Allergy prevention--an attainable objective?

Abstract

Few authorities doubt that here has been a significant rise in IgE mediated diseases in almost all populations in which they have been studied. There is less agreement why this should have occurred and a number of genetic and environmental influences almost certainly play a part. Although the present discussions are concentrating on dietary factors these cannot be expected to play more than a partial role in the pathogenesis and expression allergy. The approach to the prevention of allergy, generally implying IgE mediated disease, has been described as primary, secondary or tertiary. Primary prevention means prevention of sensitisation, secondary prevention means prevention of manifestation of disease in an already sensitised individual, and tertiary means attempting to reduce or abolish expression of allergy in an individual already showing symptoms. Such as classification is convenient although the borders become blurred. It had until recently been assumed that sensitisation rarely if ever took place before birth. Recent studies from Melbourne (Tang et al., 1994), Southampton (Warner JA et al., 1994) and Japan (Kondo et al., 1992) suggest this may no be so. Their studies have given evidence of intrauterine programming. Warner showed a raised peripheral blood mononuclear proliferative response in infants born to atopic families in those who developed atopic eczema with positive skin prick test to foods. The Melbourne group has recently shown a reduced IFN-chi in cord blood mononuclear cells from infants of atopic families. Thus previous attempts at primary prevention may indeed be secondary prevention as immune responses are already developed at birth. Additionally it may be necessary to move attempts at intervention back into early pregnancy or even pre-conception. This would compound the problems of an already difficult area of preventive medicine.