ACUTE‐PHASE RESPONSE AND THE HYPERCOAGULABLE STATE IN PULMONARY TUBERCULOSIS

Abstract
In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 ± 14.3 v 3.2 ± 1.7 μg/ml : P < 0.01), t-PA (19.4 ± 14.9 v 11.3 ± 0.8 ng/ml : P < 0.01), and functional PAI-1 activity (11.6 ± 6.3 v 4.2 ± 4.1 : P < 0.01) with lower platelet counts (347 ± 110 v 563 ± 230 × 109/l : P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.