The causal relationship between diabetes mellitus and the risk of sensorineural hearing loss: A Mendelian randomization study

被引:0
作者
Guo, Qingqing [1 ]
Niu, Dingren [1 ]
Zhou, Ling [2 ]
机构
[1] Heilongjiang Univ Chinese Med, Harbin, Heilongjiang, Peoples R China
[2] Heilongjiang Univ Chinese Med, Affiliated Hosp 1, Dept Orthopaed, Harbin 150040, Heilongjiang, Peoples R China
关键词
causal relationship; diabetes mellitus; Mendelian randomization; sensorineural hearing loss; INSTRUMENTS; MORTALITY;
D O I
10.1097/MD.0000000000039950
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
An increasing body of evidence suggests that diabetes mellitus (DM) plays a role in sensorineural hearing loss (SNHL). However, the specific causal relationship between DM and SNHL remains partially uncertain. This study aimed to investigate the causal relationship between DM and the risk of SNHL using a Mendelian randomization (MR) study. Single nucleotide polymorphisms closely related to DM were selected as instrumental variables using open genome-wide association study datasets. Three methods based on inverse variance weighted were utilized to investigate the causal relationship between DM and SNHL. Subsequently, multivariable MR (MVMR) was executed to adjust for confounding genetic associations. In addition, a range of sensitivity analyses were performed to assess the stability and reliability of the MR results. The inverse variance weighted analysis indicated a potential genetic causality between DM and SNHL (odds ratio [OR]: 2.179; 95% confidence interval [CI]: 1.123-4.231; P = .021). The sensitivity analyses showed that the included single nucleotide polymorphisms had no heterogeneity, horizontal pleiotropy, and outliers (P > .05). Moreover, the leave-one-out method further verified the robustness of the MR analysis results. Finally, the results of the MVMR study predicted that there was a genetic causal relationship between type 1 DM and SNHL (OR: 1.032; 95%CI: 1.018-1.047; P = 5.45 x 10(-6)), while there was no causality between type 2 DM and SNHL (OR: 1.000; 95%CI: 0.958-1.036; P = .853). Our study suggested that DM and type 1 DM may be genetically responsible for SNHL. Although our study did not detect a genetic causal relationship between type 2 DM and SNHL, this does not rule out a relationship between them at other mechanistic levels. Further studies are required to confirm the findings and look into the physiological and pathological mechanism underlying these relationships.
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