Effect of Dupilumab on Type 2 Biomarkers in Chronic Rhinosinusitis With Nasal Polyps: SINUS-52 Study Results

杜皮鲁玛 慢性鼻-鼻窦炎 鼻息肉 医学 窦(植物学) 皮肤病科 鼻窦炎 内科学 胃肠病学 免疫学 特应性皮炎 生物 植物
作者
Claus Bachert,Tanya M. Laidlaw,Seong Ho Cho,Joaquim Mullol,Brian N. Swanson,Souâd Naimi,Marion Classe,Sivan Harel,Alexandre Jagerschmidt,Elizabeth Laws,Marcella Ruddy,Amy Praestgaard,Nikhil Amin,Leda Mannent
出处
期刊:Annals of Otology, Rhinology, and Laryngology [SAGE]
卷期号:132 (12): 1649-1661 被引量:1
标识
DOI:10.1177/00034894231176334
摘要

Chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and non-steroidal anti-inflammatory drug-exacerbated respiratory disease (NSAID-ERD) are frequent coexisting conditions and share type 2 inflammatory pathophysiology, with interleukin (IL)-4 and IL-13 as key cytokines. Dupilumab is a monoclonal antibody that blocks the shared receptor for IL-4 and IL-13. The objective of this analysis was to evaluate dupilumab's effect on type 2 inflammation biomarkers in patients with CRSwNP with/without coexisting asthma or NSAID-ERD from the SINUS-52 (NCT02898454) study.Patients received treatment with dupilumab or placebo for 52 weeks. Blood and urinary biomarkers were evaluated through 52 weeks, and nasal secretions and mucosa brushings through 24 weeks.Of 447 patients, 60% had coexisting asthma and 27% had coexisting NSAID-ERD. At baseline, blood eotaxin-3, eosinophils, and periostin, nasal secretion eotaxin-3, and urinary leukotriene E4 were significantly higher in patients with coexisting NSAID-ERD than without. Dupilumab reduced eotaxin-3, thymus and activation-regulated chemokine, periostin, and total immunoglobulin E in blood, eotaxin-3, periostin, IL-5, and eosinophil cationic protein in nasal secretions, and leukotriene E4 in urine. Reductions were generally similar or greater in the subgroups with asthma and NSAID-ERD than without. Dupilumab also reduced MUC5AC and mast cell counts in nasal mucosa brushings.Dupilumab reduced local and systemic type 2 inflammatory biomarkers in patients with CRSwNP, including mast cells in nasal mucosa and cysteinyl leukotrienes in urine. These findings provide insight into the processes driving CRSwNP and the mechanisms of dupilumab's therapeutic effects.SINUS-52 https://www.clinicaltrials.gov/ct2/show/NCT02898454.NCT02898454.
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