Mendelian randomization study shows a causal effect of asthma on chronic obstructive pulmonary disease risk.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2023
2023
Historique:
received:
19
05
2023
accepted:
22
08
2023
medline:
7
9
2023
pubmed:
1
9
2023
entrez:
1
9
2023
Statut:
epublish
Résumé
This study was performed to explore the causal association between asthma and chronic obstructive pulmonary disease(COPD). We obtained summary statistics for asthma from 408,442 Europeans in an open genome-wide association study (GWAS) from the UK Biobank to select strongly associated single nucleotide polymorphisms that could serve as instrumental variables for asthma (P < 5×10-8). Additional summary statistics for COPD were obtained from 193,638 individuals of European ancestry in the GWAS published by FinnGen. Univariable Mendelian randomization(UVMR) analysis was performed using inverse variance weighted (IVW) as the primary method of analysis. The reliability of the results was verified by multivariable MR(MVMR), reverse and replication MR analysis, and sensitivity analysis. In the UVMR analysis, asthma increased the risk of COPD, with an odds ratio (OR) of 1.27 (95% confidence interval (CI) = 1.16-1.39, P = 5.44×10-7). Estimates were consistent in MVMR analyses by the adjustments of smoking initiation, age of smoking initiation, cigarettes per day, PM 2.5, and the combination of the above factors. In the reverse MR analysis, there was no evidence of a causal effect of COPD on asthma risk(OR = 1.02, 95% CI = 0.97-1.07, P = 0.3643). In the replication MR analysis, asthma still increased the risk of COPD. Sensitivity analyses validated the robustness of the above associations. We found that genetically predicted asthma was positively associated with the risk of COPD. Additionally, there was no evidence that COPD increases the risk of asthma. Further clarification of this link and underlying mechanisms is needed to identify feasible measures to promote COPD prevention.
Sections du résumé
BACKGROUND
This study was performed to explore the causal association between asthma and chronic obstructive pulmonary disease(COPD).
METHODS
We obtained summary statistics for asthma from 408,442 Europeans in an open genome-wide association study (GWAS) from the UK Biobank to select strongly associated single nucleotide polymorphisms that could serve as instrumental variables for asthma (P < 5×10-8). Additional summary statistics for COPD were obtained from 193,638 individuals of European ancestry in the GWAS published by FinnGen. Univariable Mendelian randomization(UVMR) analysis was performed using inverse variance weighted (IVW) as the primary method of analysis. The reliability of the results was verified by multivariable MR(MVMR), reverse and replication MR analysis, and sensitivity analysis.
RESULTS
In the UVMR analysis, asthma increased the risk of COPD, with an odds ratio (OR) of 1.27 (95% confidence interval (CI) = 1.16-1.39, P = 5.44×10-7). Estimates were consistent in MVMR analyses by the adjustments of smoking initiation, age of smoking initiation, cigarettes per day, PM 2.5, and the combination of the above factors. In the reverse MR analysis, there was no evidence of a causal effect of COPD on asthma risk(OR = 1.02, 95% CI = 0.97-1.07, P = 0.3643). In the replication MR analysis, asthma still increased the risk of COPD. Sensitivity analyses validated the robustness of the above associations.
CONCLUSIONS
We found that genetically predicted asthma was positively associated with the risk of COPD. Additionally, there was no evidence that COPD increases the risk of asthma. Further clarification of this link and underlying mechanisms is needed to identify feasible measures to promote COPD prevention.
Identifiants
pubmed: 37656706
doi: 10.1371/journal.pone.0291102
pii: PONE-D-23-15131
pmc: PMC10473539
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0291102Informations de copyright
Copyright: © 2023 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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