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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with chronic renal failure (CRF) on periodical hemodialysis may accumulate aluminum in tissues and show typical disorders such as dialysis encephalopathy, osteodystrophy, and microcytic anemia. Aluminum contamination of the water used to prepare the dialysis solution (dialysate) is one of the metal sources that may affect people under hemodialysis, especially in units in which untreated water is used. Graphite furnace atomic absorption spectrometric methods for aluminum determination in whole blood, dialysis solution, and tap water samples from CRF patients were developed, based upon the use of the same furnace temperature program. Samples were diluted 4-fold with 0.6% triton X-100 (whole blood) or with 0.01 mol/L nitric acid (dialysis solution and tap water) and analyzed by aqueous standard (blood and tap water) or matrix-matching standard (dialysis solution) calibration curves. The characteristic masses were 33.8, 11.3, and 19.5 pg Al/0.0044 A.s for whole blood, dialysate, and tap water, respectively. In the diluted solutions, the detection limits (2 sigma) for the described methods were 0.5 microgram/L Al (whole blood), 0.4 microgram/L Al (dialysate), and 0.4 microgram/L Al (tap water). The methods were applied to samples from several CRF patients under hemodialysis at Maracaibo University hospital. The data revealed extremely high aluminum levels, which corresponded to the symptoms of dialysis encephalopathy and/or osteodystrophy showed by some of them. The proposed methods are reliable and reproducible.
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PMID:Aluminum determination in whole blood, dialysis solution, and tap water samples from Maracaibo dialysis units (Venezuela) by graphite furnace atomic absorption spectrometry. 298 Jul 89

Previously we have shown that sera from patients with fulminant hepatic failure (FHF) will inhibit partially purified rat brain Na+, K+-ATPase and sodium efflux from human leucocytes in vitro. Similar inhibition may be involved in the pathogenesis of encephalopathy and cerebral oedema in these patients. In the present study we have attempted to establish whether the activity of brain Na+, K+-ATPase is decreased in vivo in rats with D-galactosamine induced hepatic failure using homogenates of snap-frozen brains. Na+, K+-ATPase activity was significantly reduced in the forebrain region at the stage of mild encephalopathy (43 h after injection), while at the deeper stage of coma (43-53 h after injection) enzyme activity was further reduced in the forebrain region and was also significantly reduced in the hindbrain region. Ouabain insensitive ATPase activity was not significantly altered at any time. While a significant increase in the water content (0.5%) of the hindbrain region was found 43 h after galactosamine, there was no clear correlation between the development of cerebral oedema and the reduction of Na+, K+-ATPase activity. The activity of partially purified normal rat brain Na+, K+-ATPase was 15% lower when incubated with sera from rats in the deep stage of coma compared with control sera. These data support other evidence that the reduction in brain Na+, K+-ATPase is likely to be due to toxic substance circulating in serum which have been shown to inhibit this enzyme in vitro and to cause coma when administered to normal animals.
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PMID:Reduced brain Na+, K+-ATPase activity in rats with galactosamine-induced hepatic failure: relationship to encephalopathy and cerebral oedema. 302

Aluminium encephalopathy is a specific syndrome occurring in dialysis patients and linked to high aluminium levels in dialysis water. We present the features of 38 cases seen in a single dialysis and transplantation unit. Serum immunoglobulin levels and the prevalence of histocompatibility antigens are discussed. The syndrome in its complete form is specific and easily recognizable. Careful attention to premonitory symptoms may lead to earlier diagnosis.
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PMID:Aluminium encephalopathy: clinical and immunological features. 326 92

The dialysis encephalopathy syndrome is at once the most widely recognized and most severe manifestation of aluminum toxicity. Evidence linking this syndrome and aluminum intoxication is virtually incontrovertible. The syndrome is characterized by speech and motor difficulties, dementia, and seizures. Less widely recognized symptoms include subtle changes in cognition and personality and directional disorientation. Since the widespread use of water treatment, aluminum exposure in the dialysis population has been primarily via intravenous (IV) medications and oral aluminum-containing, phosphate-binding antacid gels. In addition to the encephalopathy syndrome, aluminum has been linked to toxicity in bone, parathyroid gland, RBC, and kidney. These organ toxicities seem to be the result of specific protein enzyme inhibition. Currently identified factors that affect aluminum accumulation and modulate aluminum balance include uremia, renal function, parathyroid hormone withdrawal and suppression, 1,25-dihydroxycholecalciferol, and serum aluminum binding. Impaired renal function is not a prerequisite for increased tissue aluminum burdens. It is likely that aluminum-related disease will be increasingly observed in populations other than those with chronic renal failure.
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PMID:The metabolism of aluminum and aluminum-related encephalopathy. 329 87

A double-blind, controlled trial to study the efficacy of acidifying enemas of lactitol, a new galactoside-sorbitol disaccharide, and lactose vs. nonacidifying tap-water enemas was performed in 45 episodes of acute portal-systemic encephalopathy. At the time of randomization, all patients had encephalopathy of at least Grade 2+ severity, delay in the performance of number connection tests and hyperammonemia. A sequential analysis was performed which revealed after the inclusion of the first 20 patients, a significant failure of the nonacidifying enemas as compared to the lactitol enemas (p less than 0.004). The tap-water enema group was, therefore, suspended but the rest of the study continued after rerandomization for lactose and lactitol groups. A favorable response to treatment was obtained in 19 (86%) of the patients receiving lactitol enemas and in 14 (78%) of those receiving lactose enemas. A similar significant improvement in portal-systemic encephalopathy parameters and index was observed after both treatments. Both types of acidifying enemas induced a significant pH decrease in stool (p less than 0.05). These data suggest that acidifying agents like lactose and lactitol are effective and superior to tap-water enemas for the treatment of acute nitrogenous portal-systemic encephalopathy.
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PMID:Acidifying enemas (lactitol and lactose) vs. nonacidifying enemas (tap water) to treat acute portal-systemic encephalopathy: a double-blind, randomized clinical trial. 330 14

The brain changes in patients with chronic renal failure treated by chronic hemodialysis were studied with the help of computed tomography. The results showed the development of internal hydrocephalus in the patients in whose treatment "hard" water was used. In some of these patients the hydrocephalus was accompanied by clinical manifestations of the "disequilibrium" syndrome and the "hard water" syndrome. The patients dialyzed with "soft" water showed no brain changes and clinical signs. Hydrocephalus is probably the main pathogenetic factor for the development of the "hard water" syndrome which later develops in dialysis encephalopathy.
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PMID:[Brain changes in patients on chronic hemodialysis recorded by computed axial tomography]. 341 93

Newborn rats were exposed to daily intraperitoneal injections of 10 mg lead nitrate per kg body weight for the first 15 postnatal days. The growth and mortality of the lead-exposed animals did not differ from their control litter-mates, injected with vehicle only. In our previous studies, focal hemorrhages and spongy areas as well as breakdown of blood-brain barrier to plasma proteins were shown by light microscopy in the cerebellar parenchyma of 15-day-old rats exposed to this dose. In spite of these signs of edema, measurements of brain tissue specific gravity did not show increased water content. In the present investigation we examined the ultrastructure of the brain lesions in these rats with low-dose lead encephalopathy, focusing on signs of edema, and evaluated astroglial reaction by immunocytochemical staining for glial fibrillary acidic protein (GFAP). The electron microscopic findings were compatible with extracellular edema in the cerebellum of 15-day-old lead exposed rats. The number of GFAP-positive cell bodies in the gray substance of the cerebellar cortex was increased in the 15-day-old lead-exposed rats as compared with the controls of the same age, a finding which is presumably related to the leakage of plasma proteins. Both these findings were lacking at 20 days of age, suggesting reversibility of the lead-induced changes.
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PMID:Extracellular edema and glial response to it in the cerebellum of suckling rats with low-dose lead encephalopathy. An electron microscopic and immunohistochemical study. 343 20

This report presents results of surgery for bleeding esophageal varices in 80 patients. A prospective randomized study addresses the efficacy of the distal splenorenal shunt (DS) versus the mesocaval shunt (MS) in 50 patients undergoing elective surgery. An additional 30 patients underwent emergency MS for uncontrollable hemorrhage. In the elective series, patients averaged "B" according to Child's Classification. Operative mortality rates were similar (5%). Incidences of encephalopathy were also similar (10%). Those patients undergoing MS experienced an overall operative mortality of 9 per cent, which included emergency shunts (operative mortality 13%). This latter figure is the lowest in the world's literature. Our technique of mesocaval shunting emphasizes short (mean, 3.8-cm) and wide (mean, 21.5-mm) cloth prostheses. Utilizing this approach, we have been able to reduce operative portal venous pressure from a mean (x +/- SE) of 40.1 +/- 1.9 to 13.1 +/- 0.6 cm H2O. The latter value correlated inferior vena caval pressure, 11.8 +/- 0.6 and central venous pressure (recorded by the anesthesiologist) 11.4 +/- 0.5 cm H2O. This is the highest reduction (67%) in portal pressure thus far recorded and reflects our emphasis upon meticulous and extensive dissection of the involved structures. The former minimizes blood loss, which in our hands has been minimal (0.45 +/- 0.18 units per case), reducing the threat of further liver damage; the latter facilitates the "optimal shunt," one which returns portal venous pressure to normal.
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PMID:Surgical management of bleeding esophageal varices. Results with 80 cases. 348 22

This study compares early and late effects of the injection of hyperosmolar NaCl and urea of equal osmolarity on selected aspects of brain water, electrolyte, carbohydrate, amino acid, urea, and energy metabolism in normal suckling-weanling mice. One hour after treatment, salt-treated mice were critically ill, while the behavior of urea-treated animals could not be distinguished from that of controls. This clinical difference could not be explained on the basis of differences in plasma osmolality, the brain water content, or the degree of hemorrhagic encephalopathy. The injection of NaCl induced a 14-fold increase in plasma insulin and a progressive fall in the plasma glucose concentration (a reduction of 66% at 1 hr). In contrast, plasma glucose levels in urea-injected mice were unchanged. Prior to the fall in plasma glucose levels, metabolite changes in the brains of NaCl-injected mice were compatible with facilitation of transfer of glucose from the blood to the brain, increased metabolic flux in the Embden-Meyerhof and Krebs citric acid cycle pathways, and increased energy production. With the exception of the glucose content (unchanged), similar metabolite changes were seen in brain soon after urea injection. In the brains of the hypoglycemic NaCl-treated mice, glucose levels were reduced 80%, and glycogen 41%. Other metabolite changes were compatible with decreased glycolysis and metabolic flux through the Krebs citric acid cycle. In contrast, with few exceptions, at a similar time after injection, metabolite levels had returned to normal in the urea-treated mice. Permeability of the brain to urea was also examined. Brain urea reached high levels at 2 hr but returned to near baseline at 6 hr. Both hyperosmolar solutions increased the brain content of aspartic and glutamic acids 1 hr after injection. The failure of hypoglycemic mice with hypernatremia and elevated plasma osmolality (range, 416-434 mOsm/kg H2O) to respond to 1 M glucose (30 ml/kg) may have been due to the ill effects of the additional hyperosmolar load. The possibility remains that the encephalopathy induced by hyperosmolar NaCl, but not by hyperosmolar urea, is in some way related to the sudden elevation of brain Na+ and/or Cl- ions.
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PMID:Effects of acute hyperosmolar NaCl or urea on brain H2O, Na+, K+, carbohydrate, and amino acid metabolism in weanling mice: NaCl induces insulin secretion and hypoglycemia. 350 38

We investigated whether thiamine deficiency (TD), a frequent concomitant of chronic alcoholism, differentially modifies the response to ethanol in two inbred rat strains with highly different genetic susceptibilities to development of TD encephalopathy. Ethanol-induced (3 g/kg i.p.) behavioral impairment and hypothermia were studied after 2, 5 and 7 weeks of TD and after 6 weeks of repletion on normal diet. Controls of the M520/N (TD-sensitive) strain metabolized ethanol more rapidly, had a greater liver to body weight ratio, greater total body water, earlier and lower peak blood ethanol concentrations (BEC), diminished area under the BEC curve and lesser behavioral impairment and hypothermia (even at equivalent BEC values) than those of the F344/N (TD-resistant) strain. In both strains, TD resulted in reduced ethanol metabolic rate and liver to body weight ratio and equivalent ethanol-induced hypothermia and behavioral impairment at lower BEC. Lower and delayed peak BEC and unchanged area under the BEC curve suggest an increased volume of ethanol distribution during TD. Recovery appeared complete after 6 weeks of normal diet. Both strains lost an equivalent proportion of body weight during TD but M520/N rats had lesser decrements in ethanol metabolic rate, had greater reductions in liver weight, peak BEC and baseline body temperature and developed overt encephalopathy whereas F344/N rats did not. Therefore, in the chronic alcoholic, TD may modify ethanol's effects via pharmacokinetic and pharmacodynamic mechanisms. Relatively high ethanol tolerance of the strain with a genetic predisposition to TD encephalopathy is consistent with the hypothesized role of this avitaminosis in the pharmacogenetics of alcoholism.
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PMID:Influence of thiamine deficiency on the response to ethanol in two inbred rat strains. 355 71


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