Factors predicting food allergy
Introduction
Food allergy is defined as an adverse clinical reaction to food due to any type of abnormal immune response to an ingested food antigen. It affects 1–2% of the general population. In the very young, the prevalence can be as high as 8%. An entire population cohort of over 1000 infants born on the Isle of Wight between 1989–1990 have been followed since birth. At 4 years of age, the cumulative prevalence of food allergy ranged between 0.2% for tree-nuts to 51% for milk (Table 1). Despite this, until fairly recently, food allergy was considered to be in the fringe of medicine.
In the past 2–3 decades a great deal of valuable research has been carried out concerning the diagnosis, symptoms and treatment of food allergy (Metcalfe et al., 1991). No gold standards have been set in tackling any of the above areas in food allergy with the overall picture more complex than initially anticipated. Nevertheless, there is a relatively homogenous view in the medical and scientific community regarding the diagnosis and treatment of this group of patients. Hence, in the last few years the emphasis has been shifted more towards the prediction and prevention of this disorder. In the following sections, I will attempt to highlight potential factors which have been investigated for predicting the development of food allergy.
Section snippets
Family history
Genetic factors are important in the predisposition for allergic diseases (Kaufman and Frick, 1976). However, the evidence regarding how factors such as family history can predict ‘food allergy’ is weak. In addition, when describing the family history, it becomes evident that the definition of a positive family history varies between the different studies. Some quote a life-long prevalence as a positive family history, while others refer to a current history of allergy in the immediate family
Cord IgE
Cord IgE has been advocated by some as a useful indicator and, in certain studies, even more useful than family history for prediction of atopy (Michel et al., 1980, Croner et al., 1982, Businco et al., 1983, Kjellman and Croner, 1984, Chandra et al., 1985, Magnusson, 1988, Strimas and Chi, 1988, Croner and Kjellman, 1990, Hansen et al., 1992a, Hansen et al., 1992b, Hansen et al., 1992c, Hansen et al., 1993). The problem with the findings of these earlier studies is that they were not
Cord blood lymphocyte responses
Although many studies have highlighted inhalant allergen-induced proliferation of peripheral blood mononuclear cells (PBMCs) in allergic individuals, information on the responses to food allergens is quite scarce. An enhanced lymphocyte response to food antigens has been reported in patients with cow-milk protein intestinal intolerance (Scheinmann et al., 1976) and in those with enterocolitis caused by cow’s milk or soy (van Sickle et al., 1985). More recently, elevated PBMC responses to
Cytokine concentration at birth
T-helper lymphocytes are broadly divided into two types of cells based on the profile of cytokines produced by each subtype, TH1 and TH2 cells (Mosmann and Coffman, 1989). TH1 cells are involved in infections and in delayed hypersensitivity, while TH2 cells are responsible for the inflammatory response in allergic disease (Robinson et al., 1993). The concept that certain cytokines promote allergic reactions while others inhibit the allergic response is now a relatively well established one.
Conclusion
At present, there is no single predictor for development of allergic disorders. A positive family history coupled with the measurement of cord IgE offers the best choice available. If in the future, a particular indicator offers high sensitivity and specificity with excellent positive predictive value, the selection of who to test has to be rationalised. In addition, the question of when to test needs to be addressed. This is particularly true if preventive measures are to be taken from birth
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