The relationship between smoking and recurrent aphthous stomatitis: A Mendelian randomization study DOI Creative Commons
Yujiao Hu, Cheng Chen, Fei Yu

et al.

Tobacco Induced Diseases, Journal Year: 2025, Volume and Issue: 23(January), P. 1 - 10

Published: Jan. 15, 2025

INTRODUCTION Existing research suggests an association between smoking and the incidence of recurrent aphthous stomatitis (RAS); however, causal relationship remains ambiguous.We employed Mendelian randomization (MR) to clarify potential risk developing RAS.METHODS We utilized genome-wide study (GWAS) sequencing data related from Finnish database as instrumental variables (IVs) GWAS for RAS UK Biobank (UKB) outcome perform a two-sample MR analysis.The selection IVs was rigorously controlled according three principal assumptions relevance, independence, exclusivity.The primary analytical methods were inverse variance weighting (IVW) weighted median (WM), supplemented by MR-Egger, simple mode, mode techniques infer causality RAS.Sensitivity analyses conducted using MR-PRESSO, Cochran's Q, MR-Egger intercept ensure robustness findings.RESULTS The findings IVW WM suggest elevated (IVW: OR=1.003; 95% CI: 1.0002-1.005,p=0.033;WM: 1.00006-1.007,p=0.044).Compared non-smokers, smokers have 0.3% increase in RAS.Furthermore, sensitivity analysis did not reveal any inconsistencies that would contradict results.CONCLUSIONS Our provide preliminary evidence RAS, which may contribute deeper understanding underlying mechanisms.Further is needed confirm these results explore their implications clinical practice.

Language: Английский

The relationship between smoking and recurrent aphthous stomatitis: A Mendelian randomization study DOI Creative Commons
Yujiao Hu, Cheng Chen, Fei Yu

et al.

Tobacco Induced Diseases, Journal Year: 2025, Volume and Issue: 23(January), P. 1 - 10

Published: Jan. 15, 2025

INTRODUCTION Existing research suggests an association between smoking and the incidence of recurrent aphthous stomatitis (RAS); however, causal relationship remains ambiguous.We employed Mendelian randomization (MR) to clarify potential risk developing RAS.METHODS We utilized genome-wide study (GWAS) sequencing data related from Finnish database as instrumental variables (IVs) GWAS for RAS UK Biobank (UKB) outcome perform a two-sample MR analysis.The selection IVs was rigorously controlled according three principal assumptions relevance, independence, exclusivity.The primary analytical methods were inverse variance weighting (IVW) weighted median (WM), supplemented by MR-Egger, simple mode, mode techniques infer causality RAS.Sensitivity analyses conducted using MR-PRESSO, Cochran's Q, MR-Egger intercept ensure robustness findings.RESULTS The findings IVW WM suggest elevated (IVW: OR=1.003; 95% CI: 1.0002-1.005,p=0.033;WM: 1.00006-1.007,p=0.044).Compared non-smokers, smokers have 0.3% increase in RAS.Furthermore, sensitivity analysis did not reveal any inconsistencies that would contradict results.CONCLUSIONS Our provide preliminary evidence RAS, which may contribute deeper understanding underlying mechanisms.Further is needed confirm these results explore their implications clinical practice.

Language: Английский

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