Abstract
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.
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