minor
glucocorticoids n and do not flares and
in most lead to skin subacute atopic
patients. dermatitis.
atrophy.
Strategy for topical treatment
SYSTEMIC
ANTI- HISTAMINIC

SYSTEMIC
GLUCOCORTICOIDS

ANTIMICROBIALS
 ANTI- HISTAMINIC

SEDATING ANTIHISTAMINES are helpful in breaking the

‘itch–scratch cycle’ in AD, given at bedtime.

useful to patients in whom itching prevents sleep or in

those scratch to producing hemorrhagic crusts at night.

NON-SEDATING ANTIHISTAMINES are occasionally helpful,

but the most benefit is usually obtained at higher doses
 SYSTEMIC GLUCOCORTICOIDS
SHOULD BE AVOIDED EXCEPT in rare
instances in adults for only short courses.
 For severe disease, prednisone, 60–80 mg daily for 2
days, then halving the dose each 2 days for the next 6
days.
 Patients tend to become dependent on oral
glucocorticoid. Often, small doses (5–10 mg) make the
difference in control and can be reduced gradually to
even 2.5 mg/d, as is used for the control of asthma.
Intramuscular glucocorticoids are risky and
should be avoided.
 ANTIMICROBIALS
• Antimicrobials are important for AD patients with
cutaneous infections.
• antibiotics can directly improve AD by reducing
bacterial products thought to exacerbate AD is
less clear.
• Antistaphylococcal therapy (e.g. cephalosporins)
can significantly improve superinfected AD and
may provide some benefit to non-infected skin.
• Ketoconazole has been used for head- or neck-
based AD, presumably to reduce Malassezia
colonization
 PHOTOTHERAPY
Improve AD, but some patients cannot tolerate the
heat generated by the equipment.
UVB, UVA, narrowband UVB, combined UVA and
UVB, and (PUVA) have all been effective in AD.
Some patients benefit from natural sunlight.
Has a favorable side-effect profile compared
to systemic immunosuppressive agents, with
potential risks of ‘sunburn’ and, with long-
term treatment, photoaging and cutaneous
malignancies.
 Advanced Therapies
For the unusually difficult-to-manage AD patient

CYCLOSPORINE
METHOTREXATE
AZATHIOPRINE
 BIOLOGICS
 CYCLOSPORINE
Oral cyclosporine at a dose of 1.25 mg/kg per
day is effective in reducing disease extent and
severity as well as improving pruritus, sleep and
quality of life in AD.

renal toxicity after as little as 3–6 months of

therapy limit the use of cyclosporine, but short-
term courses followed by maintenance therapy
can be prescribed
 METHOTREXATE
MTX is the folic antagonist aminopterin

causes a temporary inhibition of keratinocyte proliferation

during the first 24 hours after a therapeutic dose, and has an
inhibtory effect on circulating and cutaneous lymphocytes

Methotrexate 2.5–25 mg per week (depending upon patient

age,weight and renal function)
 AZATHIOPRINE
Azathioprine is an immunosuppressant drug effective in severe AD.

Side effects are high, including myelo-suppression, hepato-

toxicity, gastrointestinal disturbances, increased susceptibility for
infections, and possible development of skin cancer.

azathioprine is metabolized by the thiopurine methyl-transferase

(TPMT); a deficiency of this enzyme should be excluded before
starting azathioprine treatment.

Dosage (2–3.5 mg/kg/day if normal, 0.5–1 mg/ kg/day if low)

 BIOLOGICS
• Anti-IgE (omalizumab), which is approved for
asthma, has been tried with variable results in
AD.
• Since these patients usually display very high
levels of IgE, neutralizing these levels would
require extremely high amounts of this biologic.
• Nevertheless, some recent case report suggested
the successful of omalizumab in selected patients
• However, effects of biologics may be serious and
need further evaluation.
 OUR
MESSAGE
AD IS A COMMON WELL KNOWN DISEASE
BUT NEED TO BE CARFULLY DIAGNOSED

SYSTEMIC STEROID IS NOT

INDICATED IN TEARTMENT OF
AD WHER AS EMOLLIENT ARE
THE 1ST LINE