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At least 1,369 records · Page 76Linked to original sources
PubMed2007

Chronic oral anticoagulant therapy for extrahepatic visceral thrombosis is safe.

BACKGROUND: Patients with hypercoagulability may thrombose visceral veins with resultant portal hypertension, esophagogastric varices, and hemorrhage. The role of chronic oral anticoagulant therapy in such patients is unclear. On the one hand, such patients are prone to significant hemorrhage and thus anticoagulant therapy may seem contraindicated. On the other hand, because the causal pathophysiology is typically hypercoagulability, it would seem rational to treat these patients with chronic anticoagulant therapy in order to both prevent other visceral and systemic thromboses and perhaps, over time, reduce the degree of portal hypertension. Experience and poor prognosis associated with the more common portal hypertension due to hepatic cirrhosis may bias judgment. METHODS: We retrospectively reviewed the course of chronic oral anticoagulant therapy regarding both the safety and effectiveness using our long-term follow-up of a cohort of seven patients with visceral thrombosis resulting in extrahepatic non-cirrhotic portal hypertension. RESULTS: Seven consecutive patients encountered over the past 19 years were observed for 78 patient-years, the first 14 patient-years prior to anticoagulant therapy and the latter 64 patient-years on oral anticoagulant therapy. No patients rethrombosed either visceral or systemic vessels while on oral anticoagulant therapy. There were no fatal or serious hemorrhagic events on oral anticoagulant therapy; in fact, upper gastrointestinal bleeding decreased from 1.2 to 0.2 bleeds/year. The endoscopic grade of esophageal varices decreased in four of five patients who underwent serial endoscopy, and platelet counts increased in all seven patients. CONCLUSIONS: Chronic oral anticoagulant therapy is safe and not associated with an increase in upper gastrointestinal bleeding in such patients. Additionally, and by inference, perhaps in conjunction with the natural history of portal hypertension, such therapy is possibly effective in reducing portal hypertension in patients with hypercoagulability-induced extrahepatic portal hypertension.

Administration, Oral↗
PubMed2006

[Oncological results of renal cancer with inferior vena cava thrombosis after nephrectomy].

OBJECTIVE: The objective of this study was to evaluate survival and risk of recurrence in patients undergoing nephrectomy with resection of inferior vena cava tumour thrombus in our department. MATERIAL AND METHODS: From June 1991 to March 2003, 40 patients underwent radical nephrectomy with resection of inferior vena cava tumour thrombus. The upper limit of the tumour thrombus was below the hepatic veins in 21 cases (52.5%) and above the hepatic veins in 19 cases (47.5%), with thrombus in the right atrium in 6 cases (15%). Cardiopulmonary bypass (CPB) was used in 12 patients (30%) RESULTS: With a mean follow-up of 28.5 +/- 36.8 months (range: 0-150), 22 patients (55%) have died. The 2- and 5-year overall survival rates were 45.2% and 38. 7%, respectively. Local and/or metastatic recurrence was observed in 28 patients (70%) after a mean interval of 18 +/- 22.9 months (range: 1-104). Patients with tumour thrombus derived from the left kidney had a higher local recurrence rate than patients with thrombus derived from the right kidney (p = 0.0194). The 2- and 5-year recurrence-free survival rates were 28.3% and 8.9%, respectively. Only stage pN had a statistically significant prognostic value on overall survival, but not on recurrence-free survival. At the end of the study, only 1 patient (2.5%) can be considered to be cured with no disease progression with a sufficient follow-up (52 months) after nephrectomy. CONCLUSION: Nephrectomy with resection of tumour thrombus from the inferior vena cava provides a gain in terms of medium-term survival, but the majority of patients are not cured by this major surgery. Only lymph node status has a prognostic value.

Adult↗
PubMed1998

[Combined hepatic resection and removal of portal vein tumor thrombi].

Portal thrombectomy with extended hepatectomy for extensively progressive primary liver cancer (Vp 3), in which the tumor thrombus has spread beyond the first portal branches, will make other non-surgical treatments possible and improve patients quality of life. We have performed extensive resections in 15 cases of such Vp 3 liver cancer. One patient with huge HCC involving retrohepatic IVC underwent in situ extended left hepatectomy without reconstruction of IVC, resulting in postoperative renal failure because of thrombosis in the bilateral renal veins, but 14 other patients' postoperative courses were uneventful. Ten of 14 patients relapsed within one year, but these patients underwent non-surgical treatments, resulting in improvement in the quality of life. The 1-, and 3-year survival rates were 55.6% and 32.5%, respectively.

Adult↗
PubMed1975

Two-stage occulsion of the protal vein in the rat:survival related to weight variation and the interval between partial and total occulusion.

A portal vein stenosis with a diameter of 1.1 mm was performed in female Wistar rats of four different weight groups. The mortality rate was found to increase with increasing weight of the animals, a near linear correlation between mortality rate and body weight being found. Severe circulatory disturbances of the small intestine with haemorrhage and necrosis of the bowel wall were a prominent finding at death. In the survivors total occulsion was carried out at varying times, from 48 h after the first operation, and the mortality rates were recorded. A major contributing cause of death appeared to be ischaemic infarction of the liver. Only a slight congestion of the duodenum was found and no circulatory disturbance of the small intestine. Thus by 48 h the porto-systemic collaterals are sifficiently developed to prevent subsequent venous congestion. The survival rates showed a significant increase when the time interval between partial and total occlusion was extended from 48 to 72 h. This may be due to an increased blood flow through the hepatic artery and collateral arteries to the liver.

Animals↗
PubMed1999

Congenital hepatic arterioportal fistula complicated with gastrointestinal bleeding treated with transcatheter embolization: case report.

Congenital hepatic arterioportal fistula (HAVF) is extremely rare in children. We present a patient with congenital hepaticoportal arteriovenous fistula complicated with gastrointestinal bleeding treated using transcatheter arterial embolization. Our patient was the youngest (2 days old) case ever reported with congenital HAVF and the first one to receive arterial embolization for HAVF during childhood. The 3-year-old girl was suggested of having congenital HAVF using Doppler ultrasonography. However, her family refused further investigation, and she was lost to follow-up. Three years later, she was sent to our hospital due to melaena. Repeated ultrasonography revealed dilated intrahepatic portal vein with arterial flow demonstrated using Doppler imaging. No esophageal varices or gastric or duodenal ulcer was seen during endoscopy. Angiography showed a HAVF and transcatheter embolization was done simultaneously. Follow-up at one and two weeks post-embolization revealed no more shunt flow within the portal vein, though cystic like dilatation of the portal vein persisted, and no thrombosis was observed. This case emphasizes that transcatheter arterial embolization can be easily and successfully used for treating childhood congenital HAVF. Abnormal dilatation of the portal vein in children needs doppler evaluation and possibly angiography.

Arteriovenous Fistula↗
PubMed2006

[Total pancreas sampling and transplantation].

Pancreas removal and transplantation consists in three main steps: sampling, preparation of the transplant with reconstruction of vessels and finally transplantation. Sampling requires good anatomical knowledge and perfect synchronization between hepatic surgeons so as to ensure adequate dissection of liver and pancreas vessels: portal vein, splenic, upper mesenteric and hepatic arteries. Washing and conservation of organs require the use of University of Wisconsin solution. The preparation of the pancreatic graft consists in reconstructing the unique arterial axis using an iliac arterial fork sutured with upper mesenteric and splenic arteries. The portal vein is lengthened step by step, avoiding venous patch source of thrombosis. The transplantation is realized in the right flank, on the aorta and the vena cava near the iliac crossroads. The digestive anastomosis is performed between duodenum of the transplant and first bowel hail of the recipient. It must be done carefully to avoid any risk of pancreas fistula.

Humans↗
PubMed2006

The transjugular route: the key hole to the liver world.

Portal hypertensive complications are major causes of morbidity and mortality in patients with liver cirrhosis. The advent of the transjugular route with its minimal access allows non-surgical management of portal hypertension, therapy of venous complications of liver transplantation, monitoring of therapy for portal hypertension, hepatic venous pressure gradient and is also the major route to treat hepatic venous obstruction syndromes. In addition, the transjugular route is a safe route to perform a liver biopsy (transjugular liver biopsy) and allows retrograde evaluation of the portal vein. All these procedures can be combined in the same session. These hepatic interventional radiological skills should be incorporated into the expertise of the liver team in specialised hepatological centres, particularly in liver transplant centres as they are especially useful in improving outcomes of cirrhotic patients on the liver transplantation waiting list. A limitation in achieving this goal, could be the number of experienced radiologists, but hepatologists can be trained, at least for the most simple procedures (transjugular liver biopsy and hepatic venous pressure gradient). This would allow wider applicability and use of these diagnostic and therapeutic techniques, all through a 2 mm hole in the neck--the key hole to the liver world.

Biopsy↗
PubMed2002

Hepatic circulatory diseases associated with chronic myeloid disorders.

These liver diseases are diseases of the hepatic circulation. Myeloproliferative disorders are among the most common prothrombotic disorders that lead to Budd-Chiari syndrome and PVT. SOS, previously known as hepatic veno-occlusive disease, is mainly seen in North America and Western Europe as a complication of the conditioning regimen for hematopoietic stem cell transplantation. SOS is caused by damage to SECs, and the initiating circulatory blockage occurs because of the embolism of sinusoidal lining cells. Myeloproliferative disorders are an uncommon cause of NRH, which is believed to be caused by uneven perfusion of the liver at the venous or sinusoidal level. Peliosis hepatis is believed to result from damage to SECs and is seen mainly in immunosuppressed patients, patients with a wasting illness, or patients with a drug toxicity.

Budd-Chiari Syndrome↗
PubMed1975

Adrenal venography and ultrasound in the investigation of the adrenal gland: an analysis of 58 cases.

Adrenal venography has been carried out in 58 patients with the left adrenal vein being successfully catheterized in 91 per cent and the right in 77 per cent. Of the 30 patients with primary hyperaldosteronism, 11 adenomas (12-35 mm diameter) have been demonstrated at venography and two of 15 mm suspected, all of which were confirmed surgically. Aldosterone levels in the adrenal vein plasma were raised on the affected side. In the group of proved micronodular hyperplasia, two patients had surgically confirmed macronodules and venography demonstrated one of 12 mm diameter. Two adenomas of 11 mm and one macronodule of 15 mm have been demonstrated at venography in the remainder who have not had an operation. Ultrasound was carried out in 12 patients with primary hyperaldosteronism, ten of which had tumours at venography. Two adenomas measuring 30 and 31 mm were outlined by ultrasound and confirmed surgically. Seven adenomas, including one macronodule (10-25 mm in diameter) were not defined. Three intra-adrenal phaeochromocytomas (45-90 mm) and one extra-adrenal (80-85 mm) were demonstrated at arteriography, identified by ultrasound and confirmed surgically. Of the ten patients with Cushing's syndrome three had enlarged glands at venography, this was confirmed surgically. Cumulative experience from this analysis and published reports indicate that venography will demonstrate tumours of 10 mm or more in diameter and outline enlarged glands; aldosterone assays will lateralize tumours as small as 3 mm; ultrasound will outline tumours of 30 mm and selective adrenal arteriography will demonstrate tumours of 10 mm. One patient developed acute adrenal cortical insufficiency with intra-adrenal extravasation on one side and thrombosis of the central vein on the opposite side. A second case developed temporary adreno-cortical insufficiency. Published reports indicate that the risk of complication is about 1 per cent. The report includes an anatomical study of the efferent adrenal veins in 50 patients paying particular attention to the diameter, number of accessory hepatic veins, and the angle of entry and position of the right adrenal vein.

Adenoma↗
PubMed1980

Carcinogenicity of benzene hexachloride and its isomers.

Technical BHC and the alpha, beta, gamma and delta isomers of BHC are carcinogenic for the liver of mice and rats. Mice given the isomers of BHC developed carcinomas and hyperplastic nodules of the liver as early as 24 weeks. Several strains of mice (dd, ICR-JLC, CL1, DDY, IRC, DBA/Z, C3H/HEN, C57BL/6 were susceptible. Male mice were more susceptible to hepatic carcinogenesis than female mice and they appeared to be more susceptible to alpha-BHC. The incidence of neoplasms of the liver was increased when beta-, gamma-, or delta-BHC were each given together with alpha-BHC. PCB-5 promoted the induction of hepatic neoplasms when administered with beta-BHC. Technical BHC and its isomers are carcinogenic for the liver of male and female Wistar rats. Beta-BHC is carcinogenic for the liver of Osborne-Mendel male rats. Osborne-Mendel rats receiving delta-BHC developed cirrhosis of the liver, portal vein thrombosis, and focal necrosis of the skeletal muscle. Male rats ingesting technical BHC or the beta or delta isomers also had atrophic testes.

Animals↗
PubMed2005

Efficacy of different treatment strategies for hepatocellular carcinoma with portal vein tumor thrombosis.

AIM: To evaluate the efficacy of different treatment strategies for hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT) and investigate factors influencing prognosis. METHODS: One hundred and seventy-nine HCC patients with macroscopic PVTT were enrolled in this study. They were divided into four groups and underwent different treatments: conservative treatment group (n = 18), chemotherapy group (n = 53), surgical resection group (n = 24) and surgical resection with postoperative chemotherapy group (n = 84). Survival rates of the patients were analyzed by the Kaplan-Meier method. A log-rank analysis was performed to identify group differences. Cox's proportional hazards model was used to analyze variables associated with survival. RESULTS: The mean survival periods of the patients in four groups were 3.6, 7.3, 10.1, and 15.1 mo respectively. There were significant differences in the survival rates among the groups. The survival rates at 0.5-, 1-, 2-, and 3-year in surgical resection with postoperative chemotherapy group were 55.8%, 39.3%, 30.4%, and 15.6% respectively, which were significantly higher than those of other groups (P<0.001). Multivariate analysis revealed that the strategy of treatment (P<0.001) and the number of chemotherapy cycles (P = 0.012) were independent survival predictors for patients with HCC and PVTT. CONCLUSION: Surgical resection of HCC and PVTT combined with postoperative chemotherapy or chemoembolization is the most effective therapeutic strategy for the patients who can tolerate operation. Multiple chemotherapeutic courses should be given postoperatively to the patients with good hepatic function reserve.

Adult↗
PubMed2005

Idiopathic portal hypertension complicating systemic sclerosis: a case report.

BACKGROUND: Patients with systemic sclerosis may develop mild abnormalities of liver function tests. More serious hepatic involvement has been well documented but is rare. Idiopathic portal hypertension had been reported only in a few female patients with systemic sclerosis. CASE PRESENTATION: An 82-year-old man with known systemic sclerosis presented with melaena. Urgent gastroscopy revealed oesophageal varices, which re-started bleeding during the procedure and were treated ensocopically, with Sengstaken tube and glypressin. Liver function tests and coagulation were normal. Non-invasive liver screen (including hepatitis viral serology and autoantibodies) was negative. Ultrasound scan of the abdomen revealed a small liver with coarse texture and no focal lesion. Hepato-portal flow was demonstrated in the portal vein. The spleen was enlarged. A moderate amount of free peritoneal fluid was present. A CT scan confirmed the absence of portal vein thrombosis. One month following discharge the patient had a liver biopsy. Histological examination showed essentially normal liver tissue; there was no evidence of any excess inflammation and no features to suggest cirrhosis or drug-induced liver disease. Taking into account the above evaluation we concluded that the patient had idiopathic portal hypertension. CONCLUSION: Both male and female patients with systemic sclerosis may -- rarely -- develop idiopathic portal hypertension.

Aged, 80 and over↗
PubMed2005

Extensive prolongation of aPTT with argatroban in an elderly patient with improving renal function, normal hepatic enzymes, and metastatic lung cancer.

OBJECTIVE: To report a case of an elderly male with improving renal function and normal hepatic function who sustained an elevated activated partial thromboplastin time (aPTT) after an infusion of argatroban was discontinued. CASE SUMMARY: A 77-year-old white male with a history of heparin-induced thrombocytopenia (HIT) and metastatic lung disease was started on argatroban for treatment of a right upper-extremity deep vein thrombosis (DVT). The infusion was initiated at 2.0 microg/kg/min and was titrated to a goal aPTT of 60-80 seconds. Argatroban was discontinued due to an aPTT elevated to >100 seconds; the aPTT remained elevated for 130 hours after discontinuation of the infusion. DISCUSSION: Argatroban dose reductions in patients with impaired liver and renal function test values have been reported. Elderly subjects may have a prolonged clearance compared with young healthy subjects, although the duration of effect has not been established. As of April 18, 2005, the effect of liver metastasis on argatroban pharmacokinetics in the setting of normal liver function enzyme levels has not been reported. An objective causality assessment using the Naranjo probability scale showed that the prolonged aPTT was probably attributable to argatroban. CONCLUSIONS: Clinicians should exercise caution when initiating argatroban at a dose of 2.0 microg/kg/min in elderly patients with underlying comorbidities, such as metastatic disease and renal impairment, since this may lead to excessive and prolonged anticoagulation and increased risk of bleeding.

Aged↗