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<p>Venous thromboembolism (VTE) is a serious yet often overlooked disorder with numerous contributing risk factors. Pulmonary embolism (PE) and deep vein thrombosis (DVT) together constitute VTE. Both PE and DVT are highly prevalent and present a significant global burden in terms of morbidity and mortality. There are various reported underlying causes for the condition. The risk factors for VTE are categorized based on the relative risk they pose. Factors such as age, sex, obesity, malignancy, hormonal therapies, and co-morbidities play a crucial role in determining the severity and outcomes of VTE. Additionally, bacterial and viral infectious diseases have emerged as critical factors for pulmonary embolism. Notable examples include human immunodeficiency virus (HIV), cytomegalovirus, hepatitis C virus, Chlamydia pneumoniae, and respiratory infections. The mechanisms by which infection-induced thrombosis develops and is resolved remain poorly understood. The presence of pathogens and their products triggers inflammation-induced platelet activation and damage to endothelial cells, leading to fibrin deposition and thrombus formation. Bacterial infection-driven generation of reactive oxygen species contributes to platelet activation and subsequent stimulation of the coagulation cascade. Malignancy, particularly its metastasis stage, significantly elevates the risk of coagulation mediated via proteases, which activate factor X. Despite its clinical importance, the underlying mechanisms of VTE are still unclear, and it is unknown whether these mechanisms are conserved. The development of novel and innovative experimental systems to decipher the intricate interplay between infection-mediated inflammation and its impact on the coagulation process would significantly aid in the development of targeted therapeutic strategies for thrombus resolution. A better understanding of these processes is crucial for improving prognosis, diagnosis, and therapeutic strategies for thrombus resolution, all while maintaining immunity against pathogens and preserving homeostasis.</p>

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Venous thromboembolism in infectious diseases

  • 期刊论文

  • 发表日期：

    2025年4月3日

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  • Priyanka P. Nigade,
  • Sagar S. Dhanagar,
  • Vandana S. Nikam

摘要

Venous thromboembolism (VTE) is a serious yet often overlooked disorder with numerous contributing risk factors. Pulmonary embolism (PE) and deep vein thrombosis (DVT) together constitute VTE. Both PE and DVT are highly prevalent and present a significant global burden in terms of morbidity and mortality. There are various reported underlying causes for the condition. The risk factors for VTE are categorized based on the relative risk they pose. Factors such as age, sex, obesity, malignancy, hormonal therapies, and co-morbidities play a crucial role in determining the severity and outcomes of VTE. Additionally, bacterial and viral infectious diseases have emerged as critical factors for pulmonary embolism. Notable examples include human immunodeficiency virus (HIV), cytomegalovirus, hepatitis C virus, Chlamydia pneumoniae, and respiratory infections. The mechanisms by which infection-induced thrombosis develops and is resolved remain poorly understood. The presence of pathogens and their products triggers inflammation-induced platelet activation and damage to endothelial cells, leading to fibrin deposition and thrombus formation. Bacterial infection-driven generation of reactive oxygen species contributes to platelet activation and subsequent stimulation of the coagulation cascade. Malignancy, particularly its metastasis stage, significantly elevates the risk of coagulation mediated via proteases, which activate factor X. Despite its clinical importance, the underlying mechanisms of VTE are still unclear, and it is unknown whether these mechanisms are conserved. The development of novel and innovative experimental systems to decipher the intricate interplay between infection-mediated inflammation and its impact on the coagulation process would significantly aid in the development of targeted therapeutic strategies for thrombus resolution. A better understanding of these processes is crucial for improving prognosis, diagnosis, and therapeutic strategies for thrombus resolution, all while maintaining immunity against pathogens and preserving homeostasis.