The allergic march in early childhood and beyond

Atopy is defined as a personal and/or a familial tendency to become sensitized and produce IgE antibodies in response to ordinary exposures to allergens, usually proteins [1]. As a consequence, these persons can develop typical symptoms of asthma, rhinoconjunctivitis, eczema and food allergy. Atopy may thus be viewed as a risk factor or an intermediate phenotype of these atopic (or allergic) diseases. The prevalence of allergic diseases has increased in developed countries and this trend is supported by documented increases in objectively measured atopy [2]. The incidence of atopic eczema and food allergy seems to peak already within the first 2 years of life, and these infants are at increased risk of later manifestations of allergic disease such as asthma and allergic rhinitis. This phenomenon of switching from one clinical manifestation of allergy to another is often referred to as ‘The allergic march’. Knowledge about the natural (or spontaneous) course of atopy and its relation to the manifestations of allergic disease is important in risk stratification of patients and may further provide clues to the causes of the allergy epidemic as well as increased insights into the mechanisms underlying the development of disease. This knowledge is best obtained by longitudinal studies of general populations. In this issue of Clinical and Experimental Allergy, Asarnoj et al. present important data on the development of sensitization (serum allergen-specific IgE) during early childhood (from 4 to 8 years of age) from a population-based birth cohort study: the BAMSE birth cohort [3]. They report a remarkably high incidence of IgE sensitization to inhalant allergens during this period of life, adding fuel to the continuation of the allergic march beyond early childhood. The high incidence and the persistence of sensitization resulted in a marked increase in the prevalence of sensitization to inhalant allergens from 15% to 25% over this 4-year period. The persistence of sensitization was generally high for all inhalant allergens [3]. For example, 97% of children sensitized to birch pollen at 4 years of age were still sensitized to birch pollen at 8 years, i.e. a remission rate of 3%. This is a remarkably low remission rate emphasizing the persistent nature of IgE sensitization to inhalant allergens in this period of life. From a biological point of view, the ‘true’ remission rate may be even lower, because measurement error and seasonal variation in levels of serum-specific IgE are likely to decrease the reproducibility of test results. There is evidence that the persistent nature of IgE sensitization to inhalant allergens goes beyond early childhood. Thus, Rhodes et al. performed repeated follow-ups including measurement of sensitization from birth to 22 years of age in a high-risk birth cohort [4]. The prevalence of IgE sensitization to inhalants continued to increase over the whole time span, supporting both the high incidence and the chronic nature of inhalant sensitization up to the age of 22 years. Even in much older populations, the remission of sensitization to inhalant allergens appears to be low. In a prospective study of a general population of 18–69 year olds, the 8-year remission rates of serumspecific IgE sensitization to pollen allergens and dust mite/ pet allergens were 6% and 11%, respectively [5]. The rates of remission for specific allergens are shown in Table 1. The 8-year remission rate for grass pollen sensitization in this adult population was 12%, which was remarkably similar to the 4-year remission rate for grass pollen sensitization observed in the much younger BAMSE cohort (13%). Hence, although we need more data on the natural course of atopy and its clinical manifestations, it is becoming clear that inhalant sensitization is more persistent than previously recognized. In contrast to the persistent nature of sensitization to inhalant allergens, food allergen sensitization tends to be more transient. The incidence of food sensitization peaks during infancy, while the incidence of inhalant sensitization peaks later in childhood. In the German Multicenter Correspondence: Allan Linneberg, Research Centre for Prevention and Health, Glostrup University Hospital, The Capital Region of Denmark, 57 Nordre Ringvej, Building 84/85, DK-2600 Glostrup, Denmark. E-mail: alli@glo.regionh. dk Cite this as: A. Linneberg, Clinical and Experimental Allergy, 2008 (38) 1419–1421. Clinical and Experimental Allergy, 38, 1419–1421 doi: 10.1111/j.1365-2222.2008. 03063.x