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Case report reveals pulmonary embolism due to tuberculosis and antiphospholipid syndrome, highlighting risks.
Introduction: Unprovoked pulmonary embolism (PE) in a young adult mandates a search for prothrombotic etiologies - chief among them acquired thrombophilias, antiphospholipid syndrome (APS), and, in tropical settings, tuberculosis (TB). Observation: We report a 39-year-old woman with weight loss and fever, presenting with acute basal chest pain on a background of prolonged cough. CT pulmonary angiography diagnosed distal PE, and Xpert MTB/RIF confirmed pulmonary TB. Work-up identified triple-positive APS associated with protein S deficiency. Management combined standard anti-tuberculosis therapy (RHZE) and vitamin K antagonist (VKA) anticoagulation, with close INR monitoring due to drug–drug interactions. Discussion: TB triples the risk of VTE/PE ; in triple-positive APS, direct oral anticoagulants (DOACs) are discouraged in favor of VKAs per international recommendations. Rifampicin, a strong inducer, reduces the effectiveness of both DOACs and VKAs, necessitating dose adjustments and tight monitoring. Protein S deficiency may be constitutional or acquired (inflammation, TB, pregnancy, VKAs) and must be re-confirmed away from the acute phase and off VKA. Conclusion: In apparently “unprovoked” PE in TB-endemic regions, TB and APS should be actively sought. In APS receiving rifampicin, VKAs remain the reference strategy with rigorous bio-clinical follow-up.
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Niang et al. (2025) studied this question.
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