Pulmonary Embolism Complicating Active Pulmonary Tuberculosis: Two Case Reports of Tuberculosis-Associated Hypercoagulability.

Background: Active tuberculosis (TB) is increasingly recognized as a systemic thrombo-inflammatory condition capable of inducing a clinically relevant hypercoagulable state and increasing the risk of venous thromboembolism, including pulmonary embolism (PE). However, this association remains underrecognized in clinical practice, and its biological and therapeutic implications are not yet fully defined. We report two cases of active pulmonary tuberculosis complicated by PE and review the literature to highlight the temporal patterns, laboratory features, and clinical relevance of TB-associated hypercoagulability. Case Presentation: The first case involved a 65-year-old man with stage II chronic obstructive pulmonary disease in whom PE was identified concurrently with the diagnosis of active pulmonary TB. The second case concerned a 43-year-old man with severe pulmonary tuberculosis and subsequent intestinal involvement, in whom bilateral PE developed during the early intensive phase of antituberculous therapy. In both patients, laboratory evaluation demonstrated a consistent prothrombotic profile characterized by reactive thrombocytosis, elevated inflammatory markers, increased fibrinogen and D-dimer levels, and reduced protein C and protein S activity. Both patients received standard antituberculous therapy combined with therapeutic anticoagulation, with favorable clinical, laboratory, and radiological outcomes. Discussion: These cases are consistent with emerging evidence that active tuberculosis may induce a reversible infection-related hypercoagulable state through systemic inflammation, endothelial dysfunction, platelet activation, impaired fibrinolysis, and transient depletion of natural anticoagulants. They illustrate two clinically relevant temporal patterns described in the literature, namely PE detected at diagnosis and PE developing during early treatment despite appropriate therapy. The normalization of coagulation abnormalities after treatment further supports an acquired TB-related thrombo-inflammatory mechanism. Conclusions: Active tuberculosis may be complicated by pulmonary embolism both at presentation and during the early phase of treatment. Reactive thrombocytosis, elevated inflammatory markers, increased D-dimer levels, and reduced protein C and protein S activity may serve as useful indicators of TB-associated hypercoagulability. Pulmonary embolism should be considered in patients with severe tuberculosis who show unexplained deterioration or delayed recovery. Larger prospective studies are needed to clarify the role of coagulation profiling and biomarker-guided management in this setting.