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Acute-phase response and the hypercoagulable state in pulmonary tuberculosis
S C Robson1, N W White, I Aronson
1University of Cape Town Leukaemia Centre, MRC-UCT Liver Research Centre, Department of Medicine, Cape Town, South Africa.
British Journal of Haematology
|June 1, 1996
Summary
Severe pulmonary tuberculosis (PTB) increases the risk of deep venous thrombosis (DVT) due to inflammation and hypercoagulable states. Key factors include elevated fibrinogen, impaired fibrinolysis, low antithrombin III, and thrombocytosis.
Area of Science:
- Medical Research
- Pulmonology
- Hematology
Background:
- Severe pulmonary tuberculosis (PTB) is frequently associated with deep venous thrombosis (DVT).
- Inflammation in PTB can lead to a hypercoagulable state, predisposing patients to thrombosis.
- Understanding these predisposing factors is crucial for patient management.
Purpose of the Study:
- To prospectively examine the hemostatic changes and predisposing factors for DVT in patients with active pulmonary tuberculosis.
- To compare coagulation parameters between PTB patients with and without DVT.
Main Methods:
- Prospective analysis of patients with active pulmonary tuberculosis.
- Sequential assessment of hemostatic markers, including fibrinogen, fibrin degradation products (FDP), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), and antithrombin III.
- Venographic confirmation of DVT in a subset of patients.
Main Results:
- PTB patients exhibited anemia, thrombocytosis, elevated fibrinogen, FDP, t-PA, and PAI-1, with decreased antithrombin III.
- Patients with proven DVT showed significantly higher FDP, t-PA, and PAI-1 activity compared to those without DVT.
- Platelet counts were lower in patients with DVT.
- Fibrinogen levels increased early in therapy but normalized within 12 weeks.
Conclusions:
- Elevated plasma fibrinogen, impaired fibrinolysis, decreased antithrombin III, and reactive thrombocytosis are key factors favoring DVT development in PTB.
- These findings highlight the complex interplay between tuberculosis, inflammation, and coagulation.
- Therapeutic strategies may need to address these hemostatic disturbances to prevent DVT in PTB patients.