[Iatrogenic angioedema: clinical features].
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Biomedical subjects
Publications and source records attributed to G Kanny.
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BACKGROUND: The prevalence of sesame allergy is increasing in European countries. Cases of severe allergy lack any evidence of specific immunoglobulin (Ig)Es by prick tests and CAPSystem-FEIA. The reasons for this negativity are unknown. METHODS: In 32 patients displaying immediate symptoms such as anaphylactic shock, asthma, urticaria, angioedema, sesame allergy was diagnosed by double-blind placebo-controlled food challenge (DBPCFC) or convincing clinical history. However, 10 patients had negative prick tests and CapSystem-FEIA. The specificity of IgEs was further investigated by enzyme-linked immunosorbent assay (ELISA), isoelectrofocalisation (IEF)-blotting, and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) blotting using total sesame extracts and purified fraction of oil bodies. Monospecific rabbit antibodies directed to two oleosin isoforms (15 and 17 kDa) were used. RESULTS: By ELISA, white sesame seed extract allowed the detection of higher levels of IgE than brown sesame extract. In all sera, numerous bands binding IgEs were detected by IEF or SDS-PAGE. In reducing conditions, two bands (15-17 kDa), could be separated from 2S albumin. Oleosins, present in oil bodies fractions, were recognized by IgEs from all sera. CONCLUSION: Oleosins are major allergens of sesame seeds and may be relevant to severe anaphylaxis. Falsely negative prick tests could be due to the lack of oleosins in presently available extracts, or to the fact that epitopes might be buried in the inner molecule. Detection tests currently used to identify sesame allergens based on sesame vicillins or other storage proteins could be insufficient for the detection of sesame seed contamination. Oleosins have been named Ses i 4 (17 kDa) and Ses i 5 (15 kDa), in accordance with the IUIS Nomenclature Committee.
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Exercise-induced anaphylaxis (EIA) is defined as the onset of allergic symptoms during, or immediately after, exercise, the clinical signs being various degrees of urticaria, angioedema, respiratory and gastrointestinal signs and even anaphylactic shock. Food-dependent exercise-induced anaphylaxis (FDEIA) introduces food in the syndrome and is revealed by a chronological sequence in which food intake, followed by exercise, induces symptoms after a varying period. When the food intake and the exercise are independent of each other, there are no symptoms. FDEIA is not very frequent. Identifying the culprit food allergen depends on the patient's eating habits. Crustaceans and wheat flour are the two commonest but others foods can be implicated. The patho-physiology of FDEIA has not been clearly established but it appears to result from degranulation of mast cells. As with food allergy, FDEIA diagnosis is based on interview, skin and biological tests and challenge. For the clinical signs of allergy, antihistamines, corticosteroids and epinephrine may be administered. Prophylaxis aims to prevent a recurrence; the patient should be given an emergency kit to deal with any recurrent episode. After the food allergen has been identified, it should be avoided for at least 4 to 5 hours before any exercise.
Prick-tests to foods are usually carried out as the first step in the diagnosis of food allergy. Severe anaphylaxis accounts for 4.9 % of allergies in children and occurs more frequently in adults, raising the possibility of systemic reactions to prick-tests in highly sensitized people. Several studies published in the literature have used commercial extracts. As for airborne allergens, concentrations causing a skin reaction of 15 mm do not present a risk of systemic reactions. Prick-tests to native foods--prick-in-prick tests--have been less extensively studied. The CICBAA1 data, from 1,138 food allergic patients of all ages, cover 34,905 prick-in-prick tests to foods. The wheal of these prick-tests has been regulary registered. The risk of systemic reactions can be evaluated at 0.008 %. There were no severe reactions and anti-histamine and corticosteroid therapy were sufficient. These results are similar to those of the large study in 2000 carried out by Devenney in neonates (0.005%). A review of the literature reveals only a few severe reactions in adults. The authors draw attention to the necessary precautions: temporary contra-indication for skin prick-tests in children and adults with grade 3 or 4 asthma, with particular attention to such foods as all kinds of nuts, fish, etc.
The risk of allergy to food proteins in cosmetics and topical medicinal agents is poorly evaluated. IgE dependent contact urticaria and contact dermatitis are observed. Eleven cases (7 infants and 4 women) are reported. Wheat, egg, oats, milk, peanut proteins are incriminated by prick-tests or atopy patch-tests. Cases are related to a previous food allergy and other ones may indicate primary sensitization to topical creams mainly used for skin care of atopic dermatitis. A consecutive exercise induced anaphylaxis to wheat and a long lasting sensitization to wheat have been observed. A clear and accurate identification of food allergens in cosmetics and topical agents is necessary. Given the hyper-permeability of infant skin, topical products containing food proteins of known allergenicity are contra-indicated for neonates, and for infants with atopic dermatitis, which may be associated with skin hyper-permeability.
BACKGROUND: A woman with a past history of allergy to artichoke presented with two episodes of immediate allergic reactions, one of which was a severe anaphylactic shock after eating two types of health foods containing inulin. RESULTS: Dot blot assay techniques identified specific IgEs to artichoke, to yoghurt F, and to a heated BSA + inulin product. Dot blot inhibition techniques confirmed the anti-inulin specificity of specific IgE. CONCLUSIONS: The absence of a positive reaction to an unheated milk-inulin mixture indicates the probability of protein-inulin binding. There is no cross-reactivity with the carbohydrates of the glycosylated allergens.
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Severe anaphylaxis is a systemic reaction affecting two or more organs or systems and is due to the release of active mediators from mast cells and basophils. A four-grade classification routinely places 'severe' anaphylaxis in grades 3 and 4 (death could be graded as grade 5). Studies are underway to determine the prevalence of severe and lethal anaphylaxis in different populations and the relative frequencies of food, drug, latex and Hymenoptera anaphylaxis. These studies will also analyse the risk arising from the lack of preventive measures applied in schools (personalized management protocols) and from the insufficient use of self-injected adrenalin. Allergy-related conditions may account for 0.2-1% of emergency consultations. Severe anaphylaxis affects 1-3 per 10 000 people, but for the United States and Australia figures are even higher. It is estimated to cause death in 0.65-2% of patients, i.e. 1-3 per million people. An increased prevalence has been revealed by monitoring hospitalized populations by reference to the international classification of disease (ICD) codes. The relative frequency of aetiological factors of allergy (food, drugs, insects and latex) varies in different studies. Food, drug and Hymenoptera allergies are potentially lethal. The risk of food-mediated anaphylaxis can be assessed from the number of personalized management protocols in French schools: 0.065%. Another means of assessment may be the rate of adrenalin prescriptions. However, an overestimation of the anaphylaxis risk may result from this method (0.95% of Canadian children). Data from the literature leads to several possibilities. First, a definition of severe anaphylaxis should be agreed. Secondly, prospective, multicentre enquiries, using ICD codes, should be implemented. Moreover, the high number of anaphylaxis cases for which the aetiology is not identified, and the variation in aetiology in the published series, indicate that a closer cooperation between emergency specialists and allergists is essential.
BACKGROUND: Food allergy to wheat induces different symptoms as atopic eczema/dermatitis syndrome (AEDS), urticaria and more severe reactions as wheat-dependent exercise-induced anaphylaxis (WDEIA). Different gliadin classes are involved in this allergy but IgE-binding epitopes are known only on omega5-gliadins and for WDEIA cases. OBJECTIVES: The aim of the study was to identify IgE-binding epitopes on several gliadin classes and for several patients with different symptoms and ages. METHODS: Eleven sera were analysed by pepscan with overlapping synthetic peptides. RESULTS: Sera from five patients with anaphylaxis, urticaria or WDEIA, displayed strong IgE-binding to sequential epitopes of the repetitive domains of alphabeta, gamma, omega2 or omega5-gliadins with two immunodominant epitopes on omega5-gliadin and a consensus motif of the type QQX1PX2QQ (X1 being L, F, S or I and X2 Q, E or G). One patient allergic to deamidated wheat proteins also had IgE to a repetitive peptide of gamma and omega2-gliadins of the type QPQQPFP. Sera from four patients with AEDS detected no linear epitopes on gliadins, despite the fact that they contained specific IgE to alpha, beta, gamma or omega-gliadins. One child with AEDS recognized cysteine-containing sequences in the nonrepetitive domains of alphabeta and gamma-gliadins. CONCLUSION: B epitopes in wheat allergy were different from B epitopes of coeliac disease. Differences exist in IgE-binding epitopes between patients with food allergy to wheat. IgE from those suffering from WDEIA, anaphylaxis and urticaria detected sequential epitopes in the repetitive domain of gliadins whereas IgE from AEDS patients probably recognized conformational epitopes.
A total of 4,737 people consulting allergologists were routinely tested for peanut sensitization. The study involved 84 allergologists in the Allergo-Vigilance Network over a period of 30-60 consecutive days. Investigation procedures were identical. Results classified subjects into four groups according to the clinical history and prick-tests to common inhalants: group 1: subjects suspected of having a food allergy; group 2: subjects with ongoing atopic disease; group 3: subjects with an underlying predisposition to atopy, as showed by one or more positive results to prick-tests with airborne allergens; group 4: non atopic subjects. The sensitization rates were 22.7%, 8.7%, 4%, and 0.4% respectively. Assuming that 25% of the French population is allergic the rate of sensitization to peanut in the general population should be between 1% and 2.5%. Considering a ratio of 3.3 between sensitization and clinical allergy as plausible, the prevalence of peanut allergy could be 0.3% to 0.75% of the French population. This figure is lower than that for the UK, the US and Canada (0.8% to 1.5%). The correlation between the data in this study and those from previous epidemiological studies validates the methodology used in this type of enquiry. One of the aims of the Allergo-Vigilance Network set up in 2001 is to collect data from a large number of people. We present here the results of a study carried out in 2002 by 84 allergologists in the Allergo-Vigilance Network. The primary aim was to assess the prevalence of peanut sensitization in the French population seeking treatment for various allergic disorders. The second objective was to determine whether there was any difference in risk of peanut sensitization in people with ongoing atopic disease, in those with an underlying predisposition to atopy (shown by positive prick-tests) and finally in non atopic people.
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Atopic dermatitis (AD) is one of the first manifestations of the atopic march. The natural history of food allergies (FA) is closely related to AD. Sensitivity to food is demonstrated with cutaneous tests (prick-tests and atopy patch-tests) or the presence of IgE specific to food. A true allergy to a foodstuff is revealed by oral provocation tests (OPT) or by improvement during an avoidance diet. Ingestion of the food allergen during OPT can provoke an onset of eczema, an immediate reaction (urticaria, oedema) or involve other target organs (digestive disorders, rhinitis, asthma or anaphylactic shock). Seven allergens are responsible for around 90 p. 100 of FA: milk, eggs, wheat, peanuts, nuts, soy and fish. The fundamental knowledge acquired demonstrates the implication of food allergens in the physiopathogenesis of AD. The assessment of the efficacy of avoidance diets is difficult to demonstrate in standardised double-blind studies. Their efficacy is demonstrated compared with the natural history of AD. A diagnostic algorythm of FA during AD is proposed. An avoidance diet can be prescribed on 3 levels: primary, secondary and tertiary prevention. Diagnostic dietetics are aimed at initiating a hypoallergenic diet over a short period of 15 to 21 days when AD is severe and does not permit an allergy assessment. This diet is followed by an allergy assessment and OPT to determine the foodstuff responsible. Therapeutic dietetics consists in initiating an avoidance diet based on the results of the allergy assessment: positive predictive value of specific IgE, positivity of oral provocation tests or the re-introduction of the foodstuff for one week. Preventive dietetics is aimed at preventing the onset of AD: a consensus has been established by the American and European Academies of Paediatrics. In conclusion, present knowledge demonstrates that FA is a triggering factor for AD and that the avoidance diets based on allergy assessments are an essential tool in the treatment of AD. Understanding the triggering mechanisms of oral tolerance will permit the development of strategies for the prevention and cure of food allergies.
Many active ingredients and excipients present in allopathic drugs derive from food allergens normally associated with compulsory food labelling. This study was undertaken to evaluate the presence of these components in the various pharmaceutical formulations of the 50 highest-selling drugs in French pharmacies in 2002 (in quantity and/or value), and to assess their labelling on the packaging of these drugs. The 174 pharmaceutical formulations of 86 drugs were studied and the composition of each one was identified using data-processing software. An excipient deriving from an allergen with obligatory labelling in food is present in 58.6% of the studied pharmaceutical formulations. Almost one third (32.2%) of these medications are correctly labelled since the excipients in question are already known to have adverse effects. This study demonstrates the actual presence of components derived from allergens with compulsory food labelling in the 50 highest-selling p maceutical products in France (in value and/or volume). Given the absence of clear labelling of food allergens in drugs, allergologists must inform both the medical and public communities of this potential risk. It is equally important that the pharmaceutical laboratories implement clear, informative labelling of food allergens, similar to that of the food industry.
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