Prediction and prevention of allergic disease in at risk children

Allergic asthma and rhinitis, atopic dermatitis (AD), urticaria and gastrointestinal allergy, are common diseases of infants and children. Their phenotypic expression varies widely, being very mild in some cases, severe and frustrating in many, but even life-threatening in others. Specific IgE to foods and positive challenge test to a number of food allergens are frequently present in children with these disorders. Cow's milk (CM) appears to be the most common offending food both in gastrointestinal and in cutaneous manifestations of atopic disease. It was recently estimated that 14% of children suffer from AD and about 25% from more or less adverse reactions to CM. Babies of atopic parents are at high risk of developing atopic diseases. The main goal of modern medicine is prevention of chronic and severe diseases. Food allergy (FA) and AD may negatively interfere with the child's life and his physical and physiological development. We stress that few diseases like AD, although not being lethal, are causes of invaluable physical and emotional suffering either for children or their parents. Indeed, severe AD confronts doctors with one of their most demanding challenges: too long has this condition been neglected. Sensitization to foods occurs more commonly early in life, however it may even occur prenatally. The possibility of preventing such disorders in predisposed children has stimulated the investigators' imagination since the beginning of this century, when atopic diseases were not so common. However, the possible influence of early diet on later FA has received much attention only in the last decade. Prevention of FA might be achieved by altering the dietary factors, which are responsible for the sensitization and for the phenotypic expression of the disease. As the crucial expression of allergic disease results from an intricate interrelationship between the atopy-prone genetic constitution and the encountered environment, prevention of IgE-mediated disease could potentially be approached by selectively interfering with the major forces, genetic and environmental, that appear to be responsible in concert for the ultimate phenotypic expression of atopy.