Chapter 145 Adverse Reactions to Foods
Adverse reactions to foods consist of any untoward reaction following the ingestion of a food or food additive and are classically divided into food intolerances, which are adverse physiologic responses, and food hypersensitivities, which include adverse immunologic responses and allergies (Tables 145-1 to 145-3). Like other atopic disorders, food allergies have increased over the past 3 decades, primarily in “Westernized” countries, and now affect an estimated 3.5% of the U.S. population. Up to 6% of children experience food allergic reactions in the 1st 3 yr of life, including about 2.5% with cow’s milk allergy, 1.5% with egg allergy, and 1% with peanut allergy. Most children “outgrow” milk and egg allergies, with about 50% doing so within 3-5 yr. In contrast, about 80-90% of children with peanut, nut, or seafood allergy retain their allergy for life.
Table 145-1 ADVERSE FOOD REACTIONS
FOOD INTOLERANCE
Host Factors
Enzyme deficiencies—lactase (primary or secondary), fructase (maturational delay)
Gastrointestinal disorders—inflammatory bowel disease, irritable bowel syndrome
Idiosyncratic reactions—caffeine in soft drinks (“hyperactivity”)
Psychologic—food phobias
Migraines (rare)
Food Factors
Infectious organisms—Escherichia coli, Staphylococcus aureus, Clostridium
Toxins—histamine (scombroid poisoning), saxitoxin (shellfish)
Pharmacologic agents—caffeine, theobromine (chocolate, tea), tryptamine (tomatoes), tyramine (cheese)
Contaminants—heavy metals, pesticides, antibiotics
FOOD HYPERSENSITIVITIES
IgE-Mediated
Cutaneous—urticaria, angioedema, morbilliform rashes, flushing, contact urticaria
Gastrointestinal—oral allergy syndrome, gastrointestinal anaphylaxis
Respiratory—acute rhinoconjunctivitis, bronchospasm
Generalized—anaphylactic shock, exercise induced anaphylaxis
Mixed IgE- and Cell-Mediated
Cutaneous—atopic dermatitis, contact dermatitis
Gastrointestinal—allergic eosinophilic esophagitis and gastroenteritis
Respiratory—asthma
Cell Mediated
Cutaneous—contact dermatitis, dermatitis herpetiformis
Gastrointestinal—food protein–induced enterocolitis, proctocolitis, and enteropathy syndromes, celiac disease
Respiratory—food-induced pulmonary hemosiderosis (Heiner syndrome)
Unclassified
Cow’s milk–induced anemia
IgE, immunoglobulin E.
Table 145-2 DIFFERENTIAL DIAGNOSIS OF ADVERSE FOOD REACTIONS
GASTROINTESTINAL DISORDERS (WITH VOMITING AND/OR DIARRHEA)
Structural abnormalities (pyloric stenosis, Hirschsprung disease)
Enzyme deficiencies (primary or secondary):
Disaccharidase deficiency—lactase, fructase, sucrase-isomaltase
Galactosemia
Malignancy with obstruction
Other: pancreatic insufficiency (cystic fibrosis), peptic disease
CONTAMINANTS AND ADDITIVES
Flavorings and preservatives—rarely cause symptoms:
Sodium metabisulfite, monosodium glutamate, nitrites
Dyes and colorings—very rarely cause symptoms (urticaria, eczema):
Tartrazine
Toxins:
Bacterial, fungal (aflatoxin), fish-related (scombroid, ciguatera)
Infectious organisms:
Bacteria (Salmonella, Escherichia coli, Shigella)
Virus (rotavirus, enterovirus)
Parasites (Giardia, Akis simplex [in fish])
Accidental contaminants:
Heavy metals, pesticides
Pharmacologic agents:
Caffeine, glycosidal alkaloid solanine (potato spuds), histamine (fish), serotonin (banana, tomato), tryptamine (tomato), tyramine (cheese)
PSYCHOLOGIC REACTIONS
Food phobias
Etiology
Adverse reactions to foods may result from intolerances, which are based on functional properties of foods, or from physiologic responses of the host, including hypersensitivities and adverse immunologic responses (see Table 145-1). Although food represents the largest antigenic load confronting the body, the gut-associated lymphoid tissue (GALT) is able to readily discriminate between “harmless” foods and pathogenic organisms. Ingestion of food normally leads to oral tolerance, which is the induction of T-cell anergy and T regulatory cells that enable the systemic immune system to “ignore” the roughly 2% of antigenic protein normally entering the systemic circulation at each meal. In young infants, functional barriers (stomach acidity, intestinal enzymes, glycocalyx) and immunologic barriers (secretory immunoglobulin [Ig] A) are immature, allowing increased penetration of food antigens, and the GALT appears less capable of “tolerizing” than the mature system. Consequently, food hypersensitivity reactions most commonly develop at this susceptible age.
Pathogenesis
Children in whom IgE-mediated food allergies develop may be sensitized by food allergens penetrating the gastrointestinal barrier, which are class 1 food allergens, or by partially homologous allergens such as plant pollens penetrating the respiratory tract, which are class 2 food allergens. Any food may serve as a class 1 food allergen, but egg, milk, peanuts, tree nuts, fish, soy, and wheat account for 90% of food allergies during childhood. Many of the major allergenic proteins of these foods have been characterized. There is variable but significant cross reactivity with other proteins within an individual food group. Exposure and sensitization to these proteins often occur very early in life, because intact food proteins are passed to the infant through maternal breast milk, and after introduction of solid foods, many parents strive to provide their infants with a highly varied diet. Virtually all milk allergies develop by 12 mo of age and all egg allergies by 18 mo of age, and the median age of 1st peanut allergic reactions is 14 mo. Class 2 food allergens are typically plant or fruit proteins that are partially homologous with pollen proteins (see Table 145-3). With the development of seasonal allergic rhinitis from birch, grass, or ragweed pollens, subsequent ingestion of certain uncooked fruits or vegetables provokes the oral allergy syndrome. Intermittent ingestion of allergenic foods may lead to acute symptoms, whereas prolonged exposure may lead to chronic disorders such as atopic dermatitis and asthma. Cell-mediated sensitivity typically develops to class 1 allergens.
