2. Atopic dermatitis (AD) is a pruritic disease of
unknown origin that usually starts in early infancy; it
is characterized by pruritus, eczematous lesions,
xerosis, and lichenification.
AD may be associated with other atopic
(immunoglobulin E [IgE]–associated) diseases (eg,
acute allergic reaction to foods, asthma, urticaria, and
allergic rhinitis
3.
4. The prevalence rate for atopic dermatitis (AD) is 10-12% in
children and 0.9% in adults (US)
The prevalence rate of AD is rising, and AD affects 15-30%
of children and 2-10% of adults (international). The
frequency is increased in patients who immigrate to
developed countries from underdeveloped countries.
The male-to-female ratio for AD is 1:1.4.
In 85% of cases, AD occurs in the first year of life; in 95% of
cases, it occurs before age 5 years. The incidence of AD is
highest in early infancy and childhood.
5. AD is basically the inflammation of the skin due to
allergic reaction, when the immune system attacks the
skin causing dry skin rashes ,which are common
among small children
The skin rashes are found on the flexor surfaces of the
body such as –creases of the wrists, insides of the
elbows, backs of knees
It is due to TYPE 4 HYPERSENSITIVITY REACTION
1. Sensitization
2. Re- exposure
6.
7. Genetic
A family history of atopic dermatitis (AD) is common.
The strongest known genetic risk factor for developing
AD is the presence of a loss-of-function mutation in
filaggrin (helps in water retention).
These genes encodes proteins involved in epidermal
proliferation and differentiation or inflammatory
cytokines.
8. The skin of patients with AD is colonized by S. aureus.
Clinical infection with S aureus often causes a flare of
AD, and S aureus has been proposed as a cause of AD
by acting as a super antigen. Similarly, super infection
with herpes simplex virus can also lead to a flare of
disease and a condition referred to as eczema
herpeticum.
An aeroallergen is any airborne substance, such as
pollen or spores, which triggers an allergic reaction.
9. Two main hypotheses have been proposed regarding
the development of inflammation that leads to AD:
The first suggests a primary immune dysfunction
resulting in IgE sensitization, allergic inflammation,
and a secondary epithelial barrier disturbance.
The second proposes a primary defect in the epithelial
barrier leading to secondary immunologic
dysregulation and resulting in inflammation
10. Erythema
Crusted lesions on the face neck
Erythematous macules that lichenifies with
scratching
Swelling
Pruritis
Weeping clear fluid
Dry and itchy skin
11. There is no cure for AD
Lifestyle changes –avoid soaps ,avoid allergy triggers
Skin care –use oil based moisturizers
Medications -such as oral corticosteroids or
antihistamines, are taken as pills, use of anti-
inflammatory drugs