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

This study addresses mechanisms of the clinical, encephalopathic uremic illness and its suppression by dialysis. Renoprival rats were treated with peritoneal dialysis (8 exchanges per day, 30 min dwell), or untreated (attrition group), and their EEG's were automatically sampled overnight and subjected to power spectrum analysis as an index of encephalopathy. As in man the background rhythm of the quantified EEG (Q.EEG) in the attrition group slowed with time as extracellular fluid composition became increasingly abnormal; these changes were normalized by therapeutic dialysis (TD) using standard, commercial dialysate. However, Q.EEG slowing was only partially normalized by solute-specific dialysis using "mock uremic dialysate" (M-UD), prepared from laboratory chemicals to equal plasma concentrations in preterminal uremic rats of urea, creatinine, potassium, phosphorus, calcium, magnesium, bicarbonate, sodium, and chloride. When only phosphate was added to TD, the Q.EEG slowed to the same level achieved after M-UD. We conclude that uremic encephalopathy in this model is produced by an unknown neurotoxin and augmented by one or more of the M-UD solutes, phosphate being a likely candidate. To localize the encephalopathic effect, regional brain glucose uptake was estimated in 20 discrete brain areas. Significance of reduced uptake in three areas is discussed.
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PMID:Role of dialysable solutes in the mediation of uremic encephalopathy in the rat. 231 78

Hyperammonemic encephalopathy in the urological patient is a rare but grave condition. In the pediatric urological population it has been associated with massively dilated upper tracts and urinary infection with urea-splitting organisms. We report 2 cases of hyperammonemic encephalopathy in association with the prune belly syndrome. Both patients presented comatose with markedly elevated serum ammonia levels and Proteus mirabilis urinary tract infection. Intravenous antibiotics and catheter drainage resulted in dramatic reversal of the encephalopathy. The pathophysiology of hyperammonemic encephalopathy in association with the prune belly syndrome and a review of the literature are presented.
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PMID:Hyperammonemic encephalopathy: a complication associated with the prune belly syndrome. 266 23

The authors conducted a prospective, longitudinal, multicentre study in patients with liver cirrhosis; a total of 192 patients were on follow-up, of this number 125 died during the study. Mean age, 56 years, was markedly more advanced in the dead; men prevailed among the patients. Duration of complaints and the interval since the diagnosis had been established was shorter in the dead than in those alive; a positive HBs antigen was likewise more often present in the former. Clinical and laboratory parameters in this group were assessed with a view to the differences between the dead and those alive and with a view to the time course of changes in these differences. Multifactorial discriminative analysis of these data for various intervals before death was also performed. The most pronounced differences were noted in clinical manifestations and laboratory signs of hepatic insufficiency, especially in the presence and degree of ascites, jaundice, encephalopathy, and in the values of bilirubin, Quick' test and blood albumin levels; thus the degree of liver insufficiency appears to be the most important prognostic marker in patients with liver cirrhosis. Moreover, a significant increase in urea and leucocyte levels was found in the terminal stages of the disease. Ascites, encephalopathy and a progressive increase in serum bilirubin levels seem to be the best markers for discriminative analysis of prognosis for the last six months of life. Results of this study, while confirming some findings by other authors, offer also new insights into the whole issue.
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PMID:[A prospective prognostic study of liver cirrhosis]. 267 84

Young ferrets develop hyperammonemia soon after eating an arginine-free diet, whereas adult ferrets do not develop hyperammonemia after an identical treatment. Earlier reports indicate that young or adult rats do not develop hyperammonemia and encephalopathy after a single meal of an arginine-free diet. The effects of a single feeding of an arginine-free diet on the urea cycle enzyme activities in the liver of young and adult ferrets is reported. Ornithine carbamyl transferase, carbamyl phosphate synthetase and ornithine aminotransferase activities in the livers of adult ferrets were significantly higher than those in the livers of young ferrets. A single meal of an arginine-free diet did not alter the urea cycle enzyme activities in the liver of young or adult ferrets. The levels of urea cycle enzymes in the liver and kidney of young ferrets were comparable to those in rat liver and kidney. The results suggest that the hyperammonemia observed in young ferrets following a single meal of an arginine-free diet may not be due to the deficiency of enzyme activities.
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PMID:Effects of arginine-free diet on urea cycle enzymes in young and adult ferrets. 272 82

Ten sessions of extracorporeal connection to a xenous (pig) spleen were conducted as part of combined treatment in 7 patients with urosepsis in combination with severe renal failure. The session lasted for 40 to 90 minutes. The blood volume, required to fill the spleen and the main vessels, was below 100-150 ml with 7500-10,000 units of heparin spent. There was a marked clinical effect, manifested in reduced fever, better spirits, sleep and appetite, and a greater urinary output. Encephalopathy diminished. The connection to a xenous spleen had virtually no effect on urea, creatinin, electrolytes, bilirubin, transaminases, protein and acid-base values. There is evidence of mechanical withdrawal of compounds that are markers of septic intoxication: mean molecular levels dropped by an average of 20%, total spermine, spermidine and putrescine levels dropped by 35-40%, and blood became sterile. Circulating immune complexes decreased by 30-60%. The T-RFC count increased by 30-50%, largely owing to the helper cells. Leucocyte counts increased by 25%. FHA-induced blast transformation increased by 15-20%. Four (57%) of the 7 patients died. With hemodialysis alone, the mortality rate was 85% in this category of patients. Therefore, extracorporeal connection to a xenous spleen is indicated in cases of urosepsis as an effective as well as sparing method of biosorption and immunity activation in septic intoxication.
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PMID:[Extracorporeal use of a donor spleen in the treatment of patients with urinary tract infection]. 272 34

Two subsequent phases of hepatogenic encephalopathy (HE), the metabolic and precomatous phase, were produced in rats by thioacetamide treatment. Plasma and brain levels of arginine and its metabolites in the arginine-glutamate pathway, and activities of 2 brain enzymes of this pathway: arginase (L-arginine amidohydrolase, EC3521) and ornithine amino-transferase (OAT, ornithine-oxo-acid aminotransferase, EC26113) were measured in these rats. Plasma arginine sharply decreased in the metabolic phase and rose above control level in the precomatous phase, whereas ornithine and glutamate increased and urea decreased in both phases. Brain amino acids levels remained unchanged throughout, confirming earlier report of their insensitivity to external manipulation. Both brain enzymes showed a similar stepwise increase in their activities up to 150% the control level. The results are indicative of increased involvement of arginine as a precursor of amino acid neurotransmitters glutamate and GABA, with possible implication for the course of HE.
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PMID:Arginine in thioacetamide-induced hepatogenic encephalopathy in rats: activation of enzymes of arginine metabolism to glutamate. 287 5

An investigation of the mechanism of development of hepatic encephalopathy induced by CCl4 was performed in rats. CCl4 (1.0 ml/kg three times per week for over 10 weeks) caused hepatic encephalopathy in 80% of the treated rats. Accompanying the hepatic encephalopathy were hematemesis, abdominal dropsy, and hyperammonemia, conditions observed in hepatic coma patients. The blood ammonia levels were tremendously increased in only those rats with hepatic encephalopathy. Hepatic activities of carbamylphosphate synthetase (CPS) and argininosuccinate synthetase (ASS), important enzymes of the urea cycle, were significantly inhibited by CCl4. However, the causality between the inhibition of CPS or ASS activity and the increase in blood ammonia levels was not observed. On the other hand, the content of ATP, which is a substrate of CPS and ASS, was decreased by 60% in liver of rats with hepatic encephalopathy. The activity of Mg2+-ATPase which can decompose hepatic ATP was increased by 60 and 300% in mitochondria and microsomes, respectively, of livers of rats with CCl4-induced encephalopathy. There was a good correlation between the decreased hepatic ATP content and the increased mitochondrial Mg2+-ATPase activity. Furthermore, there was also a good correlation between the increase in blood ammonia levels and the increase in Mg2+-ATPase activity in microsomes. These findings suggest that hyperammonemia, which was produced by the decrease in hepatic content and by the inhibition of CPS and ASS, may play an important role in induction of hepatic encephalopathy.
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PMID:Blood ammonia levels and hepatic encephalopathy induced by CCl4 in rats. 296 38

A case of cerebral oedema developed during an apparently common attempted suicide with valpromide is reported. The most conspicuous biochemical abnormality was hyperammonaemia. The oedema proved refractory to the standard medical treatment of intracranial hypertension, and decompressive craniectomy was performed with only minor sequelae. The cerebral oedema cum hyperammonaemia syndrome led to the discovery, in this hitherto asymptomatic adult subject, of a 50 per cent deficiency in type a carbamyl phosphate synthetase liver activity. By completing such a deficiency, valproate may produce an extremely serious syndrome resembling the neonatal encephalopathy due to complete enzyme deficiencies in the urea cycle. All valpromide or valproate intoxications probably are cerebral oedemas with hyperammonaemia akin ti Reye's syndrome. All accidents of this type occurring during treatment or poisoning with valproate should be investigated for urea cycle enzyme abnormalities.
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PMID:[Cerebral edema with hyperammonemia in valpromide poisoning. Manifestation in an adult, of a partial deficit in type I carbamylphosphate synthetase]. 297 63

This study compared the effect of a vegetable diet with an animal protein diet on various aspects of nitrogen metabolism to identify what components of the vegetable diet might be causing beneficial therapeutic effects in hepatic encephalopathy. Vegetable diets contained 4.5-fold greater amounts of fiber (56 +/- 3 g/day) and reduced amounts of methionine, tyrosine, and tryptophan. In 6 stable cirrhotic subjects without encephalopathy, vegetable diets caused a significant reduction in the urea production rate from 106 +/- 5 to 89 +/- 5 mg X kg-1 X 24 h-1 of urea nitrogen. This was mainly accounted for by a fall in urinary urea output. Vegetable diets also caused a fall in total urinary nitrogen, which was accounted for by the fall in urea nitrogen, and a comparable increase in fecal nitrogen from 12 +/- 2 to 28 +/- 5 mg X kg-1 X 24 h-1. The fecal bacterial fraction contained 63% of the increase in stool nitrogen. Most plasma amino acids, including methionine, tyrosine, phenylalanine, as well as total and free tryptophan, were unchanged. The effect of vegetable diets on nitrogen metabolism can be mainly accounted for by the increased intake of dietary fiber and increased incorporation and elimination of nitrogen in fecal bacteria.
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PMID:Effects of vegetable diets on nitrogen metabolism in cirrhotic subjects. 299 Oct 68

A prognostic study based on 127 untreated patients with hepatocellular carcinoma was undertaken to evaluate their survival time and to find clinical and biologic criteria which allow the selection of patients with a survival time longer than 60 days who could enter a therapeutic trial. Twenty-eight clinical and biologic variables were assessed using univariate and multivariate semiparametric regression (Cox's) models. Ten variables were isolated by univariate analysis. Multivariate analysis found a negative relationship between a survival time longer than 60 days and five of these variables; these variables were in decreasing order: encephalopathy, alcohol consumption, aspartate amino transferase (AST), blood urea nitrogen, and total bilirubin. Prevalence, positive, and negative predictive values of encephalopathy were 20%, 27.5%, and 97% respectively. When three other criteria: ASAT greater than four times the upper limit of the normal (N), blood urea nitrogen greater than N, and total bilirubin greater than 2N were added, their prevalence, positive, and negative predictive values were 72%, 89.7%, and 57.1% respectively. These results suggest that in countries where incidence of hepatocellular carcinoma is low and recruitment of patients difficult, absence of encephalopathy must be the only criterion for selection of patients with hepatocellular carcinoma in therapeutic trials; whereas, in countries with a high incidence of hepatocellular carcinoma the other criteria may be added.
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PMID:Prognostic factors in patients with hepatocellular carcinoma. Attempts for the selection of patients with prolonged survival. 303 3


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