Wheat Allergy in Children: A Comprehensive Update

Abstract

Gluten-related disorders are very common in pediatric patients. Wheat allergy is triggered by an immunoglobulin E (IgE)-dependent mechanism; its prevalence varies according to the age and region, and in Europe has been estimated to be lower than 1%. Many studies investigated the potential role of several external factors that can influence the risk to developing wheat allergy, but results are still inconclusive. It can be responsible for several clinical manifestations depending on the route of allergen exposure: food-dependent exercise-induced anaphylaxis (FDEIA), occupational rhinitis or asthma (also known as baker’s asthma), and contact urticaria. The prognosis of IgE-mediated wheat allergy in children is generally favorable, with the majority of children becoming tolerant by school age. Patients who experienced an anaphylactic reaction prior to 3 years of age and patients with higher level of wheat- or ω-5 gliadin-specific IgE antibodies seem to be at higher risk of persistent wheat allergy. The current management of patients is dietary avoidance. Nowadays, oral immunotherapy has been proposed for wheat allergy with promising results, even if further studies are necessary to establish the best protocol in order to promote tolerance in wheat-allergic children.

Natural ingredients in cosmetic products—A suggestion for a screening series for skin allergy

“…It is the most common food grain worldwide due to its ability to grow in various climates. 75 Sensitization to wheat proteins can be oral, percutaneous, perimucosal, and/or rhinoconjunctival, and it may cause different disorders with different immunologic mechanisms. 75,76 Impaired skin barrier as in atopic dermatitis may increase the risk of sensitization via skin.…”

“…75 Sensitization to wheat proteins can be oral, percutaneous, perimucosal, and/or rhinoconjunctival, and it may cause different disorders with different immunologic mechanisms. 75,76 Impaired skin barrier as in atopic dermatitis may increase the risk of sensitization via skin. 59 The IgE-mediated type I allergic reactions are most common with symptoms such as urticaria, abdominal pain, or systemic anaphylaxis.…”

“…79 The remaining 15% of wheat proteins are water-soluble, nongluten proteins, including albumins and globulins, which also are implicated in wheat allergy and cross-react with grass pollen allergens. 75,80 Wheat protein and wheat gluten can be hydrolyzed enzymatically or chemically to its constituent amino acids to overcome insolubility, a process called deamidation. 81 Hydrolyzed wheat protein (HWP) and hydrolyzed wheat gluten (HWG) are added to skin care and hairdressing products for their emulsifying, stabilizing, moisturizing, and volumizing properties.…”

Is Gluten the Only Culprit for Non-Celiac Gluten/Wheat Sensitivity?

“…WA is a classic food allergy characterized by cutaneous, gastrointestinal or respiratory manifestations. These include wheat-dependent, exercise-induced anaphylaxis (WDEIA), which results from the combination of wheat ingestion and physical exercise, baker’s asthma and rhinitis, occurring after inhalation of wheat and cereal flours, which is one of the most common occupational allergies and contact urticaria [ 139 ]. Children with WA mainly display moderate-to-severe atopic dermatitis; wheat ingestion may also elicit IgE-mediated urticaria, angioedema, bronchial obstruction, nausea and abdominal pain, or even severe systemic anaphylaxis [ 140 ].…”

An updated overview of spectrum of gluten-related disorders: clinical and diagnostic aspects

“…In contrast to CD, different wheat components such as water-soluble (albumin and globulin) and water-insoluble (glutenin and gliadin) proteins contribute to the development of wheat allergy [ 102 – 104 ]. WA is more common in pediatric practice than adult medicine (the mean age of onset for WA is 5.5 years (3–16 years)) and the global prevalence of WA is reported at 0.5–1% [ 105 – 108 ]. Wheat allergy as a subgroup of food hypersensitivity is categorized into two groups; IgE-Mediated and non-IgE-Mediated WA [ 108 – 110 ].…”