<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14</volume><submitter>Zhou T</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Observational studies suggest that inflammatory markers may increase the risk of idiopathic sudden sensorineural hearing loss (ISSHL). However, the causal relationship between the two has not been established. We sought to assess the possible causal effect between several genetically predicted inflammatory markers and ISSHL by Mendelian random (MR) analysis.&lt;h4>Methods&lt;/h4>We extracted single nucleotide polymorphisms (SNPs) associated with C-reactive protein (CRP), Tumor necrosis factor-α (TNF-α), and fibrinogen from abstract data from the European Individual Large genome-wide association studies (GWAS). Genetic data for ISSHL were obtained from the FinnGen study (&lt;i>n&lt;/i> = 196,592). Effect estimates were assessed using inverse variance weighting (IVW) as the primary me</pubmed_abstract><journal>Frontiers in neurology</journal><pagination>1111255</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9992207</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Inflammatory markers and the risk of idiopathic sudden sensorineural hearing loss: A Mendelian randomization study.</pubmed_title><pmcid>PMC9992207</pmcid><pubmed_authors>Xia Z</pubmed_authors><pubmed_authors>Lin R</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Chen M</pubmed_authors><pubmed_authors>Zhou T</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Yuan Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inflammatory markers and the risk of idiopathic sudden sensorineural hearing loss: A Mendelian randomization study.</name><description>&lt;h4>Background&lt;/h4>Observational studies suggest that inflammatory markers may increase the risk of idiopathic sudden sensorineural hearing loss (ISSHL). However, the causal relationship between the two has not been established. We sought to assess the possible causal effect between several genetically predicted inflammatory markers and ISSHL by Mendelian random (MR) analysis.&lt;h4>Methods&lt;/h4>We extracted single nucleotide polymorphisms (SNPs) associated with C-reactive protein (CRP), Tumor necrosis factor-α (TNF-α), and fibrinogen from abstract data from the European Individual Large genome-wide association studies (GWAS). Genetic data for ISSHL were obtained from the FinnGen study (&lt;i>n&lt;/i> = 196,592). Effect estimates were assessed using inverse variance weighting (IVW) as the primary me</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-04T18:51:14.067Z</modification><creation>2025-04-04T18:51:14.067Z</creation></dates><accession>S-EPMC9992207</accession><cross_references><pubmed>36908593</pubmed><doi>10.3389/fneur.2023.1111255</doi></cross_references></HashMap>