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PubMed1978

Carcinomas and other lesions of the liver in mice ingesting organochlorine pesticides.

Carcinomas of the liver were readily induced in male and female mice given organochlorine pesticides orally. The carcinomas were predominantly hepatocellular, with a few being cholangiocellular, and varied from well differentiated to poorly differentiated to undifferentiated. They are capable of invading, metastasizing, and killing the mice. Hemangiosarcomas, leimyosarcomas, and reticulum cell sarcomas were also occasionally seen in mice receiving these chemicals. Hepatic vein thrombosis and hepatic necrosis was observed in some mice.

Adenoma, Bile Duct↗
PubMed2000

Cause of portal or hepatic venous thrombosis in adults: the role of multiple concurrent factors.

According to a recent hypothesis, venous thrombosis results from the concurrence of several factors. This hypothesis was assessed in patients with portal or hepatic venous thrombosis by simultaneously investigating most of the currently identified prothrombotic disorders, local precipitating factors, and other risk factors such as oral contraceptive use. Patients with a tumorous obstruction and patients with cirrhosis with portal vein thrombosis were excluded. The prothrombotic disorders that were investigated included classical and occult myeloproliferative disorders; antiphospholipid syndrome; protein C; protein S and antithrombin deficiency; factor V Leiden; factor II; and methylene-tetrahydrofolate-reductase gene mutations. We found 1 or several prothrombotic disorders and a local precipitating factor in 26 and 10 of the 36 patients with portal vein thrombosis, respectively; and in 28 and none of the 32 patients with hepatic vein thrombosis, respectively. We found a combination of prothrombotic disorders in 5 and 9 patients with portal and hepatic vein thrombosis, respectively, whereas such a combination is expected in less than 1% of asymptomatic subjects. Of the 10 patients with a local precipitating factor, 8 had a prothrombotic disorder. Of the 13 patients who use oral contraceptives, 10 had a prothrombotic disorder. We conclude that portal or hepatic venous thrombosis should be regarded as an index for 1 or several prothrombotic disorders, whether or not local precipitating factors or oral contraceptive use are found. Concurrence of prothrombotic disorders is more common than expected. Extensive investigation of prothrombotic disorders and anticoagulation should be considered in patients with portal or hepatic venous thrombosis.

Budd-Chiari Syndrome↗
PubMed1983

Acute liver dystrophy with thrombosis of hepatic veins: a fatal complication of dacarbazine treatment.

In the course of adjuvant single-agent chemotherapy with dacarbazine after extirpation of malignant melanoma, a fatal complication was observed in four of our patients. During the second cycle of therapy liver failure due to massive hepatic necrosis supervened, with widespread thrombosis of liver veins. The clinical and pathologic features of our patients are compared with the findings in eight published cases. The possible pathogenesis is discussed in detail, and Budd-Chiari syndrome caused by an allergic thrombophlebitis with secondary liver cell necrosis seems to be most probable.

Chemical and Drug Induced Liver Injury↗
PubMed1997

Poor prognosis and limited therapeutic options in patients with Budd-Chiari syndrome and portal venous system thrombosis.

OBJECTIVES: Therapeutic options in Budd-Chiari syndrome (BCS) are highly dependent on the site and extent of hepatic vein thrombosis. The aim of this study was to evaluate the effect of additional portal venous system thrombosis on the clinical presentation, treatment and outcome in patients with BCS. PATIENTS: Clinical notes of 51 patients with BCS admitted to our centre were evaluated. We identified 13 patients (25%) with BCS and additional portal venous system thrombosis. Ten patients were female and three male with a mean age at presentation of 42 years (range 32-67). RESULTS: An underlying haematological aetiology was identified in 10 of the 13 patients. Only four patients (31%) were anticoagulated before referral to our centre. In addition to hepatic vein thrombosis seven patients had portal vein thrombosis (PVT), three had PVT, splenic vein (SV) and superior mesenteric vein (SMV) thrombosis and three had either SV, SMV or inferior vean cava (IVC) thrombosis. The presentation was acute in three patients, subacute in six and chronic in four with a high incidence of encephalopathy (6/13; 46%). Treatment included liver transplantation (four), mesoatrial shunt (one) and balloon dilatation of hepatic veins (two). Six patients were treated medically as all other options were considered too risky or technically impossible. Nine of 13 patients (70%) died either after surgery or before any treatment could be instituted (median survival 1 month), compared to 14/38 (37%) in patients with isolated hepatic vein thrombosis (median survival 6.3 years). CONCLUSION: We conclude that patients with BCS and portal venous system thrombosis constitute a unique group with limited therapeutic options and poor prognosis. The importance of early recognition and anticoagulation of patients with BCS is emphasized.

Adolescent↗
PubMed1997

Spontaneous erythroid colony formation as the clue to an underlying myeloproliferative disorder in patients with Budd-Chiari syndrome or portal vein thrombosis.

Budd-Chiari syndrome is a severe disease characterized by occlusion of large hepatic veins leading to death if untreated. Using the classical criteria for the diagnosis of polycythemia vera (PV), essential thrombocythemia (ET), and idiopathic myelofibrosis (IMF), overt PV was the underlying cause in about 10% of the cases and ET or IMF in only a very few. Using spontaneous endogenous erythroid colony (EEC) formation in vitro and/or bone marrow biopsies, a primary myeloproliferative disorder (PMD) was present in 78% of the patients with apparently idiopathic Budd-Chiari syndrome and in about half of the patients with portal, splenic, and/or mesenteric vein thrombosis. The diagnoses in 40 reported cases with hepatic vein thrombosis and spontaneous EEC were overt PV in 25 and latent unclassified PMD in 15 patients. The diagnoses of 40 reported cases with splanchnic vein thrombosis and spontaneous EEC were overt PV in 12, ET in 2, IMF in 2, and latent unclassified PMD with the presence of EEC in 24 patients. Thrombocytosis as a manifestation of myeloproliferative disease was recorded in 34 of 80 (42.5%) patients with spontaneous EEC and Budd-Chiari syndrome or portal vein thrombosis. Thrombocythemia was present in 15 of 41 patients with a proven and in 19 of 39 patients with a latent myeloproliferative disorder. Patients with hepatic vein or splanchnic vein thrombosis associated with a PMD are predominantly females younger than 45. It is concluded that both spontaneous EEC and histopathology from bone marrow biopsy provide specific information as sensitive clues to the diagnosis of all variants of overt and latent myeloproliferative disorders. The association of hepatic and splanchnic vein thrombosis and PMD is not fully understood. Therapeutic options of Budd-Chiari syndrome include anticoagulation with heparin, fibrinolysis followed by oral anticoagulation, and appropriate treatment of the underlying PMD. In case of failure, invasive options include local procedures such as angioplasty or stenting, venous decompression by portal-systemic shunts, or liver transplantation.

Biomarkers↗
PubMed1986

Ulcerative colitis complicated by Budd-Chiari syndrome.

We present two cases of ulcerative colitis associated with a chronic pattern of hepatic vein thrombosis (Budd-Chiari syndrome). Progression of the hepatic disorder appeared to be unrelated to the activity of the colitis. Liver function tests were normal until a late stage in the disease except for a high serum alkaline phosphate and a low serum albumin. This combination of abnormalities together with ascites merit further investigation and should raise the suspicion of hepatic vein thrombosis complicating ulcerative colitis.

Adult↗
PubMed2000

Antibodies to tissue-type plasminogen activator in plasma from patients with primary antiphospholipid syndrome.

A reduction in fibrinolysis has been described in association with thrombosis in the primary antiphospholipid syndrome (PAPS). In this study, we measured anti-tissue-type plasminogen activator (t-PA) antibodies and anti-fibrin-bound t-PA antibodies as possible causes of hypofibrinolysis in 39 patients with PAPS. We also evaluated the differences in anti t-PA antibodies between patients without previous thrombosis (20 patients) and patients with previous episodes of thrombosis (19 patients: deep vein thrombosis in nine, ischaemic stroke in six, arterial leg thrombosis in one, hepatic vein thrombosis in one, thrombophlebitis in one and cerebral venous thrombosis in one). Anti-t-PA antibodies were measured by an enzyme-linked immunosorbent assay (ELISA), and anti-t-PA fibrin-bound antibodies were measured by a solid-phase fibrin immunoassay (SOFIA) in 39 patients with PAPS and in 39 controls matched for gender and age. High levels of IgG anti-t-PA were found in three out of 39 patients with PAPS, and all three patients had a history of thrombosis; four other patients, one of whom had a history of thrombotic events, had high titres of antibodies directed against fibrin-bound t-PA. In addition, patients with ischaemic stroke had significantly higher levels of IgG anti-t-PA than patients without thrombosis (P = 0.029). In conclusion, our data showed that, in patients with PAPS, the highest levels of anti-t-PA antibodies were present in subjects with previous thrombotic events. The discrepancy in the results obtained with two methods of detection of anti-t-PA antibodies, ELISA and SOFIA, indicates a different interaction of the antibodies with the t-PA molecules, which are directly bound to polystyrene plates in ELISA and bound to fibrin as a bridging molecule in SOFIA.

Adult↗
PubMed1990

Hepatic vascular disease and portal hypertension in polycythemia vera and agnogenic myeloid metaplasia: a clinicopathological study of 145 patients examined at autopsy.

The pathogenesis of portal hypertension arising in patients with myeloproliferative disorders has been difficult to understand because liver biopsy findings often show minimal changes. It has been suggested that increased splenic blood flow, hepatic infiltration with hematopoietic cells or sinusoidal fibrosis may be important. We have reviewed the autopsy findings and clinical histories of 97 patients with polycythemia vera and 48 patients with agnogenic myeloid metaplasia collected from three institutions and from the Polycythemia Vera Study Group. Cirrhosis was present in seven patients, one of whom had bleeding varices. Esophageal varices were present clinically in 10 patients without cirrhosis (seven polycythemia and three agnogenic myeloid metaplasia). All of these patients had lesions in small or medium-sized portal veins and four had stenosis of the extrahepatic portal vein with histology compatible with organized thrombi. Nodular regenerative hyperplasia occurred in 14.6% and correlated closely with the presence of portal vein lesions. Thirty patients had greater than 500 ml of ascites, seven of these patients also had varices and six of them had hepatic vein thrombosis. Ascites also correlated with hepatic vein disease confined to small intrahepatic branches. No correlation was seen between hepatic hematopoietic infiltration and signs of portal hypertension. We conclude that esophageal varices are common and are almost always associated with portal vein lesions visible by light microscopy. These portal vein lesions, and the secondary effects of nodular regenerative hyperplasia and portal hypertension, are most likely a result of portal vein thrombosis in patients with myeloproliferative disorders.

Adult↗
PubMed2000

Abdominal venous thrombosis in neonates and infants: role of prothrombotic risk factors - a multicentre case-control study. For the Childhood Thrombophilia Study Group.

The factor V (FV) G1691A mutation, the prothrombin (PT) G20210A variant, the methylenetetrahydrofolate reductase (MTHFR) T677T genotype, together with fasting homocysteine (HCY) concentration, lipoprotein (Lp)(a), anti-thrombin (AT), protein C (PC), protein S (PS) and anti-cardiolipin antibodies were investigated in 65 consecutively recruited infants (neonate to < 12 months) with renal venous thrombosis (RVT; n = 31), portal vein thrombosis (PVT; n = 24) or hepatic vein thrombosis (HVT n = 10), and 100 age- and sex-matched healthy controls. FV G1691A was found in 14 babies (heterozygous: RVT n = 9, PVT n = 4; homozygous HVT n = 1) and five controls, the MTHFR TT677 genotype together with increased HCY in four infants with thrombosis (RVT n = 2; PVT n = 1; HVT n = 1) compared with one control, and the PT G20210A variant was present in one control only. PC type I deficiency was diagnosed in three patients (RVT n = 2; PVT n = 1) and AT deficiency in two patients (RVT n = 1; PVT n = 1). Three neonates with spontaneous thrombosis showed FV G1691A combined with Lp(a) and the FV G1691A was combined with the PT G20210A genotype in two infants. Additional triggering factors were reported in 27 patients (41.5%). The overall odds ratios (ORs) and 95% confidence intervals (CIs) with respect to the different thrombosis locations were: RVT (OR/CI: 10.9/3.85-31.1; P < 0.0001), PVT (5.47/1.7-17.6; P < 0.0007) and HVT (3.3/0.58-18.7; P = 0.18). The data presented here suggest that genetic prothrombotic risk factors also play an important role in abdominal venous thrombosis during infancy.

Antibodies, Anticardiolipin↗
PubMed1987

Budd-Chiari syndrome: CT observations.

The authors describe four patients with Budd-Chiari syndrome in whom contrast material-enhanced computed tomographic (CT) scans demonstrated low-density venous thrombosis in three sites not, to our knowledge, previously described with this modality. Thrombosis was seen in the portal circulation, the hepatic veins, and the intrahepatic inferior vena cava. It is known that concomitant portal vein thrombosis may be seen in 20% of patients with Budd-Chiari syndrome. Three of the four patients in the current study had this finding, one with extensive thrombosis of portal, mesenteric, and splenic veins and the other two with portal vein branch involvement. In one patient hepatic vein thrombosis was demonstrated with CT, and in three inferior vena cava clot was demonstrated. All four patients had the distinctive hepatic parenchymal contrast enhancement pattern seen in this condition, which the authors think may be at least partially caused by associated portal thrombosis. The presence of portal venous thrombosis should prompt the observer to consider the diagnosis of Budd-Chiari syndrome. Detection of hepatic vein clot confirms the diagnosis and may be seen in this condition in association with inferior vena cava thrombus.

Adult↗
PubMed2000

Technical refinement in adult-to-adult living donor liver transplantation using right lobe graft.

OBJECTIVE: To report the authors' experience with living donor liver transplantation in adults using right lobe liver grafts, performed by a modified technique. SUMMARY BACKGROUND DATA: The initial results of seven living donor liver transplants in adults using extended right lobe grafts were satisfactory, but serious complications occurred in two donors, and six recipients required repeat laparotomy. Another 11 similar operations were performed. Further evaluation was made with the aim of improving the postoperative outcome. METHODS: From December 1996 to August 1998, 11 patients underwent living donor liver transplantation using right lobe grafts. The first four patients underwent surgery using methods previously designed and the next seven underwent a modification designed to minimize devitalized tissues on the liver transection surface, improve hepatic venous drainage, and reduce the number of hepatic duct orifices. RESULTS: There were no donor deaths. Donor complications included cholestasis (n = 1) and minor wound infection (n = 1). All the first four recipients required a repeat laparotomy for infected necrotic liver transection surface (n = 1), acute pancreatitis (n = 1), hepatic vein thrombosis (n = 1), and leakage from one of the two bilioenteric anastomoses (n = 1). The patient with hepatic vein thrombosis died. In the last seven recipients, all of whom survived the operation, one required a repeat laparotomy with the discovery of a methicillin-resistant Staphylococcus aureus culture of fibrinous exudate at the left subphrenic peritoneum, and another had right hepatic duct stump necrosis. The latter was likely related to hypovolemic shock secondary to bleeding from the right saphenous vein on removal of a hemofiltration catheter. Comparison of the incidence of repeat laparotomy between the first four and the remaining seven recipients showed a significant trend of improvement. Combining the result of the seven patients reported previously, the improvement in terms of relaparotomy rate is significant. CONCLUSION: With modification of surgical technique, living donor liver transplantation in adults using right lobe liver grafts can become a relatively safe procedure.

Adolescent↗
PubMedDate not supplied

Vascular involvement in Behçet's disease: 8-year audit.

Behçet's disease is a multisystemic disorder characterized by recurrent ulcers of the mouth and genitalia and relapsing iritis. Four types of vascular lesion are recognized in Behçet's disease: arterial occlusions, aneurysms, venous occlusions, and variceal development. The incidence of vascular involvement reported in the literature ranges from 7% to 29%. The aim of this study was to determine the rate of vascular involvement in Behçet's disease at our hospital between 1983 and 1992. Of 1200 patients with Behçet's disease, 173 (14.4%) had venous manifestations and 19 (1.6%) had arterial manifestations (in some patients more than one organ was involved). In the group of patients with venous manifestations, there were 154 (12.8%) with venous thrombosis, 17 (1.4%) with vena cava superior syndrome, 5 (0.4%) with inferior vena cava syndrome, 5 (0.4%) with varices, 2 with upper extremity venous thrombosis, 1 with internal jugular vein thrombosis, 1 with cavernous sinus thrombosis, and 1 with hepatic vein thrombosis. In the arterial manifestation group there were 7 femoral, 3 abdominal, 3 popliteal, 2 iliac, 2 pulmonary, 1 axillary, and 1 carotid artery aneurysm as well as 3 arterial occlusions. We concluded that vascular surgeons dealing with young adults should bear Behçet's disease, an uncommon clinical entity, in mind.

Adult↗