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Aspirin‐intolerant asthma: role of cyclo‐oxygenase enzymes
Author(s) -
Picado C.
Publication year - 2002
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.57.s72.14.x
Subject(s) - aspirin , bronchoconstriction , leukotriene , arachidonic acid , arachidonate 5 lipoxygenase , pharmacology , asthma , lipoxygenase , proinflammatory cytokine , medicine , zileuton , enzyme , eicosanoid , cyclooxygenase , chemistry , immunology , inflammation , biochemistry
Aspirin‐induced asthma and rhinitis (AIAR) appear to be precipitated by the inhibition of cyclo‐oxygenase (COX). By inhibiting COX pathway aspirin diverts arachidonic acid metabolites to the lipoxygenase pathway. There are two isoforms of COX, namely COX‐1 and COX‐2. Metabolites derived from COX‐1 are involved in cellular housekeeping functions. COX‐2 can be induced in cells exposed to proinflammatory substances and growth factors. Recent studies have reported that patients with AIAR have decreased activity of COX‐2 and lower production of PGE 2 in the upper airway and peripheral blood cells. Considering the protective effect of exogenous PGE 2 on aspirin‐induced bronchoconstriction and the interdependence of PGE 2 and cisteinyl leukotriene production, a reduced PGE 2 synthesis may render aspirin‐sensitive patients more susceptible to the inhibitory effect of NSAIDs drugs and also lead to an increase in cysteinyl leukotriene release.