PO92 | Challenging management of portal vein thrombosis in a cirrhotic patient on hormone therapy after breast cancer

L.J. Valletta, C. De Luca, M. Aversano, C. Caputo, E. Cimino, P. Conca, A. Tufano, M.D. Di Minno | AOU Federico II Napoli, Italy

Background: Portal vein thrombosis (PVT) is a multifactorial condition frequently associated with liver cirrhosis, malignancies, or prothrombotic states. In cirrhotic patients, reduced portal flow, endothelial dysfunction, and systemic inflammation can promote thrombosis even in the absence of documented thrombophilia. Hormonal therapy, particularly in hormone-sensitive breast cancer, may further increase thrombotic risk. Anticoagulation in cirrhotic patients with thrombocytopenia remains controversial, often limited by drug intolerance and bleeding risk.

Case Report: A 52-year-old woman with liver cirrhosis of probable metabolic origin, moderate splenomegaly, and chronic thrombocytopenia (approximately 50,000/mm³) presented with acute abdominal pain and was diagnosed with portal vein thrombosis by contrast-enhanced CT scan. There was no personal or family history of venous thromboembolism. Both hereditary and acquired thrombophilia screening were negative. The patient was in the first year of adjuvant hormonal therapy with letrozole following quadrantectomy and radiotherapy for hormone-sensitive breast cancer. Anticoagulation with apixaban (5 mg twice daily) was discontinued after two doses due to a significant drop in hemoglobin, severe epistaxis, and gingival bleeding. Fondaparinux (2.5 mg/day) also led to significant bleeding after the second dose. Low-molecular-weight heparin (enoxaparin 4000 IU/day) was poorly tolerated for similar reasons. Each attempt at anticoagulation resulted in relevant bleeding complications, despite the low dosing and short treatment duration. Given the high hemorrhagic risk and a markedly elevated HAS-BLED score, anticoagulant therapy was definitively discontinued, and the patient was placed under close clinical and radiological surveillance.

Conclusions: This case highlights the clinical challenges of managing acute PVT in patients with liver cirrhosis, thrombocytopenia, and hormone therapy. While guidelines support anticoagulation in such settings, an individualized approach is crucial. In selected cases, a high bleeding risk—as documented by validated scores like HAS-BLED—may outweigh the thrombotic risk, leading to the justified suspension of therapy. Clinical decisions must carefully balance efficacy and safety through multidisciplinary evaluation and continuous reassessment.