Contents

Disclaimer

Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Show Summary Details
Page of

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 August 2013. The previous version of this content can be found here.
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2016. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 26 September 2018

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....

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.