Non-steroidal anti-inflammatory drugs (NSAIDs) are one of the leading causes of
hypersensitivity reactions to drugs, and they are classified in two groups: those induced by nonspecific
immunological mechanisms (non-allergic or cross-intolerance (CI) reactions), or by
specific immunological mechanisms (allergic or selective reactions (SR)). The pathogenesis of
CI is associated with their pharmacological activity (COX-1 inhibition), with symptoms due to
an imbalance in the arachidonic acid pathway, independently of their chemical structure. SRs
are mediated by specific IgE- or by a T-cell response and can be induced by a single NSAID or
a class of chemically related NSAIDs, with patients tolerating chemically unrelated compounds.
NSAIDs hypersensitivity reactions have been classified in five main groups: i)
NSAIDs-exacerbated respiratory disease (NERD); ii) NSAIDs-exacerbated cutaneous disease
(NECD); iii) NSAIDs-induced urticaria/angioedema (NIUA); iv) Single NSAID–induced
urticaria/angioedema or anaphylaxis (SNIUAA); v) Single NSAID–induced delayed reactions
(SNIDRs). Although this classification described above is widely accepted by most authors some phenotypes such as
blended reactions do not fit. Therefore more research is needed in this topic.
Keywords: Non-steroidal anti-inflammatory drugs, hypersensitivity reactions, cross-intolerance, selective reactions, IgE, T-cell response,
classification, blended reactions.
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