Food Allergy

The terms food allergy and food hypersensitivity are synonymous. Food “allergy” is distinguished from food “intolerance” in that it includes a true allergic, immunologic response ( Fig. 69.1 ). Food intolerances are not immunologic responses. Allergic responses may be acute and may result in anaphylaxis (a rare occurrence) or may be chronic.

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Intestinal Disturbances Resulting From Food Allergy.

This diagram demonstrates the entry of proteins through the intestinal epithelium that become attached or react with lymphocytes within Peyer's patches or with macrophages. The reaction is different if it is a T cell or a B cell. The T cells produce non–IgE-mediated reactions through the mechanisms listed in the box on the right. The B cells can stimulate this process or stimulate the IgE-mediated process and activate mast cells. There are also mixed IgE and non–IgE-mediated conditions, such as eosinophilic enteritis.

Although its incidence is difficult to determine, food hypersensitivity occurs in approximately 2% of the general population and in as many as 6% of young children. However, anecdotal experience indicates a much higher incidence, with many patients not seeking assistance or medical advice because they eliminate foods they identify as causing symptoms. Common foods associated with symptoms are milk, eggs, fish, tree nuts, shellfish, soybeans, fruits, and wheat. Children tend to outgrow the symptoms; in adulthood, the foods most often associated with food hypersensitivity are peanuts, tree nuts, fruits, fish, and shellfish.

The pathophysiology of food allergy is becoming clearer. True hypersensitivity reactions usually are mediated through immunoglobulin E (IgE) and associated with atopy. However, these findings are not essential when an alleged exposure can be demonstrated by an exclusion diet. Although IgG and IgA antibodies are demonstrated in celiac disease, the demonstration of these antibodies in other food allergies has been controversial. Immediate-phase reactions are IgE mediated, with inflammatory mediators released from mast cells. However, some hypersensitivity reactions are non-IgE mediated and involve histamine release from mast cells. Therefore both IgE hypersensitivity and non-IgE hypersensitivity exist. It is also clear that new understandings of the physiology of response are coming forth, particularly, in such areas as calcitonin gene–related peptides (CGRP), where the understanding of nociception is being elaborated.

Non-IgE food allergy is T cell–mediated, but mixed IgE-mediated and non–IgE-mediated conditions appear to involve the gut, including eosinophilic esophagitis, gastritis, or gastroenteritis.