Browsing by Author "Lepp, Ute"

Chronic urticaria, recurrent angioedema and non-allergic asthma may be due to pseudoallergic reactions to food ingredients. For atopic dermatitis and gastrointestinal symptoms the role of these non-allergic reactions is discussed controversially. Pseudoallergic reactions can be elicited by food additives as well as naturally occurring food components. An altered histamine metabolism may be associated with pseudoallergy. Extensive diagnostic measures are not indicated for an acute urticaria or a short episode of angioedema. Only when symptoms become chronic or at least intermittent, basic diagnostic measures are justified. If this procedure is unsuccessful, pseudoallergy to food components should be considered as a causative factor. In order to confirm this suspicion, patients should adhere to a low pseudoallergen diet for 3 weeks. During this period, a daily documentation of symptoms is recommended. As the underlying pathomechanism is not IgE-mediated, skin and blood tests are not useful for diagnosis. After apparent improvement or remission of symptoms, the causative role of a low pseudoallergen diet can be proven by re-esposure to foods rich in Pseudoallergens over 2 days. As food additives only play a minor role in pseudoallergic reactions, a mixture of relevant food additives can be given at one time in most patients. Patients with asthma bronchiale or a history of anaphylactoid reactions should be challenged with single food additives in increasing doses. If adverse reactions to histamine are Suspected, an oral provocation with histamine dihydrochloride is recommended. For patients with respiratory symptoms inhalant challenge tests are suggested, Double-blind, placebo-controlled food challenge is recommended if the patient suffers from gastrointestinal symptoms only and pseudoallergy is suspected.

In adults, the majority of IgE-mediated food allergies is caused by cross-reacting allergen-molecular structures that are present in inhalant as well as food allergens. On the one hand, synthesis of IgE stimulated by a cross-reactive allergen in pollen can result in a diverse pattern of sensitizations against various foods. On the other hand, even anaphylactic reactions may occur after first consumption of a food containing a cross-reactive allergen. In clinical practice, it is not sufficient to detect cross-reactivities by immunologic assays. Clinically relevant sensitizations have to be distinguished from clinically irrelevant IgE responses. Hence, in cases of unclear history, oral challenge tests are necessary. A few open studies have demonstrated the therapeutic potential in pollen-related food allergy: in at least 50% of the cases, tree pollen immunotherapy led to an improvement of associated food allergies, However, these results have to be confirmed in placebo-controlled studies. As we are facing an increase of pollen allergies, a shift in sensitization patterns and changes in nutritional habits, the occurrence of new, so far unknown cross-reactions, is expected.

In adults, the majority of IgE-mediated food allergies is caused by cross-reacting allergen molecular structures that are present in inhalant as well as food allergens. On the one hand, synthesis of IgE stimulated by a cross-reactive allergen in pollen can result in a diverse pattern of sensitizations against various foods. On the other hand, even anaphylactic reactions may occur after first consumption of a food containing a cross-reactive allergen. In clinical practice, it is not sufficient to detect cross-reactivities by immunologic assays. Clinically relevant sensitizations have to be distinguished from clinically irrelevant IgE responses. Hence, in cases of unclear history oral challenge tests are necessary. A few open studies have demonstrated the therapeutic potential in pollen-related food allergy: in at least 50% of the cases, tree pollen immunotherapy led to an improvement of associated food allergies. However, these results have to be confirmed in placebo-controlled studies. As we are facing an increase of pollen allergies, a shift in sensitization patterns and changes in nutritional habits, the occurrence of new, so far unknown cross-reactions is expected.

Adverse food reactions are far more often perceived than objectively verified. In our scientific knowledge on non-allergic adverse reactions including the so called histamine intolerance, there are large deficits. Due to the fact that this disorder is increasingly discussed in the media and the internet, more and more people suspect it to be the trigger of their symptoms. The scientific evidence to support the postulated link between ingestion of histamine and adverse reactions is limited, and a reliable laboratory test for objective diagnosis is lacking. This position paper by the “Food Allergy”Working Group of the German Society for Allergology and Clinical Immunology (DGAKI) in collaboration with the German Association of Allergologists (AeDA), the Society for Pediatric Allergology and Environmental Medicine (GPA), and the Swiss Society for Allergology and Immunology (SGAI) reviews the data on the clinical picture of adverse reactions to ingested histamine, summarizes important aspects and their consequences, and proposes a practical diagnostic and therapeutic approach.

Detection of allergen-specific IgE represents the most important tool for in vitro diagnostic testing of food allergy. Applied methods vary in design (single allergen sources or mixtures, panel tests, single allergen components) and diagnostic efficacy. High specific IgE to liens egg, cows milk, peanut and fish is associated with an increased risk for clinical reactions, but rarely supersedes oral challenge tests. Cellular tests with basophil leukocytes, demonstrating IgE-mediated sensitizations indirectly, are useful only in selected cases. Particular protein families (i.e. Bet v 1 homologs, lipid transfer proteins and profilms) consist of allergenic molecules with similar sequence and structure. Their shared IgE binding sites form the basis of cross-reactivity. Cross-reactive carbohydrate determinants (CCD), frequently from plant origin, can also bind IgE being rarely clinically relevant. Allergy to plants (i.e. tree nuts, fruits, legumes) and animals (cows milk, liens egg, fish) is diagnosed with extracts, if their quality is sufficient. Detecting IgE to single allergenic components allows molecule-specific diagnoses, their value varies for each allergen source and single allergen component. Allergen-specific IgE detections are indicated in case of suspected food-allergic reactions despite uncertain history and skin tests, sensitizations to foods not applicable for skin testing, severe reactions to foods, conditions hampering skin testing or its interpretation, and in children. Interpreting should consider incorrect results due to inferior reagents or laboratory errors and clinically irrelevant results due to highly elevated total IgE, low assay thresholds or cross-reactive allergens (errors of interpretation). Positive test results indicate allergen-specific sensitizations, being clinically relevant only in case of corresponding symptoms. The following methods are not useful for diagnosing food allergy: bioresonance, electroacupuncture, kinesiology, cytotoxic food allergy test (methods without validity and/or evidence), lymphocyte stimulation test, food-specific IgG and IgG4 (methods with invalid interpretation).

The following guideline of the "Arbeits-gruppe Nahrungsmittelallergie der DGAKI und des ADA" (Task Force on Food Allergy of the German Society for Allergology and Clinical Immunology and the Medical Association of German Allergologists) summarizes different procedures, when food allergy is suspected in atopic dermatitis (neurodermatitis, atopic eczema). The problem is clinically relevant because many patients assume allergic reactions against foods being responsible for triggering eczematous reactions or worsening eczema. It is important to identify such patients who indeed benefit from an elimination diet and to avoid unnecessary diets. Elimination diets (especially in early childhood) are associated with the risk of malnutrition and additional emotional stress for the patients. The gold standard for the diagnosis of food-dependent reactions is to perform placebo-controlled, double-blind oral food challenges because specific IgE, prick tests and anamnestic data often do not correlate with clinical reactivity. This is particularly true in the case of delayed eczematous skin reactions. The instrument of diagnostic elimination diets should be used before an oral provocation test. If multiple sensitizations against foods are discovered in a patient, an oligoallergenic diet and a subsequent stepwise supplementation of the nutrition should be performed. If a specific food is suspected of triggering food allergy, oral provocation should be performed after a diagnostic elimination diet. As eczematous skin reactions may develop slowly (i.e., within one or two days), we recommend that the skin is inspected the day after the provocation test and that a repetitive test should be performed if the patient has not reacted to a given food on the first day of oral provocation. The guideline discusses various clinical situations for patients with atopic dermatitis, allowing for differentiated diagnostic procedures.

Skin tests have a central role in the diagnostics of food allergy. Particularly the prick test is established as a routine diagnostic tool. However, instable allergens and the lack of standardized extracts raise problems in the identification of sensitizations to food in suspected food allergy. Therefore, prick to prick tests with native foods are still recommended. The indications and contraindications do not differ with regard to common rules of skin testing in clinical allergology. We recommend a careful and restrictive application of skin tests in patients with a history of severe anaphylaxis to foods.