Abstract
Objectives: Endothelial injury may promote declining lung function. We aimed to investigate in well-treated persons living with HIV (PLWH) whether elevated levels of thrombomodulin (TM) and syndecan-1 (SDC1) are associated with excess lung function decline and worsening dyspnea.
Methods: A prospective cohort study comprising patients from the Copenhagen municipality. We included 698 PLWH with undetectable viral load. Biomarkers and demographics were measured at baseline, spirometry [forced expiratory volume in one second (FEV1) and forced vital capacity (FVC)] and dyspnea score both at baseline and 2-year follow-up.
Both biomarkers were dichotomized at the 3rd quartile. Decline in lung function was estimated using a linear mixed model with patient-specific random effect. Increase in dyspnea score was estimated using a general mixed logistic regression model.
Results: We did not find an association between elevated SDC1 or TM and an excess decline in neither FEV1: SDC1: 4.5 mL/year (95% CI: −3.9–12.9, p = 0.30), TM: 2.2 mL/year (95% CI: −6.0–10.4, p = 0.60) nor FVC: SDC1: 4.1 mL/year (95% CI: −6.0–14.2, p = 0.42), TM: 1.4 mL/year (95% CI: −8.3–11.1, p = 0.78). A subgroup analysis of never-smokers was consistent with the main analysis.
Likewise, we did not find any association between elevated SDC1 and TM and increase in dyspnea score: SDC1: OR 1.43 (95% CI: 0.89–2.30, p = 0.14), TM: OR 1.05 (95% CI: 0.65–1.71, p = 0.26).
Conclusion: We did not find a significant association between elevated biomarkers of endothelial injury and decline in lung function nor dyspnea.
Methods: A prospective cohort study comprising patients from the Copenhagen municipality. We included 698 PLWH with undetectable viral load. Biomarkers and demographics were measured at baseline, spirometry [forced expiratory volume in one second (FEV1) and forced vital capacity (FVC)] and dyspnea score both at baseline and 2-year follow-up.
Both biomarkers were dichotomized at the 3rd quartile. Decline in lung function was estimated using a linear mixed model with patient-specific random effect. Increase in dyspnea score was estimated using a general mixed logistic regression model.
Results: We did not find an association between elevated SDC1 or TM and an excess decline in neither FEV1: SDC1: 4.5 mL/year (95% CI: −3.9–12.9, p = 0.30), TM: 2.2 mL/year (95% CI: −6.0–10.4, p = 0.60) nor FVC: SDC1: 4.1 mL/year (95% CI: −6.0–14.2, p = 0.42), TM: 1.4 mL/year (95% CI: −8.3–11.1, p = 0.78). A subgroup analysis of never-smokers was consistent with the main analysis.
Likewise, we did not find any association between elevated SDC1 and TM and increase in dyspnea score: SDC1: OR 1.43 (95% CI: 0.89–2.30, p = 0.14), TM: OR 1.05 (95% CI: 0.65–1.71, p = 0.26).
Conclusion: We did not find a significant association between elevated biomarkers of endothelial injury and decline in lung function nor dyspnea.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 1337609 |
| Tidsskrift | Frontiers in Medicine |
| Vol/bind | 11 |
| Antal sider | 9 |
| ISSN | 2296-858X |
| DOI | |
| Status | Udgivet - 2024 |
Bibliografisk note
Funding Information:The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This study was supported by Rigshospitalet, the Novo Nordisk Foundation, and Gilead Sciences. The funder Gilead Sciences was not involved in the study design, collection, analysis, interpretation of data, the writing of this article, or the decision to submit it for publication.
Publisher Copyright:
Copyright © 2024 Rønn, Knudsen, Arentoft, Thudium, Heidari, Sivapalan, Ulrik, Benfield, Ostrowski, Jensen and Nielsen.