Food Allergy or Food Intolerance

The prevalence of food allergy is increasing in industrialized countries. True food allergy can be defined as the presence of food-specific IgE, which results in a reproducible, immediate hypersensitivity reaction. Although 20 percent of adults believe that they have food allergy, only 3.7 percent of adults and 6 percent of children in the United States have a true IgE-mediated food allergy.

The diagnosis of food allergy can be complicated. Not all food reactions are mediated through IgE. For example, an infant with bloody stools due to milk ingestion — known as milk protein-induced protocolitis syndrome — does not have an IgE-mediated milk reaction, although many practitioners and patients refer to this as a “milk allergy.” This clinical scenario is more appropriately called “food intolerance.” In addition, the reactions to foods, even when mediated through IgE, can vary.

One-third of children with severe eczema will have foods that worsen their dermatologic disease. On the other hand, some patients with food allergy will have an anaphylactic reaction to an ingested allergen. To further complicate the issue, the presence of food-specific IgE does not imply a clinical reaction to the food; it merely demonstrates that a person is sensitized to the food. However, the presence of a clinical reaction within at least four hours, and often much sooner, consisting of urticaria, angioedema, wheezing, difficulty swallowing, hypotension, or any combination of these findings raises the clinical index of suspicion for IgE-mediated food allergy. The repeated ingestion of the triggering food will lead to a recrudescence of symptoms. The symptoms most commonly resolve over a few hours, not days or weeks. At times, the clinical symptoms can be life-threatening and require immediate, appropriate medical intervention.

The most common instigators of food-induced allergy and/or anaphylaxis in children and adults are milk, soy, egg, wheat, peanuts, tree nuts, fish, and shellfish. The evaluation of a patient suspected of having had a food-induced allergic reaction should include a complete history for the instigating food and the timing of the reaction. An evaluation of the presence of specific IgE to the suspected food should also be done.

Standardized, validated testing for antigen-specific IgE includes serum tests or skin prick testing. While serum tests document the level and presence of IgE, they do not document the functionality of the molecule. On the other hand, skin prick testing documents both the presence and the function of the specific IgE. Serum testing is done by incubating the patient’s serum with an antigen on a solid phase. A secondary antibody against the constant portion of the IgE molecule is then utilized to quantitate the amount of antigen-specific IgE present in the patient’s serum using a color reaction. Skin prick testing uses standardized, commercially available food extracts. The extract is pricked onto the patient’s skin. If cutaneous mast cells preloaded with specific IgE are present, the presence of the antigen results in mast cell degranulation, release of histamine, and the formation of an urticarial “wheal and flare” reaction.

There is a high rate of sensitization without clinical reaction to foods. Up to half of the people who have IgE to a specific food are able to eat that food without any clinical reaction. Thus, eliciting the history of the reaction is of paramount importance when diagnosing a true food allergy. On the other hand, most food IgE testing has an excellent negative predictive value, often 95–97 percent, making a negative test significantly reassuring that a person can ingest a suspected food without clinical sequallae.

It is important to note that, although reassuring, no test has a 100 percent positive or negative predictive value. When the result of the specific food ingestion is potential anaphylaxis, it is essential that even a food thought not to drive a clinical response be evaluated under safe and monitored conditions. This often involves an open or blinded food challenge in an allergist’s office.

Treatment of food allergy consists of food avoidance and the utilization of auto-injectable epinephrine. Since accidental ingestion of foods is common, patients with food allergies must read food labels carefully and should carry an auto-injectable form of epinephrine with them at all times. For children, this means having epinephrine available at school and having personnel on campus who are trained to use it. Reactions that require the use of epinephrine include diffuse urticaria, hoarseness, trouble swallowing, wheezing, stridor, and hypotension, all of which are clinical signs of significant mast cell degranulation causing anaphylaxis. Deaths and intensive care unit admissions due to anaphylaxis are associated with late and low-dose utilization of epinephrine, as well as with poorly controlled asthma.

The natural history of food allergy varies by age and etiology. The majority of children (approximately 80 percent) will outgrow a food allergy to milk, egg, soy, or wheat by the age of five years. Only 20 percent of children will outgrow a peanut allergy. Adult food allergy tends to be persistent. Since children often lose their food allergies over time, the state of their food sensitization should be re-evaluated every 1–2 years. Finally, the diagnosis, evaluation, and management of food allergy should involve an integrated care team of primary care physicians, allergist-immunologists, and nutritionists.