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At least 19 recordsLinked to original sources
PubMed1996

[Food hypersensitivities].

Food hypersensitivity includes adverse reactions to food which are most often mediated by IgE. Food allergy is the first atopic disease. Food-sensitized individuals can develop allergic reactions such as atopic dermatitis, urticaria, angioedema, rhinitis, asthma or digestive symptoms. Anaphylactic shock is the most severe reaction of immediate hypersensitivity. The prevalence of food allergy has drastically increased during the last years. Numerous food products can be involved, with special emphasis on masked allergens in processed foods. The diagnosis of food hypersensitivity is based on clinical history, analysis of patient's food intake, skin tests and placebo-controlled food challenge tests. Oral food-challenge tests allow a distinction between food sensitization and true food hypersensitivity. Treatment consists in avoidance of the offending food allergen associated with adjunctive therapy by antihistamines and disodium cromoglycate. The prescription of a first-aid kit is required in case of anaphylaxis. Specific immunotherapy seems to be an interesting therapeutic prospect. Prevention remains essential.

Adult↗
PubMed2002

Improving in-vitro tests for the diagnosis of food hypersensitivity.

Food hypersensitivity reactions affect up to 8% of children under 3 years of age and approximately 2.5% of the general United States population. Food allergic disorders may be subdivided into either IgE-mediated or cell-mediated reactions. The diagnostic 'gold standard' of 'symptomatic' food allergies remains the blinded oral food challenge because of the poor specificity of patient histories, skin testing and standard radioallergosorbent tests, and the outcomes of elimination diets. Little progress has been made in the development of in-vitro tests for the diagnosis of cell-mediated food hypersensitivities. However, new developments in in-vitro technologies have improved the capabilities of these tests to diagnose IgE-mediated reactivity and perhaps predict the development of future 'tolerance', i.e. 'outgrowing' the allergy.

Allergens↗
PubMed1991

Food hypersensitivity.

Food allergy is one of several causes of adverse reactions to foods. The underlying immunologic mechanism varies from one manifestation to another, hence no current single laboratory test can be expected to be positive in every case. The diagnosis could be suggested by information gathered from the medical history or screening procedures, such as trials of elimination diets, the food/symptom diary, skin testing, and in vitro-specific IgE antibody measurement. All foods suspected by any of the aforementioned methods should be subjected to verification by appropriate elimination-challenge testing, preferably in a double-blind, placebo-controlled manner. Basically, treatment is dietary elimination, and its success requires identification and avoidance of all offending foods and control of other contributory factors.

Antibodies↗
PubMed2003

Antigen-specific histamine release in dogs with food hypersensitivity.

An in vitro evidence of IgE-mediated hypersensitivity to food allergens was detected by positive results of antigen-specific histamine release in dogs with food hypersensitivity. Eight dogs were diagnosed to have food hypersensitivity based on identification of offending food allergens with food elimination followed by oral food provocation. The percentages of histamine release against the stimulation of offending food allergens in the cases ranged from 2.1% to 70.9%. Six of the 8 cases showed histamine release higher than those of healthy control dogs. Four dogs showed relatively high histamine release at the percentage beyond 10% that was compatible with a positive value of histamine release in humans with food hypersensitivity. These findings would suggest that IgE-mediated hypersensitivity against food allergens could be involved in canine food hypersensitivity.

Animals↗
PubMed1989

Spontaneous release of histamine from basophils and histamine-releasing factor in patients with atopic dermatitis and food hypersensitivity.

Patients with hypersensitivity to food documented by a double-blind, placebo-controlled oral food challenge have been reported to have a high rate of release of histamine from basophils in vitro. To determine whether patients with atopic dermatitis and food hypersensitivity had similar high rates of spontaneous histamine release in vitro, whether dietary elimination of relevant food antigens affected this release, and whether a cytokine, histamine-releasing factor, could account for it, we evaluated 63 patients with atopic dermatitis and food hypersensitivity (38 of whom had eliminated the offending foods from their diets), 20 patients with atopic dermatitis without food hypersensitivity, and 18 normal volunteers. Patients with atopic dermatitis and food hypersensitivity were found to have higher rates of spontaneous release of histamine from basophils than controls (mean +/- SE, 35.1 +/- 3.9 percent vs. 2.3 +/- 0.2 percent; P less than 0.001). Those who had eliminated the offending food allergen from the diet for an extended period had a significantly lower rate of histamine release (3.7 +/- 0.5 percent; P less than 0.001). In patients with atopic dermatitis without food hypersensitivity, the rate (1.8 +/- 0.2 percent) did not differ from that in normal controls. Mononuclear cells from persons with food allergies spontaneously produced a histamine-releasing factor in vitro that provoked the release of histamine from the basophils of other food-sensitive persons, but not from those of normal controls. Patients who adhered to a restricted diet had a decline in the rate of spontaneous generation of the factor by their mononuclear cells. The histamine-releasing factor was found to activate basophils through surface-bound IgE. We conclude that in patients with food hypersensitivity, exposure to the relevant antigens produces a cytokine (histamine-releasing factor) that interacts with IgE bound to the surface of basophils, causing them to release histamine.

Adolescent↗
PubMed1991

Diagnostic testing of dogs for food hypersensitivity.

Thirteen food-allergic dogs were studied to evaluate the efficacy of feeding a commercially available egg and rice diet, intradermal skin testing, and serologic testing by ELISA for diagnosing and/or characterizing food hypersensitivity. Feeding of a home-cooked whole lamb meat and rice diet for 3 weeks, followed by challenge with each dog's regular diet, served as the standard for diagnosing food hypersensitivity. Each dog underwent provocative testing with 6 individual ingredients to determine as many of its dietary allergens as possible. Prior to skin testing and serologic testing by ELISA, most dogs had been recently exposed to the offending diet and subsequently manifested clinical signs of allergy. All dogs that tolerated the aforementioned commercial diet were exposed to it for at least 7 weeks; 84.6% of food-hypersensitive dogs ate the commercial diet with impunity. Of the 2 reactors to the commercial diet, only 1 became pruritic in response to provocation testing with chicken eggs. Low sensitivity and high specificity were found for skin testing and the ELISA, indicating a lack of true- and false-positive reactions. Neither the positive nor negative predictive values adequately predicted positive and negative reactions, respectively, for either test. On the basis of these results, the commercial diet, skin testing, and anti-IgE ELISA cannot replace an owner-prepared food elimination diet for food hypersensitivity testing in dogs.

Animal Feed↗
PubMedDate not supplied

[Digestive manifestations of food hypersensitivity in adults].

Food allergy, synonymous with food hypersensitivity (FHS), is defined as an immunologically-mediated adverse reaction to food. Initiation of FHS could result from a break in the immune mucosal barrier with abrogation of oral tolerance. Food hypersensitivity is mostly due to immediate-type reaction involving IgE-dependent mastocytes activation. Changes in intestinal function and structure have been mainly studies in an animal model of rat sensitized to egg albumin. Intraluminal antigen challenge resulted in abnormalities of gut absorption, secretion and motility in sensitized rats. In man, experimental data are scarce. Gastrointestinal manifestations of immediate FHS are varying and unspecific. A role for FHS in irritable bowel syndrome is debated. Participation of delayed-type FHS to digestive diseases is still questionable, but eosinophilic gastroenteritis might be an example. In clinical practice, diagnosis of FHS demands rigorous criteria. Double blind placebo-controlled food challenge has eventually proved to be the "gold standard" test for FHS diagnosis.

Animals↗
PubMed1983

Role of immediate food hypersensitivity in the pathogenesis of atopic dermatitis.

Twenty-six children with atopic dermatitis and markedly elevated serum IgE concentrations were evaluated for clinical evidence of hypersensitivity to foods with double-blind placebo-controlled food challenges. Selection of foods for challenges was based on positive prick skin tests (greater than 3 mm wheal) or a convincing history. At least one positive skin test to a food antigen was found in 24/26 patients. A total of 111 double-blind placebo-controlled challenges were performed in these children after suspect foods were eliminated from their diets for 10 to 14 days. There were 23 positive challenges in 15 children, 21 of which manifested as cutaneous symptoms, primarily pruritus and an erythematous macular and/or maculopapular rash involving 5% (or greater) of the body surface. In all, 14 children (54%) developed cutaneous symptoms after food challenges. All symptoms occurred within 10 min to 2 hr of challenge; nasal symptoms, mild wheezing, and gastrointestinal symptoms were seen in some children. No symptoms occurred in 104 placebo challenges. There were 86/111 clinically insignificant positive skin tests (77%) and three false-negative skin tests. These studies demonstrate that in some children with atopic dermatitis, immediate food hypersensitivity can provoke cutaneous pruritus and erythema, which leads to scratching and subsequent eczematoid lesions.

Adolescent↗
PubMed2001

Murine model of atopic dermatitis associated with food hypersensitivity.

BACKGROUND: Atopic dermatitis (AD) is an eczematous skin eruption that generally begins in early infancy and affects up to 12% of the population. The cause of this disorder is not fully understood, although it is frequently the first sign of atopic disease and is characterized by an elevated serum IgE level, eosinophilia, and histologic tissue changes characterized early by spongiosis and a CD4(+) T(H)2 cellular infiltrate. Hypersensitivity to foods has been implicated as one causative factor in up to 40% of children with moderate-to-severe AD. OBJECTIVE: The purpose of this study was to establish a murine model of food-induced AD. METHODS: Female C3H/HeJ mice were sensitized orally to cow's milk or peanut with a cholera toxin adjuvant and then subjected to low-grade allergen exposure. Histologic examination of skin lesions, allergen-specific serum Ig levels, and allergen-induced T-cell proliferation and cytokine production were examined. RESULTS: An eczematous eruption developed in approximately one third of mice after low-grade exposure to milk or peanut proteins. Peripheral blood eosinophilia and elevated serum IgE levels were noted. Histologic examination of the lesional skin revealed spongiosis and a cellular infiltrate consisting of CD4(+) lymphocytes, eosinophils, and mast cells. IL-5 and IL-13 mRNA expression was elevated only in the skin of mice with the eczematous eruption. Treatment of the eruption with topical corticosteroids led to decreased pruritus and resolution of the cutaneous eruption. CONCLUSION: This eczematous eruption resembles AD in human subjects and should provide a useful model for studying immunopathogenic mechanisms of food hypersensitivity in AD.

Animals↗
PubMed1988

Comparative study of commercial food antigen extracts for the diagnosis of food hypersensitivity.

Single lots of food allergen extracts from three different commercial sources were compared for their efficacy in evaluating immediate food hypersensitivity. Eighty-seven children with atopic dermatitis and food hypersensitivity underwent prick skin testing to a battery of 18 food extracts from each company. Results of skin tests were compared with results of double-blind, placebo-controlled oral food challenges and open challenges to determine the sensitivity, specificity, and predictive indices of each reagent. Negative predictive indices were generally good for all reagents, whereas positive predictive indices were generally poor and showed considerable variation (0% to 79%) between commercial sources. Under the conditions of the study, skin test reagents from two companies showed slightly better agreement with double-blind, placebo-controlled food challenge results than did reagents from the third company. However, with known lot-to-lot variations in extract potency and intrapatient variation in skin test results, these differences probably are not of clinical significance.

Administration, Oral↗
PubMed1992

The immunopathogenic role of food hypersensitivity in atopic dermatitis.

Food hypersensitivity is reported to play an immunopathogenic role in atopic dermatitis in approximately one-third of children. In 320 selected children with moderate to severe atopic dermatitis, 63% of children were found to have food hypersensitivity by double-blind placebo-controlled food challenges. Both IgE-mediated mast cell and mononuclear cell activation appear responsible for the eczematous lesions resulting from ingestion of food allergens.

Adult↗
PubMed1983

[Food hypersensitivity in infants].

In a group of 41 infants with immediate, IgE mediated, food hypersensitivity, food anamnesis was specific in 60 per 100 and food challenge positive in 29 out of 34 times. Total serum IgE levels were raised in 80 per 100. In 26 instances symptoms appeared with the first food intake (15 cases) or there was sensitization before ingestion (11 cases); all but three were breast fed. Moreover, breast feeding in patients of the whole group had higher prevalence (p less than 0,001) than in a non-sensitized control group. These results suggest that food hypersensitivity in infants occurs very often without previous antigen intake and it is not always followed by clinical intolerance. Breast milk and/or transplacental antigen passage are probably important ways of sensitization. If so, it seems that minute quantities of antigen may be more fit for sensitization, provided the possible genetic high responsiveness for IgE synthesis in those infants.

Animals↗
PubMed1989

Natural history of food hypersensitivity in children with atopic dermatitis.

Patients with atopic dermatitis and food hypersensitivity who were adhering to an elimination diet underwent repeat double-blind, placebo-controlled oral food challenges annually for follow-up of their food allergy. After 1 year, 19 of 75 patients lost all signs of clinical food hypersensitivity (15 of 45 patients allergic to one food, and 4 of 21 allergic to two foods). Of the individual foods, 38 of 121 no longer elicited symptomatic responses. After 2 years, patients underwent a second rechallenge; 4 of 44 patients tested lost their clinical food hypersensitivity. In 20 patients undergoing a third rechallenge, no food hypersensitivity was lost. Loss rate of food hypersensitivity varied among foods; after 1 year, there was a 26% loss of symptomatic food allergy to five major allergens (egg, milk, soy, wheat, and peanut) compared with a 66% loss rate to other food allergens. Loss of symptomatic allergy was not affected by the patient's age at diagnosis, except with milk allergy, for which older patients were more likely to lose clinical food hypersensitivity (p less than 0.05). Total serum IgE and prick skin tests were not useful for predicting loss of symptomatic food hypersensitivity. There was no significant decrease in skin test wheal size corresponding to loss of clinical food hypersensitivity. Patients developing only skin symptoms during the initial challenge were most likely to lose symptomatic food hypersensitivity.

Adolescent↗
PubMed1996

Pathogenic role of thromboxane A2 in immediate food hypersensitivity reactions in children.

BACKGROUND: Food hypersensitivity, from the standpoint of pathogenesis as well as clinical management, remains controversial. During the food allergen-induced immediate hypersensitivity reaction, various chemical mediators are released. OBJECTIVE: The purpose of our study was to determine whether thromboxane A2 participates in food antigen-induced responses in children with food hypersensitivity. METHODS: Nine open food challenges were performed in nine patients with suspected food hypersensitivity. Plasma thromboxane B2 and histamine levels were measured during a 24-hour period following the challenge. RESULTS: All the patients demonstrated immediate reactions after food challenge. The mean plasma thromboxane B2 level (a marker of thromboxane A2 activity) rose significantly at two hours and three hours after the challenge. Simultaneously, the mean plasma histamine level rose significantly at two hours and three hours after the challenge. CONCLUSIONS: The results suggest that thromboxane A2 may play a pathogenic role in part in the immediate reaction after food challenge and that thromboxane A2 is probably released from a common cellular source (eg, mast cell) with histamine and/or by a common mechanism (eg, IgE-dependent platelet activation).

Child↗
PubMed1992

[Prevalence of putative food hypersensitivity in young children].

UNLABELLED: Prevalence, symptoms and family prevalence of food hypersensitivity and other hypersensitivities were investigated in a group of 5-6-year old children (n = 1039) in a rural area of the Netherlands using a questionnaire for the parents. Subsequently parents were asked about their actions once they suspected their child of food hypersensitivity. According to 23.1% of the parents their child was hypersensitive, and mostly food hypersensitive (11.4%). In particular, gastrointestinal symptoms, crying spells in infancy and behaviour problems were reported. These symptoms were usually caused by cows' milk, food additives and chocolate. Most of the food hypersensitive children experienced their first problems before their first birthday. Although only 39% of these children were examined, 91.5% of the parents of the so-called food hypersensitive children restricted the food intake of their children. CONCLUSION: Many parents consider their children to be food hypersensitive and they restrict the food intake without any examination.

Child, Preschool↗
PubMed1983

Food allergy: how much in the mind? A clinical and psychiatric study of suspected food hypersensitivity.

Objective evidence of food hypersensitivity was sought by the use of exclusion diets and provocation tests in 23 patients who attributed a wide variety of symptoms to food allergy. Hypersensitivity to ingested substances was confirmed in 4, each of whom presented with typical atopic symptoms. None of these had psychological symptoms, but a high incidence of psychiatric disorder was found in patients whose belief that they had a food allergy could not be confirmed.

Adult↗
PubMed1983

Food hypersensitivity in irritable bowel syndrome.

Food hypersensitivity as a cause of abdominal symptoms was investigated by means of exclusion diets and double-blind food provocation in patients with irritable bowel syndrome. Twenty-seven patients entered the study; nineteen complied with dietary manipulation. Food hypersensitivity as a cause of their presenting symptoms was confirmed by double-blind food provocation in only three patients, who also had evidence of associated atopic disease and positive skin tests to common inhalant allergens. Evidence of minor psychiatric disorder was found in twelve of fourteen patients examined by an independent psychiatrist.

Adolescent↗