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Primary skin diseases that principally
affect the epidermis may be categorized as either a dermatitis or
a papulosquamous disorder. Dermatitis commonly
denotes inflammation of the epidermis. Eczema generically
denotes edema within the epidermis. Many primary dermatitides are
eczematous in nature, although the term eczema is
often misused interchangeably for atopic dermatitis. In its mildest
or chronic form, edema is seen histopathologically as prominent, toothlike
interconnections between keratinocytes (spongiosis). With more intracellular
fluid accumulation, intraepidermal vesicles are formed. Vesicles
are often subclinical in subacute or chronic eczemas where edema
is mild but present as grossly evident vesicles and bullae in acute
eczemas. Papulosquamous eruptions are characterized by the presence
of erythematous papules or plaques with overlying scale. While eczematous
processes clinically manifest with weeping or crusting, papulosquamous
disorders are associated with little to no edema and thus clinically
tend to be dry.
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Atopic dermatitis is the most common chronic inflammatory childhood
skin disease, characterized by intense itching, dry skin, inflammation, and
exudation. The typical clinical finding is an ill-defined patch
or plaque of scaling and erythema. Pruritus is a constant feature.
Chronic scratching results in dramatic accentuation of the skin
markings (lichenification), sometimes with postinflammatory hyperpigmentation,
whereas the chronic eczematous process itself may result in hypopigmentation.
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The exact prevalence of atopic dermatitis is not known but has been
reported to be 15% to 20% lifetime prevalence.
Symptoms begin during the first 6 months in 45% of children,
first year of life in 60%, and before the age of 5 years
in at least 85% of affected individuals.1
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The pathogenesis of atopic dermatitis is not completely understood. It
is likely multifactorial involving interplay between immune, genetic,
metabolic, infectious, and environmental factors.2 Abnormalities
of the epidermal barrier paired with immune dysregulation culminate
in expression of this disease. A genetic basis for abnormal barrier
function in some patients with atopic dermatitis has recently been
linked to the FLG gene, the gene in which null
mutations result in ichthyosis vulgaris, a scaly skin disorder in
which 20% to 25% of people are also atopic.3 The FLG gene
encodes filaggrin, a protein essential for epidermal barrier formation
and hydration. The role of filaggrin (or of its absence) in the development
of atopic dermatitis is not completely understood.
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In infancy, involvement of the face, particularly the cheeks
(Fig. 358-1), and of extensor surfaces of
the extremities is typical, but involvement of the scalp and trunk is also common. In
older children, atopic dermatitis favors the flexures such as the
antecubital and popliteal fossae. Ankles, wrists, and dorsa of hands
and feet are also commonly involved (eFig. 358.1).
Occasionally, disease is widespread and severe. A papular variant
may be seen, particularly in African American patients (eFig. 358.2). Several subtle physical findings may
support the diagnosis, including accentuation of skin markings on
palms and soles, double or triple creases under the lower eyelid (Dennie-Morgan
folds), ...