The therapeutic goal in chronic airway diseases is shifting from symptom control to disease remission. Disease-modifying therapies, including biologics and allergen immunotherapy, have made remission achievable in patients with severe asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), or allergic rhinitis (AR). This EUFOREA consensus aims to establish practical guidance for inducing and maintaining remission in global airway diseases. An international panel of experts in pneumology, rhinology, and allergology convened in Rome (October 2025) to review current evidence and develop consensus statements. The panel achieved consensus on key principles: (i) remission is a therapeutic target independent of disease severity prior to treatment initiation and should not be reserved for severe cases; (ii) CRSwNP with nonallergic eosinophilic asthma, and AR with allergic asthma should be considered features of a single disease rather than comorbidities; (iii) remission should be assessed by each subspecialty separately while warranting combined approaches; (iv) pragmatic definitions prioritizing achievability and clinical utility are recommended; and (v) a 4-week recall window is preferred to assess symptom control within the evaluation of remission and a 12-month period is suggested as the minimal period to define remission. Remission represents an ambitious yet achievable goal, with practical guidance for optimizing patient outcomes.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a prevalent inflammatory disease of the sinuses that significantly diminishes patients' quality of life. Endoplasmic reticulum stress (ERS) is strongly associated with the initiation and progression of numerous inflammatory diseases. This study aimed to identify ERS-related hub genes in CRSwNP using bioinformatics approaches. We combined the GSE136825 and GSE179265 datasets. Subsequently, we performed differential expression analysis and weighted gene co-expression network analysis. The genes identified were then cross-referenced with those associated with ERS, allowing us to identify ERS-related differentially expressed genes in CRSwNP. We employed 4 machine learning algorithms: support vector machine, random forest, extreme gradient boosting, and least absolute shrinkage and selection operator. These methods facilitated the identification of hub genes, which were then used to construct a nomogram for disease prediction. Twenty-eight genes related to ERS showed significant expression differences (P < .05). By overlapping the genes selected from 4 machine learning algorithms, we identified 3 hub ERS-differentially expressed genes: ATP2A3, ACTC1, and DES. The nomogram prediction model built on these pivotal genes demonstrated strong predictive performance. This study offers new insights into the molecular mechanisms of CRSwNP and suggests potential new avenues for early diagnosis and targeted treatment in future clinical practice.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a prevalent type 2 inflammatory disorder that substantially impairs patient quality of life (QoL) through cardinal symptoms of nasal obstruction, olfactory dysfunction, and sleep disturbance, further compounded by frequent comorbidities including asthma and non-steroidal anti-inflammatory drug-exacerbated respiratory disease (NERD). While conventional therapies with intranasal corticosteroids, systemic corticosteroids, and endoscopic sinus surgery remain foundational, their limitations in achieving durable disease control have prompted the emergence of biologic agents targeting key type 2 inflammatory pathways. This narrative review synthesizes evidence from a targeted literature search including randomized controlled trials and complementary real-world studies to evaluate the impact of biologic therapies on patient-reported QoL outcomes in severe CRSwNP. Biologic agents targeting key mediators of type 2 inflammation have consistently demonstrated clinically meaningful improvements in disease-specific QoL, as measured by the Sinonasal Outcome Test-22 (SNOT-22), across nasal, sleep, olfactory, and emotional domains, with consistent benefits regardless of comorbidities or prior surgery. Real-world evidence corroborates trial findings, demonstrating sustained QoL benefits and reduced dependence on systemic corticosteroids and revision surgery. The integration of patient-reported outcome measures into therapeutic decision-making bridges the gap between objective clinical metrics and lived disease burden, informing patient-centered care models. Biologic therapies have redefined success in CRSwNP management by consistently delivering multidimensional, durable improvements in patient-reported QoL, head-to-head comparisons and optimized treatment sequencing warrant further research.

BackgroundChronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by significant tissue remodeling, in which Epithelial-mesenchymal transition (EMT) plays a pivotal role in this process. Autophagy, a cellular degradation mechanism crucial for maintaining cellular homeostasis, may also contribute to EMT in CRSwNP.ObjectivesTo investigate the role of autophagy in EMT during CRSwNP.MethodsTissue specimens were obtained from control subjects and patients with CRSwNP. The expression levels of human neutrophil elastase (HNE), Transforming growth factor-β1 (TGF-β1), the autophagic protein LC3, and EMT-related markers (E-cadherin, N-cadherin, and vimentin) were detected using immunohistochemistry and Western blotting. The expression characteristics of TGF-β1 in CRSwNP and their relationship with autophagy caused by HNE was assessed by in-vitro culture of the human nasal epithelial cell line RPMI-2650 treated with human recombinant HNE.ResultsPatients with CRSwNP had more protein expression of TGF-β1, LC3, N-cadherin, and vimentin, whereas the expression of E-cadherin was significantly decreased (P < .05). Treatment of nasal epithelial cells with recombinant HNE also induced the upregulation of TGF-β1, LC3, N-cadherin and Vimentin, while reducing E-cadherin levels (P < .05). Alternatively, treatment of nasal epithelial cells with an autophagy inhibitor or a TGF-β1 inhibitor mitigated EMT.ConclusionHNE induced EMT by activating the autophagy in CRSwNP and TGF-β1 also played an important role in this process.