ALLERGY PREVENTION - AN ATTAINABLE OBJECTIVE

Few authorities doubt that there has been a significant rise in IgE me diated diseases in almost all populations in which they have been stud ied. There is less agreement why this should have occurred and a numbe r of genetic and environmental influences almost certainly play a part . Although the present discussions are concentrating on dietary factor s these cannot be expected to play more than a partial role in the pat hogenesis and expression allergy. The approach to the prevention of al lergy, 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 at tempting to reduce or abolish expression of allergy in an individual a lready showing symptoms. Such as classification is convenient although the borders become blurred. It had until recently been assumed that s ensitisation rarely if ever took place before birth. Recent studies fr om Melbourne (Tang et al., 1994), Southampton (Warner JA et al., 1994) and Japan (Kondo et al., 1992) suggest this may not be so. Their stud ies have given evidence of intrauterine programming. Warner showed a r aised peripheral blood mononuclear proliferative response in infants b orn to atopic families in those who developed atopic eczema with posit ive skin prick test to foods. These infants also had a reduced interfe ron-gamma production. The Melbourne group has recently shown a reduced IFN-X 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. Additi onally it may be necessary to move attempts at intervention back into early pregnancy or even pre-conception. This would compound the proble ms of an already difficult area of preventive medicine.