edited by Elisa Magnanelli M.D.
Wheat allergy is an adverse reaction to wheat proteins with an immunological basis. According to many studies 0.5 - 4 percent of population experiences this allergic disorder.
Anti-IgE antibodies play an essential role in its pathogenesis, but depending on the route of entry of the allergen and the underlying immunological mechanism, wheat allergy can take several clinical forms:
Allergic response to wheat ingestion can be divided into two types. Wheat-Dependent Exercise Induced Anaphylaxis(WDEIA), which is a well-defined syndrome caused by a particular wheat protein: Omega-5-Gliadin, and other non-specific allergic forms as atopic dermatitis, urticaria and anaphylaxis, which seem to be related to a large variety of wheat proteins. Studies with purified proteins, testing bond with serum IgE of patients affected by such non-specific forms, showed that 60% of patients had anti-alpha-gliadin, anti-beta-gliadin and anti-subunit low molecular weight IgE antibodies, while 55% had anti-gamma-gliadin, 48% anti-omega-gliadin and 26% anti-subunit high molecular weight antibodies.
Patients with WDEIA exhibit clinical symptoms varying from generalized urticaria to serious allergic reaction including anaphylaxis.
Using synthetic peptides, researchers identified seven epitopes (i.e. the part of an antigen that is recognized by antibodies) in the primary sequence of omega-5-gliadin, which are the main responsible for allergic reaction: QQIPQQQ, QQLPQQQ, QQFPQQQ, QQSPEQQ, QQSPQQQ, QQYPQQQ e PYPP.
Four of these epitopes proved to be dominant (QQIPQQQ, QQFPQQQ, QQSPEQQ e QQSPQQQ), and mutational analysis of QQIPQQQ and QQFPQQQ epitopes suggests that amino acids at position glutamine-1, proline-4, glutamine-5, glutamine-6 e glutamine-7 play a critical role in IgE binding.
Since the Roman Empire, Rhinitis and Baker's Asthma are well-known diseases, arising from an allergic response to flour and grain dust from wheat and other cereals.
A Polish research showed that in a population of apprentice bakers, the frequency of baker's asthma was 4,2% after one year and 8,6% after two years, whereas rhinitis appeared in 8,4% after one year and in 12,5% after two years.Baker's asthma, often preceded by rhinitis, appears as dyspnea (shortness of breath, air hunger) especially with difficulty in exhalation (i.e. breathing out), due to contraction of bronchiole muscles caused by allergic reaction.
Diagnosing baker's asthma includes skin prick tests and RAST tests to detect specific IgE antibodies directed against wheat, barley or rye flour, or anti-alpha-amylase IgE antibodies.
Recent studies have identified single proteins responsible for baker's asthma and a specific wheat protein family (alpha-amylase inhibitor) is likely to contain most important allergens. Nevertheless baker's asthma can also be attributed to other wheat proteins, including wheat germ agglutinin, peroxidase and non-specific lipid transfer proteins (LPTs). It is interesting to point out that the last two types of proteins probably cause also food wheat allergy.
Prick Tests and RAST are first-line diagnostic test as far as wheat allergy is concerned; however their predictive value is inferior to 75%, especially in adults, due to cross reactivity with grass pollen. Moreover many reagents for skin prick testing for sale have low sensitivity because they are mixtures of water-soluble wheat proteins lacking in allergens contained in the water-soluble gliadin fraction. This problem can be partly solved testing single allergens one by one, but often oral administration of wheat components is necessary to make a definitive diagnosis of e.g. food wheat allergy.
In the last few years many wheat proteins have been isolated and identified as allergens; some of them are currently used in IVD (in vitro diagnostic tests), improving their accuracy and sensitivity.
On the other hand there is no evidence that the detection of IgG anti-gliadin antibodies in serum determines the presence of disease.