Eczema – Atopic eczema

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Eczema – Atopic eczema

Definition

Atopic eczema is predominantly a disease of childhood that gives rise to poorly demarcated chronic pruritic papular inflammation of the skin. Uncontrollable scratching is prominent. Most cases improve with age, although approximately 50% of children retain evidence of the condition into adult life. For diagnostic criteria, see Table 1.

Table 1 Diagnostic criteria for atopic dermatitis

Evidence of itchy skin, or parental report of scratching or rubbing plus three or more of the following:

History of involvement of the skin creases.

History of asthma or hay fever (or first-degree relative if under 4 years).

History of generally dry skin in the past year.

Onset under 2 years old (not used if child is under 4 years).

Visible rash on the flexures (including face if under 4 years).

(Adapted from Williams et al Br J Dermatol 1994; 131 (3): 406–416).

Aetiopathogenesis

Skin barrier

Individuals with atopic eczema have an impaired skin barrier which allows excess water loss through the skin (drying effect) and an increased potential for exogenous irritants and allergens to penetrate (inducing inflammation). Discovery of a strong association between loss-of-function mutations in the gene encoding filaggrin, which is a skin barrier protein expressed in the outer layers of the epidermis, and individuals with atopic eczema has shown how critical epidermal function is to development of atopic eczema.

Immunology

Individuals with atopic eczema make aberrant immune responses to environmental allergens which become skewed towards Th2 responses (p. 10), inducing allergen-specific IgE production. The basic cause of these immune defects is still unclear. However, the serum IgE is normal in 20% of atopic eczema subjects.

Incidence

About 20–30% of UK infants are affected. The condition usually starts within the first 6 months of life and, by 1 year, 60% of those likely to develop atopic eczema will have done so. Two-thirds have a family history of atopy. Remission occurs within 10–20 years in 40–60%, although some relapse later.

Clinical presentation

The appearance of atopic eczema differs depending on the age of the patient.

Infancy

Babies develop an itchy vesicular exudative eczema on the face (Fig. 1), head and hands, often with secondary infection. About half continue to have eczema beyond 18 months.

Fig. 1 Atopic eczema in an infant.

Secondary bacterial infection was present.

After 18 months, the pattern often changes to the familiar involvement of the flexures (antecubital and popliteal fossae, neck, wrists and ankles) (Figs 2 and 3). The face often shows erythema and infraorbital folds. Lichenification, excoriations and dry skin (Fig. 4) are common, and palmar markings may be increased. Postinflammatory hyperpigmentation occurs in those with dark skin. Scratching and rubbing cause most of the clinical signs and are a particular problem at night when they can interfere with sleep. Behavioural difficulties can occur, and a child’s eczema can disrupt family life. Occasionally, a ‘reverse pattern’ of eczema is seen, with involvement of the extensor aspects of the knees and elbows.

Fig. 2 Atopic eczema in a child, showing excoriations and lichenification at the wrist.

Fig. 3 Atopic eczema involving the popliteal fossa in a child.

Fig. 4 A ‘dry’ pruritic type of atopic eczema.

Note the loss of eyebrows due to constant rubbing of the face.

Adults

The commonest manifestation in adult life is hand dermatitis, exacerbated by irritants, in someone with a past history of atopic eczema. However, a small number of adults have a chronic severe form of generalized and lichenified atopic eczema (Fig. 5), which may interfere with their employment and social activities. Stressful situations, such as examinations or marital problems, often coincide with exacerbations.

Fig. 5 Grossly lichenified and nodular atopic eczema on the face of an adult.

Differential diagnosis

Infantile seborrhoeic eczema (p. 116) may sometimes develop into the atopic variety and, occasionally, the distinction from scabies is necessary. Rarely, infants with immune deficiency syndromes (e.g. Wiskott–Aldrich) or with Langerhans cell histiocytosis (p. 116) have an eczematous eruption.

Investigations

Prick tests or the allergen-specific IgE tests to inhalant and (sometimes) food allergens are frequently positive, although the relevance is often unclear. Total serum IgE levels are raised in 80% of patients. Swabs for bacterial and viral culture may be helpful during an exacerbation.

Management

General measures include explaining the disorder and its treatment to the patient and the parents, stressing the normally good prognosis. Nails should be kept short. The exclusion of house dust mite from the home environment is difficult. Careers advice to avoid wet work jobs (e.g. nursing, hairdressing, cleaning) and those with exposure to irritant oils is important. Some sufferers obtain support from groups such as the National Eczema Society (p. 132).

Specific treatments for atopic eczema are summarized in Table 2.

Table 2 Treatment of atopic eczema

Treatment	Indication
Emollients	Most eczema; ichthyosis
Topical steroids	Most types of eczema
Topical tacrolimus	Steroid-resistant eczema
Tar bandage	Lichenified/excoriated eczema
Oral antihistamine	Pruritus
Oral antibiotic	Bacterial superinfection
Exclusion diet	Food allergy/resistant eczema
UVB, ciclosporin and azathioprine	Resistant and severe eczema unresponsive to topical therapy

Topical therapy

Washing and emollient therapy

Soap and ‘bubbly’ products should be completely avoided. Emollients (p. 22) should be used regularly on the skin and to wash with. They moisturize the dry skin, diminishing the desire to scratch and reducing the need for topical steroids. The greasy emollients (ointments) are more effective at repairing the skin barrier and therefore are usually more effective. Creams containing antiseptics such as chlorhexidine and bath oils may also help.