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Published on: October 5, 2015
The Hemostatic Changes in Active Pulmonary Tuberculosis
Severe pulmonary tuberculosis (PTB) can lead to deep venous thrombosis (DVT) due to hemostatic disturbances. Treatment improved coagulation markers and platelet activation, suggesting a hypercoagulable state in PTB that resolves with therapy.
Area of Science:
- Hematology
- Pulmonology
- Infectious Diseases
Background:
- Severe pulmonary tuberculosis (PTB) is occasionally complicated by deep venous thrombosis (DVT).
- Hemostatic disturbances are potential predisposing factors for venous thrombosis in PTB patients.
Purpose of the Study:
- To investigate the role of hemostatic disturbances in PTB patients.
- To analyze coagulation and platelet function in PTB patients before and during treatment.
Main Methods:
- Coagulation and platelet function tests were performed on 40 severe PTB patients and 40 healthy controls.
- Tests were conducted before therapy and on day 30 of treatment, comparing results to controls.
Main Results:
- Active PTB patients exhibited anemia, leukocytosis, thrombocytosis, elevated fibrinogen, factor VIII, and PAI-1, with depressed antithrombin III (ATIII) and protein C (PC) levels.
- Treatment improved anemia, leukocytosis, and thrombocytosis. Fibrinogen and factor VIII normalized, while PC and ATIII levels increased.
- Platelet aggregation studies showed increased platelet activation; DVT was not detected during follow-up.
Conclusions:
- Decreased ATIII and PC levels, elevated fibrinogen, and increased platelet aggregation contribute to a hypercoagulable state in PTB.
- This hypercoagulable state improves with effective PTB treatment.
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