4.5 Review

Hypersensitivity Reactions to Non-Steroidal Anti-Inflammatory Drugs

Journal

CURRENT PHARMACEUTICAL DESIGN
Volume 22, Issue 45, Pages 6784-6802

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612822666160928142814

Keywords

Non-steroidal anti-inflammatory drugs; hypersensitivity reactions; cross-intolerance; selective reactions; IgE; T-cell response; classification; blended reactions

Funding

  1. Institute of Health Carlos III of the Ministry of Economy and Competitiveness (European Regional Development Fund (ERDF) RIRAAF network) [RD12/0013]
  2. Consejeria de Salud de la Junta de Andalucia [PI-0463-2013]

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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 non-specific 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.

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