A NEW study has uncovered a significant genetic link between asthma and bronchiectasis, shedding light on how certain factors like sinusitis, nasal polyps, and eosinophils may mediate this relationship. The findings offer insights into the shared mechanisms behind these respiratory conditions and highlight potential pathways for targeted interventions.
Using a two-sample Mendelian randomisation (MR) approach, researchers analysed genome-wide association study (GWAS) data to explore whether asthma plays a causal role in the development of bronchiectasis. The results revealed that asthma increases the odds of developing bronchiectasis by 22.8% (OR = 1.228, 95% CI: 1.077–1.400, P = 0.002). This relationship was validated through an independent dataset, strengthening the evidence of causality.
Further mediation MR analyses identified nasal polyps, acute and chronic sinusitis, and elevated peripheral eosinophil counts as significant mediators. Chronic sinusitis showed the highest mediation effect, accounting for 40.7% of the relationship between asthma and bronchiectasis.
To validate these findings, a retrospective observational study compared bronchiectasis patients with and without asthma. Results indicated that those with asthma had significantly higher rates of sinusitis (5.043% versus 2.971%), nasal polyps (0.536% versus 0.152%), and rhinitis (13.197% versus 1.860%). These patients also exhibited elevated eosinophil levels, both in proportion and total counts, suggesting a systemic inflammatory link.
The study provides evidence that asthma can contribute to bronchiectasis development, with sinusitis, nasal polyps, and eosinophilic inflammation playing key roles. This highlights the need for comprehensive management of these mediators in patients with asthma to potentially reduce the risk of bronchiectasis.
Reference
Fan R et al. Association of asthma and bronchiectasis: Mendelian randomization analyses and observational study. Respir Res. 2024;DOI: 10.1186/s12931-024-03034-3.
