Analgesics

Chem Immunol Allergy. 2010:95:170-179. doi: 10.1159/000315950. Epub 2010 Jun 1.

Abstract

Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are often incriminated in hypersensitivity reactions leading to anaphylaxis. Two populations are at the high risk of developing such reactions: patients with asthma and those with urticaria. In a subset of asthmatics, NSAIDs that inhibit cyclooxygenase-1 (COX-1) precipitate non-allergic, hypersensitivity reactions, characterized by violent attacks of dyspnea. These patients suffer from a distinct clinical syndrome, called aspirin induced asthma (AIA), which includes chronic eosinophilic rhinusinusitis and persistent asthma. Inpatients with chronic idiopathic urticaria, and less commonly in patients without chronic urticaria, NSAIDs usually acting through inhibition of COX-1 can induce or exacerbate skin eruptions. While alterations in eicosanoid biosynthesis characterized both AIA and aspirin-triggered urticaria, other patients may rarely manifest IgE-mediated reactions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Analgesics / adverse effects*
  • Analgesics / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects*
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Asthma, Aspirin-Induced / pathology
  • Asthma, Aspirin-Induced / physiopathology*
  • Cyclooxygenase 1 / metabolism
  • Drug Hypersensitivity / pathology
  • Drug Hypersensitivity / physiopathology*
  • Dyspnea
  • Eicosanoids / metabolism
  • Eosinophils / drug effects*
  • Eosinophils / immunology
  • Eosinophils / metabolism
  • Eosinophils / pathology
  • Humans
  • Rhinitis
  • Sinusitis
  • Urticaria

Substances

  • Analgesics
  • Anti-Inflammatory Agents, Non-Steroidal
  • Eicosanoids
  • Cyclooxygenase 1