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Blood Cells and Venous Thromboembolism Risk: A Two-Sample Mendelian Randomization Study
Jiahao He1, Qian Jiang1, Yiting Yao1
1State Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Genetic predisposition to higher red blood cell width, mean reticulocyte volume, and mean red blood cell volume, along with lower monocyte counts, increases venous thromboembolism (VTE) risk. These findings suggest potential VTE prevention strategies targeting these blood cell indices.
Area of Science:
- Genetics
- Hematology
- Epidemiology
Background:
- Previous studies linked various cell indices to increased venous thromboembolism (VTE) risk.
- The causal relationship between cell indices and VTE risk remained unclear.
- Mendelian randomization (MR) is a robust method to investigate causal associations.
Purpose of the Study:
- To assess the causal association between genetically predicted blood cell indices and VTE risk.
- To clarify the role of specific erythrocyte, leukocyte, and platelet indices in VTE pathogenesis.
Main Methods:
- A two-sample Mendelian randomization (MR) analysis was performed.
- Genetic instruments for cell indices were sourced from large genome-wide association studies (GWAS) in European ancestry.
- Inverse variance weighting (IVW) was the primary analytical method, with sensitivity analyses for pleiotropy and heterogeneity.
Main Results:
- Genetically predicted higher red blood cell distribution width (OR=1.002, P=0.022), mean reticulocyte volume (OR=1.003, P=0.001), and mean red blood cell volume (OR=1.001, P=0.005) were associated with increased VTE risk.
- Genetically predicted lower monocyte count (OR=0.998, P=0.041) was associated with increased VTE risk.
Conclusions:
- Genetic liability towards specific red blood cell indices and monocyte counts are causally associated with VTE risk.
- Targeting these genetically influenced blood cell factors may offer novel strategies for VTE prevention.
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