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

Parenteral realimentation in the patient with severely impaired nutrition is sometimes associated with the development of a metabolic encephalopathy with coma. The onset of this complication is sudden. The coma is deep, accompanied by signs of neuromuscular hyperexcitability and very marked hyperventilation. It generally regresses rapidly, without sequellae. The onset of such a realimentation coma should be feared in the presence of a certain combination of conditions : severely impaired nutrition, parenteral alimentation with a high level of nitrogen and calories, transfer to the anabolic phase (perfect carbohydrate utilisation, fall in blood phosphate levels with hypophosphaturia, sometimes very marked positivisation of nitrogen balance) and, sometimes, mild premonitory clinical signs. The relationship between this type of complication and hypophosphoraemia is quite definite, but the fall in serum phosphates would not appear to be directly responsible for the coma. The exact mechanism is not known. In order to avoid such complications, great caution should be observed in both the quality as well as the quantity of the intake, as well as in the clinical and laboratory surveillance of the malnourished patient undergoing realimentation.
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PMID:[Comas of realimentation]. 2 97

Brain-aluminium concentrations were found to be significantly higher in 7 patients dying with dialysis encephalopathy (mean 15.9 microgram aluminium/g dry weight) than in 11 dialysed controls (4.4 microgram/g) and in 2 uraemic patients who were not dialysed (2.7 microgram/g). The grey matter from the patients with dialysis encephalopathy contained about three times as much aluminium as white matter. The results suggest that dialysis with untreated and/or softened tap-water (aluminium concentration 0.1-1.2 mg/1) makes the major contribution to brain-aluminium levels; dialysis with deionised water (aluminium concentration normally less than 0.02 mg/1) and intake of phosphate-binding AL(OH)3 gel are less important. Brain aluminium levels remain elevated for up to four years after restoration of good renal function by transplantation. The association of dialysis encephalopathy with high levels of aluminium in the brain and in the dialysis water emphasises the potential neurotoxicity of aluminium in man.
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PMID:Brain-aluminium concentration in dialysis encephalopathy. 7 45

Clinical and Neuropathological data on sixteen cases of progressive myoclonic encephalopathy are reported. This neurological syndrome appears after an average duration of thirty two months of haemodialysis and leads to death in four and a half months, and is characterized by myoclonus, speech disorder, epileptic seizures, and mental-status changes. At first, clinical signs and symptoms are related to haemodialysis, later they become permanent. An early diagnosis is based on EEG which is the only useful laboratory test, demonstrating bisynchronous slow-wave bursts. The caracteristic histopathologic findings are neuronal depopulation, lipofuscin accumulation, and appearance of Neurofibrillary degeneration, especially in Motor cortex, red nucleus and dentato-olivary systems. It seems to be justified to attribute P.M.D.E. to aluminium chronic poisonning; the source of the aluminium intoxication is not aluminium containing phosphate-binding gels but intravenously administreted tape-water. The intracellular binding of aluminium is shown from a histochemical study employing fluorescent stain Morin.
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PMID:[Progressive myoclonic encephalopathy in dialysis patients. Clinical, electroencephalographic and neuropathological study. Pathogenetic discussion]. 10 55

The aluminum present as a contaminant in ATP preparations can cause strong inhibition of yeast hexokinase P-II activity at pH 7.0 or below but has little or no inhibitory effect at a pH of 7.5 or greater. The inhibition is reversed by citrate, 3-phosphoglycerate, malate, phosphate, and catecholamines, all of which have previously been described as activators of hexokinase at low pH. We suggest that these agents activate the enzyme only by virtue of their ability to coordinate with aluminum present in the assay system. The presence of aluminum is also responsible for the "negative cooperativity" observed at low pH with respect to Mg . ATP concentration--i.e., the inhibition by aluminum is uncompetitive at low Mg . ATP concentrations but becomes competitive at high Mg . ATP concentrations. The inhibition is thought to be due to formation of a complex of Al . ATP with the enzyme, with a dissociation constant (Ki) of 0.1 microM. Yeast hexokinase P-I is somewhat less sensitive to A1 than is hexokinase P-II, and yeast glucokinase is not detectably affected. The hexokinase in rat brain (type I) shows a pH-dependent inhibition by Al similar to that observed with the yeast hexokinases, whereas the rat muscle (type II) enzyme is less sensitive, suggesting a possible relationship to aluminum encephalopathy in man.
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PMID:Proton-dependent inhibition of yeast and brain hexokinases by aluminum in ATP preparations. 11 25

Severe hypophosphatemia may be observed after the ingestion of certain antacids which complex phosphorus in the intestinal lumen. In severe burn cases, during realimentation after denutrition, during intense and prolonged hyperventilations responsible for respiratory alkalosis, in diabetic ketoacidosis and in alcoholics. Hypophosphatemia lead to erythrocyte abnormalities which may eventually approach hemolysis, to phagocytosis and platelet function disorders and to neurological troubles which suggest a metabolic encephalopathy, a myopathy, a metabolic acidosis or a change in hepatic functioning. Treatment for hypophosphatemia with milk and sodium or potassium phosphate must be begun as soon as possible and must be sufficient to maintain blood phosphate levels above 10 mg/liter.
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PMID:[Hypophosphatemias (author's transl)]. 12 9

There is increasing evidence that aluminium accumulation in patients with impaired renal function has pathological consequences. The serum aluminium content of 45 patients with chronic renal failure was found to be significantly elevated when compared with normal subjects. A further rise in serum aluminium concentration was seen in patients with chronic renal failure when they were taking aluminium-containing phosphate binding agents. Patients with stable but moderately impaired renal function who are taking aluminium-containing phosphate binders for several years may be at risk from aluminium accumulation and the development of osteomalacia and encephalopathy as seen in patients on intermittent haemodialysis.
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PMID:Evidence for aluminium accumulation in renal failure. 54 3

On the basis of the organ values of nine decreased, formerly with Al (OH)3 treated patients with renal insufficiency without dialysis and 15 patients with dialysis their Mn-state was investigated in comparison to 60 control persons comparable as to age and sex. The dialysis patients for a considerable part died of the so-called dialysis encephalopathy three to five years after the beginning of the Al-treatment. In all investigated nine organs with the exception of the blood of the dialysed patients (liver, hair of the head, myocardium, brain, rib, lung and testicle) the Mn-content was, in comparison to the control persons, essentially, partly highly significantly reduced. These findings were discussed in various kinds of animals in connection with the skeletal and nervous disturbances conditioned by the Mn-deficiency. It may not be excluded that the Al-hydroxyde used for the phosphate binding protects also another essential trace elements and particularly Mn from resporption and has an antagonistic influence on the Mn-metabolism, respectively. Animal experiments must clarify the complex mentioned.
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PMID:[The effect of chronic renal insufficiency with and without dialysis therapy on the manganese content of various human organs]. 55 Jun 17

After ingestion of 150 mEq. of calcium chloride (CaCl-2), urinary acidification was studied for 6 hours in 22 normokalemic patients with alcoholic liver disease (L) of varying severity, and in 7 control (C) subjects during 10 studies. The degree of the induced systemic acidosis was similar in all groups. Nine L patients were unable to normally lower urine pH below 5.25 (L-I) and these were compared with the 13 L patients achieving lower pH (L-II) and with control subjects. This defect was consistently reproduced. Titratable acid excretion was less in L-I than in the other groups. The percentage contribution of ammonium to maximal net acid excretion was significantly higher in L-I and L-II than in C. No L-I patient had spontaneous metabolic acidosis, nor was there evidence of encephalopathy or of proximal tubular dysfunction. Sodium excretion was significantly lower in L-I than in either L-II or C. Sodium sulfate and sodium phosphate infused after acid-loading rapidly reduced urine pH into the appropriately acidic range in L-I patients with alcoholic liver disease by means of a simple, safe, and short acid-loading test. Although the mechanism of this renal tubular acidfying defect remains unknown a low distal delivery of sodium by limiting the transtubular potential difference may have been partially responsible.
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PMID:Abnormal renal acidification in alcoholic liver disease. 109 79

The aluminum content of muscle, bone and brain was measured in control subjects and in uremic patients on dialysis who had been maintained on phosphate-binding aluminum gels. The mean muscle aluminum was 14.8 ppm, and the trabecular-bone aluminum 98.5 ppm in the patients on dialysis, as compared with 1.2 and 2.4 in control subjects (P less than 0.05). Brain gray-matter aluminum values in a group of uremic patients on dialysis who died of a neurologic syndrome of unknown cause were 25 ppm as compared with 6.5 ppm in a group of uremic patients on dialysis who died of other causes and 2.2 ppm in control subjects. The fact that brain gray-matter aluminum was higher in all patients with the dialysis-associated encephalopathy syndrome than any of the control subjects or other uremic patients on dialysis suggests that this syndrome may be due to aluminum in intoxication.
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PMID:The dialysis encephalopathy syndrome. Possible aluminum intoxication. 124 32

Reye's syndrome (RS) consists of encephalopathy, fatty degeneration of viscera, and elevation of ammonia, certain amino acids, and liver enzymes in the blood. It is most characteristically a disease of children and has been considered to have a poor prognosis despite the use of various treatment regimens. Exchange transfusion (ET) with fresh blood (less than 24 hours old) for the removal of toxic metabolic byproducts in TS is a relatively recent development which appears to have improved the survival rates. However, because RS may occur in epidemic proportions at any time the demand for fresh blood can place an excessive stress on blood resources. We have, therefore, utilized saline-washed (to remove potentially toxic metabolites) red blood cells (RBC's) less than six days old, and fresh frozen citrate-phosphate-dextrose (CPD) plasma in treating this disorder. Nine patients in the Milwaukee community with severe encephalopathy secondary to RS were treated with ET. These patients collectively required 151 units of washed RBC's for 21 ET. Eight of nine patients survived without sequelae. Age of blood used did not correlate with the number of exchanges required or the eventual outcome. A continual computerized EEG in five patients provided objective evidence of the effectiveness of ET. We conclude that ET with saline-washed RBC's reconstituted with fresh frozen plasma (FFP) is a fast, safe, and effective means of treating patients with RS.
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PMID:Exchange transfusion in Reye's syndrome with saline-washed red blood cells. 125 13


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