Budd-Chiari syndrome and heparin-induced thrombocytopenia in polycythemia vera: Successful treatment with repeated TIPS and interferon alpha
Autor: | Nathalie Mahfoud, Daniel Mahfoud, Riad Akoum, Albert Ghaoui, Nadine Haddad, Hussein Farhat, Joe Khoury |
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Rok vydání: | 2009 |
Předmět: |
Adult
medicine.medical_specialty Vitamin K Alpha interferon heparin-induced thrombocythopenia Budd-Chiari Syndrome Fondaparinux lcsh:RC254-282 Polycythemia vera Polysaccharides hemic and lymphatic diseases Heparin-induced thrombocytopenia Humans Immunologic Factors Medicine Radiology Nuclear Medicine and imaging Polycythemia Vera Heparin business.industry Anticoagulants Interferon-alpha Ultrasonography Doppler General Medicine lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens medicine.disease Magnetic Resonance Imaging Thrombocytopenia Thrombosis Portal vein thrombosis Surgery Oncology Budd–Chiari syndrome Female Portasystemic Shunt Transjugular Intrahepatic Tomography X-Ray Computed business Postpartum period medicine.drug |
Zdroj: | Journal of Cancer Research and Therapeutics, Vol 5, Iss 4, Pp 305-308 (2009) |
ISSN: | 0973-1482 |
Popis: | Polycythemia vera (PV) is a common cause of Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT). The postpartum period is a precipitating cofactor. An additional heparin-induced thrombocytopenia/thrombosis (HIT/T) leads to a life-threatening condition in which transjugular intrahepatic portosystemic shunting (TIPS) seems to be the only life-saving procedure. We describe the case of a subacute BCS and PVT in the late postpartum period. The diagnosis was established using CT scan, MRI, and Doppler ultrasonography of abdominal vessels and the laboratory findings were compatible with PV. After a successful creation of TIPS, a HIT/T worsened the hemorrhagic and thrombotic picture. TIPS procedure was successfully repeated and heparin was replaced with Fondaparinux and then vitamin K antagonist. The treatment with interferon alpha-2A, started after the normalization of liver functions, resulted in a complete remission within 6 months. The JAK2 V617F mutation clone remained undetectable after 2 years′ follow-up. |
Databáze: | OpenAIRE |
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