Mingyi Yang, Yani Su, Pengfei Wen, Jiale Xie, Xianjie Wan, Ke Xu, Wensen Jing, Zhi Yang, Lin Liu, Peng Xu
{"title":"Is the occurrence of deep vein thrombosis related to the fracture site? A two-sample Mendelian randomization study.","authors":"Mingyi Yang, Yani Su, Pengfei Wen, Jiale Xie, Xianjie Wan, Ke Xu, Wensen Jing, Zhi Yang, Lin Liu, Peng Xu","doi":"10.1080/17474086.2025.2459251","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Deep vein thrombosis (DVT) is a known complication of fractures. This study aimed to explore the genetic causal relationship between DVT and fracture sites.</p><p><strong>Research design and methods: </strong>The exposures analyzed in this study included fracture of femur (FFE), fracture of lower leg, including ankle (FLLA), fracture of shoulder and upper arm (FSUA), fracture of forearm (FFO), fracture of rib, sternum and thoracic spine (FRSTS) and fracture of lumbar spine and pelvis (FLSP). DVT as the outcome. A two-sample Mendelian randomization (MR) approach was employed to investigate the genetic causal relationship, and a series of sensitivity analyses were conducted.</p><p><strong>Results: </strong>The findings indicated no genetic causal relationship between FFE (<i>p</i> = 0.569, OR 95% CI = 1.001 [0.998-1.003]), FLLA (<i>p</i> = 0.371, OR 95% CI = 0.999 [0.995-1.002]), FSUA (<i>p</i> = 0.871, OR 95% CI = 1.000 [0.998-1.002]), FFO (<i>p</i> = 0.281, OR 95% CI = 1.001 [0.999-1.002]), FRSTS (<i>p</i> = 0.346, OR 95% CI = 0.999 [0.996-1.001]) or FLSP (<i>p</i> = 0.759, OR 95% CI = 1.000 [0.999-1.002]) and DVT. Sensitivity analyses reinforced the robustness.</p><p><strong>Conclusions: </strong>This study indicate that no genetic causal relationship exists between DVT and fracture site, the observed association may be attributable to non-genetic factors.</p>","PeriodicalId":12325,"journal":{"name":"Expert Review of Hematology","volume":" ","pages":"155-165"},"PeriodicalIF":2.3000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Expert Review of Hematology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/17474086.2025.2459251","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/27 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"HEMATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Deep vein thrombosis (DVT) is a known complication of fractures. This study aimed to explore the genetic causal relationship between DVT and fracture sites.
Research design and methods: The exposures analyzed in this study included fracture of femur (FFE), fracture of lower leg, including ankle (FLLA), fracture of shoulder and upper arm (FSUA), fracture of forearm (FFO), fracture of rib, sternum and thoracic spine (FRSTS) and fracture of lumbar spine and pelvis (FLSP). DVT as the outcome. A two-sample Mendelian randomization (MR) approach was employed to investigate the genetic causal relationship, and a series of sensitivity analyses were conducted.
Results: The findings indicated no genetic causal relationship between FFE (p = 0.569, OR 95% CI = 1.001 [0.998-1.003]), FLLA (p = 0.371, OR 95% CI = 0.999 [0.995-1.002]), FSUA (p = 0.871, OR 95% CI = 1.000 [0.998-1.002]), FFO (p = 0.281, OR 95% CI = 1.001 [0.999-1.002]), FRSTS (p = 0.346, OR 95% CI = 0.999 [0.996-1.001]) or FLSP (p = 0.759, OR 95% CI = 1.000 [0.999-1.002]) and DVT. Sensitivity analyses reinforced the robustness.
Conclusions: This study indicate that no genetic causal relationship exists between DVT and fracture site, the observed association may be attributable to non-genetic factors.
期刊介绍:
Advanced molecular research techniques have transformed hematology in recent years. With improved understanding of hematologic diseases, we now have the opportunity to research and evaluate new biological therapies, new drugs and drug combinations, new treatment schedules and novel approaches including stem cell transplantation. We can also expect proteomics, molecular genetics and biomarker research to facilitate new diagnostic approaches and the identification of appropriate therapies. Further advances in our knowledge regarding the formation and function of blood cells and blood-forming tissues should ensue, and it will be a major challenge for hematologists to adopt these new paradigms and develop integrated strategies to define the best possible patient care. Expert Review of Hematology (1747-4086) puts these advances in context and explores how they will translate directly into clinical practice.