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Allergic Reactions02:06

Allergic Reactions

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Overview
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Allergic Reactions: Anaphylaxis01:30

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Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin,...
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Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial...
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Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
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Hypersensitivity Reactions: Immune-Complex Reactions01:19

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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
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Hypersensitivity Reactions: Cytolytic Reactions01:01

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Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
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Wheat-dependent exercise-induced anaphylaxis.

K A Scherf1, K Brockow2, T Biedermann2

  • 1Deutsche Forschungsanstalt für Lebensmittelchemie, Leibniz Institut, Freising, Germany.

Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology
|September 19, 2015
PubMed
Summary
This summary is machine-generated.

Wheat-dependent exercise-induced anaphylaxis (WDEIA) is a severe allergic reaction triggered by wheat consumption combined with exercise or other cofactors. Diagnosis involves medical history and specific tests, with a gluten-free diet being the most effective prevention.

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Area of Science:

  • Allergy and Immunology
  • Food Science

Background:

  • Wheat-dependent exercise-induced anaphylaxis (WDEIA) is a rare but severe food allergy.
  • Reactions occur when wheat ingestion is combined with cofactors like exercise, NSAIDs, alcohol, or infections.
  • Symptoms range from mild skin reactions to life-threatening anaphylaxis.

Purpose of the Study:

  • To summarize the clinical characteristics, potential mechanisms, allergens, diagnosis, and management of WDEIA.
  • To highlight the role of cofactors in triggering anaphylactic reactions.
  • To discuss diagnostic approaches and prophylactic strategies.

Main Methods:

  • Review of existing literature on WDEIA.
  • Analysis of clinical case reports and diagnostic criteria.
  • Identification of major wheat allergens and proposed pathomechanisms.

Main Results:

  • WDEIA is characterized by anaphylaxis following wheat intake and cofactors.
  • Potential mechanisms involve increased allergen permeability, altered blood flow, or mast cell degranulation.
  • Major allergens include ω5-gliadin and high-molecular-weight glutenin subunits.
  • Diagnosis relies on history, skin tests, specific IgE, basophil activation, and exercise challenge tests.

Conclusions:

  • WDEIA requires careful diagnosis combining clinical history with specific immunological tests.
  • Management strategies include acute treatment with adrenaline and long-term prophylaxis through a strict gluten-free diet or cofactor avoidance.
  • Understanding cofactor roles is crucial for effective prevention and management.