Early in life, immaturity of both immunologic and nonimmunologic components of the mucosal barrier in the gastrointestinal tract results in a marked increase in uptake of food antigens. However, despite the immune system of preterm infants being characterized as “immature compared to full term, the infants can respond appropriately to antigenic stimuli, as demonstrated in vaccination programs.
Very little is known of the immunologic response of preterm or low-birth-weight infants to dietary antigens. Studies in preterm newborns have shown increased food antigen uptake caused by increased intestinal permeability, which is inversely related to gestational age. The amount of antigenically intact proteins that is absorbed may be up to 100-fold greater when compared with full-term children. Because of this increased permeability, it has been proposed that an increased risk of IgE-mediated food allergy exists in premature children. In fact, Lucas et al assessed “latent systemic anaphylactic sensitization” to cows’ milk in 61 preterm infants. They found that infants of low birth weight who receive cow’s milk formula develop systemic sensitization more rapidly than infants born at term.
Low birth weight is considered to be related to immaturity of digestive and absorptive function, which might cause increased macromolecular absorption, leading to food allergy. Also, insufficient secretory IgA resulting from an immature gut immune system in low-birth-weight infants may result in greater penetration of allergens in early life and in subsequent development of food allergy.
However, some studies have not found this relationship. For example, de Martino et a; studied 80 preterm infants and compared them with 80 sex-matched and age-matched full-term infants at a mean age of 16 months. They found that the frequency of positive skin tests to foods and of atopic dermatitis were similar between the 2 groups. They suggested that increased intestinal permeability and antigen uptake have no role in triggering IgE sensitization to foods in these infants and that oral tolerance to food antigens may develop in preterm infants. Such tolerance might result from interaction of high antigen concentration with the immature immune system of the preterm infant.
Joel J. Liem found that prematurity or low birth weight do not play a role in the likelihood of food allergy. Additional large population studies should be undertaken to confirm this observation. Oral intake of highly allergenic proteins in early life may tolerize rather than sensitize children. Carefully designed and monitored studies are also required to inform the health care community as to the best approach to the introduction of foods for infants and young children. Goyal et al reported birth at late-preterm and low-normal gestational ages might be an important risk factor for the development of asthma and for increased health service use in early childhood. Robinson et al demonstrated an interaction between maternal smoking during pregnancy and prematurity on childhood wheezing in this urban, multiethnic birth cohort.
Lucas et al reported reactions to drugs were least likely to occur in infants who had been ventilated and were on multiple medications in the neonatal period, suggesting that drug tolerance may have developed. They speculate that preterm infants may be a high risk group for asthma and eczema, which could imply an association between atopy and prematurity. Hikino et all find that low birthweight was significantly associated with a lower risk of both food allergy and atopic dermatitis at 18 mo of age.
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