What question did this study set out to answer?

This study aims to clarify whether genetic predispositions to autoimmune diseases influence the risk of hearing loss.

May 31, 2026Open Access

Exploring causal associations between autoimmune diseases and hearing loss: a mendelian randomization study

Puntos clave

This study aims to clarify whether genetic predispositions to autoimmune diseases influence the risk of hearing loss.
Conducted a Mendelian Randomization (MR) analysis using SNPs as instrumental variables for autoimmune diseases.
Utilized Inverse Variance Weighted (IVW) as the primary analysis method, supplemented with MR-Egger and other techniques.
Evaluated heterogeneity and pleiotropy using various statistical tests.
Identified nine significant associations between autoimmune diseases and hearing loss outcomes, including multiple sclerosis and sudden idiopathic hearing loss (OR = 1.0494).
Ankylosing spondylitis was notably associated with several hearing loss types, with the highest odds ratio for mixed conductive and sensorineural hearing loss (OR = 1.5994).
Outlier analysis revealed significant findings for AS-SNHL after removing outliers (OR = 1.1722, p < 0.00001).

Resumen

Objective The causal relationship between Autoimmune Diseases (ADs) and Hearing Loss (HL) remains unclear. This study investigates whether genetic predispositions associated with ADs contribute to HL risk. Methods Mendelian Randomization (MR) analysis was conducted to explore the causal effects of ADs on HL. SNPs from Genome-Wide Association Studies (GWAS) were used as instrumental variables for ADs, including Rheumatoid Arthritis (RA), Type 1 Diabetes (T1D), Systemic Lupus Erythematosus (SLE), Sjögren’s Syndrome (SS), Ankylosing Spondylitis (AS), Multiple Sclerosis (MS), Crohn's Disease (CD), and Ulcerative Colitis (UC). Outcome data included Sensorineural Hearing Loss (SNHL), Conductive Hearing Loss (CHL), Mixed conductive and sensorineural Hearing Loss (MHL), and Sudden Idiopathic Hearing Loss (SIHL). MR analyses employed Inverse Variance Weighted (IVW) as the primary method, supplemented with MR-Egger, weighted median, and weighted mode. Heterogeneity, pleiotropy, and sensitivity were evaluated using Cochran's Q test, MR-Egger regression, MR-PRESSO, and leave-one-out analysis. Results The IVW method identified nine significant associations: MS-SIHL (OR = 1.0494, 95% CI 1.0072–1.0934), AS-CHL (OR = 1.2832, 95% CI 1.0643–1.5472), AS-MHL (OR = 1.5994, 95% CI 1.3696–1.8678), AS-SNHL (OR = 1.1903, 95% CI 1.1104–1.276), AS-SIHL (OR = 1.481, 95% CI 1.22–1.798), SLE-CHL (OR = 1.0593, 95% CI 1.0116–1.1092), UC-MHL (OR = 1.0907, 95% CI 1.0027–1.1865), CD-CHL (OR = 1.0529, 95%CI: 1.0074–1.1005), and CD-SIHL (OR = 1.0597, 95% CI 1.0177–1.1034). Among these, outliers were detected only in AS-SNHL. After outlier removal, the AS-SNHL association remained significant (OR = 1.1722, p < 0.00001), with resolved heterogeneity and pleiotropy. No heterogeneity and pleiotropy were found for the other associations. Conclusion This study identified nine significant AD-HL associations, emphasizing the need for targeted screening and management of HL in individuals with AD. Level of Evidence Level 5.

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