2018
DOI: 10.3389/fped.2018.00142
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The Role of Inflammation in Venous Thromboembolism

Abstract: Venous thromboembolism (VTE), comprising deep vein thrombosis (DVT), and pulmonary embolism (PE), is becoming increasingly recognized as a cause of morbidity and mortality in pediatrics, particularly among hospitalized children. Furthermore, evidence is accumulating that suggests the inflammatory response may be a cause, as well as consequence, of VTE, but current anticoagulation treatment regimens are not designed to inhibit inflammation. In fact, many established clinical VTE risk factors such as surgery, ob… Show more

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Cited by 292 publications
(259 citation statements)
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“…In this context, inflammation-dependent platelet activation plays a fundamental role by enhancing tissue factor expression, thrombin production and activation of coagulation factors leading to a hypercoagulable state [34]. This concept is supported by accumulating evidence highlighting the role of inflammation in venous thromboembolism (VTE), a condition where endothelial damage is not mandatory and can occur without the traditional risk factors for atherothrombosis [32,33,35].…”
Section: Inflammation and Thrombosis: An Emerging Relationshipmentioning
confidence: 99%
“…In this context, inflammation-dependent platelet activation plays a fundamental role by enhancing tissue factor expression, thrombin production and activation of coagulation factors leading to a hypercoagulable state [34]. This concept is supported by accumulating evidence highlighting the role of inflammation in venous thromboembolism (VTE), a condition where endothelial damage is not mandatory and can occur without the traditional risk factors for atherothrombosis [32,33,35].…”
Section: Inflammation and Thrombosis: An Emerging Relationshipmentioning
confidence: 99%
“…45 Interestingly, increased IL-6 and IL-8 levels in plasma are associated with increased risk of VTE in non-cancer patients. 47 It should, however, be noted that no correlations were found between interleukins and VTE in the Vienna Cancer and Thrombosis Study cohort, 48 except for patients with pancreatic cancer. This might be attributed to the relatively low incidence of VTE in the cohort (7.2%) and that plasma was collected prior to cancer-related therapy, ruling out contributions of surgery and/or chemotherapy.…”
Section: Tumor-specific Geneticsmentioning
confidence: 96%
“…Moreover, elevated levels of inflammatory mediators, eg, IL‐6 and IL‐8, may be found in tumor cells harboring a K‐ras mutation 45. Interestingly, increased IL‐6 and IL‐8 levels in plasma are associated with increased risk of VTE in non‐cancer patients 47. It should, however, be noted that no correlations were found between interleukins and VTE in the Vienna Cancer and Thrombosis Study cohort,48 except for patients with pancreatic cancer.…”
Section: Tumor‐specific Geneticsmentioning
confidence: 99%
“…Only once the immune system establishes that a thrombus is sterile does the resolution progress, and this requires additional detection of the thrombus microenvironment to take the appropriate next step. Both policing and repairing phases are mediated by various cytokines and chemokines [56]. Biochemically or genetically shifting the immune response in ways that simulate sepsis or hypersensitize it toward infection slow thrombus resolution because immune cells cannot remodel the tissue until they recognize that their primary job of sterilization has been achieved.…”
Section: Immune Cells: Attack Then Repairmentioning
confidence: 99%