Disease relevance of Hepatic Vein Thrombosis

• The goals of treatment of the Budd-Chiari syndrome are relief of portal hypertension, relief of inferior vena cava syndrome, if present, and preservation of hepatic function [1].
• Erythroid colony formation in the absence of erythropoietin, which is a reliable indicator for a primary myeloproliferative disorder, was seen in 16 patients in whom Budd-Chiari syndrome was due to hepatic vein thrombosis, including 13 women aged 18 to 45 years [2].
• In a collaborative multicenter case-control study, we investigated the effect of factor V Leiden mutation, prothrombin gene mutation, and inherited deficiencies of protein C, protein S, and antithrombin on the risk of Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT) [3].
• These findings indicate that hepatic erythropoietin production occurs in the acute phase of Budd-Chiari syndrome and suggest that, in some cases of Budd Chiari syndrome, polycythemia which resolves after the acute phase may be secondary to liver disease [4].
• We report on a 29 year old woman with Budd-Chiari syndrome and occlusion of the inferior vena cava who presented with acute liver failure [5].

High impact information on Hepatic Vein Thrombosis

• Histopathology of membranous obstruction of the inferior vena cava in the Budd-Chiari syndrome [6].
• Idiopathic granulomatous venulitis that is reversible with prednisone therapy should be considered in the differential diagnosis of the Budd-Chiari syndrome [7].
• High concentrations of serum erythropoietin were observed in 6 of 7 patients with acute primary Budd-Chiari syndrome [4].
• Hereditary protein C deficiency should be considered in patients with Budd-Chiari syndrome [5].
• Lupus anticoagulant, an immunoglobulin that prolongs the partial thromboplastin time, has been associated with thrombotic events, including deep venous thrombosis, pulmonary emboli, and Budd-Chiari syndrome [8].

Chemical compound and disease context of Hepatic Vein Thrombosis

• A gallium-67 study, performed in a rare case of Budd-Chiari syndrome (BCS) in a 6-yr-old child, showed marked concentration of the tracer in the left and caudate lobes of the liver [9].
• The Japanese Ministry of Health and Welfare Research Committee on Aberrant Portal Blood Flow carried out an epidemiological survey and clinical study on Budd-Chiari syndrome in 1990 [10].
• Xenon-133 splenoportography in Budd-Chiari syndrome [11].
• BACKGROUND: Patients who undergo orthotopic liver transplantation (OLT) for Budd-Chiari syndrome (BCS) traditionally have been anticoagulated with warfarin postoperatively [12].
• CONCLUSIONS: The prognosis of Budd-Chiari syndrome can be based on age, Pugh score, ascites, serum creatinine and the presence of features indicating acute injury superimposed on chronic lesions (type III form) [13].

Biological context of Hepatic Vein Thrombosis

• Distended abdominal veins found in a substantial number of cases, often point to collateral circulation due to a membrane in the inferior vena cava (budd-Chiari syndrome) [14].
• We report the case of a 26-year-old man with a chronic Budd-Chiari syndrome with ascites, caused by a hereditary Protein S deficiency, in a Turkish family with consanguinity [15].

Anatomical context of Hepatic Vein Thrombosis

• In the current study, hepatic portion of the inferior vena cava and hepatic veins were studied in 17 autopsy cases of the Budd-Chiari syndrome, 16 of which had no demonstrable cause (idiopathic) [6].
• A patient with this tumour who presented with Budd-Chiari syndrome (the first to the authors' knowledge in Western literature and only the third patient overall) secondary to extensive thrombosis in his inferior vena cava extending from the right atrium down to his iliac vessels is described [16].
• Surprisingly, after 3 months clinical signs of Budd-Chiari syndrome resolved; venography disclosed the resolution of thrombosis in the vena cava inferior and hepatic veins [17].
• Paroxysmal nocturnal hemoglobinuria and Budd-Chiari syndrome: therapeutic challenge with bone marrow transplantation, transjugular intrahepatic portosystemic shunt, and vena cava stent [18].
• Visualization of collaterals in budd-chiari syndrome with Tc-99m MDP bone scintigraphy and Tc-99m HMPAO-labeled leukocyte scintigraphy [19].

Gene context of Hepatic Vein Thrombosis

• Hyperhomocysteinemia and the MTHFR C677T mutation in Budd-Chiari syndrome [20].
• Tissue plasminogen activator and plasminogen activator inhibitor status in Budd-Chiari syndrome [21].
• Liver transplantation for acute Budd-Chiari syndrome in identical twin sisters with Factor V leiden mutation [22].
• Budd-Chiari syndrome in a young patient with celiac sprue: A case report [23].
• We report a case of Budd Chiari syndrome associated with a deficit in protein C, in a young women admitted to hospital for investigation of thromboembolic disease and ascites [24].

Analytical, diagnostic and therapeutic context of Hepatic Vein Thrombosis

• OBJECTIVES: This study sought to report the long-term result (up to 8 years) of percutaneous transluminal balloon angioplasty (PTBA) for Budd-Chiari syndrome (BCS) caused by membranous obstruction of the inferior vena cava (MOVC) [25].
• Dilatation of the inferior vena cava using an expandable metal stent in Budd-Chiari syndrome [26].
• Radionuclide imaging of the inferior vena cava (RIVC) was performed by injecting [99mTc] phytate into a dorsal pedal vein, as an initial diagnostic procedure for eight patients with clinical features of Budd-Chiari syndrome [27].
• The use of gallium-67 liver imaging for the early diagnosis of Budd-Chiari syndrome [9].
• Budd-Chiari syndrome in autosomal dominant polycystic kidney disease: a complication of nephrectomy in patients with liver cysts [28].

References