S4985 Recurrent Thromboembolism and Ulcerative Colitis Flares Following Anticoagulation Withdrawal: A Case Highlighting the Interplay Between IBD and Hypercoagulability

Introduction: The relationship between anticoagulation and IBD activity remains poorly defined. We present a unique case of a patient with longstanding ulcerative colitis (UC) who experienced recurrent thromboembolism and UC flares following withdrawal of warfarin therapy, despite negative hypercoagulable workup and left atrial appendage occlusion. Case Description/Methods: A 72-year-old man with a 20-year history of UC, managed on mesalamine 2.4 g daily, developed multiple thromboembolic events including ischemic stroke, pulmonary embolism, and deep vein thromboses, requiring long-term warfarin therapy. He was later diagnosed with atrial fibrillation and underwent Watchman device placement. Based on cardiology recommendations, warfarin was discontinued. On 2 separate occasions following anticoagulation cessation, the patient developed new deep vein thromboses along with symptomatic UC flares. Extensive hypercoagulable testing, including evaluations for inherited and acquired thrombophilia’s, was negative. Despite appropriate placement of the Watchman device and presumed stroke risk reduction, recurrent thrombotic events continued in the absence of anticoagulation. Notably, each episode was temporally linked with UC flare-ups. Given this pattern, his gastroenterologist recommended indefinite warfarin therapy, citing a likely inflammation-driven hypercoagulable state. Discussion: This case illustrates the complex interaction between systemic inflammation and thrombosis in IBD. Although left atrial appendage occlusion theoretically reduces the need for chronic anticoagulation in atrial fibrillation, our patient continued to experience thromboembolic events, suggesting that the inflammatory burden of UC may serve as an independent driver. The recurrence of thrombotic events in tandem with UC flares highlights the need to consider ongoing anticoagulation in select IBD patients, even in the absence of traditional risk factors or positive laboratory findings. In patients with IBD and prior thrombosis, anticoagulation may play a dual role: preventing clots and potentially modulating disease activity. Clinical decisions should be individualized, especially when discontinuation of therapy leads to both thromboembolism and IBD flare.