The role of cord blood total IgE as a marker for the development of food allergy is not clear. Studies do not consistently show a positive association (Dean 1997, Kjellmann et aJ. 1988, Kulig et aJ. 1999). Furthermore, in the recent German multicentre allergy study where an association between cord blood total IgE and sensitisation to foods at one year of age was found, the authors comment on the poor predictive performance of cord blood IgE (Kulig et aJ. 1999). This study puzzlingly also showed that an elevated cord blood total IgE was a significant protective factor for early-onset atopic eczema (Edenharter et al. 1998). Thus, cord blood total IgE is an unhelpful marker in predicting the development of food allergy and in planning appropriate prevention strategies.
Prenatal sensitisation with antigen-specific IgE has been reported but seems to be uncommon, and limited to cows' milk (Businco et al. 1983, Host et al. 1992). It is therefore unlikely to play a role in the vast majority of food allergy. None of the large birth cohort studies have demonstrated any specific IgE to foods in cord blood, including cows' milk, even in children who subsequently developed clinical or immunological sensitisation (Kjellmann et al. 1988, Hide et al. 1996, Kulig et al. 1999). It is therefore not surprising to find that dietary intervention in pregnancy has shown no benefit in modifying the natural history of IgE-mediated food allergy. Food sensitisation as measured by allergen-specific T-cell responses have been demonstrated in cord and fetal blood (Jones et al. 1998). However, none of these responses have been assessed to be risk factors in the development of food allergy. It is unclear whether these responses are derived from a memory T-cell population or from a naive population.
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