This document provides information on atopic dermatitis (AD), including its definition, epidemiology, pathogenesis, clinical features, complications, diagnosis, and differential diagnosis. AD is defined as an itchy, chronic inflammatory skin condition with a flexural distribution and early age of onset. Genetic and environmental factors contribute to skin barrier dysfunction and immune dysregulation underlying AD. Clinical features vary by age but commonly include dry skin, rashes, and skin thickening/lichenification due to scratching. Secondary infections can occur. Diagnosis is based on characteristic features and history. Differential diagnoses include other eczemas and psoriasis.

3. 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

4. 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

5. 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.

6. 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.

7. 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.

8. AETIOLOGY
The
inheritance
Eliciting
Factors
Exacerbating
Factors

9. 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.

10. 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.

11. 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.

12. PATHOGENESIS
SKIN
BARRIER
GENITIC
ENVIRONM
ENAL
PHARMAC
OLOGIC
IMMUNOL
OGIC

13. 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.

14. 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

15. IMMUNOLGICAL
1) Elevated serum Ig E in majorty of case
type 1 hypersensetivity reaction

16. 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.

19. 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.

20. 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.

21. 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

22. 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.

24. 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.

25. 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.

26. 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.

27. Ichthyosis vulgaris
• Up to 50% of AD
patients have this
autosomal dominant
disorder
• characterized by
excessive scaling, which
spares the flexures

28. 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.

29. Palmoplantar hyperlinearity
• Increased prominence
of palmar and plantar
creases may be seen in
AD patients, particular
those with associated
ichthyosis vulgaris

30. 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

31. Cheilitis
• Dry, crusty, ‘chapped’ lips
or fissuring of the
commisures (angular
cheilitis) is more
common in infants and
children with AD than in
adults

32. 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.

33. Prurigo nodularis
• Multiple intensely
and pruritic nodules
occurring chiefly on
the extremities
(especially the
anterior surfaces of
the thighs and legs)

34. COMPLICATIONS
Secondary infection
with S. aureus
herpes simplex virus
(eczema herpeticum).
Rarely
• keratoconus
• cataracts
• Keratoconjunctivitis
• with secondary
herpetic infection and
corneal ulcers.

35. DIAGNOSIS
Diagnostic fatures of atopic dermatitis by
the American Academy of Dermatology
(AAD)

36. Essential
features (must
present)
Important
features
(support)
Associated
features
(helpful, less
specific)

37. 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

38. Important features (support)
Early age of onset
Personal and/or family history of atopy
(IgE reactivity)
Xerosis

39. Associated features (helpful, less specific)
Keratosis pilaris/ichthyosis vulgaris/palmar hyperlinearity
Atypical vascular responses
Perifollicular accentuation/lichenification/prurigo
Ocular/periorbital changes
Perioral/periauricular lesions

40. The UK refinement diagnostic
criteria for atopic dermatitis

41. In order to qualify as a case of atopic dermatitis
with the UK diagnostic criteria, the child must have:
• An itchy skin
condition (or
parental
report of
scratching or
rubbing in a
child)
• Plus three or more of the
following:
1. Onset below age 2 years
2. History of skin crease
involvement
3. History of a generally dry
skin
4. Personal history of other
atopic disease
5. Visible flexural dermatitis
(or dermatitis of
cheeks/forehead and outer
limbs in children under 4
years)

42. 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.

43. DIFFERENTIAL DIAGNOSIS
Nummular eczema dermatophytosis,
Early stages of
mycosis
fungoides.

44. ICD ACD

45. PSORAIASIS
SEBORREHIC
DERMATITS

47. TREATMENT

48. 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.

49. Supportive Care
1) After the onset of AD, a reduction of trigger
factors

50. 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

51. 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.

52. Management of chronic AD
TOPICAL
SYSTEMIC
PHOTOTHERAPY
ADVANCED TTT

53. TOPICAL
Emollients
Topical steroids
topical calcineurin
inhibitors (TCIs)

54. 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.

55. Topical steroids
Principles of treatment with topical corticosteroids.
Use the weakest
steroid that controls
the eczema
effectively
Review their use
regularly; check for
local and systemic
side-effects
In primary care,
avoid using potent
and very potent
steroids for children
with atopic eczema
Be wary of repeat
prescriptions

57. Topical calcineurin inhibitors (TCIs)
Tacrolimus and
Pimecrolimus,
are gradually
replacing
glucocorticoids
in most
patients.
potently
suppress
itching and
inflammatio
n and do not
lead to skin
atrophy.
not effective
enough to
suppress acute
flares but work
very well in minor
flares and
subacute atopic
dermatitis.

58. Strategy for topical treatment

59. SYSTEMIC
ANTI- HISTAMINIC
SYSTEMIC
GLUCOCORTICOIDS
ANTIMICROBIALS

60. 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

61. 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.

62. 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

63. 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.

64. Advanced Therapies
For the unusually difficult-to-manage AD patient
CYCLOSPORINE
METHOTREXATE
AZATHIOPRINE
 BIOLOGICS

65. 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

66. 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)

67. 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)

68. 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.

69. OUR
MESSAGE

70. 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