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NSAID-exacerbated respiratory disease — SCE Respiratory MCQ

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HardAsthma PhenotypesNSAID-exacerbated respiratory diseaseSCE Respiratory

A 49-year-old woman is reviewed in a severe-asthma service. Asthma began at 38 years, followed by recurrent chronic rhinosinusitis with nasal polyps requiring two operations. On separate occasions, ibuprofen and naproxen caused nasal obstruction, wheeze and a greater than 20% fall in peak expiratory flow within 90 minutes. She has no childhood atopy; skin-prick testing and specific IgE to common aeroallergens are negative. Despite electronically confirmed adherence to high-dose ICS/formoterol, tiotropium and montelukast, she had five corticosteroid-treated exacerbations last year and now requires prednisolone 10 mg daily. Before maintenance prednisolone, blood eosinophil counts were repeatedly 0.62–0.78 × 10^9/L. The current count is 0.05 × 10^9/L, but fractional exhaled nitric oxide is 58 ppb. Induced sputum obtained while taking prednisolone contains 0.4% eosinophils and 78% neutrophils; bacterial and mycobacterial cultures are negative. There are no pulmonary infiltrates, neuropathic symptoms, purpura, renal abnormalities or cardiac features, and ANCA is negative. Which formulation best captures her dominant asthma phenotype and explains the apparently discordant current biomarkers?

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Correct answer: E — T2-high eosinophilic asthma with NSAID-exacerbated respiratory disease, modified by maintenance corticosteroids

Explanation lettering: C = shown as A · D = shown as C · E = shown as D · A = shown as E

The longitudinal phenotype is more informative than cell counts obtained during systemic corticosteroid treatment. Adult-onset severe asthma, recurrent nasal polyposis and reproducible respiratory reactions to two non-selective NSAIDs establish the characteristic clinical pattern of NSAID-exacerbated respiratory disease (N-ERD), a predominantly eosinophilic T2 inflammatory disorder. Repeated pre-prednisolone eosinophilia and persistently high FeNO despite confirmed inhaled-treatment adherence further support T2-high disease. Maintenance prednisolone can markedly suppress blood and airway eosinophils and can contribute to airway neutrophilia; therefore, the current blood and sputum findings must not be used in isolation to relabel her as T2-low. B is attractive because sputum is currently neutrophilic, but it ignores corticosteroid-induced phenotype distortion and the historical T2 biomarkers. C is incorrect because mixed-granulocytic asthma requires contemporaneous eosinophilic and neutrophilic airway inflammation, which this treated sputum sample does not show. D fails because N-ERD is not an IgE-mediated reaction, and there is no aeroallergen sensitisation. E is less likely: adult-onset eosinophilic asthma and polyposis can precede EGPA, but there are no vasculitic, infiltrative, neurological, renal, cardiac or constitutional features. ANCA negativity does not exclude EGPA, but the supplied findings support N-ERD rather than systemic vasculitis.

Reference: Management of severe asthma: a European Respiratory Society/American Thoracic Society guideline (2020) — https://publications.ersnet.org/content/erj/55/1/1900588 Diagnosis and management of NSAID-Exacerbated Respiratory Disease (N-ERD)—a EAACI position paper (January 2019) — https://pubmed.ncbi.nlm.nih.gov/30216468/ Effects of steroid therapy on inflammatory cell subtypes in asthma (May 2010) — https://pubmed.ncbi.nlm.nih.gov/19996343/