Factor V Leiden (FVL) and the prothrombin 20210A gene mutation are two common genetic predispositions to hypercoagulability. We present a complex case of recurrent venous thromboembolism (VTE) in a 50‐year‐old woman with double heterozygosity for FVL and prothrombin G20210A, complicated by heparin‐induced thrombocytopenia (HIT) and May–Thurner syndrome. Following a recent orthopedic surgery and a sedentary postoperative course, the patient developed extensive bilateral deep vein thrombosis (DVT) and a saddle pulmonary embolism. Initial anticoagulation with heparin was complicated by progressive thrombocytopenia and confirmed HIT, prompting transition to bivalirudin and subsequently argatroban. Despite therapeutic anticoagulation and multiple interventional procedures, the patient experienced repeated thrombotic events. After increasing the therapeutic aPTT goal for argatroban, she ultimately stabilized and was successfully transitioned to oral apixaban. This case highlights the synergistic risk posed by the combination of inherited thrombophilia, structural venous abnormalities, and acquired prothrombotic conditions. It provides insight into the complex nature of proper anticoagulation strategies in these individual cases. Our use of argatroban with higher aPTT goals may provide guidance in future cases of refractory VTE. Further studies are needed to better understand the optimal therapies and management for patients with hereditary and acquired thrombophilia.
Okabe et al. (Wed,) studied this question.