Atopic
dermatitis
also referred to as atopic eczema; eczema = "boiling
over"
intensely pruritic inflammatory skin disorder associated with
"atopy": asthma,
hayfever, and allergic conjunctivitis
strong familial aggregation
"The rash that itches, or the itch that
rashes?"
Pathogenesis
basic defect in atopic dermatitis is unknown, but there are
several characteristic
physiologic and immunologic derangements in "atopic" individuals:
- cutaneous inflammation mediated by Th2 cells
(type 2 helper T cells producing Il-4 and IL-5)
- elevated serum levels of IgE
-
impaired cutaneous barrier function
(increased transepidermal water loss leads to dry skin)
- skin colonization and infection by Staphylococcus aureus
(the
toxins of which may serve as superantigens to promote cutaneous inflammation)
- the role of dietary factors in atopic dermatitis is probably overemphasized
Clinical
unlike psoriasis the appearance or basic morphology of
atopic dermatitis is more
difficult to describe
pruritus is usually the most outstanding clinical feature
depending on the acuity of the skin disease there can be:
- ill-defined erythema
-
tiny coalescing edematous papules or papulovesicles
-
excoriations
-
crusting (if secondarily infected)
-
xerosis (or dry, scaly skin)
depending on the acuity of the skin disease there can be:
- lichenification
3 phases of atopic dermatitis:
- infantile (2 months to 2 years):
- facial and extensor distribution
- childhood
-
greater tendency to xerosis
- flexural distribution
- more lichenification and excoriations
- adult
- atopic dermatitis generally improves gradually with age, and may remit by
late childhood or early adulthood
- lesser tendency to flexural localization
- in adults, atopic dermatitis may primarily affect the hands
Treatment
Avoid irritating factors
Aggressive restoration of the cutaneous permeability barrier with bland emollients
and
moisturizers
Topical glucocorticoids (creams or ointments)
Topical or systemic anti-staphylococcal antibiotics
Oral antihistamines
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