<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>He J</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Previous studies have shown that various cell indices are associated with a higher risk of venous thromboembolism (VTE), however, whether these findings reflect a causal relationship remains unclear. Therefore, we performed a two-sample Mendelian randomization (MR) analysis to assess the causal association of various blood cells with VTE risk.&lt;h4>Study design and methods&lt;/h4>Summary statistics of genetic instruments representing cell indices for erythrocytes, leukocytes, and platelets were extracted from genome-wide association studies of European ancestry, by Two-Sample Mendelian Randomization. Inverse variance weighting (IVW) was used as the primary analytical method for MR. Sensitivity analyses were performed to detect horizontal pleiotropy and heterogeneity.&lt;h4>Results&lt;/h4>Genetically predicted red blood cell distribution width, mean reticulocyte volume, and mean red blood cell volume were positively associated with VTE, with odds ratio (OR) of 1.002 [CI 1.000-1.003, &lt;i>P&lt;/i> = 0.022), 1.003 (CI 1.001-1.004, &lt;i>P&lt;/i> = 0.001, respectively)] and 1.001 (CI 1.000-1.002, &lt;i>P&lt;/i> = 0.005). Genetically predicted monocyte count was negatively correlated with VTE, with OR = 0.998 (CI 0.996-0.999, &lt;i>P&lt;/i> = 0.041).&lt;h4>Conclusion&lt;/h4>Genetically liability to high- red blood cell distribution width, mean reticulocyte volume, mean red blood cell volume, and low monocyte count are associated with the higher risk of VTE. Targeting these factors might be a potential strategy to prevent VTE.</pubmed_abstract><journal>Frontiers in cardiovascular medicine</journal><pagination>919640</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9304581</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Blood Cells and Venous Thromboembolism Risk: A Two-Sample Mendelian Randomization Study.</pubmed_title><pmcid>PMC9304581</pmcid><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Ma R</pubmed_authors><pubmed_authors>Yao Y</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>He J</pubmed_authors><pubmed_authors>Jiang Q</pubmed_authors><pubmed_authors>Zhang N</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Shen Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Blood Cells and Venous Thromboembolism Risk: A Two-Sample Mendelian Randomization Study.</name><description>&lt;h4>Background&lt;/h4>Previous studies have shown that various cell indices are associated with a higher risk of venous thromboembolism (VTE), however, whether these findings reflect a causal relationship remains unclear. Therefore, we performed a two-sample Mendelian randomization (MR) analysis to assess the causal association of various blood cells with VTE risk.&lt;h4>Study design and methods&lt;/h4>Summary statistics of genetic instruments representing cell indices for erythrocytes, leukocytes, and platelets were extracted from genome-wide association studies of European ancestry, by Two-Sample Mendelian Randomization. Inverse variance weighting (IVW) was used as the primary analytical method for MR. Sensitivity analyses were performed to detect horizontal pleiotropy and heterogeneity.&lt;h4>Results&lt;/h4>Genetically predicted red blood cell distribution width, mean reticulocyte volume, and mean red blood cell volume were positively associated with VTE, with odds ratio (OR) of 1.002 [CI 1.000-1.003, &lt;i>P&lt;/i> = 0.022), 1.003 (CI 1.001-1.004, &lt;i>P&lt;/i> = 0.001, respectively)] and 1.001 (CI 1.000-1.002, &lt;i>P&lt;/i> = 0.005). Genetically predicted monocyte count was negatively correlated with VTE, with OR = 0.998 (CI 0.996-0.999, &lt;i>P&lt;/i> = 0.041).&lt;h4>Conclusion&lt;/h4>Genetically liability to high- red blood cell distribution width, mean reticulocyte volume, mean red blood cell volume, and low monocyte count are associated with the higher risk of VTE. Targeting these factors might be a potential strategy to prevent VTE.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-26T07:33:26.985Z</modification><creation>2025-04-06T12:19:03.575Z</creation></dates><accession>S-EPMC9304581</accession><cross_references><pubmed>35872889</pubmed><doi>10.3389/fcvm.2022.919640</doi></cross_references></HashMap>