Prevalence of parent-reported immediate hypersensitivity food allergy in Chilean school-aged children

BackgroundFood allergies (FAs) affect 2–4% of school-aged children in developed countries and strongly impact their quality of life. The prevalence of FA in Chile remains unknown.MethodsCross-sectional survey study of 488 parents of school-aged children from Santiago who were asked to complete a FA screening questionnaire. Parents who reported symptoms suggestive of FA were contacted to answer a second in-depth questionnaire to determine immediate hypersensitivity FA prevalence and clinical characteristics of school-aged Chilean children.ResultsA total of 455 parents answered the screening questionnaire: 13% reported recurrent symptoms to a particular food and 6% reported FA. Forty-three screening questionnaires (9%) were found to be suggestive of FA. Parents of 40 children answered the second questionnaire; 25 were considered by authors to have FA. FA rate was 5.5% (95% CI: 3.6–7.9). Foods reported to frequently cause FA included walnut, peanut, egg, chocolate, avocado, and banana. Children with FA had more asthma (20% vs. 7%, P < 0.02) and atopic dermatitis (32% vs. 13%, P < 0.01) by report. The parents of children with FA did not report anaphylaxis, but 48% had history compatible with anaphylaxis. Of 13 children who sought medical attention, 70% were diagnosed with FA; none were advised to acquire an epinephrine autoinjector.ConclusionUp to 5.5% of school-aged Chilean children may suffer from FA, most frequently to walnut and peanut. It is critical to raise awareness in Chile regarding FA and recognition of anaphylaxis, and promote epinephrine autoinjectors in affected children.     

Gastric mucosal reactions in patients with food allergy

The aim of our study was to determine whether patients suffering from food allergy show any pathologic reactions on the mucosa of the gastrointestinal (GI) tract after allergen contact. For this reason, we included in the study 30 patients whose food-allergic history had been proven through double-blind challenge tests; 20 healthy volunteers also were included as controls. The patients and volunteers underwent standard laboratory investigations and allergy tests with PRICK and RAST. To observe possible mucosal reactions, we applied the proposed allergens via endoscope to the gastric mucosa. Macroscopic reactions were observed blindly by two independent physicians. Biopsies were taken from the challenged areas for histological and histochemical analysis. The examinations included the estimations of tissue histamine concentrations and of mast cell and lymphocyte counts. In all 30 patients, macroscopic reactions (swelling, erosions, bleedings) were observed. Patients with food allergy had, in contrast to healthy volunteers, elevated lymphocyte counts, tissue histamine concentrations, and mast cell counts. After provocation, tissue histamine concentrations and mast cell counts fell significantly. Skin and RAST tests showed positive results in only 46.7% and 50.0%, respectively, of food-allergic patients. We conclude, first, that through intragastric provocation under endoscopic control (IPEC), food-allergic reactions on the mucosa of the GI tract can be verified and, second, that the liberation of tissue histamine seems to play an important role in the establishment of food-allergic reactions on the mucosa.     

Oral disodium cromoglycate in food allergy. An open trial in four patients.

The effect of DSCG olution per os was studied in four infants with immediate hypersensitivity reaction to cow's milk and egg, manifested by digestive and cutaneous symptoms. Previous administration of a 1 per cent DSCG solution by mouth resulted in diminution of both the digestive and cutaneous symptoms associated with allergen challenge. The best time interval between oral DSCG and the allergen challenge was about 30 min. The drug lost effectiveness when the solution was prepared more than a week in advance of its administration. A 2-year follow-up in two of the patients revealed the reappearance of cutaneous and digestive symptoms and, for the first time, the onset of wheezing while continuing to administer the allergens and despite continuous oral DSCG. The characteristics of these cases raise questions about the means of sensitization, and the possible mechanism of action of oral DSCG in the inhibition of non-digestive symptoms. Clinical indications for its use are discussed.     

Increased frequency of asymptomatic bronchial hyperresponsiveness in nonasthmatic patients with food allergy.

Subclinical inflammation in gut mucosa has been demonstrated in bronchial asthma suggesting the whole mucosal system is involved in allergic diseases. The presence of subclinical bronchial involvement was assessed by nonspecific bronchial hyperresponsiveness (BHR) in nonasthmatic patients with food allergy (FA). BHR was studied in 35 patients with various manifestations of FA without food-induced asthma. Sixteen had a previous history of asthma and/or rhinitis to aeroallergens (group A), whereas 19 patients (group B) did not. BHR was defined by a provocative dose causing a 20% fall in forced expiratory volume in one second of (PC20) <8 mg.mL(-1) of methacholine. Asymptomatic BHR occurred frequently in nonasthmatic patients with FA (10 of 19, 53%); this did not significantly differ from patients with FA and a previous history of asthma and/or rhinitis to aeroallergens (13 of 16, 81%). PC20 was significantly lower in group A (1.84+/-0.53 mg.mL(-1)) than in group B (3.35+/-0.74 mg.mL(-1); p<0.05). The number of patients with positive skin tests to aeroallergens was similar between groups. Sequential evaluation, performed 1 year after initial evaluation, in 7 nonasthmatic patients (group B) demonstrated a similar level of BHR. The present study demonstrated that BHR is a frequent finding in nonasthmatic patients with food allergy which may be due, at least in part, to a subclinical inflammatory process in the bronchi.     

Approach to patients with symptoms of food allergy

“Allergy” is a term often used by patients to describe symptoms that arise after eating. The term “adverse reaction to food” is preferred unless the event has an immunologic basis. True food allergy, primarily mediated by immunoglobulin (Ig)E antibodies to food proteins, is present in 3% to 4% of US adults. Symptoms range from mild mouth itching (“oral allergy syndrome”) to anaphylaxis. The diagnosis is established by history and appropriately performed skin testing or in vitro assays for specific IgE antibodies to the suspected food. Because food-allergic reactions can be fatal, it is important to identify and avoid the causative food. Food-allergic reactions are treated by prompt use of intramuscular epinephrine. Patients may be referred to an allergy/immunology specialist when the diagnosis is uncertain or if avoidance measures are not successful. Investigational therapies may ultimately be preventative or curative.     

Preventing food allergy

In this review, we examine the critical periods of immune development and how these might be modified to prevent food allergy. The relevant dietary intervention studies, roles of microorganisms and their products, and other strategies are critically analyzed. Additionally, we highlight the potential importance of different routes of allergic sensitization and the role of oral tolerance induction in the pathogenesis and prevention of food allergy.     

Adult food allergy

Adult food allergy is estimated at approximately 3.2% worldwide. The persistence of childhood food allergy is unusual, peanut allergies excepted. Once established in adults, food allergy is rarely cured. Factors favoring the acquisition of allergy could be sensitization to pollens, occupational sensitization by inhalation, drugs (such as tacrolimus), and sudden dietary changes. Severe anaphylaxis and oral allergy syndrome are frequent. The fatality risk is estimated at 1% in severe anaphylaxis. Risk factors for severe anaphylaxis are agents causing increased intestinal permeability, such as alcohol and aspirin. β-blockers, angiotensin-converting enzyme (ACE) inhibitors, and exercise are other factors. Gastrointestinal food allergy remains, to a large extent, undiagnosed in adults. Food allergens are mainly fruit and vegetable, related to pollen sensitizations, or to latex allergy. Wheat flour allergy is increasing. The diagnosis relies on prick skin tests, detection of specific IgEs, and standardized oral challenges. Strict avoidance diets are necessary. Specific immunotherapy to pollens may be efficient for cross-reactive food allergies.     

Symptoms of food allergy

Adverse reactions to foods can be due to many causes, but only those involving an immunological mechanism can be defined as food allergic disease. An increasing number of gastrointestinal and other diseases are being shown to involve food intolerances. Immediate reactions with symptoms within hours of eating a particular food are most readily shown to be due to food allergy and are often associated with the presence of food-specific IgE as shown by skin prick tests and RASTs. When reactions are delayed for 24 to 48 hours or more, underlying food intolerance is harder to recognize and much less often shown to be due to allergy. At present, diagnosis and management depends on dietary manipulation, showing that symptoms improve on food avoidance and are reproduced by food challenge (preferably double-blind). Further understanding of the mechanisms involved in food allergy, in Crohn's disease and irritable bowel syndrome may allow the development of simple tests to identify the foods concerned and perhaps, in the case of allergic disease, cure by the induction of tolerance.     

Genetics of food allergy

Allergic reactions to foods are an important medical problem throughout the industrialized world. The occurrence of food allergy appears to be strongly in.uenced by genetics, but the basis of the genetic predisposition to food allergy has not been differentiated from that for atopy in general. In addition, genetic susceptibility alone does not explain the prevalence of food allergy satisfactorily, leaving ample room to consider the importance of environmental in.uences (external, maternal, and gastrointestinal environment) and interactions between the host and the environment. Several features of food allergy are highlighted in this review: 1) patients with severe food allergies are overwhelmingly atopic, but food allergy occurs only in approximately 10% of patients with other atopic diseases; 2) most patients are clinically reactive to a single food, and although a substantial minority have multiple food allergies, the variety of bonefide food allergies in a given individual is limited; 3) foods contain multiple proteins whereas only a small subset are allergenic; 4) there is likely an important contribution of the environment, becoming manifest in genetically susceptible individuals.     

Nutrition basics in food allergy

Strict elimination of foods because of food allergies can interfere with good nutrition. It is essential that the diagnosis of a food allergy be proven thoroughly to avoid unnecessary food restrictions. Comprehensive education should show where allergenic foods are found, how to find appropriate substitutes for the eliminated foods and corresponding nutrients, and how to avoid accidental ingestion of allergenic foods. A nutrition assessment is an essential part of the clinical follow-up. Identifying nutrition-related problems early can correct difficult situations and prevent long-term health consequences.     

Follow-up study of latex-allergic health care workers in Japan.

BACKGROUND: While many cases of latex allergy have been reported in Japanese health care workers (HCWs) since 1992, there have been no follow-up studies after removing latex from the workplace. We had previously replaced all working environment latex gloves and latex products with low-allergen or non-latex products. The purpose of the investigation was to evaluate the benefits of the latex allergy countermeasures that were taken in our hospital, and the effects of life guidance education. METHODS: We investigated 16 latex-allergic HCWs in our hospital. We gave them a detailed questionnaire and tested them by a skin prick test (SPT) with latex extract and specific IgE antibodies against latex using the Pharmacia CAP RAST system, RAST FEIA. We compared these results with earlier results from the time of diagnosis. RESULTS: According to the questionnaire, none of the HCWs had changed their work habits, though all were avoiding the use of latex products as much as possible. Of the 16 patients, 81.2% were eating foods for which cross reactivity with latex has been reported. However, the foods had not induced severe allergic symptoms. In the SPT, 62.5% of scores decreased and 81.2% of patients had decreases in specific IgE antibody levels. CONCLUSIONS: After avoiding latex products and following our educational suggestions, the patients' allergy symptoms had generally improved. This indicates that our countermeasures against latex allergy were largely successful.