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World Allergy Organization
WAO's mission: To be a global resource and advocate in the field of allergy, advancing excellence in clinical care through education, research and training as a world-wide alliance of allergy and clinical immunology societies.

Aspirin Exacerbated Respiratory Disease

Marek L. Kowalski MD, PhD
Professor and Chairman, Department of Immunology, Rheumatology and Allergy, Faculty of Medicine
Medical University of Łódź
Łódź, Poland


Abstract

Dr. Marek L. Kowalski, MD, PhD
Medical University of Łódź

The coexistence of hypersensitivity to aspirin with rhinosinusitis/nasal polyps and bronchial asthma has been referred to as “aspirin triad” and more recently the term aspirin-exacerbated respiratory disease (AERD) has been proposed. The incidence of AERD varies from 5% in mild asthmatics up to 24% in more severe groups of patients with asthma. Patients with AERD suffer from persistent asthma of greater than average severity and of higher than ordinary medication requirements, including poor response to steroids. Rhinosinusitis has usually protracted course and is complicated by mucosal hypertrophy and polyp formation.

The mechanism of the aspirin-induced reaction is not immunological, but seems to be related to inhibition by aspirin (or other NSAID) of cyclooxygenase-1, leading to release of mast cell derived mediators and enhanced production of leukotrienes. The pathomechanism of persistent eosinophilic inflammation of the lower and upper airway mucosa, a typical feature for AERD, is not related to intake of aspirin, but may result from inherited and/or acquired AA metabolism abnormalities including overproduction of cysteinyl leukotrienes and deficiency of anti-inflammatory lipoxins. More recently, an immunological response to Staphylococcus aureus enterotoxins has been implicated in the development of underlying chronic inflammation in the airways of patients with AERD.

Although management of asthma and rhinosinusitis in a patient with AERD follows general guidelines, several AERD phenotype specific measures should be considered. Careful avoidance of ASA and other NSAIDs in sensitive patients is important, since aspirin may be a cause of severe asthmatic attacks. For the majority of aspirin-hypersensitive patients an alternative anti-inflammatory drug can be found, and selective COX-2 inhibitors (e.g. celecoxib) are well tolerated by patients with AERD. Management of chronic rhinosinusits includes topical steroids, which are quite effective in controlling symptoms of rhinitis and slow down recurrence of nasal polyps in most patients. Various nasal surgical procedures may be needed to relieve chronic rhinosinusitis and to remove nasal polyps, although patients with AERD respond less well to surgical intervention. Inhaled glucocorticosteroids, often in combination with long acting beta-2 agonists, are the most effective drugs for controlling asthmatic inflammation and asthma symptoms in aspirin-sensitive patients. Although leukotriene receptor antagonists and synthesis inhibitors have been shown to be of clinical benefit in patients with AERD, the magnitude of improvement does not exceed that observed in ASA-tolerant patients. A more specific approach to AERD is aspirin given orally after desensitization. In a subgroup of patients ingestion of aspirin after desensitization results in alleviation of chronic symptoms from both upper and lower airway and in a decreased need for nasal/sinus surgery.
 

Slide Presentation
Posted: March 2010

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