Definition, prevalence and burden of disease

Atopy is defined as the ability of an individual to form specific immunoglobulin (Ig) E antibodies to one or more common inhaled aeroallergens such as animal dander, pollen, mould or house dust mite. An allergen is defined as an antigen (usually a protein) that is recognized by the immune system, is usually harmless, and induces an allergic inflammatory response. The atopic or allergic diseases include eczema, asthma and allergic rhinoconjunctivitis. These are complex inflammatory conditions that are associated with immune dysregulation. Not all atopic individuals express clinical disease, but the majority of children who have these diseases are atopic. For example, 30–40% of individuals in developed countries can be shown to be atopic (have detectable allergen-specific IgE antibodies), yet only 5–20% may manifest an atopic disease. The reasons for this variable disease expression are not known.

There is a marked variation in the global and regional prevalence of the atopic diseases, with the highest disease burden in industrialized countries and urbanized communities. In these countries, atopic diseases are now the commonest ailments of childhood, and Australian and New Zealand children have the fifth highest global rates of atopic disease (Table 13.1.1). Since the industrial revolution, the prevalence of atopic diseases has been increasing in most communities, for reasons that are not yet apparent. Environmental factors are thought to account for the variable and increasing prevalence of atopic disease. A commonly cited hypothesis, the ‘hygiene hypothesis’, proposes that the lack of early childhood exposure to infections and/or other environmental factors (such as bacterial endotoxin) may predispose to atopic disease in genetically susceptible individuals. Such a hypothesis can be supported by epidemiological and possibly immunological evidence.

Table 13.1.1 Prevalence of atopic disorders among Australian children

Because atopic diseases are common, often chronic and usually begin in early childhood, the burden to the community, family and individual is considerable. The cost of allergic disease to the Australian community is estimated to be $7 billion per annum. Importantly, the impact of severe atopic disease such as atopic dermatitis on a family may exceed that of other chronic childhood disorders such as diabetes mellitus or juvenile rheumatoid arthritis.

Pathogenesis

Although atopy is defined by an excessive production of IgE, this is only one of many immunological changes that characterize the allergic diseases, as these are also associated with a complex dysregulation of the humoral and cellular immune systems (Fig. 13.1.1). For this process to occur, both a genetic predisposition and early life environmental exposure are important. During early life, naive T-helper lymphocytes respond in a particular way to environmental allergen exposure as well as a host of other non-allergen immunomodulatory factors (such as endotoxin). T-regulatory cell function and the pattern of cytokine secretion are central to the factors that result in the production of antibodies, including IgE.

Fig. 13.1.1 Pathogenesis of atopic disease. Ig, immunoglobulin; IL, interleukin; Th2, T-helper type 2.

History and examination

The history and examination should cover the following aspects:

On examination, atopic children may have a typical appearance (Table 13.1.2).

Table 13.1.2 Examination of the atopic child

Assessment

Once the history and examination are completed, there is seldom difficulty in diagnosing the presenting atopic disease. However, as many children manifest more than one atopic disease, it is important to consider whether any other atopic condition is present. A differential diagnosis should be considered, as uncommon disorders may present similarly to an atopic disease (Table 13.1.3).

Table 13.1.3 Differential diagnosis of atopic disease

* These immunodeficiency diseases may have atopic dermatitis as a component.

Investigations

Investigations in the atopic child are limited. Total IgE concentration is raised in the majority of children with atopic disease but there is substantial overlap with values in non-atopic children. Measurement of total IgE levels is seldom indicated. Allergen-specific IgE (ASE) is more useful and can be determined using both in vivo (skin testing) and in vitro (serological) methods (Table 13.1.4). Measurement of ASE may be helpful in identifying a specific allergen trigger. However, interpretation of the skin test or ASE result is critical:

Table 13.1.4 Determination of allergen-specific IgE

Management

The aims of management in atopic disease may vary depending on the clinical context.

Management of symptomatic atopic disease

Once the child has developed symptomatic atopic disease, management involves allergen identification and avoidance, and symptomatic treatment. Immunotherapy may be appropriate for selected children.

Allergen identification and avoidance

When possible, this remains an important component of management. Avoidance measures may involve considerable parental education, effort and expense. Note that:

• with ingested allergens identification and avoidance are particularly important when atopic disease is associated with a food allergy, as this is the only means of therapy

• with inhalant allergens, methods have been evaluated to reduce exposure to indoor allergens, most importantly house dust mite (Box 13.1.2). A number of studies in sensitized individuals have demonstrated improvements in atopic dermatitis and allergic rhinitis following house dust mite reduction measures. The benefit of house dust mite avoidance in asthma is much more controversial

• other indoor allergens (cat, cockroach, mould) and outdoor allergens are less easily avoided and alternative forms of therapy may be required.

Box 13.1.2 Methods to reduce house dust mite exposure

Definitely useful

• Encase bedding in impermeable covers (dust mite covers): most important measure, because the bed is the major source

• Hot water washing of bedding and clothes (> 56°C): will destroy house dust mite and remove allergens

Probably useful

• Replacement of fitted carpets with smooth flooring

• Hard-surface cleaning with a damp cloth, at least once a week

Possibly useful

• Air filtration, ionizers and air conditioning

Unlikely to be useful

• Acaricides (dust mite sprays) for the carpet and mattress

Symptomatic treatment

When allergen avoidance is difficult, the response is partial or the allergen cannot be identified, symptomatic treatment is indicated. A number of medications are available, including antihistamines, sympathomimetics, mast cell stabilizers, corticosteroids and leukotriene antagonists (Table 13.1.5).

Table 13.1.5 Medications for the symptomatic treatment of allergic disease

	Important mechanisms of action in allergic disease	Examples
Antihistamines
First and second generation	H1-receptor antagonism	Diphenhydramine
		Promethazine
		Hydroxyzine
Second generation	Above plus antiallergic effects	Cetirizine
	Decrease mediator release	Loratadine
	Decreased migration and activation of inflammatory cells	Terfenadine
	Reduced adhesion molecule expression
Sympathomimetics
β-agonists	Bronchial smooth muscle relaxation	Salbutamol
	Reduce mast cell secretion	Albuterol
		Terbutaline
α- and β-agonists	Bronchial smooth muscle relaxation	Adrenaline (epinephrine)
	Vasoconstriction – skin and gut
	Inotropic and chronotropic effects
	Reduce mast cell secretions
	Glycogenolysis
Cromolyn	Mast cell stabilizer	Cromolyn sodium
	Inhibits chemotaxis of eosinophils	Nedocromil sodium
	Inhibits pulmonary neuronal reflexes
Corticosteroids	Reduce T-cell cytokine production	Hydrocortisone
	Reduce eosinophil adhesion, chemotaxis	Beclomethasone
	Reduce mast cell proliferation	Budesonide
	Reduce vascular permeability	Fluticasone/flunisolide
	Reverse adrenoreceptor downregulation	Triamcinolone acetonide
Leukotriene antagonists	5-Lipo-oxygenase enzyme inhibition, or LTD4 receptor antagonist	Montelukast

LT, leukotriene.

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