Background. Scientific evidence accumulated in recent years indicates that food and in ha l ant allergens can trigger atopic dermatitis (AD). It may be hypothesized that, also in AD, the allergens could induce a cutane ous hyper reactivity analogous to the bronchial hyperreactivity (BHR) described in al ler gic pa tients with asthma. Nonspecific stimuli can therefore trigger and wors en the skin lesions. Eosinophils, as in asthma, seem to play an impor tant role in in ducing and maintaining the skin lesions. Objective. Taken to gether, these data suggest that in AD there exists a vicious circle, by which immunologic and nonim munologic factors act in various ways and at differ ent levels triggering dif ferent, though synergistic, reactions to initiate, am plify and maintain the chronic skin lesions characteristic of the condi tion. Patients and Methods. We have pros pectively 395 atopic children attend ing our Di vision because they were affected with AD, and found 213/395 babies af fected contemporane ously with AD and respiratory allergy. The di agnosis of atopic diseases in the children was done according to family and clinical his tory, physical examination and positive SPTs and/or RAST to the most com mon inhalant and/or food allergens Results. Of them 14 babies experienced a positive OFC (open chal lenge test) to different foods (9 cow milk CM, 5 hydrolysate formulas, HFs, and one fish, but we stress that three of them reacted to one drop or two ml of CM) Positivity of family history and elevated total IgE confirm that AD is a ge netic disease. Conclusion. The data confirms the studies that have suggest ed that al ler gens in turn could elicit respiratory symptoms, that can be dist in gu ished as food induced asthma and asthma with food allergy (FA). In sum mary, FA pro vokes wheezing in a small, but significant number of chil dren suffering from AD and asthma, thus con fronting pediatri cians with one of the most de mand ing chal len ges