Aetiology

Food allergy is likely to develop as a result of both genetic and environmental factors. With regard to genetic determinants:

  • Peanut allergy is 7 times more likely to occur in a child with a sibling who is peanut-allergic than in the general population[15]

  • Specific genes contributing to food allergy development have not been identified.

Environmental factors hypothesised to contribute to the development of allergy include:[16]

  • Reduced exposures to bacteria and infections (the hygiene hypothesis)

  • A rise in consumption of omega-3 polyunsaturated fatty acids

  • Reduced dietary antioxidants

  • Excess or deficiency of vitamin D

  • Possible cutaneous exposure[17]

While sensitisation to food proteins is the most common form of allergy to foods of both plant and animal origin, sensitisation to carbohydrate epitopes leading to allergic reaction to mammalian meat has been described. This form of food allergy involves sensitisation to the carbohydrate epitope galactose-alpha-1,3-galactose (alpha-gal). Alpha-gal is a carbohydrate moiety that is present on cells and tissues of all mammals except the higher order primates (including humans). Tick bites can lead to sensitisation of humans to alpha-gal, and subsequent ingestion of meat (e.g., beef, pork, lamb) leads to a delayed allergic reaction. The reaction typically occurs 3 to 6 hours after ingestion. Cross-reactivity with cetuximab has been reported (alpha-gal is present on the Fab portion of the cetuximab heavy chain).[18]

Pathophysiology

Immunoglobulin (Ig) E-mediated food allergy reactions are rapid in onset (usually within minutes to 2 hours of ingestion) and are the manifestation of a cascade of events.[19]

  • IgE antibodies to specific epitopes in the food allergen are produced by a patient with atopic disease.

  • These antibodies then bind to IgE receptors on mast cells and basophils found in the respiratory tract, gastrointestinal tract, and skin.

  • On exposure to the food allergen, the IgE antibodies are cross-linked, resulting in mediator release from the mast cells and basophils.

  • Cytokines, chemokines, histamine, prostaglandins, and leukotrienes are released, resulting in vasodilation, smooth muscle contraction, and mucus secretion.

Reactions may be generalised or localised to a specific organ system. Symptoms are believed to be related to mediator release from tissue mast cells and circulating basophils resulting in reactions such as urticaria and angio-oedema, rhinoconjunctivitis, gastrointestinal anaphylaxis, and generalised anaphylaxis. Non-IgE-mediated food allergies present with more chronic or subacute symptoms usually isolated to the gastrointestinal tract. IgE antibody-associated/cell-mediated food allergies may relate to homing of food-responsive T cells to the skin in the case of atopic dermatitis, or to mediators that home and activate eosinophils in the case of eosinophilic gastroenteropathies.[16]

Classification

Clinical classification by immune response[1]​​

IgE-mediated reactions. Presentations include:

  • Urticaria

  • Angio-oedema

  • Morbilliform rash

  • Acute rhinoconjunctivitis

  • Acute asthma

  • Anaphylaxis

  • Food-associated exercise-induced anaphylaxis.

Non-IgE-mediated reactions. Presentations include:

  • Contact dermatitis

  • Dermatitis herpetiformis

  • Food protein-induced enterocolitis syndrome

  • Coeliac disease

  • Heiner's syndrome.

Mixed IgE-mediated/non-IgE-mediated reactions. Presentations include:

  • Atopic dermatitis

  • Eosinophilic oesophagitis

  • Eosinophilic gastritis

  • Eosinophilic gastroenteritis.

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