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Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

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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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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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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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Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
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[Angioedema and urticaria].

I Boccon-Gibod1, L Bouillet1

  • 1Centre national de référence des angioedèmes (CREAK), CHU de Grenoble, Hôpital Nord, Boulevard de la Chantourne, 38700 La Tronche, France; Clinique universitaire de médecine interne, Pôle pluridisciplinaire de médecine, CHU de Grenoble - Hôpital Albert Michallon, BP 217, Boulevard de la Chantourne, 38043 Grenoble cedex 9, France.

Annales De Dermatologie Et De Venereologie
|December 26, 2014
PubMed
Summary
This summary is machine-generated.

Angioedema (AE) is deep urticaria, often non-allergic and mast-cell mediated in chronic cases. Treatment focuses on antihistamines, avoiding steroids in chronic urticaria.

Keywords:
AngiœdemaAngiœdèmeAnti-histamineAnti-histaminiqueChronic urticariaHistaminergicHistaminiqueMast cellsMastocytesUrticaire chronique

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Area of Science:

  • Dermatology
  • Allergology
  • Immunology

Background:

  • Angioedema (AE) is a manifestation of urticaria (U) involving subcutaneous swelling.
  • Chronic urticaria is classified as spontaneous (CSU) or inducible (CIU).
  • AE in chronic urticaria is typically non-allergic, resulting from mast-cell activation (non-IgE mediated).

Purpose of the Study:

  • To differentiate angioedema from urticaria.
  • To outline the classification and characteristics of chronic urticaria and associated angioedema.
  • To discuss triggers and treatment strategies for angioedema in chronic urticaria.

Main Methods:

  • Review of updated urticaria classification.
  • Description of angioedema characteristics, triggers, and duration.
  • Discussion of treatment principles for histaminergic angioedema.

Main Results:

  • Angioedema presents as transient, painful, non-inflammatory swelling, distinct from itchy wheals.
  • Common triggers include physical factors and certain medications.
  • Recurrent angioedema lasting over six weeks defines chronic urticaria.

Conclusions:

  • Angioedema in chronic urticaria is primarily non-allergic and managed with antihistamines.
  • Steroids should be avoided in chronic urticaria due to potential for worsening symptoms.
  • Understanding AE triggers and non-IgE mechanisms is crucial for effective management.