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At least 271 records · Page 15Linked to original sources
PubMed1996

Evaluation of the efficacy and safety of flumazenil in the treatment of portal systemic encephalopathy: a double blind, randomised, placebo controlled multicentre study.

BACKGROUND: Portal systemic encephalopathy (PSE) is a complex neuropsychiatric syndrome associated with hepatic failure. Small scale studies have shown the benzodiazepine receptor antagonist flumazenil to be effective in ameliorating PSE. AIMS: To determine the efficacy of flumazenil in patients with non-comatous mild to moderate PSE (stages I to III) due to severe chronic liver disease. PATIENTS: 49 male and female adults without symptoms of severe bleeding and sepsis and who screened negative for benzodiazepine in both blood and urine, were included in the study. METHODS: Patients were randomised to receive either three sequential bolus injections of flumazenil (0.4, 0.8, and 1 mg) or placebo at one minute intervals, followed by intravenous infusions of either flumazenil (1 mg/h) or placebo for three hours. Clinical PSE grading and vital signs were assessed hourly during baseline and post-treatment periods and half hourly during treatment. The main outcome measures were improvement in group average PSE score and reduction of two points in individual PSE score (clinically relevant improvement). RESULTS: The mean average improvement in the PSE score in the subjects treated with flumazenil was not statistically significantly different from placebo. However, for patients showing clinically relevant improvement, the difference between flumazenil and placebo was statistically significant (seven of 28 v none of 21; p = 0.015). Flumazenil was well tolerated. CONCLUSIONS: A subgroup of patients with PSE resulting from chronic liver disease may benefit from the administration of flumazenil.

Chronic Disease↗
PubMed1993

Portal-systemic encephalopathy: a disorder of neuron-astrocytic metabolic trafficking.

Portal-systemic encephalopathy (PSE) is a major neuropsychiatric complication of chronic liver disease. Neuropathologic evaluation of brain tissue from cirrhotic patients who died in hepatic coma reveals astrocytic (rather than neuronal) changes referred to as Alzheimer type II astrocytosis. Evidence to date suggests that Alzheimer type II astrocytosis is the result of ammonia neurotoxicity. Exposure of cultured astrocytes to concentrations of ammonia equivalent to those encountered in brain in experimental PSE results in Alzheimer type II astrocytosis as well as changes in other astrocytic parameters such as glial fibrillary acidic protein and glycogen metabolism. A second characteristic of PSE is the appearance of increased densities of 'peripheral-type' benzodiazepine receptors (PTBRs) in both brain and peripheral tissues. In brain, PTBRs are highly localized on astrocytic outer mitochondrial membranes. Experimental PSE resulting from portacaval anastomosis in the rat results in increased densities of PTBRs in brain and in increased expression of the endogenous PTBR ligand octadecaneuropeptide in nonneuronal elements. It is suggested that the PTBR and its endogenous ligands could mediate the astrocytic response to chronic exposure to ammonia in PSE. Astrocytic changes in PSE are accompanied by disruption of neuron-astrocytic metabolic trafficking. In particular, reuptake of the neurotransmitter glutamate into the perineuronal astrocyte is inhibited in PSE resulting in glutamatergic synaptic dysregulation and potentially compromised astrocytic energy metabolism. Astrocytic metabolism of monoamine neurotransmitters may also be increased as a result of increased activities of monoamine oxidase MAOB.

Animals↗
PubMed1989

Lactitol in prevention of recurrent episodes of hepatic encephalopathy in cirrhotic patients with portal-systemic shunt.

Recurrent episodes of hepatic encephalopathy (HE) frequently occur in surgically shunted cirrhotic patients. The prevention of these episodes is based mainly on the long-term use of lactulose. Recently, lactitol, a nonabsorbable disaccharide similar to lactulose, has been proposed as an alternative in the management of HE. It has the advantage of being better tolerated and producing a more predictable catharsis. The effects of the two agents were compared in a controlled randomized study lasting six months involving 31 cirrhotic patients with portal-systemic shunt, of whom 40% experienced HE. The PSE index (mental state, EEG, asterixis, Raitan test, and ammonia) was assessed in each patient on entry to the study and every three months during treatment. Episodes of HE, side effects, and the patients' comments on efficacy, tolerability, and palatability were recorded. The dose required to induce two bowel movements per day was 48 +/- 25 ml of lactulose syrup and 36 +/- 7 g of lactitol. During the study, the number of patients who had an episode of HE and the PSE index was similar in both groups. The patients judged lactitol better from the point of view of palatability. Meteorism and flatulence, experienced by patients treated with lactulose, was not reported by the lactitol group. We concluded that lactitol is as effective as lactulose in the long-term prevention of episodes of HE in cirrhotics with portal-systemic shunt and may be better tolerated.

Adolescent↗
PubMed1987

Schistosoma mansoni: mechanism of attrition and routes of migration from lungs to hepatic portal system in the laboratory mouse.

The number of schistosomula in the axillary lymph nodes of mice was determined by compressed tissue autoradiography at 13 intervals from 0.5 to 28 days after exposure of abdominal skin to 75Se-labeled cercariae of S. mansoni. Significant accumulations were observed between days 3 and 6 and peaked on day 4 at which time 9.4 +/- 1.1% of the schistosomula present in the whole body were found in the axillary lymph nodes. The total number and distribution of schistosomula in all tissues of mice were likewise determined at 12 intervals from 3 to 24 days following exposure. The frequent appearance of small numbers of schistosomula in trachea and esophagus suggested that normal attrition resulted at least in part from physical expulsion of schistosomula from the body by way of the tracheobronchial tree and gastrointestinal tract. The distribution of schistosomula observed in heart chambers, caudal vena cava, hepatic portal vein, aorta, intestinal wall, thoracic cavity rinses, and diaphragm supported all 3 standing hypotheses regarding route of migration from lungs to hepatic portal system, i.e., that schistosomula migrate via (1) the pulmonary artery, right heart, caudal vena cava, and hepatic veins, (2) the pulmonary vein, left heart, aorta, and cranial mesenteric artery, and (3) the thoracic cavity and diaphragm.

Animals↗
PubMed1979

[Coloportal fistula in ulcerative colitis (massive penetration, through the splenic vein, of barium and air into the portal system during barium enema)].

The authors describe one case of massive penetration of barium and air through the splenic vein into the portal system during administration of a radiopaque enema to a woman suffering from hemorrhagic proctitis in the florid phase. They provide a detailed description of this rare clinical case and discuss the possible etiology and pathophysiology of the observed event.

Barium Sulfate↗
PubMed2005

Quality of life in refractory ascites: transjugular intrahepatic portal-systemic shunting versus medical therapy.

Uncontrolled studies suggest that transjugular intrahepatic portal-systemic shunting (TIPS) may improve quality of life in patients with refractory ascites. We hypothesized that any improvement of quality of life in patients with TIPS would be matched in controls due to the competing effects of improved ascites and worsened hepatic encephalopathy. Thus, an analysis of quality of life was performed using original data from the North American Study for the Treatment of Refractory Ascites, a multicenter trial of 109 patients randomized to TIPS or repeated large volume paracentesis (LVP) for refractory ascites. Short form 36 (SF-36) surveys were completed at baseline and at 6- and 12-month follow-up. Variables analyzed were: randomization group, number of LVP performed, cumulative volume from LVP, shortness of breath, abdominal distention, abdominal pain, diuretic usage, confusion, hospitalizations, and emergency room visits. Outcomes were changes in physical component scale (PCS) and mental component scale (MCS) of SF-36 results. We constructed multivariable, mixed effects models, including randomization group and baseline MCS and PCS. Changes in PCS and MCS from baseline were similar between the two randomization groups. In multivariate analysis, PCS improvement was associated with lack of confusion, improved ascites, and lack of hospitalizations, but not directly with randomization group. Improvement in MCS was associated with randomization to TIPS and lack of confusion. In conclusion, patients with refractory ascites randomized to TIPS or repeated LVP had similar changes in quality of life. Competing effects of hepatic encephalopathy, requirement for repeated LVP, and need for hospitalizations explain similar changes in quality of life between the two groups.

Analysis of Variance↗
PubMed1993

An autopsy case of coexisting portal systemic encephalopathy and senile dementia of the Alzheimer type.

An autopsy case of portal systemic encephalopathy and senile dementia of the Alzheimer type coexisting in a 77-year-old man is described. The patient had suffered recurrent episodes of delirium after a subtotal gastrectomy for gastric carcinoma. He died of DIC 45 months after the gastrectomy. A pathological examination revealed a vascular plexus around the liver which might have served as collateral circulation. Neuropathologically, spongy necrosis and Alzheimer type II changes of astrocytes were found in the basal ganglia and fronto-occipital cortices. In the same anatomical regions, only immunohistological staining using antibody against amyloid beta-protein and the periodic-acid methenamine silver method revealed abundant neuriticplaques, cerebral amyloid angiopathy and diffuse plaques. We discussed the clinicopathological findings in this case.

Aged↗
PubMedDate not supplied

Portal system thrombosis after splenectomy for neoplasm or chronic hematologic disorder: is routine surveillance imaging necessary?

PURPOSE: This study was undertaken to assess the frequency and sequelae of portal system thrombosis (PST) after splenectomy in patients with cancer or chronic hematologic disorders and to determine whether routine surveillance imaging for this potential complication is warranted. METHOD: The radiology reports of 203 consecutive patients with cancer or chronic hematologic disorders who underwent splenectomy between January 1990 and January 1997 were reviewed. Imaging examinations and medical records were reviewed for those in whom PST was found after splenectomy. RESULTS: One hundred twenty-three patients (60.6%) underwent CT (n = 88), sonography (n = 10), or both (n = 24) after splenectomy; one other patient underwent MRI. Twelve of these patients (9.8%) had thrombosis of the splenic, portal, and/or superior mesenteric veins. Their underlying diseases were myelofibrosis/ myelodysplastic syndrome (n = 8), lymphoma (n = 3), and leukemia (n = 1). At follow-up imaging (obtained in 10 of the 12 patients), PST had resolved (n = 5), worsened (n = 2), improved (n = 1), remained unchanged (n = 1), or resulted in cavernous transformation of the portal vein (n = 1). Nine of 12 patients were symptomatic. No patient died of PST. CONCLUSION: PST was an uncommon and typically unsuspected finding after splenectomy in this patient population, and no serious sequelae of PST were found. Routine surveillance imaging for PST after splenectomy does not seem warranted, but in symptomatic patients (particularly those with myelofibrosis/myelodysplastic syndrome), a high clinical suspicion and a low threshold for obtaining imaging examinations are needed.

Adult↗
PubMed1976

Histochemical studies in experimental portal-systemic encephalopathy.

Results of a histochemical study of glutamic dehydrogenase in experimental portal-systemic encephalopathy with hyperammonemia indicate that the enzyme's activity in brain was increased in all stages of the encephalopathy, and this increase appeared to be localized exclusively in astrocytes. The results are consistent with the view that the astrocyte has a critical role in ammonia metabolism in brain, probably in ammonia detoxification. The findings, moreover, indicate that one pool of glutamate, possibly the small pool, is located in the astrocyte.

Alzheimer Disease↗
PubMed1997

Portal systemic encephalopathy.

The goal of this article is to update the status of Portal systemic encephalopathy (PSE) in the light of new data. First, PSE is the context of other types of hepatic encephalopathy. Subsequently, current views of the pathogenesis of the disorder are discussed, followed by an analysis of therapeutic options. Diagnosis will not be considered, as no major new developments have recently been documented in this area.

Ammonia↗
PubMed1977

A light and electron microscopic study of experimental portal-systemic (ammonia) encephalopathy. Progression and reversal of the disorder.

A sequential light and electron microscopic study of cerebral cortex was performed in a rat model of portal-systemic encephalopathy produced by creating a portacaval shunt and followed by ammoniate resin feedings. Prior to coma, astrocytes were characterized ultrastructurally by marked cytoplasmic enlargement, proliferation of mitochondria and endoplasmic reticulum, and an accumulation of cytoplasmic glycogen. The Alzheimer type II astrocyte change was seen only in coma and was characterized ultrastructurally by additional hydropic and degenerative mitochondrial and nuclear changes. Attempts at reversal of the encephalopathy were successful only if ammoniated resin feedings were discontinued prior to coma. Results suggest (1) that the astrocyte response initially reflects an ammonia-induced increased metabolic activity in that cell; (2) that subsequently a gliopathy develops having the light microscopic appearance of the Alzheimer type II change; and (3) that the Alzheimer type II astrocyte change may be responsible for an irreversible clinical course in this experimental condition.

Alzheimer Disease↗