EVALUATING CHRONIC RHINOSINUSITIS AS A COMORBID DRIVER IN COPD

Abstract

Introduction: Chronic rhinosinusitis (CRS) is increasingly recognized as a significant comorbidity in patients with chronic obstructive pulmonary disease (COPD), particularly under the framework of the “united airways” model, which emphasizes shared inflammatory mechanisms across the upper and lower respiratory tract.

Aim: To evaluate inflammatory biomarker profiles among COPD patients with and without CRS, and to assess differences across distinct COPD phenotypes—non-exacerbators (NE), frequent exacerbators (E), and asthma-COPD overlap (ACO).

Material and methods: A cross-sectional study was conducted on 36 COPD patients at a university clinic in Skopje, including 21 with CRS and 15 patients without CRS. All participants underwent clinical phenotyping, nasal endoscopy, sinus CT, and serum biomarker analysis (IL-4, IL-5, IL-6, IL-8, CRP, leukocytes). Statistical comparisons were made using Mann–Whitney U and Kruskal–Wallis tests.

Results: CRS was predominantly found in patients with the ACO phenotype (71.4%, p = 0.0006). No statistically significant differences were observed in systemic biomarkers (IL‑4, IL‑5, IL‑6, IL‑8, CRP, leukocytes) between COPD patients with and without CRS. IL‑5 and IL‑6 were undetectable. Similarly, inflammatory profiles did not significantly differ among COPD phenotypes.

Conclusion: CRS appears disproportionately represented in the ACO phenotype, likely due to shared type‑2 inflammatory pathways. However, conventional systemic biomarkers lack the sensitivity to detect upper airway involvement or differentiate COPD phenotypes. These findings highlight the need for comprehensive airway assessment and more specific biomarkers in future studies to better understand the interplay between CRS and COPD.