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Simons E.,University of Toronto | Sicherer S.H.,Elliot and Roslyn Jaffe Food Allergy Institute | Simons F.E.R.,University of Manitoba
Annals of Allergy, Asthma and Immunology | Year: 2012

Background: The optimal time for transferring responsibilities for anaphylaxis recognition and epinephrine auto-injector use from adults to children and teenagers has not yet been defined. Objective: To determine whether pediatric allergists have age-specific goals for beginning to transfer responsibilities for anaphylaxis recognition and epinephrine auto-injector use from parents and caregivers to children and teenagers at risk of anaphylaxis in the community. Methods: Members of the American Academy of Pediatrics Section on Allergy and Immunology (AAP-SOAI) were surveyed about when they typically begin to transfer these responsibilities from adults to children and teenagers. Results: Eighty-eight allergists responded to the survey, 97.7% of whom provided service to children and teenagers with food allergies. Few allergists expected to begin transferring responsibilities for anaphylaxis recognition and epinephrine auto-injector use to children younger than 9 to 11 years. By the time their patients reached age 12 to 14 years, however, most allergists expected them to be able to describe some anaphylaxis symptoms (95.4%), demonstrate how to use an epinephrine auto-injector trainer (93.1%), begin carrying self-injectable epinephrine (88.2%), recognize the need for epinephrine (88.1%), learn to self-inject epinephrine (84.5%), and be able to self-inject epinephrine (78.6%) (cumulative data). The allergists rated the following as "very important" readiness factors for beginning to transfer responsibilities: medical history, developmental level, and ability to demonstrate auto-injector technique. Conclusion: Most pediatric allergists expected that by age 12 to 14 years, their patients should begin to share responsibilities with adults for anaphylaxis recognition and epinephrine auto-injector use; however, they individualized the timing based on assessment of patient readiness factors. © 2012 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. Source


Sicherer S.H.,Elliot and Roslyn Jaffe Food Allergy Institute | Leung D.Y.M.,National Jewish Health
Journal of Allergy and Clinical Immunology | Year: 2010

This review highlights some of the research advances in anaphylaxis and hypersensitivity reactions to foods, drugs, and insects, as well as advances in allergic skin disease that were reported in the Journal in 2009. Among key epidemiologic observations, several westernized countries report that more than 1% of children have peanut allergy, and there is some evidence that environmental exposure to peanut is a risk factor. The role of regulatory T cells, complement, platelet-activating factor, and effector cells in the development and expression of food allergy were explored in several murine models and human studies. Delayed anaphylaxis to mammalian meats appears to be related to IgE binding to the carbohydrate moiety galactose-α-1,3-galactose, which also has implications for hypersensitivity to murine mAb therapeutics containing this oligosaccharide. Oral immunotherapy studies continue to show promise for the treatment of food allergy, but determining whether the treatment causes tolerance (cure) or temporary desensitization remains to be explored. Increased baseline serum tryptase levels might inform the risk of venom anaphylaxis and might indicate a risk for mast cell disorders in persons who have experienced such episodes. Reduced structural and immune barrier function contribute to local and systemic allergen sensitization in patients with atopic dermatitis, as well as increased propensity of skin infections in these patients. The use of increased doses of nonsedating antihistamines and potential usefulness of omalizumab for chronic urticaria was highlighted. These exciting advances reported in the Journal can improve patient care today and provide insights on how we can improve the diagnosis and treatment of these allergic diseases in the future. © 2010 American Academy of Allergy, Asthma & Immunology. Source


Sicherer S.H.,Elliot and Roslyn Jaffe Food Allergy Institute | Wood R.A.,Johns Hopkins University | Stablein D.,EMMES Corporation | Burks A.W.,Duke University | And 9 more authors.
Journal of Allergy and Clinical Immunology | Year: 2010

Background: Immune features of infants with food allergy have not been delineated. Objectives: We sought to explore the basic mechanisms responsible for food allergy and identify biomarkers, such as skin prick test (SPT) responses, food-specific IgE levels, and mononuclear cell responses, in a cohort of infants with likely milk/egg allergy at increased risk of peanut allergy. Methods: Infants aged 3 to 15 months were enrolled with a positive SPT response to milk or egg and either a corresponding convincing clinical history of allergy to milk or egg or moderate-to-severe atopic dermatitis. Infants with known peanut allergy were excluded. Results: Overall, 512 infants (67% male) were studied, with 308 (60%) having a history of a clinical reaction. Skin test responses, detectable food-specific IgE, or both revealed sensitization as follows: milk, 78%; egg, 89%; and peanut, 69%. SPT responses and food-specific IgE levels were discrepant for peanut (15% for IgE ≥0.35 kUA/L and negative SPT response vs 8% for positive SPT response and IgE <0.35 kUA/L, P = .001). Mononuclear cell allergen stimulation screening for CD25, cytokine-inducible SH2-containing protein (CISH), forkhead box protein 3 (FOXP3), GATA3, IL10, IL4, IFNG, and T-box transcription factor (TBET) expression by using casein, egg white, and peanut revealed that only allergen-induced IL4 expression was significantly increased in those with clinical allergy to milk (compared with nonallergic subjects) and in those sensitized to peanut, despite the absence of an increase in GATA3 mRNA expression. Conclusions: Infants with likely milk/egg allergy are at considerably high risk of having increased peanut-specific IgE levels (potential allergy). Peanut-specific serum IgE levels were a more sensitive indicator of sensitization than SPT responses. Allergen-specific IL4 expression might be a marker of allergic risk. Absence of an increase in GATA3 mRNA expression suggests that allergen-specific IL-4 might not be of T-cell origin. © 2010 American Academy of Allergy, Asthma & Immunology. Source


Sicherer S.H.,Elliot and Roslyn Jaffe Food Allergy Institute | Sampson H.A.,Elliot and Roslyn Jaffe Food Allergy Institute
Journal of Allergy and Clinical Immunology | Year: 2010

Adverse immune responses to foods affect approximately 5% of young children and 3% to 4% of adults in westernized countries and appear to have increased in prevalence. Food-induced allergic reactions are responsible for a variety of symptoms and disorders involving the skin and gastrointestinal and respiratory tracts and can be attributed to IgE-mediated and non-IgE-mediated (cellular) mechanisms. Genetic disposition and environmental factors might abrogate oral tolerance, leading to food allergy. Disease outcomes are influenced by the characteristics of the immune response and of the triggering allergen. Diagnosis is complicated by the observation that detection of food-specific IgE (sensitization) does not necessarily indicate clinical allergy. Therefore diagnosis requires a careful medical history, laboratory studies, and, in many cases, an oral food challenge to confirm a diagnosis. Novel diagnostic methods, including ones that focus on immune responses to specific food proteins or epitopes of specific proteins, are under study. Currently, management of food allergies consists of educating the patient to avoid ingesting the responsible allergen and to initiate therapy (eg, with injected epinephrine for anaphylaxis) in case of an unintended ingestion. Improved therapeutic strategies under study include oral and sublingual immunotherapy, Chinese herbal medicine, anti-IgE antibodies, and modified vaccines. © 2010 American Academy of Allergy, Asthma & Immunology. Source


Sicherer S.H.,Elliot and Roslyn Jaffe Food Allergy Institute | Munoz-Furlong A.,Food Allergy and Anaphylaxis Network | Godbold J.H.,Mount Sinai School of Medicine | Sampson H.A.,Elliot and Roslyn Jaffe Food Allergy Institute
Journal of Allergy and Clinical Immunology | Year: 2010

Background: Allergy to peanuts and tree nuts (TNs) is the leading cause of fatal allergic reactions in the United States, and the prevalence appears to be increasing. Objectives: We sought to determine the US prevalence of self-reported peanut, TN, and sesame allergy in 2008 and compare results with comparable surveys conducted in 1997 and 2002. Methods: A nationwide, cross-sectional, random telephone survey for peanut and TN allergy was conducted with a previously used questionnaire, with additional questions about sesame. Results: A total of 5,300 households (13,534 subjects) were surveyed (participation rate, 42% vs 52% in 2002 and 67% in 1997). Peanut allergy, TN allergy, or both was reported by 1.4% of subjects (95% CI, 1.2% to 1.6%) compared with 1.2% in 2002 and 1.4% in 1997. For adults, the prevalence was 1.3% (95% CI, 1.1% to 1.6%), which was not significantly different from prior surveys. However, the prevalence of peanut or TN allergy for children younger than 18 years was 2.1% (95% CI, 1.6% to 2.7%) compared with 1.2% in 2002 (P = .007) and 0.6% in 1997 (P < .001). The prevalence of peanut allergy in children in 2008 was 1.4% (95% CI, 1.0% to 1.9%) compared with 0.8% in 2002 (P = not significant) and 0.4% in 1997 (P < .0001). The prevalence of childhood TN allergy increased significantly across the survey waves (1.1% in 2008, 0.5% in 2002, and 0.2% in 1997). Sesame allergy was reported by 0.1% (95% CI, 0.0% to 0.2%). Conclusions: Although caution is required in comparing surveys, peanut allergy, TN allergy, or both continue to be reported by more than 1% of the US population (eg, >3 million subjects) and appear to be increasingly reported among children over the past decade. Sesame allergy is reported much less commonly. © 2010 American Academy of Allergy, Asthma & Immunology. Source

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