Dietary Protein Enterocolitis and Gastrointestinal Food Allergy in Childhood
Gastrointestinal food allergies are a spectrum of disorders that result from adverse immune responses to dietary antigens. The named disorders include immediate gastrointestinal hypersensitivity (anaphylaxis), oral allergy syndrome, allergic eosinophilic esophagitis, gastritis, and gastroenterocolitis; dietary protein enterocolitis, proctitis, and enteropathy; and celiac disease. Additional disorders sometimes attributed to food allergy include colic, gastroesophageal reflux, and constipation. The pediatrician faces several challenges in dealing with these disorders because diagnosis requires differentiating allergic disorders from many other causes of similar symptoms, and therapy requires identification of causal foods, application of therapeutic diets and/or medications, and monitoring for resolution of these disorders.
The symptoms observed in infants with dietary protein enterocolitis seem similar to but more severe than those observed in protein enteropathy. Because both the small and large bowel are involved, the term “enterocolitis” is used. The disorder must be differentiated from nonallergic causes of enterocolitis (eg, infection, neonatal enterocolitis). Cow milk protein is the most common cause, but approximately half of patients also react to soy. A variety of additional foods have been implicated, including rice, oat and other cereal grains, and poultry. During chronic or intermittent ingestion of the causal food protein, infants may experience such severe vomiting and diarrhea that dehydration, lethargy, acidosis, and methemoglobinemia may result, and infants may seem septic with high peripheral blood polymorphonuclear leukocyte counts. Resolution of symptoms occurs after appropriate dietary exclusion.
A distinct feature of this disorder is that reintroduction of the causal protein leads to a delayed (∼2 hours) onset of dramatic symptoms that has been used to confirm the diagnosis by oral food challenge. Confirmation of the allergy includes a negative search for other causes; improvement when not ingesting the causal protein; a positive oral challenge resulting in vomiting/diarrhea; and evidence of gastrointestinal inflammation through stool examination for blood, eosinophils, and a rise in the peripheral polymorphonuclear leukocyte count over 3500 cells/mL. Caution is needed when performing oral food challenges because approximately 20% of reactions lead to shock. The diagnosis is usually made without biopsy, but colonic biopsies in symptomatic patients reveal crypt abscesses and a diffuse inflammatory cell infiltrate with prominent plasma cells; small bowel biopsies reveal edema, acute inflammation, and mild villous injury. The mechanism underlying this disorder seems to involve a milk-specific T cell response with elaboration of the cytokine tumor necrosis factor-α that may also account for some of the systemic symptoms. That several foods are often involved may reflect a more global problem in immune tolerance for these infants.
The disorder is not associated with IgE antibody (but a small subset of patients may eventually establish IgE antibody responses). Considering the high rate of co-allergy to cow milk and soy, treatment with a hypoallergenic formula (casein hydrolysate) is suggested and usually effective (if not, then an amino acid-based formula can be used). It may be advisable to delay the introduction of other allergenic foods, especially grains, in these children. Treatment of acute reactions (reexposure) may require fluid resuscitation, and administration of steroids has been suggested. Most infants outgrow the allergy by age 2 or 3 years, but some seem to maintain hypersensitivity into childhood. Because resolution must be proved through oral challenges that can induce severe reactions, evaluation must be undertaken cautiously under supervision in a controlled setting, usually with intravenous access in place.
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