Serum vitamin D levels and Sjogren's syndrome: bi-directional Mendelian randomization analysis.


Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
15 05 2023
Historique:
received: 24 11 2022
accepted: 05 05 2023
medline: 17 5 2023
pubmed: 16 5 2023
entrez: 15 5 2023
Statut: epublish

Résumé

Based on the results of existing observational studies, it can be found that the association between serum vitamin D levels and the risk of Sjogren's syndrome (SS) in humans is still controversial. Based on this situation, this study aimed to assess the causal relationship between serum vitamin D levels and SS by using the Mendelian randomization (MR) approach. In this study, genome-wide association studies (GWAS) summary statistics on serum vitamin D levels [sample size = 417,580 (UK Biobank)] and SS [sample size = 416,757 (cases = 2495, controls = 414,262) (FinnGen)] were used. The bi-directional MR analysis was then used to assess possible causal relationships. The major analysis method of MR was performed using inverse-variance weighted (IVW), supplemented by MR-Egger and the weighted median approaches. In addition, sensitivity analyses were used to ensure the stability of the results, including Cochran's Q test, MR-PRESSO, MR-Egger intercept test, and the leave-one-out test. The MR suggested that no significant causal effects of serum 25(OH)D levels on SS risks were observed [odds ratio (OR) = 0.9824; 95% confidence interval (CI) = 0.7130 to 1.3538; P = 0.9137]. Similarly, no evidence supported the causal effects of SS on serum vitamin D levels (β: 0.0076, 95% CI: - 0.0031 to 0.0183; P = 0.1640). This study found no obvious evidence that serum vitamin D level is causally associated with SS risks or vice versa. We call for larger sample size studies to further unravel the potential causal relationship and the exact mechanism.

Sections du résumé

BACKGROUND
Based on the results of existing observational studies, it can be found that the association between serum vitamin D levels and the risk of Sjogren's syndrome (SS) in humans is still controversial. Based on this situation, this study aimed to assess the causal relationship between serum vitamin D levels and SS by using the Mendelian randomization (MR) approach.
METHODS
In this study, genome-wide association studies (GWAS) summary statistics on serum vitamin D levels [sample size = 417,580 (UK Biobank)] and SS [sample size = 416,757 (cases = 2495, controls = 414,262) (FinnGen)] were used. The bi-directional MR analysis was then used to assess possible causal relationships. The major analysis method of MR was performed using inverse-variance weighted (IVW), supplemented by MR-Egger and the weighted median approaches. In addition, sensitivity analyses were used to ensure the stability of the results, including Cochran's Q test, MR-PRESSO, MR-Egger intercept test, and the leave-one-out test.
RESULTS
The MR suggested that no significant causal effects of serum 25(OH)D levels on SS risks were observed [odds ratio (OR) = 0.9824; 95% confidence interval (CI) = 0.7130 to 1.3538; P = 0.9137]. Similarly, no evidence supported the causal effects of SS on serum vitamin D levels (β: 0.0076, 95% CI: - 0.0031 to 0.0183; P = 0.1640).
CONCLUSION
This study found no obvious evidence that serum vitamin D level is causally associated with SS risks or vice versa. We call for larger sample size studies to further unravel the potential causal relationship and the exact mechanism.

Identifiants

pubmed: 37189174
doi: 10.1186/s13075-023-03062-2
pii: 10.1186/s13075-023-03062-2
pmc: PMC10184420
doi:

Substances chimiques

Nonoxynol 26027-38-3
Vitamin D 1406-16-2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

79

Informations de copyright

© 2023. The Author(s).

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Auteurs

Meng Zhao (M)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.

Feiran Wei (F)

Division of Rheumatology, Zhongda Hospital Southeast University, Nanjing, 210008, Jiangsu, China.

Han Li (H)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.

Zemin Wang (Z)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.

Shuai Wang (S)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.

Yangyang Liu (Y)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.

Gaoqiang Fei (G)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.

You Ge (Y)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China.

Pingmin Wei (P)

Department of Epidemiology and Health Statistics, School of Public Health, Southeast University, Nanjing, 210009, Jiangsu, China. mpw1963@126.com.

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