Evaluating and managing pediatric food allergy
Evaluating and managing ?pediatric food allergy
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At a glance
- The primary risk factor for development of food allergy in a child is having a biological parent or sibling with a history of allergic disease.
For example, children with food allergy are four times more likely to have asthma, two times more likely to have atopic dermatitis, and nearly four times more likely to have respiratory allergies compared with children who have no food allergy.
- The factor most commonly identified with severe allergic reactions is coexistence of asthma, especially when the child has a peanut or tree-nut allergy.
The oral food challenge is the gold standard for diagnosing food allergy.
Although food allergy is seen in patients of all ages, it presents unique and specific concerns for the pediatric population. The National Institute of Allergy and Infectious Diseases has clinical guidelines in place for the evaluation and management of food allergy.1 The guidelines most pertinent to the pediatric population are outlined in this article.
Food allergy defined
Food allergy is an adverse health effect arising from a specific immune response that occurs reproducibly after exposure to a given food. Immunologic reactivity may be either immunoglobulin (Ig) E-mediated or non-IgE-mediated. In contrast, food intolerance is a nonimmunologic adverse reaction (e.g., the inability to digest lactose). A diagnosis of IgE-mediated food allergy requires the presence of allergen-specific IgE, which is produced during the process known as "sensitization," and onset of clinical symptoms after exposure to the allergen.
Food allergens are specific components of food (or an ingredient in food) — typically proteins — that are recognized by allergen-specific immune cells. The allergens elicit immunologic reactions. Some allergens cause reactions primarily if eaten raw, but most can cause reactions even after being cooked digested.
Methods for reporting food allergy vary, making determination of prevalence difficult. A 2007 meta-analysis found the overall prevalence of allergy to cow's milk, egg, peanut, fish or shellfish to be 12% in children who self-reported symptoms.2 Prevalence is much lower — 2.5% for adults and children combined — when self-reported symptoms and evidence of sensitization are considered. In the United States, the prevalence of allergy to the most commonly allergenic foods is estimated as follows: peanut, 1.3%; tree nut, 1.2%; seafood (children), 0.2%; cow's milk, 0.4%; and eggs, 0.2%.3,4
The primary risk factor for development of food allergy in a child is having a biological parent or sibling with a history of allergic disease. Allergic diseases include allergic rhinitis, atopic dermatitis, asthma and food allergy. Children at highest risk have preexisting severe allergic disease (significant atopic dermatitis or asthma) or a family history of food allergy. Approximately one-third of children younger than age 5 years who have moderate-to-severe atopic dermatitis develop IgE-mediated food allergy.5 Whether food allergy can exacerbate atopic dermatitis and what the mechanism might be is unclear.
Other allergic conditions are commonly seen in children with food allergy. For example, children with food allergy are four times more likely to have asthma, two times more likely to have atopic dermatitis, and nearly four times more likely to have respiratory allergies compared with children who have no food allergy. In children with asthma, coexistence of food allergy may be a risk factor for severe asthma exacerbations. Therefore, management of asthma in these children becomes extremely important.
Allergic responses can also occur following exposure to a food allergen that shares structural similarity with a different food or an aeroallergen. This cross-reactivity is demonstrated by the finding that a patient who is allergic to cow's milk has a 92% likelihood of having an allergy to goat's milk or that a patient with a tree-nut allergy has a 37% likelihood of being allergic to other tree nuts (e.g., walnuts and pecans are related).6
Perhaps a less obvious example of cross-reactivity is the patient who is allergic to cow's milk as well as beef (13%-20% chance7) or the egg-allergic patient who cannot tolerate poultry. Interestingly, some fruits (e.g., kiwi, banana, avocado) are allergenically related to latex. Therefore, patients who cannot tolerate these fruits must be questioned about their tolerance to latex because of the dangers that might be posed when children are exposed to balloons.
In short, patients allergic to one food may be allergic to another, with a higher propensity of allergy toward foods that are similar to one another.
Severity of allergic reactions is multifactorial and variable. The severity of a reaction cannot be accurately predicted, and the severity of past reactions does not predict severity of future reactions. Similarly, one cannot predict severity based upon food-specific IgE level or the wheal size in a skin-prick test (SPT). The factor most commonly identified with severe reactions is coexistence of asthma, especially when the child has a peanut or tree-nut allergy.
IgE-mediated vs. non-IgE-mediated reactions
Allergic hypersensitivity — a response in which an immunologic mechanism is defined or strongly suspected — can be either IgE-mediated or non-IgE-mediated. IgE-mediated responses are either nonatopic or atopic in nature. Nonatopic responses include insect stings, drug reactions, and helminth infiltration. Atopic reactions include allergic diseases. In IgE-mediated hypersensitivity, antibodies develop in response to antigen. With regard to food allergy, IgE-mediated reactions include food-induced anaphylaxis, oral allergy syndrome and allergic gastroenteritis.
Non-IgE-mediated hypersensitivity responses include T-cell, eosinophil and IgG-mediated reactions, such as allergic eosinophilic esophagitis (EoE), food protein-induced enterocolitis syndrome (FPIES), proctocolitis and celiac disease (gluten-sensitive enteropathy). To complicate matters, each of these illnesses may be accompanied by an IgE-mediated component.
Distinguishing between IgE-mediated and non-IgE-mediated reactions can be difficult. While symptoms vary from patient to patient, IgE-mediated symptoms generally include acute nausea, abdominal pain and vomiting. These symptoms typically occur with allergic manifestations in other target organs. Physical findings may include cutaneous reactions, such as urticaria, angioedema, rashes and flushing (Figure 1). Common respiratory manifestations include acute rhinoconjunctivitis and bronchospasm.
Patients with non-IgE-mediated disease will present with symptoms of gastroesophageal reflux, excessive spitting up, or emesis. In addition, the symptoms of EoE include dysphagia, intermittent abdominal pain, irritability, sleep disturbance, and failure to respond to conventional reflux medications. Children with eosinophilic gastroenteritis may also have a history of early satiety, failure to thrive, and/or weight loss.
Patients with food protein-induced enteropathies (including proctocolitis and enterocolitis) present very differently. The most common symptoms of proctocolitis include gross or occult blood in the stool; the disorder is most commonly seen in the first few months of life in an infant who is typically thriving. In FPIES, however, the infant may present with protracted vomiting and diarrhea that may or may not contain blood, dehydration, abdominal distention, and failure to thrive. Of note, vomiting typically is delayed for up to one to three hours after feeding. Patients with celiac disease typically have diarrhea or steatorrhea, abdominal distention, flatulence, weight loss or failure to thrive, oral ulcers, and possibly nausea and vomiting.