Related Experiment Video
Updated: Aug 4, 2025
13:08
Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
19.0K
Predictive value for increased activated factor XI activity in acute venous thromboembolism
Magdolna Nagy1, Alejandro Pallares Robles2, Mayken Visser1
1Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
Journal of Thrombosis and Haemostasis : JTH
|April 1, 2023
Summary
Contact system activation, specifically elevated Factor XIa (FXIa) levels, is linked to acute venous thromboembolism (VTE). Higher FXIa activity at baseline predicts recurrent VTE events, supporting FXIa inhibition as a therapeutic strategy.
Area of Science:
- Hematology
- Thrombosis Research
- Coagulation Studies
Background:
- Venous thromboembolism (VTE) involves hypercoagulability, partly due to contact system activation.
- Limited understanding exists regarding the specific role of contact activation in acute VTE.
- The contact system, involving Factor XI, plays a role in coagulation and inflammation.
Purpose of the Study:
- To investigate the involvement and impact of contact system activation in patients with acute VTE.
- To assess the association between contact activation markers and the risk of recurrent VTE.
- To evaluate the potential of targeting Factor XIa (FXIa) for VTE treatment.
Main Methods:
- Investigated contact activation in 321 acute VTE patients and 300 controls.
- Measured Factor XI (FXI) levels, FXIa activity, and plasma kallikrein (PKa) activity using various assays.
- Utilized enzyme-linked immunosorbent assays to quantify FXIa and PKa in complex with inhibitors.
Main Results:
- Patients with VTE showed higher free FXI concentration (FXI:c) but lower calibrated automated thrombogram-FXIa.
- Elevated FXIa complexed with alpha-1-antitrypsin (FXIa:α1AT) and antithrombin (FXIa:AT) were observed in VTE patients.
- Baseline FXIa:α1AT and FXIa:C1-inhibitor levels predicted recurrent VTE events over a 2-year follow-up.
Conclusions:
- Elevated FXIa levels and activity are present in acute VTE and correlate with recurrent events.
- Factor XI activation significantly contributes to VTE risk.
- Findings support the therapeutic potential of FXIa inhibition for managing acute VTE.
Related Concept Videos
01:29Venous Thrombosis III: Interprofessional Care
13
Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
13
01:20Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies
18
The key difference between Superficial Vein Thrombosis (SVT) and Deep Vein Thrombosis (DVT) lies in their location and severity.Clinical ManifestationsSVT typically presents with localized pain, tenderness, and redness along the course of a superficial vein, often accompanied by a palpable, cord-like structure under the skin. This condition is usually less dangerous than DVT but can be uncomfortable and may lead to complications such as cellulitis or, rarely, a clot extension into the deep...
18
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
783
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
783
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
1.3K
Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
1.3K
01:30Venous Thrombosis I: Introduction
14
Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
14
01:20Extrinsic and Intrinsic Pathways of Hemostasis
8.5K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
8.5K