Finding a Path to Safety in Food Allergy Assessment of the Global Burden, Causes, Prevention, Management, and Public Policy (2017) / Chapter Skim
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From page 39... ...
The chapter also distinguishes food allergy from the many other adverse effects or conditions that could be related to foods but that have a nonimmunological origin. Considering the diversity of food adverse conditions with similar symptomatology and clinical manifestations (see Figure 2-1)
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FOOD ALLERGIES: DEFINITIONS Commonly Accepted Definitions Food allergy is "an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food," according to the 2010 National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIAID/NIH) -supported Guidelines for the Diagnosis and Management of Food Allergy in the United States (NIAID/ NIH-supported Guidelines)
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The presence and quantity of such allergen-specific IgE antibodies is a key metric in diagnosing and evaluating food allergy sensitivities. However, the quantity of IgE antibodies ranges widely, making quantification an incomplete TABLE 2-1 Overall Differences Between IgE- and Non-IgE-Mediated Food Allergies Class IgE-Mediated Non-IgE-Mediated Time to onset of reaction Immediate Delayed <2 hoursa Often >4-6 hours Volume usually required Small Sometimes larger for reaction Typical symptoms Urticaria Diarrhea Angioedema Food refusal Vomiting Failure to thrive Diarrhea Gastroesophageal reflux Oral itching Irritability/abdominal Anaphylaxis distension Eczema Common Above signs or symptoms Sometimes can do home-based diagnostic procedures by history or oral food elimination and rechallenge challenge sequence; some require and rechallenge in hospital setting positive IgE antibody (skin prick test or serum specific IgE)
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Eosinophilic esophagitis EoE symptoms vary depending on the age of the person, (EoE) from reflux-like symptoms and vomiting in school-age children, to refusal to eat and impaction in teenagers and adults.
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indicator of function, allergen sensitivity, or reaction severity. Moreover, some individuals with measurable IgE specific for particular food allergens do not exhibit clinical signs and symptoms of food allergy when they ingest such allergens.
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Desensitization is a state of clinical and immunological nonresponsiveness to an allergen, including food allergens, that can be induced by the careful, physician guided administration of gradually increasing amounts of the offending allergen over a relatively short period of time (hours to days)
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IgE causes the IgE-mediated allergic response by binding strongly to IgE receptors (FcɛRI) found on the surface of mast cells and basophils, and triggering these cells to release powerful inflammatory mediators once the cell bound IgE recognizes the offending food allergen.
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Identifying and tracking these allergenic proteins and how they are affected by factors such as variation in food preparation is crucial to understanding mechanisms of food allergy reactions and potential avenues of prevention or treatment. For example, it will be important to understand how and why certain processes of food preparation can neutralize or diminish the ability of allergens either to induce sensitization or elicit clinical reactions (see also Chapter 7)
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From page 47... ...
. Various surveys indicate misunderstandings among medical professionals in recognizing risk factors for food allergy reactions,
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. Specific food allergies likely are a result of complex interactions among genes and the environment (including not only factors in the "external environment," such as pollen, pollution, and pathogenic microbes, but also effects of the microbes that normally reside in us -- the "internal environment" of the microbiome)
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. It has been increasingly recognized that skin exposure can be a powerful driving factor in food sensitization.
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7 slgE production B cell specific for a FcԑRI (and dissemination via blood stream) component of the allergen Allergen non-specific lgE Plasma cell B cell receptor specific secreting slgE for a component of the allergen 6 Th2 cell drives production of sIgE Intestinal smooth muscle allergen The patient is asymptomatic 9 during sensitization Basophil (in blood)
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. The presence of these sIgE molecules on the surface of mast cells and basophils gives little or no activation signal to the cells, but prepares them to undergo activation upon subsequent exposure to the allergen recognized by the sIgE.
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products secreted by activated mast cells, such products derived from epithelial cells can have effects on local blood vessels that favor the local development of inflammation, such as (14) the recruitment of circulating leukocytes.
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to become "sensitized" so that they then can be activated to release inflammatory mediators by allergens recognized by the bound IgE. For the FcεRI to initiate the cell signaling that results in activation of mast cells and basophils to release their mediators requires that the receptors are aggregated when their bound IgE reacts with allergens that are at least bivalent (e.g., have two epitopes that can bind IgE)
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Some of the mechanisms by which treatments for food allergy may be associated with changes in the clinical symptoms include the occurrence during the treatment of natural tolerance noted above (this is one reason why clinical studies of new treatments would include a placebo group) , reduction in production of allergen-specific IgE, decreased antigenand food-specific IgE-dependent basophil activation, increased allergenspecific IgG4 (one effect of which may be to bind allergen before it can be encountered by sIgE and the surface of basophils and mast cells)
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For example, it is well known that upon re-exposure following sensitization to an antigen, the antigen-induced aggregation of antigen-specific IgE binds to receptors on specialized cells (including mast cells in tissues and basophils in the blood)
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• Identify the mechanisms, in patients with food allergies, for acquir ing tolerance to the offending food allergen, without therapeutic intervention, as well as for responding to therapeutic interventions by developing transient desensitization versus sustained unrespon siveness versus true tolerance to the offending food allergens. • Define how particular products and functions of mast cells, baso phils, and other effector cells can contribute to the signs and symp toms of food allergic reactions, including anaphylaxis, and identify factors that may contribute to individual variation in the patho physiological responses to such products.
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From page 57... ...
• Identify and describe the roles of the skin and intestinal barriers in protecting individuals from developing food sensitization or a food allergy, and identify ways in which protective aspects of barrier function can be enhanced and factors that diminish barrier func tion be reduced. • Examine the interactions between the microbiota and the host immune system that may favor or protect against the development of a food allergy, and define the extent to which the microbiota or its products can be manipulated to enhance resistance to the development of food allergy.
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From page 58... ...
J Allergy Clin Immunol Pract 1(3)
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