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Anaphylaxis 

Anaphylaxis

Chapter:
Anaphylaxis
Author(s):

Anthony F.T. Brown

DOI:
10.1093/med/9780199204854.003.1702_update_001

Update:

Updates include (1) expansion of the list of drugs that can cause Ig-E dependent anaphylaxis; (2) description of chest pain due to coronary artery spasm; (3) treatment of serious attacks of hereditary angioedema with C1 esterase inhibitor or icatibant; (4) reference to new guidelines published by the World Allergy Organization and the European Resuscitation Council.

Updated on 29 Aug 2013. The previous version of this content can be found here.
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date: 23 August 2017

The term anaphylaxis describes both IgE immune-mediated reactions and nonallergic, nonimmunologically triggered events. Comorbidities such as asthma or infection, exercise, alcohol, or stress and concurrent medications such as β-blockers and aspirin increase the risk known as ‘summation anaphylaxis’.

Aetiology and pathogenesis—activated mast cells and basophils release preformed, granule-associated mediators and newly formed lipid mediators, and generate cytokines and chemokines. These cause vasodilatation, increased capillary permeability, and smooth muscle contraction, as well as attract new cells to the area. Positive feedback mechanisms amplify the reaction in a ‘mast cell—leucocyte cytokine cascade’, although conversely reactions can be self-limiting. Parenteral penicillins, hymenopteran stings, and food are the most common causes of IgE immune-mediated fatalities, with radiocontrast media, aspirin, and other nonsteroidal anti-inflammatory drugs most commonly responsible for nonallergic fatalities....

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