Cancer-associated venous thromboembolism: unfolding the role of the intrinsic coagulation pathway
- Conditions
- blood clothcancer1001799110014523
- Registration Number
- NL-OMON54025
- Lead Sponsor
- Academisch Medisch Centrum
- Brief Summary
Not available
- Detailed Description
Not available
Recruitment & Eligibility
- Status
- Recruiting
- Sex
- Not specified
- Target Recruitment
- 100
1. Patients with active cancer and acute venous thromboembolism (VTE) in whom
anticoagulant therapy is anticipated
2. Patients with active cancer and no suspicion or history of VTE
3. Patients with acute venous thromboembolism in whom anticoagulant therapy is
anticipated, with no history of cancer or cancer treatment in the past 5 years
and no suspicion of cancer at study entry.
4. Healthy volunteers
• No history of cancer or cancer-related therapy in the past 5 years.
• No history of VTE
• No suspicion of cancer or VTE at study entry
• No hospital admission in the past 6 months
• Arterial thrombosis (ischemic stroke, myocardial infarction, peripheral
arterial thrombosis) in the past six months
• Ongoing anticoagulant or antiplatelet therapy
• Mechanical heart valves
• Central venous catheters within 4 weeks prior to inclusion, or anticipated
placement.
• One or more of the following risk factors for VTE:
- Known hereditary or acquired thrombophilia
- Viral or bacterial infection at time of inclusion
- Surgery, trauma or fracture of the leg within the previous 4 weeks
- Current known pregnancy
- Current estrogen therapy
• Inability for blood withdrawal at baseline
• Inability or refusal to provide written informed consent.
Study & Design
- Study Type
- Observational invasive
- Study Design
- Not specified
- Primary Outcome Measures
Name Time Method <p>The primary outcome is the level of factor IXa-antithrombin (FIXa:AT). The<br /><br>FIXa:AT complex reflects an early part of the coagulation cascade, and<br /><br>relatively late part of the intrinsic coagulation pathway, immediately prior to<br /><br>factor X and prothrombin conversion. FIXa:AT thereby provides the most accurate<br /><br>estimation of intrinsic pathway activation. </p><br>
- Secondary Outcome Measures
Name Time Method <p>Secondary study outcomes are:<br /><br>1. Factor XIIa-, factor XIa-, and kallikrein (PKa)-inhibitor complexes:<br /><br>FXIIa-C1inh, FXIIa:AT, FXIa-C1inh, FXIa-AT, FXIa:a1AT, and PKa:C1inh complexes<br /><br>2. FXIa-dependent thrombin generation test<br /><br>3. Cancer-related activators of the intrinsic pathway: NET-formation markers<br /><br>(myeloperoxidase, nucleosomes, and citrullinated histone H3), cell-free DNA and<br /><br>polyphosphate extracellular vesicles<br /><br>4. Extrinsic pathway activation and cancer-related activators: FVIIa-AT<br /><br>complexes and TF extracellular vesicles.<br /><br>See protocol section 5.1.2 for details. </p><br>