DESCRIPTION

Food allergy has recently been defined as “an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food.” Most commonly, the protein component of the food is responsible for the adverse immunologic response. An exception is the delayed reaction to meat, which is associated with IgE against the carbohydrate moiety, α-galactose.

• Classifications of food allergies:
  • IgE mediated, including
    • Anaphylaxis
    • Acute urticaria
    • Oral allergy syndrome
    • Galactose-α-1,3-galactose allergy
  • Non–IgE mediated (cell mediated), including
    • Food protein–induced enterocolitis syndrome (FPIES)
    • Food protein–induced allergic proctocolitis
  • Mixed IgE and non–IgE mediated, including
    • Atopic dermatitis
    • Eosinophilic gastroenteropathies (eosinophilic esophagitis, eosinophilic gastroenteritis)
• Most common IgE-mediated food allergies:
  • Children
    • Milk
    • Egg
    • Soy
    • Peanut
    • Wheat
    • Fish
    • Shellfish
    • Sesame
  • Adults
    • Peanuts
    • Tree nuts
    • Fish
    • Shellfish
• Most common non–IgE-mediated food allergies associated with food protein enterocolitis and proctocolitis:
  • Milk
  • Soy
  • Rice
  • Oat
  • Wheat
  • Barley
  • Chicken

EPIDEMIOLOGY

Food-induced anaphylaxis is the most common cause of anaphylactic reactions treated in emergency departments in the United States. The prevalence of food allergy has increased over the past 10 to 20 years.

RISK-FACTORS

• Timing of food introduction
• Genetic
• Family history
• Presence of atopic dermatitis
• Other unknown factors suspected

GENERAL-PREVENTION

• Recent studies have found that delaying introduction of food in babies increases risk of IgE-mediated reactions.
• Current recommendations are to begin adding solid foods between 4 and 6 months of age.
• High-risk infants (those with severe atopic dermatitis and IgE-mediated food allergy to egg) should be evaluated by allergist prior to peanut introduction (otherwise recommended to add into diet between 4 and 11 months of age).

ETIOLOGY

• Oral tolerance to food proteins believed to develop through T-cell anergy or induction of regulatory T cells. Food hypersensitivity develops when oral tolerance fails to develop or breaks down.
• IgE mediated: T cells induce B cells to produce IgE antibodies that initially bind on the surface of mast cells and basophils; when reexposed, the food protein binds to IgE antibodies, leading to degranulation of those cells and release of histamine and other chemical mediators.
• Non–IgE mediated (cell mediated): T cells react to protein-inducing proinflammatory cytokines, leading to inflammatory cell infiltrates and increased vascular permeability. These factors lead to subacute and chronic responses primarily affecting the GI tract.
• Mixed IgE and non–IgE mediated: Eosinophilic esophagitis and eosinophilic gastroenteropathy are characterized by eosinophilic infiltration of intestinal wall, occasionally reaching to serosa.

ASSOCIATED-CONDITIONS

• Asthma (4-fold more likely)
• Allergic rhinitis (2.4-fold more likely)
• Atopic dermatitis (1/3 of patients with severe atopic dermatitis has a food trigger.)