Atopy is the tendency to develop hypersensitivity to allergens as a result of genetic predisposition and environmental factors. Atopic diseases include atopic dermatitis (AD), hay fever and asthma. AD is a common, chronic, relapsing and remitting inflammatory skin disease; its prevalence is about 5–15% in children and 2–10% in adults. The diagnostic criteria for AD are summarised in Table 13.1.

Clinical Patterns According to Age

Infantile AD

Onset is within the first 6 months and persists until the age of 2–3 years. Usually affects the head and neck (Figure 13.1).

Childhood AD

Onset is within the first few years of life and persists until or into puberty. Typically affects flexures (e.g. antecubital and popliteal fossae, neck) (Figure 13.2).

Adult AD

Onset is usually in those in their twenties or thirties. It can affect head and neck, flexures of limbs and trunk (Figure 13.3). There is often a previous history of infantile or childhood AD.

Clinical Features (Figures 13.1–13.4)

Acute (or acute on chronic) AD presents with itchy erythematous papules, patches and vesicles with or without erosions on the affected areas.
Chronic AD appears as thickened dry skin with prominence of skin markings (lichenification), often with excoriations and post-inflammatory pigmentary changes (hyper- or hypopigmentation).

Aetiology and Pathogenesis (Figure 13.5)

In normal skin, keratinocytes and intercellular lipids form the epidermal barrier which retains water and prevents the penetration of exogenous agents (e.g. allergens and irritants) into the skin. The aetiology of AD is multi-factorial, with genetic and environmental influences, epidermal barrier defects, penetration of exogenous agents into the skin and activation of the immune response.

Mutations in filaggrin genes have been linked to AD in about 10% of individuals with AD in Europe. Filaggrin is an epidermal skin barrier protein that has a role in the aggregation of the keratin cytoskeleton during epidermal differentiation.

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