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[Plasma factor VII levels in disseminated intravascular coagulation]
K Kario1, T Matsuo, K Yamamoto
1Department of Internal Medicine, Awaji-Hokutan Public Clinic, Hyogo-pref.
Summary
Disseminated intravascular coagulation (DIC) significantly lowers factor VII levels due to consumption, though some patients show elevated levels from increased liver synthesis. Endothelial stimulation correlates with extrinsic pathway activation in DIC.
Area of Science:
- Hematology
- Coagulation Science
- Pathophysiology
Context:
- Disseminated intravascular coagulation (DIC) is a complex syndrome characterized by widespread activation of coagulation.
- The extrinsic pathway of coagulation plays a role in hemostasis and thrombosis.
- Understanding the activation of coagulation pathways in DIC is crucial for diagnosis and management.
Purpose:
- To evaluate the activation of the extrinsic pathway of coagulation in patients with DIC.
- To measure plasma factor VII coagulant activity (FVIIc) and antigen levels (FVIIag) in DIC patients.
- To correlate factor VII levels with other hemostatic parameters and clinical conditions.
Summary:
- Plasma FVIIc and FVIIag were significantly lower in 56 DIC patients compared to controls, indicating consumption.
- Lower factor VII levels correlated with reduced antithrombin III and plasminogen activities.
- Elevated factor VII levels in some DIC patients suggest compensatory liver synthesis.
- Pathologic endothelial stimulation, indicated by tPA-PAI-I complex, negatively correlated with FVIIag, suggesting extrinsic pathway activation.
- The FVIIc/FVIIag ratio correlated with FDP and fibrin monomer, reflecting factor VII zymogen activation.
Impact:
- This study reveals that factor VII consumption is a key feature of DIC, linked to reduced anticoagulant and profibrinolytic factors.
- Findings highlight the role of endothelial stimulation in activating the extrinsic pathway during DIC.
- The study provides insights into the complex hemostatic alterations in DIC, particularly concerning factor VII dynamics.