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• W2110334538 abstract "Background: Mucus hypersecretion is a hallmark of nasal polyposis (NP). Corticosteroids (CS) are first‐line treatment for NP, decreasing their size and inflammatory component. However, their effect on mucin production is not well‐understood. The aim of this (pilot) study was to investigate CS effect on mucin expression in NP. Methods: Patients were randomized in control ( n = 9) and treatment (oral prednisone for 2 weeks and intranasal budesonide for 12 weeks; n = 23) groups. Nasal polyposis from nonasthmatic (NP; n = 13), aspirin‐tolerant (NP‐ATA; n = 11) and aspirin‐intolerant (NP‐AIA; n = 8) asthmatics were studied. Nasal polyposis biopsies were obtained before (w0) and after 2 (w2) and 12 (w12) weeks of CS treatment. Secreted (MUC5AC, MUC5B and MUC8) and membrane‐tethered (MUC1, MUC4) mucins (immunohistochemistry) and goblet cells (Alcian blue‐periodic acid Schiff) were quantified in both epithelium and glands. Rhinorrea and nasal obstruction were also assessed. Results: At w2, steroids increased MUC1 (from 70 to 97.5) and MUC4 (from 80 to 100) in NP‐ATA patients’ epithelium compared with baseline (w0). At w12, steroids decreased MUC5AC (from 40 to 5) and MUC5B (from 45 to 2.5) in NP‐ATA patients’ epithelium and glands, respectively, compared with baseline. No mucin presented significant changes in NP‐AIA patients. MUC5AC and MUC5B expression correlated with goblet and mucous cell numbers, respectively, and MUC5AC also with rhinorrea score. Conclusions: These results suggest: (i) CS up‐regulate membrane (MUC1, MUC4) while down‐regulate secreted (MUC5AC, MUC5B) mucins; (ii) there exists a link between secreted mucin expression and goblet cell hyperplasia; and (iii) NP from AIA may develop resistance to CS treatment." @default.
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• W2110334538 date "2008-09-08" @default.
• W2110334538 modified "2023-10-17" @default.
• W2110334538 title "Corticosteroid therapy increases membrane-tethered while decreases secreted mucin expression in nasal polyps" @default.
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• W2110334538 doi "https://doi.org/10.1111/j.1398-9995.2008.01678.x" @default.
• W2110334538 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18547287" @default.
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