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Aspirin intolerance and the cyclooxygenase-leukotriene pathways.

AbstractPURPOSE OF REVIEW:
In up to 10% of patients with bronchial asthma, aspirin and other nonsteroidal antiinflammatory drugs precipitate asthmatic attacks. This is a hallmark of a distinct clinical syndrome that develops according to a characteristic sequence of symptoms. Here we discuss its clinical picture and management as related to the abnormalities in arachidonic acid transformations.
RECENT FINDINGS:
At the biochemical level, the characteristic feature is profound alteration in eicosanoid biosynthesis and metabolism. Major advances in the molecular biology of eicosanoids, exemplified by the cloning of cysteinyl-leukotriene receptors and discovery of a whole family of cyclooxygenase enzymes, offer new insights into mechanisms operating in aspirin-induced asthma. Clinical interest has been enhanced by the introduction into therapy of highly specific cyclooxygenase-2 inhibitors and antileukotriene drugs.
SUMMARY:
Recent studies have improved our understanding of mechanisms operating in asthma and unvieled the role of eicosanoid mediators in pulmonary disease.
AuthorsAndrew Szczeklik, Marek Sanak, Ewa Nizankowska-Mogilnicka, Bogumila Kiełbasa
JournalCurrent opinion in pulmonary medicine (Curr Opin Pulm Med) Vol. 10 Issue 1 Pg. 51-6 (Jan 2004) ISSN: 1070-5287 [Print] United States
PMID14749606 (Publication Type: Journal Article, Review)
Chemical References
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Isoenzymes
  • Leukotrienes
  • Lipoxins
  • Membrane Proteins
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Aspirin
Topics
  • Aspirin (adverse effects)
  • Asthma (chemically induced, diagnosis, drug therapy, epidemiology, physiopathology)
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors (adverse effects)
  • Desensitization, Immunologic
  • Humans
  • Isoenzymes (antagonists & inhibitors)
  • Leukotrienes (metabolism)
  • Lipoxins (physiology)
  • Mast Cells (physiology)
  • Membrane Proteins
  • Prostaglandin-Endoperoxide Synthases
  • Rhinitis (epidemiology)
  • Sinusitis (epidemiology)

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