A Hypercoagulable Triad in a Young Woman: Pulmonary Embolism Revealing Pulmonary Tuberculosis with Triple-Positive Antiphospholipid Syndrome and Protein S Deficiency, Senegal
Mouhamed AlMakhy Niang *
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Mouhamed Dieng
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Mourno Tarsa Nousradine
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Michel Assane Ndour
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Matar Ndiaye
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Oumar Boun Khatab Diouf
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Boundia Djiba
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Demba Diédhiou
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Anna Sarr
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
Maïmouna Ndour Mbaye
Department of Internal Medicine, Abass Ndao Hospital Center, Cheikh Anta Diop University, Senegal.
*Author to whom correspondence should be addressed.
Abstract
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.
Keywords: Pulmonary embolism, tuberculosis, antiphospholipid syndrome, protein S deficiency, Senegal