Allergic Food Reactions
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The topic of allergic food reactions is undoubtedly one of the most confused of clinical immunology. The term ‘allergic’ is frequently used inappropriately to describe all conditions where reproducible reactions are triggered by food ingestions, disappear on an elimination diet and recur on a blind challenge. ‘Food intolerance’ is the appropriate term to define the entirety of these conditions.
Allergic food reactions should be confined to those cases where an immune mechanism can be demonstrated. Most instances of food intolerance are not explained by a clear immunological mechanism, being caused by toxics (spices, sulphites) and pharmacological (caffeine, sodium nitrite) stimuli or by enzymatic deficiencies (lactose deficiency in some cases of milk intolerance). In these non-immune food reactions, however, many of the manifestations may be accounted for by activation of the alternative complement pathway. It is postulated that this pathway is triggered by non-immune stimuli such as food contaminants, leading to formation of anaphylotoxins such as C5a.
In the first year of life, food intolerance is relatively common, with cow’s milk being the most frequent initiating stimulus. It appears as gastrointestinal symptoms and possibly wheezing. In adults the foods most frequently involved in intolerance are milk, eggs, fish, nuts, wheat and chocolate. These food reactions frequently have an allergic pathogenesis. Symptoms include urticaria, angioedema, asthma, anaphylaxis and less frequently, nausea and vomiting. Such manifestations, but even more those comprising the oral allergy syndrome-swelling of the lips within minutes of food ingestions and tingling in the mouth and the throat-closely correlate with the presence of specific IgE and implicate a type I hypersensitivity as the mechanism responsible for the clinical manifestations.
Involvement of type I hypersensitivity can be documented by the detection of specific IgE using the RAST or, less expensively, with a skin prick test. The prick test, unfortunately, is only as good as the antigen it uses. Therefore, while antigenic preparations from eggs, milk or shellfish may provoke a positive skin reaction in sensitized individuals, highly purified preparations from apple are rarely do, even if a hypersensitive subject gives strikingly positive reactions when challenged with cruder preparations from apple juice or apple peel. The main diagnostic procedure in food intolerance is an elimination diet from which suspect foods are gradually removed until symptoms disappear. A positive diagnosis is made when symptoms reappear upon reintroducing a specific food. This challenge should be done in a double-blind manner using placebo controls. The challenge should be avoided, however, if the food is suspected to have caused systemic anaphylaxis in the past.
Allergic food reactions should be confined to those cases where an immune mechanism can be demonstrated. Most instances of food intolerance are not explained by a clear immunological mechanism, being caused by toxics (spices, sulphites) and pharmacological (caffeine, sodium nitrite) stimuli or by enzymatic deficiencies (lactose deficiency in some cases of milk intolerance). In these non-immune food reactions, however, many of the manifestations may be accounted for by activation of the alternative complement pathway. It is postulated that this pathway is triggered by non-immune stimuli such as food contaminants, leading to formation of anaphylotoxins such as C5a.
In the first year of life, food intolerance is relatively common, with cow’s milk being the most frequent initiating stimulus. It appears as gastrointestinal symptoms and possibly wheezing. In adults the foods most frequently involved in intolerance are milk, eggs, fish, nuts, wheat and chocolate. These food reactions frequently have an allergic pathogenesis. Symptoms include urticaria, angioedema, asthma, anaphylaxis and less frequently, nausea and vomiting. Such manifestations, but even more those comprising the oral allergy syndrome-swelling of the lips within minutes of food ingestions and tingling in the mouth and the throat-closely correlate with the presence of specific IgE and implicate a type I hypersensitivity as the mechanism responsible for the clinical manifestations.
Involvement of type I hypersensitivity can be documented by the detection of specific IgE using the RAST or, less expensively, with a skin prick test. The prick test, unfortunately, is only as good as the antigen it uses. Therefore, while antigenic preparations from eggs, milk or shellfish may provoke a positive skin reaction in sensitized individuals, highly purified preparations from apple are rarely do, even if a hypersensitive subject gives strikingly positive reactions when challenged with cruder preparations from apple juice or apple peel. The main diagnostic procedure in food intolerance is an elimination diet from which suspect foods are gradually removed until symptoms disappear. A positive diagnosis is made when symptoms reappear upon reintroducing a specific food. This challenge should be done in a double-blind manner using placebo controls. The challenge should be avoided, however, if the food is suspected to have caused systemic anaphylaxis in the past.
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