Aspirin-Exacerbated Respiratory Disease Management

Summary

Aspirin-Exacerbated Respiratory Disease (AERD) is a chronic syndrome characterised by asthma, nasal polyposis and hypersensitivity reactions to aspirin and other non-steroidal anti-inflammatory drugs. Management demands a multidisciplinary strategy that integrates precise diagnosis, pharmacological intervention and surgical techniques. Diagnosis typically involves controlled aspirin provocation testing to confirm drug sensitivity and to differentiate true hypersensitivity from intolerance. Pharmacological approaches centre on tailored anti-inflammatory therapy, including high-dose intranasal corticosteroids, leukotriene modifiers and biological agents targeting type 2 cytokines. Aspirin desensitisation has emerged as a cornerstone of long-term control, enabling ingestion of daily aspirin doses to reduce polyp recurrence, improve asthma control and diminish reliance on systemic steroids. Where medical therapy is insufficient, endoscopic sinus surgery may be employed to restore sinus ventilation and facilitate topical drug delivery. Emerging immunomodulatory strategies, including monoclonal antibodies against interleukin-5 or immunoglobulin E, have demonstrated promising reductions in polyp burden and exacerbation frequency. A tailored combination of these modalities, underpinned by patient education and regular monitoring of lung function and nasal patency, is essential to optimise quality of life and to reduce healthcare utilisation globally.

Research from Nature Portfolio

Recent studies have explored sphingolipid metabolites as novel biomarkers of AERD. Lipidomic analysis revealed that patients with aspirin sensitivity exhibit altered serum and urinary levels of sphingosine-1-phosphate and sphingosine when compared with aspirin-tolerant asthmatics. These metabolites correlated with bronchial hyperresponsiveness and reductions in forced expiratory volume, suggesting a mechanistic link between sphingolipid dysregulation and airway inflammation. This work provides a foundation for non-invasive diagnostic assays and highlights sphingolipid pathways as potential therapeutic targets to modulate inflammatory networks in AERD.

Aspirin-Exacerbated Respiratory Disease Management publication trend

The graph below shows the total number of articles in aspirin-exacerbated respiratory disease management across all publications each year (not limited to Nature Index journals).

Technical terms

Aspirin desensitisation: A controlled protocol that gradually increases aspirin exposure to induce drug tolerance and reduce hypersensitivity reactions.

Cysteinyl leukotrienes: Inflammatory mediators derived from arachidonic acid that contribute to bronchoconstriction and nasal oedema in AERD.

Nasal polyposis: The formation of benign mucosal protrusions in the nasal passages and sinuses, commonly associated with chronic eosinophilic inflammation.

Type 2 inflammation: An immune response characterised by eosinophils and cytokines such as IL-4, IL-5 and IL-13, central to AERD pathophysiology.

Aspirin provocation testing: A diagnostic procedure involving controlled administration of aspirin to elicit and observe hypersensitivity symptoms.

References

  1. Aspirin Exacerbated Respiratory Disease: Epidemiology, Pathophysiology, and Management. Medical Sciences (2019).
  2. Nasal lysine aspirin challenge in the diagnosis of aspirin ‐ exacerbated respiratory disease. Clinical & Experimental Allergy (2013).
  3. A retrospective study of the clinical benefit from acetylsalicylic acid desensitization in patients with nasal polyposis and asthma. Allergy, Asthma & Clinical Immunology (2014).
  4. Exploration of the Sphingolipid Metabolite, Sphingosine-1-phosphate and Sphingosine, as Novel Biomarkers for Aspirin-exacerbated Respiratory Disease. Scientific Reports (2016).
  5. NSAID-Exacerbated Respiratory Disease (NERD): From Pathogenesis to Improved Care. Frontiers in Pharmacology (2020).
  6. Pathomechanisms of AERD—Recent Advances. Frontiers in Allergy (2021).
  7. Comprehensive Analysis of Nasal Polyps Reveals a More Pronounced Type 2 Transcriptomic Profile of Epithelial Cells and Mast Cells in Aspirin-Exacerbated Respiratory Disease. Frontiers in Immunology (2022).

About these summaries

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