Antiplatelet drugs and risk of venous thromboembolism: results from the EDITH case-control study

Lacut, Karine; Maaten, Jantien van der; Gal, Grégoire Le; Cornily, Géraldine; Mottier, Dominique; Oger, Emmanuel

doi:10.3324/haematol.12331

Cited by 20 publications

(12 citation statements)

References 7 publications

(4 reference statements)

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“…As arterial and venous thrombosis seem to share common risk factors, NSAID use may affect the risk of VTE . However, only a few studies have investigated the association between NSAID use and VTE risk, and the results are conflicting . We aimed to further investigate the risk of VTE associated with use of NSAIDs in our nationwide case–control study of risk factors for VTE in women (Thrombo Embolism Hormone Study, TEHS).…”

Section: Introductionsupporting

confidence: 90%

Non‐steroidal anti‐inflammatory drugs and venous thromboembolism in women

Bergendal

Adami

Bahmanyar

et al. 2013

Pharmacoepidemiology and Drug

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Section: Introductionsupporting

confidence: 90%

Non‐steroidal anti‐inflammatory drugs and venous thromboembolism in women

Bergendal

Adami

Bahmanyar

et al. 2013

Pharmacoepidemiology and Drug

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“…A review showed that in patients with a high risk of venous thrombosis, such as surgery patients, the use of antiplatelet therapy is associated with a reduction of the risk of venous thrombosis of approximately 30% [23]. Regarding first unprovoked venous thrombotic events, a relatively small case–control study revealed risk reductions of up to 50% associated with antiplatelet therapy [24]. However, in a long‐lasting randomized controlled trial among apparently healthy women, the risk of venous thrombosis was only slightly attenuated by low‐dose aspirin [25].…”

Section: Discussionmentioning

confidence: 99%

HMG-CoA reductase inhibitors, other lipid-lowering medication, antiplatelet therapy, and the risk of venous thrombosis

Ramcharan

Stralen

Snoep

et al. 2009

Journal of Thrombosis and Haemostasis

101

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“…Patients with arterial thrombosis have been shown to also be at increased risk for venous thrombosis, and overlapping risk factors (age, obesity, hypertension, diabetes, metabolic syndrome, hypertriglyceridemia) have been found to be associated with both arterial and venous thrombotic events [32,33]. Furthermore, it has been shown that inflammation and platelet activation are also involved in the pathogenesis of venous thrombosis [33,60]. In line with these observations, many diseases are characterized by both venous and arterial thrombosis, such as cancer [61][62][63][64] and infections [65], as well as anti-phospholipid antibody syndrome [66,67], AAV [68][69][70], LVV [71][72][73] and BS [74,75].…”

Section: Fibrinogen Oxidation As a New Link Between Venous And Arterimentioning

confidence: 99%

Behçet’s syndrome as a tool to dissect the mechanisms of thrombo-inflammation: clinical and pathogenetic aspects

Becatti

Emmi

Bettiol

et al. 2018

Clinical and Experimental Immunology

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Summary Behçet’s syndrome (BS) is a complex disease with different organ involvement. The vascular one is the most intriguing, considering the existence of a specific group of patients suffering from recurrent vascular events involving the venous and, more rarely, the arterial vessels. Several clinical clues suggest the inflammatory nature of thrombosis in BS, especially of the venous involvement, thus BS is considered a model of inflammation‐induced thrombosis. Unique among other inflammatory conditions, venous involvement (together with the arterial one) is currently treated with immunosuppressants, rather than with anti‐coagulants. Although many in‐vitro studies have suggested the different roles of the multiple players involved in clot formation, in‐vivo models are crucial to study this process in a physiological context. At present, no clear mechanisms describing the pathophysiology of thrombo‐inflammation in BS exist. Recently, we focused our attention on BS patients as a human in‐vivo model of inflammation‐induced thrombosis to investigate a new mechanism of clot formation. Indeed, fibrinogen displays a critical role not only in inflammatory processes, but also in clot formation, both in the fibrin network and in platelet aggregation. Reactive oxygen species (ROS)‐derived modifications represent the main post‐translational fibrinogen alterations responsible for structural and functional changes. Recent data have revealed that neutrophils (pivotal in the pathogenetic mechanisms leading to BS damage) promote fibrinogen oxidation and thrombus formation in BS. Altogether, these new findings may help understand the pathogenetic bases of inflammation‐induced thrombosis and, more importantly, may suggest potential targets for innovative therapeutic approaches.

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Antiplatelet drugs and risk of venous thromboembolism: results from the EDITH case-control study

Cited by 20 publications

References 7 publications

Non‐steroidal anti‐inflammatory drugs and venous thromboembolism in women

Non‐steroidal anti‐inflammatory drugs and venous thromboembolism in women

HMG-CoA reductase inhibitors, other lipid-lowering medication, antiplatelet therapy, and the risk of venous thrombosis

Behçet’s syndrome as a tool to dissect the mechanisms of thrombo-inflammation: clinical and pathogenetic aspects

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