Aspirin-exacerbated respiratory disease
- Tanya M Laidlaw, MD
Tanya M Laidlaw, MD
- Assistant Professor of Medicine
- Harvard Medical School
- Elliot Israel, MD
Elliot Israel, MD
- Professor of Medicine
- Harvard Medical School
- Section Editor
- Peter J Barnes, DM, DSc, FRCP, FRS
Peter J Barnes, DM, DSc, FRCP, FRS
- Editor-in-Chief — Pulmonary and Critical Care Medicine
- Section Editor — Asthma
- Professor of Medicine
- National Heart and Lung Institute, Imperial College, London
- Deputy Editors
- Anna M Feldweg, MD
Anna M Feldweg, MD
- Director, Editorial Management — UpToDate
- Deputy Editor — Allergy and Immunology
- Assistant Professor of Medicine, Part-time
- Harvard Medical School
- Helen Hollingsworth, MD
Helen Hollingsworth, MD
- Deputy Editor — Pulmonary, Critical Care, and Sleep Medicine
- Associate Professor of Medicine
- Boston University School of Medicine
Aspirin-exacerbated respiratory disease (AERD), which is also called NSAID-exacerbated respiratory disease (NERD), refers to the combination of asthma, chronic rhinosinusitis (CRS) with nasal polyposis, and acute upper and lower respiratory tract reactions to ingestion of aspirin (acetylsalicylic acid, ASA) and other cyclooxygenase-1 (COX-1)-inhibiting nonsteroidal anti-inflammatory drugs (NSAIDs).
The first case of aspirin sensitivity in a patient with asthma was described in 1902, a few years after the introduction of aspirin into clinical use. In 1968, Samter and Beers described a triad consisting of asthma, aspirin sensitivity, and nasal polyps , which came to be known as Samter's triad.
An overview of AERD with emphasis on pathophysiology and the management of asthma will be presented here. Other types of hypersensitivity reactions to NSAIDs and the treatment of patients with asthma, CRS, and nasal polyposis are discussed separately. (See "NSAIDs (including aspirin): Allergic and pseudoallergic reactions" and "Diagnostic challenge and desensitization protocols for NSAID reactions" and "An overview of asthma management" and "Chronic rhinosinusitis: Management".)
NSAIDs — The primary effect of nonsteroidal anti-inflammatory drugs (NSAIDs) is to inhibit cyclooxygenase (also called prostaglandin synthase), thereby impairing the ultimate transformation of arachidonic acid (AA) to prostaglandins, prostacyclin, and thromboxanes and enhancing production of leukotrienes. Two related isoforms of the cyclooxygenase (COX) enzyme have been described, COX-1 and COX-2. Some NSAIDs have a greater inhibitory effect on COX-1 and others on COX-2. COX-1 inhibition is the stimulus for acute reactions to aspirin (ASA)/NSAIDs in aspirin-exacerbated respiratory disease (AERD).
In this topic review, the term "NSAID" includes aspirin (ASA). However, in some clearly marked sections, aspirin is discussed exclusive of other NSAIDs.To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- Normal arachidonic acid metabolism
- - 5-lipoxygenase pathway
- - Cyclooxygenase pathway
- Abnormalities in AERD
- Involvement of mast cells
- Other areas of investigation
- CLINICAL PRESENTATION
- Temporal development of symptoms and signs
- Acute reactions to NSAIDs
- Atopy and eosinophilia
- Reactions to alcoholic beverages
- Chest pain
- Clinical diagnosis of NSAID reactions
- Diagnostic aspirin challenge
- Chronic rhinosinusitis with nasal polyposis
- Leukotriene-modifying agents
- NSAID avoidance
- Aspirin desensitization
- - Indications
- - Efficacy of aspirin desensitization for AERD treatment
- - Maintenance of desensitization
- Biologic agents
- - Omalizumab
- - Mepolizumab
- SOCIETY GUIDELINE LINKS
- SUMMARY AND RECOMMENDATIONS