Patients with inflammatory bowel disease are at increased risk for thromboembolic complications. Its prevalence rate ranges from 1% to 7% in clinical studies and reaches 39% in autopsy series. The cause of thrombotic complications in inflammatory bowel disease is generally considered to be associated with hypercoagulability. We experienced a case of ulcerative colitis associated with Budd-Chiari syndrome and superior mesenteric vein thrombosis. This rare complication of ulcerative colitis was successfully managed by conventional treatment for ulcerative colitis and anticoagulation therapy.
Adult ; Colitis, Ulcerative/*complications ; English Abstract ; Female ; Hepatic Vein Thrombosis/*complications ; Humans ; Mesenteric Vascular Occlusion/*complications ; Mesenteric Veins ; Venous Thrombosis/*complications

BACKGROUND/AIMS: Membranous obstruction is the most common cause of Budd-Chiari syndrome in Orientals. Recently, percutaneous transluminal balloon angioplasty (PTBA) has been successfully applied as a treatment of membranous obstruction. We evaluated etiologies and clinical manifestations in our cases and the usefulness of PTBA. METHODS: Twelve cases of Budd-Chiari syndrome were analyzed. RESULTS: 50.3 years was the average age of the cases (ranging from 37 to 67 years). Major symptoms or signs were superficial collateral vessels on the chest or the abdomen in 6 cases, ascites in 3, abdominal pain in 4, hepatomegaly in 4, splenomegaly in 3, melena or hematemesis in 2, and leg edema in 2. Upper gastrointestinal endoscopy showed esophageal varices in 6 cases and two of these 6 cases had gastric varices. Of 8 cases with liver cirrhosis, 4 were classified as Child-Pugh class A and 4 as B. Four patients with cirrhosis had concurrent hepatocellular carcinoma including 1 patient who was HBs Ag positive. Etiologies were membranous obstruction in 11 cases and protein C deficiency in 1 case. The main site of obstruction was IVC in 8 and hepatic vein in 4. PTBA was successfully performed in 8 cases of membranous obstruction. During the mean follow-up period of 27.6 months (12-40 months), there were no reobstructions except in 2 cases. CONCLUSIONS: The most common cause of Budd-Chiari syndrome in our cases was membranous obstruction of IVC. Percutaneous transluminal balloon angioplasty is a very useful treatment method.
Adult ; Aged ; *Angioplasty, Balloon ; English Abstract ; Female ; Hepatic Vein Thrombosis/complications/diagnosis/*therapy ; *Hepatic Veins ; Human ; Male ; Middle Aged ; *Vena Cava, Inferior

Antiphospholipid syndrome is characterized by recurrent episodes of arterial and venous thrombosis, spontaneous fetal losses, thrombocytopenia and persistently elevated levels of antiphospholipid antibodies. We experienced a case of Budd-Chiari syndrome in a 32-year old female lupus patient who was presented with left leg edema, ascites and esophageal varix. The clinical and laboratory findings were compatible with the cirteria for systemic lupus erythematosus (SLE) and she was found to have anticardiolipin antibody, thrombocytopenia and prolonged partial thromboplastin time. Initially, she was treated with intravenous heparin and uroki nase and she was followed up with warfarin, baby aspirin and steroids.
Adult ; Angiography ; Animal ; Antibodies, Antiphospholipid/blood* ; Case Report ; Drug Therapy, Combination ; Female ; Hepatic Vein Thrombosis/complications ; Hepatic Vein Thrombosis/diagnosis* ; Hepatic Vein Thrombosis/drug therapy ; Human ; Lupus Erythematosus, Systemic/complications ; Lupus Erythematosus, Systemic/diagnosis* ; Lupus Erythematosus, Systemic/drug therapy ; Tomography, X-Ray Computed

Portal vein thrombosis (PVT) is a rare but serious postoperative complication of pancreaticoduodenectomy (PD). We reported a case of late-onset postoperative PVT with hemorrhage from the common hepatic artery (CHA) in a 73-year-old man who underwent pylorus-preserving pancreaticoduodenectomy (PPPD) for duodenum papilla cancer, followed by reconstruction using the modified Child's technique. The pancreaticojejunostomy was achieved by end-to-side, 2-layer invagination anastomosis without pancreatic duct stenting. Drain removal and hospital discharge were scheduled on postoperative day (POD) 18, but blood-stained fluid in the drain and sudden hematemesis were noted. Emergency surgery was performed because PVT and imaging findings were suggestive of necrosis of the lifted jejunum. Although no jejunal necrosis was identified during surgery, bleeding from the side of the CHA was detected and the bleeding point was suture-closed to achieve hemostasis. We suspected late-onset postoperative arterial hemorrhage and subsequent hematoma formation, which caused portal vein compression and PVT formation. We chose a conservative treatment strategy for PVT, taking into account the operation time, intraoperative vital signs and blood flow in the portal vein. Despite the complicated postoperative course, he was discharged home in a fully ambulatory state on POD 167.
Aged ; Duodenum ; Emergencies ; Hematemesis ; Hematoma ; Hemorrhage* ; Hemostasis ; Hepatic Artery* ; Humans ; Jejunum ; Necrosis ; Pancreatic Ducts ; Pancreaticoduodenectomy* ; Pancreaticojejunostomy ; Portal Vein* ; Postoperative Complications ; Postoperative Hemorrhage ; Stents ; Venous Thrombosis* ; Vital Signs

BACKGROUND/AIMS: The aim of this study is to elucidate the efficacy of repeated hepatic arterial infusion chemotherapy (HAIC) and different chemotherapeutic regimens for treating patients having advanced hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT). METHODS: From Jan. 1999 and Dec. 2003, a total of 103 patients diagnosed as having HCC with PVTT, but without extrahepatic spreading, were enrolled in this study. They were stratified into two groups. Group I (67 patients) received intraarterial cisplatin (CDDP, 80 mg/m2 for 2 hours on Day 1), Group II (36 patients) received intraarterial CDDP (60 mg/m2 for 2 hours on Day 2) and 5-fluorouracil (5-FU, 500 mg/m2 for 5 hours on Day 1-3). They were scheduled to receive at least three consecutive courses of the HAIC at 1 month intervals. RESULTS: Among the 66 patients who completed the protocol, one (2.5%) and seven (17.5%) patients of group I, and one (3.8%) and four (15.4%) of group II, exhibited complete and partial responses, respectively. The median survival period of all the patients was 6 months. Group II showed a tendency to improve the median survival compared to group I (8.5 vs 5.0 months, respectively, P=0.45). The most common adverse reaction was nausea (58.2%). However, an elevation of the total bilirubin level was more frequent in Group I than in Group II (61.3% vs 20.7%, respectively, P<0.05). CONCLUSIONS: Repeated HAIC using CDDP achieved favorable results in a few patients with HCC with PVTT, and additional 5-FU may be useful.
Adult ; Antineoplastic Combined Chemotherapy Protocols/*administration & dosage ; Carcinoma, Hepatocellular/*drug therapy ; Cisplatin/administration & dosage ; English Abstract ; Female ; *Hepatic Artery ; Humans ; Infusions, Intra-Arterial ; Liver Neoplasms/*drug therapy ; Male ; Middle Aged ; *Portal Vein ; Venous Thrombosis/*complications

Budd-Chiari syndrome (BCS) is a disorder caused by occlusion of the hepatic vein or inferior vena cava. The clinical presentation include abdominal pain, hepatomegaly, ascites, leg edema, collateral venous dilatation of the body trunk, and portal hypertension. In addition, BCS can cause hepatocellular carcinoma (HCC) in some patients, although its pathogenesis is not yet completely understood. The average reported time lag from diagnosis of BCS to full-blown HCC ranges from several years to several decades. Hepatic carcinogenesis in patients with BCS perhaps reflects a prolonged and persistent liver injury in that it occurs in the primary inferior vena cava obstruction rather than the primary hepatic vein thrombosis. Among patients with BCS, membranous obstruction of the vena cava (MOVC) usually presents an insidious and chronic illness, whereas primary hepatic vein thrombosis presents an acute or subacute illness. We experienced a case of a patient with BCS, which progressed rapidly that HCC developed only nine months after the diagnosis of BCS. The factors causing this rapid progression are still unclear and remain to be investigated.
Adult ; Carcinoma, Hepatocellular/*etiology/pathology/radiography ; Disease Progression ; Fatal Outcome ; Female ; Hepatic Vein Thrombosis/*complications/pathology/radiography ; Human ; Liver/*pathology/radiography ; Liver Neoplasms/*etiology/pathology/radiography ; Tomography, X-Ray Computed