Allergic evaluation and management of the atopic patient

Atopy is defined as an inherited predisposition to produce immunoglobulin E (IgE) antibodies in response to natural exposure to minute quantities of environmental allergens, manifesting clinically with atopic diseases. These include food allergy, eczema, asthma, seasonal and persistent rhinitis and urticaria. Not all allergic diseases are atopic in nature. Examples of non-atopic allergic diseases include allergy to drugs (e.g. penicillin), venoms (e.g. bee sting allergy) and some occupational allergies. The cornerstone of the clinical diagnosis of any atopic disease is a detailed history, followed by specific IgE sensitivity testing. This requires knowledge of the patient’s presenting symptoms, his family history and a careful knowledge of the environment in which the patient lives or works. History taking is time consuming, but always rewarding and the most cost effective part of the clinical evaluation. The history guides the clinician as to the most appropriate clinical or laboratory test and can save the patient and health funder unnecessary expenses since there are hundreds of allergen sensitivities which can be tested. In clinical practice, it is important to distinguish those patients with eczema, rhinitis, asthma and adverse food reactions who are truly allergic or “atopic” from those who are not. This distinction has a direct bearing on the treatment options for the patient (Figure 1). There are a number of unscientific and unvalidated tests which attempt to identify allergic factors playing a role in the patient’s disease, but many of these are expensive and those which do not specifically determine IgE levels or evidence of mast cell or eosinophil activation are not recommended by allergologists. This article has been peer reviewed. Full text available at www.safpj.co.za SA Fam Pract 2008;50(5):18-26 Evaluation of allergy in patients with eczema The term eczema describes an aggregation of several skin diseases with common clinical characteristics, which involve a genetically determined skin barrier defect. The prevalence of atopic eczema (AE) has risen significantly during the past few decades.1 A recent study among Xhosa children2 found a point prevalence of dermatologist diagnosed eczema in 0.7%, 1.1% and 3.7% in rural, peri-urban and urban settings respectively. In children and young adults the inflammatory component of the eczema is triggered by immunoglobulin E in more than 50% of cases. In such patients the term atopic eczema is applied. Other children and most adults do not have an “atopic” component to the eczema, as evidenced by absence of a family history of atopic diseases, normal IgE levels and no documented specific IgE sensitivities detected by skin or Immunocap RAST testing. The diagnosis of “atopic” eczema thus cannot be made without confirmation of an atopic immune response by confirming that the patient has elevated total IgE levels or specific IgE antibodies to environmental allergens. The younger the child, the more likely the eczema is to have an atopic basis and younger patients benefit more from allergic (usually dietary) intervention. Diet has almost no place in the management of “nonatopic” eczema, except for a recommendation to avoid non-specific possible triggers of pruritis such as preservatives in processed foods and acidic or irritant foods. These are also irritant if applied directly to the skin since the barrier function is deficient (See Figure 1). In view of the known barrier dysfunction in all patients with eczema, antigens can also penetrate the skin directly and cause irritant or eczematous reactions. This applies particularly to creams with preservatives (e.g. para amino benzoic acid), soaps with fragrances and also to antigens in house dust. In eczema patients who are atopic, IgE sensitisation via the inhaled route may have resulted in sensitivity to house dust mites.