Background: Allergic asthma and rhinitis, atopic dermatitis, urticaria and food allergy are genetic diseases of infants and children. Several investigators have provided evidence for a genetic localization for atopy. Babies of atopic parents are at high risk of developing atopic diseases, however the phenotypic expression of such diseases varies widely, being very mild in some infants and children, severe and frustrating in many, even life-threatening in others, being also common, disabilitating, and chronic.Methods: A meta-analysis was done of all available studies on the age of onset of the atopic march, without attempting at being comprehensive in this meta-analysis, but instead selecting what appeared the most relevant articles in the literature.
Results:In the first year of life, there is the onset of atopic dermatitis in 79,8% [ 60,2% to 100%], of cow's milk allergy in 72,7%, egg allergy in 71%, and fish allergy in 51,3% of babies. Asthma starts in the first year of life in 41,8%, in the 2nd in 49,3%, and within the 8th year in 92,5% of children. Allergic rhinitis begins in 35% of babies in the 1st year of life, and in 59% or 13-19% in those aged 2-5 years. It seems therefore that the role of pediatric allergy and immunology has been hitherto somewhat obscured, as shown by the atopic march.
Conclusion:It follows that this role is instead substantial, unmatched, focusing on the early and often very early onset of the atopic march, which needs strategic interventions in the very first months of life or even before birth. As the main goal of modern medicine is prevention of chronic and severe diseases, the possibility of preventing such disorders in predisposed children has stimulated the investigators' imagination since the beginning of the century, when atopic diseases were not as common as now.[11]. There is a significant linkage between total IgE levels and several of these markers, particularly IL-4R [12] and . A linkage of chromosome markers with bronchial hyperreactivity (BHR) and total IgE con centrations has been reported [14]. Two genes account for 78% of the genetic predisposition to high IgE levels [15]. However this linkage has not been confirmed by others, either for total serum IgE or for BHR [16,17] The genes for the ß subunit of the high affinity immunoglobulin E receptor (FceRI-ß) are located on 11q13 [18], and are associated, but without a complete unanimity of researchers, with one or more genes coding for atopy [11]. The initial study showing a dominant gene on this chromosome [19] has been confirmed [20][21][22][23][24] or not [25][26][27][28][29][30], while an association between high serum IgE levels and D11S97 on chromo some 11q has been found in Japanese sub jects [31]. There is no association of atopic dermatitis with chromosome 11q [32], but with the FceRI-ß [33]. Other genes located on 14q23, 14q32, and 14q11.2 may contain loci predisposing to high IgE levels, while those on 12q15 and 12q24 are associated with IFN-g concentrations [11] and show linkage with asthma and tota...