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Asthma: Aspirin-Intolerant

Asthma: Aspirin-Intolerant
Asthma: Aspirin-Intolerant

Aspirin-intolerant asthma (AIA) is a phenotype experienced by 10-20% of persistent asthmatics, in whom acute bronchoconstriction is induced by ingestion of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs share the ability to inhibit synthesis of prostanoids by blockade of cyclooxygenase (COX). Acute reactions to NSAIDs can be life threatening and may be associated with rhinoconjunctival and dermal symptoms. Drugs that selectively inhibit COX-2 appear to be better tolerated than nonselective inhibitors of COX-1 and COX-2. Patients with AIA usually have persistent underlying asthma, often associated with nasal polyposis. Pathologically, the bronchial and nasal airways of AIA subjects show chronic eosinophilia, with evidence of activation of eosinophils and mast cells during acute reactions. The etiology of AIA is unclear, but the proposed mechanism focuses on the inhibition by NSAIDs of the synthesis of a prostanoid, putatively prostaglandin E 2, that would normally suppress local inflammatory reactions. The consequent synthesis of cysteinyl-leukotrienes and other leukocyte-derived mediators contributes to bronchoconstriction and other acute features. Treatment of AIA involves avoidance of NSAIDs combined with conventional management of underlying asthma, with 75% of AIA patients requiring corticosteroids. Controlled desensitization with regular doses of an NSAID can provide protection against acute reactions.

Aspirin, Asthma, Cyclooxygenase
V1-181-V1-187
Elsevier
Sampson, A. P.
4ca76f6f-ff35-425d-a7e7-c2bd2ea2df60
Sampson, A. P.
4ca76f6f-ff35-425d-a7e7-c2bd2ea2df60

Sampson, A. P. (2006) Asthma: Aspirin-Intolerant. In, Encyclopedia of Respiratory Medicine: Volume 1-4. Elsevier, V1-181-V1-187. (doi:10.1016/B0-12-370879-6/00035-1).

Record type: Book Section

Abstract

Aspirin-intolerant asthma (AIA) is a phenotype experienced by 10-20% of persistent asthmatics, in whom acute bronchoconstriction is induced by ingestion of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs share the ability to inhibit synthesis of prostanoids by blockade of cyclooxygenase (COX). Acute reactions to NSAIDs can be life threatening and may be associated with rhinoconjunctival and dermal symptoms. Drugs that selectively inhibit COX-2 appear to be better tolerated than nonselective inhibitors of COX-1 and COX-2. Patients with AIA usually have persistent underlying asthma, often associated with nasal polyposis. Pathologically, the bronchial and nasal airways of AIA subjects show chronic eosinophilia, with evidence of activation of eosinophils and mast cells during acute reactions. The etiology of AIA is unclear, but the proposed mechanism focuses on the inhibition by NSAIDs of the synthesis of a prostanoid, putatively prostaglandin E 2, that would normally suppress local inflammatory reactions. The consequent synthesis of cysteinyl-leukotrienes and other leukocyte-derived mediators contributes to bronchoconstriction and other acute features. Treatment of AIA involves avoidance of NSAIDs combined with conventional management of underlying asthma, with 75% of AIA patients requiring corticosteroids. Controlled desensitization with regular doses of an NSAID can provide protection against acute reactions.

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More information

Published date: 1 January 2006
Additional Information: Publisher Copyright: © 2006 Elsevier Ltd. All rights reserved.
Keywords: Aspirin, Asthma, Cyclooxygenase

Identifiers

Local EPrints ID: 486546
URI: http://eprints.soton.ac.uk/id/eprint/486546
PURE UUID: db42e63e-56e7-4cff-b029-49f81c32a954
ORCID for A. P. Sampson: ORCID iD orcid.org/0009-0008-9653-8935

Catalogue record

Date deposited: 25 Jan 2024 17:35
Last modified: 06 Jun 2024 01:35

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