[Iatrogenic angioedema: clinical features].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D-A Moneret-Vautrin.
Explore the source record for details and available documents.
SCOPE: The eosinophil cationic protein (ECP) is one of the mediators released during eosinophil activation. These cells are effector cells taking part into the Th2-lymphocyte dependent allergic inflammation. Assaying ECP concentrations in blood and sputum may be useful in evaluating allergic inflammation (asthma and rhinitis). This summary considers the value of measuring ECP levels for the diagnosis of various diseases where an eosinophil-mediated tissue inflammation plays a role. CURRENT SITUATION AND SALIENT POINTS: Levels of eosinophil cationic protein have been determined in nasal secretions, sputum, gastric secretions, feces and serum. They are increased during seasonal allergic rhinitis and perennial rhinitis, allergic asthma and atopic dermatitis. They are also increased in various gastro-intestinal disorders, some of which are associated with IgE: eosinophil intestinal diseases (esophagitis, gastro-enteritis and colitis), gastro-intestinal food allergy and intestinal parasitoses. Finally, they are increased in non IgE-dependent disorders: non allergic asthma with aspirin intolerance, respiratory infections, sinonasal polyposis, Churg-Strauss disease and idiopathic hyper-eosinophilia (HES) syndrome. PERSPECTIVES: Assaying serum ECP could help in the diagnosis of several diseases. With parasitic disease the pathogenic progression may be accurately assessed, when serological tests are less indicative. ECP assay may point to non allergic asthma, either Fernand-Widal syndrome or Churg-Strauss disease. As for gastro-intestinal disorders, it indicates an eosinophilic tissue reaction. In the event of isolated hypereosinophilia, ECP assay may clarify whether it is benign or tending towards idiopathic HES. The assay of peroxidase and eosinophil-derived neurotoxin (EDN) should be also considered.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A case of oral allergy to dental alloys is presented, highlighting the interest of dosage of salivary nickel and of flow cytometry showing a selective CD4+ activation. The discrepancy between the rarity of oral allergy to dental alloys and the frequency of nickel sensitization and nickel-induced contact dermatitis leads to discuss the mechanisms of oral tolerance.
BACKGROUND: Mustard allergy accounts for 1.1% of food allergies in children. However, double-blind placebo-controlled food challenge trials (DB PCFCs) have not yet been proposed. OBJECTIVE: To carry out DB PCFCs to determine the real frequency of mustard allergy in patients sensitized to mustard. METHODS: A prospective study was conducted in 30 subjects aged 3-20 years presenting positive prick tests to ground mustard seeds (Brassica nigra), mustard flour (B. juncea), metabisulfite-free strong mustard seasoning (B. juncea) and a commercialized allergenic extract (B. nigra). Twenty-seven subjects were screened for mustard-specific immunoglobulin E (IgE). PCFCs were carried out either DB or single blind (SB) with up to 1340 mg of metabisulfite-free seasoning. RESULTS: The mean diameter of the wheal induced by prick tests with the allergenic extract was lower (n.s.) than that induced by the native mustard products: 5.8 mm (1.5-15) vs 6.9 mm (0.5-18) for B. nigra ground seeds, 7.8 mm (1-20) for B. juncea flour and 9.7 mm (3-20) for the strong mustard seasoning. The diameter of the wheal induced by the allergenic extract was significantly different from that induced by the mustard seasoning (P < 0.005). The mean of mustard specific-IgE values was 8.7 KU/l (0.35-72.4). Seven of 30 food challenges were considered positive. Mean prick test results in the positive and negative PCFC subgroups were 5.5 mm vs 5.9 mm for the commercialized extract, 10.9 mm vs 5.8 mm for B. nigra ground seeds (P < 0.01), 9.9 mm vs 7.1 mm for B. juncea flour (n.s. P > 0.25) and 11.5 mm vs 9.1 mm for the metabisulfite-free mustard seasoning (n.s. P > 0.1). Mean specific IgE values determined by CAP system radioallergosorbent test (Phadebas Pharmacia) were higher but not significantly so (P > 0.25) in the subgroup with mustard allergy (12.3 K/l vs 7.6 KU/l). CONCLUSIONS: About 23.3% of the sensitized subjects were allergic to a routine dose of mustard. Positive prick tests and the presence of specific IgE were not predictive. SB PCFC or DB PCFC is required before recommending avoidance diets.
A significant number of allergens arise from foods. The allergic risk of transgenic foods must be evaluated in accordance with the recommendations of the Joint Expert Committee FAO/WHO. Potential issues are the risk of cross reactivity with existing allergens, the modification of allergenicity of the transgenic protein induced by a modified metabolism in the host, the modified allergenicity of the proteins of the transgenic plant, a potential neo-allergenicity of the transgenic protein, and the risk of dissemination through pollens, inducing a respiratory sensitization then a cross food allergy. The algorithm includes three steps for evaluation: first the search for significant homology of the protein with allergens listed in allergen databanks, or the identity of a sequence of six aminoacids with known epitopes, then a cross reactivity explored through the binding to IgEs from patients allergic to the source of the gene, or allergic to organisms of the same group or botanical family, and finally the extent of the pepsine resistance. The risk of immunogenicity has to be studied with appropriate animal models. A post-marketing surveillance is recommended for monitoring of adverse effects. The structure of an Allergo-Vigilance Network, the tools for efficiency and the groups at higher risk will be discussed. The potential risk of transgenic foods to be allergenic cannot be overlooked, not ignoring the fact that current technologies modify allergenicity of foods.
The fact that more than 30 p. 100 of patients with chronic urticaria incriminate foods, and that acute urticaria is a frequent symptom of food allergy, argue in favour of a systematic search for food involvement in chronic urticaria. A global overview of publications through Medline selects 49 out of 189 papers upon strict criteria, devoted to the links between chronic urticaria and foods. Possible links exist between chronic urticaria and intolerance to additives, intolerance or allergy to contaminants, pseudo-allergic reactions to foods and IgE-dependent food allergy. The diagnosis of intolerance to additives relies on double blind placebo-controlled oral challenges, showing positivity in 2 to 3 p. 100 of cases. Flavours are being suspected but have not been validated by such oral challenges. Contaminants are nickel salts, penicillin residues in meats and milk, Anisakis larvae in fish. Intolerance to biogenic amines could be somewhat frequent and is well-documented by experimental studies of the metabolism of histamine and by the results of specific diets with a low content of amines. IgE-dependent food allergy has been evidenced in 1 to 5 p. 100 of cases. The author puts forward a methodology to search for the implication of foods in chronic urticaria, restricting the search to non-inflammatory CU, discarding moreover chronic urticaria due to physical agents, or to contact. Idiopathic chronic urticaria, that might include a subgroup of auto-immune chronic urticaria is under scope. A preliminary study of the regimen during one week needs to be carried out in order to detect an excess of consumption of categories of foods inducing pseudo-allergic reactions, or of additives. An eviction diet for biogenic amines may be proposed first. Its failure may lead to skin prick tests to foods that are daily consumed. Biological tests are not advised. When sensitization is confirmed, a 3 week eviction of the food comes ahead of a double blind placebo-controlled oral challenge. The positivity indicates that this food is likely to be a causal agent and the diagnosis can finally be based on the recovery after the implementation of strict avoidance diets.