Anaphylactic or Anaphylactoid/Allergic or Non-allergic
The European Academy of Allergy and Immunology (EAACI) redefined anaphylaxis as a severe, life-threatening, generalized, or systemic hypersensitivity reaction, sub-divided into 'allergic' and 'non-allergic' reactions.
Allergic anaphylaxis has an incidence between 1/5000–1/20 000 with a 3:1 female preponderance. Despite initially increased reporting of adverse events to new drugs (Weber effect), there is generally under reporting to databases (e.g. the UK yellow card system). Anaphylaxis-related mortality is 3–6% and an additional 2% have a poor neurological outcome.[2]
Allergic anaphylaxis implies an immunological reaction (IgE, IgG, or complement mediated). Antigen exposure results in mast cell and basophil bound antibody formation. Subsequent antigen exposure causes mast cell degranulation and the release of mediators including histamine, tryptase, leukotrienes, and prostaglandins. In 'non-allergic' reactions, mast cell and basophil degranulation are caused by direct drug action with no immune trigger. The term 'anaphylactoid' is now obsolete and encompassed non-IgE-mediated and non-allergic reactions.
The immunological mechanism is important as skin prick testing identifies only IgE-mediated hypersensitivity. Lack of skin changes does not necessarily exclude a drug as the allergic trigger.
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