ArticleAllergy2026
Comorbid Chronic Rhinosinusitis and Asthma: Shared Risk Factors and Treatment Implications-An EAACI Task Force Report.
Article in Allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Beyond dysbiosis: microbial metabolites as key remodelers of nasal mucosal immune tolerance in chronic rhinosinusitis.Frontiers in immunology · 2026Review
- The airway epithelial-immune axis: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
Chronic rhinosinusitis (CRS) and asthma are prevalent conditions that often coexist. These diseases share common inflammatory mechanisms, such as T-helper cell 2 (T2)-high inflammation, driven by interleukin (IL)-4, IL-5, and IL-13 cytokines. The frequent comorbidity between CRS, especially CRS with nasal polyps (CRSwNP), and asthma exacerbates disease severity, impairs quality of life, and complicates treatment. Patients with NSAID-exacerbated respiratory disease (N-ERD) represent a severe phenotype of this disease, characterized by the coexistence of CRSwNP, asthma, and NSAID hypersensitivity, which poses unique therapeutic challenges. This EAACI Task Force explores the shared risk factors, including genetic predispositions, epithelial barrier dysfunction, microbiome dysbiosis, underlying CRS, and asthma. It also evaluates current therapeutic strategies such as biologics, aspirin therapy after desensitization (ATAD), and endoscopic sinus surgery (ESS). Biologics have shown their effectiveness and safety in the treatment of asthma and CRS. Dupilumab, mepolizumab, depemokimab, and omalizumab have emerged as transformative therapies, particularly for patients with severe type 2 inflammation. Tezepelulumab is effective for both T2-high and T2-low asthma and CRSwNP. Itepekimab has shown its effect in asthma and is under investigation for CRSwNP. Omalizumab is effective in allergic asthma and CRSwNP. ATAD provides an additional disease-modifying approach for N-ERD, though patient adherence and tolerability remain critical challenges. ESS significantly improves asthma control, reduces medication use, and enhances sinonasal outcomes, particularly in severe asthma cases; however, these patients often need recurring surgeries. Despite these advances, treatment outcomes vary based on individual phenotypes and endotypes, underscoring the need for personalized approaches. The report highlights gaps in the literature, such as the lack of head-to-head trials comparing biologics, ATAD, and surgery. Future research should focus on refining treatment algorithms, identifying biomarkers for treatment selection, and assessing long-term outcomes to optimize care for patients with CRS, asthma, and N-ERD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.