Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This prospective study compared the effects of tube-fed nutrition with those of a regular diet in alcoholic liver disease. The high prevalence of malnutrition in patients with alcoholic liver disease requires clarification of the benefits of aggressive nutritional support. Patients were randomly assigned a regular diet without or with tube-fed supplementation, delivering 1.5 g/kg protein and 167 kJ/kg daily. Comparisons of encephalopathy, antipyrine clearance, metabolic rate, and biochemical parameters were performed weekly for 4 weeks. Sixteen patients receiving enteral supplementation had antipyrine half-life (50% vs. 3% reduction), serum bilirubin (25% vs. 0% reduction), and median encephalopathy scores that improved more rapidly than those of controls. Initially, 15 controls did not consume adequate calories to meet measured resting energy expenditure. Aggressive nutritional intervention accelerated improvement in alcoholic liver disease. Adverse effects did not offset the demonstrated benefits of a 2-cal/mL, casein-based tube-fed supplement. These findings support the use of standard, casein-based solutions in the treatment of alcoholic liver disease and as the control condition for future studies.
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PMID:Accelerated improvement of alcoholic liver disease with enteral nutrition. 161 54

Aluminum contaminates several chemical compounds that are administered intravenously to patients. The most highly contaminated are calcium and phosphate salts, followed by albumin and heparin. Parenteral administration of aluminum bypasses the gastrointestinal tract, which serves as a protective barrier to aluminum entry into the blood. In the past, parenteral administration of aluminum as a contaminant of water used in hemodialysis and of casein hydrolysate, the former source of protein in parenteral nutrition solutions, was associated with a low-turnover osteomalacic bone disease and, in the case of uremic patients, encephalopathy. Groups currently at risk for aluminum accumulation in tissue resulting from parenteral administration include premature infants receiving long-term parenteral nutrition and patients receiving plasmapheresis therapy with albumin. Both groups may develop metabolic bone disease; the pathogenesis may involve aluminum. The Food and Drug Administration is currently considering regulation of aluminum in fluids used for parenteral nutrition. No changes are presently proposed with regard to albumin.
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PMID:The aluminum content of parenteral solutions: current status. 190 89

In a double blind randomized study, branched-chain amino acids and placebo (casein) were compared as a treatment for chronic hepatic encephalopathy in cirrhosis. After a 15-day run-in period with controlled diet (45-65 g protein), the patients were administered, in addition to their diet, branched-chain amino acids (0.24 g/kg, 30 patients) or an equinitrogenous amount of casein (34 patients). One patient on branched-chain amino acids and two on casein were lost to the study. After 3 months, the index of portal-systemic encephalopathy significantly improved in patients on active treatment (from 40 [S.D. 14]% to 21 [17]), but was not in subjects receiving casein (from 37 [13]% to 36 [12]). Two or more parameters of the index improved in 24 patients treated with amino acids (80%; confidence limits, 61-92%), and only in 12 receiving casein (35%; confidence limits, 20-54%; p less than 0.001). Patients who did not improve were given an alternative treatment for 3 more months. Casein-treated patients given branched-chain amino acids rapidly improved. The changes in neuropsychologic function were associated with an improvement in semiquantitative nitrogen balance, which became consistently positive in amino acid-treated subjects; there was also a mild improvement in nutritional parameters and in liver function tests. The supplementation of oral branched-chain amino acids to the diet is superior to casein as a treatment for providing adequate nitrogen supply and improving the mental state of cirrhotic patients with chronic encephalopathy.
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PMID:Long-term oral branched-chain amino acid treatment in chronic hepatic encephalopathy. A randomized double-blind casein-controlled trial. The Italian Multicenter Study Group. 220 61

In a doubleblind cross-over placebo-controlled trial the efficiency of oral treatment with branched chain amino acids was investigated in 22 inpatients with liver cirrhosis. In all patients evidence of latent (subclinical) portalsystemic encephalopathy was obtained by using an extensive psychometric test programme. Patients received a defined diet of 35 cal/kg/day containing 1 g of protein. In addition, branched chain amino acids or casein in a dosage of 0.25 g/kg/day was administered in a cross-over fashion, each for 1 week. Semiquantitative nitrogen balance increased during both treatments, with a tendency towards a larger increase during branched chain amino acid treatment. At the same time ammonia concentration tended to decrease during branched chain amino acid treatment. Taking into account the cross-over design, significant improvements attributable to branched chain amino acid treatment could be demonstrated in psychomotor functions (line tracing, tapping, steadiness, auditory reaction time), attention (digit table), and practical intelligence (digit symbol, number connection test).
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PMID:[Branched-chain amino acids in the treatment of latent porto-systemic encephalopathy. A placebo-controlled double-blind cross-over study]. 352 38

Branched chain amino acids have been recommended for the treatment of portosystemic encephalopathy based on the false neurotransmitter hypothesis. This hypothesis implies that by correction of the deranged amino acid pattern in the blood of cirrhotics, false neurotransmission and then portosystemic encephalopathy is improved. We conducted a double-blind crossover placebo-controlled trial in 22 inpatients with liver cirrhosis and obtained evidence of latent (subclinical) portosystemic encephalopathy using an extensive psychometric test program. Patients received a defined diet of 35 cal/kg X day containing 1 g of protein. In addition, branched chain amino acids or casein in a dosage of 0.25 g/kg X day was administered in a crossover fashion, each for 1 wk. Semiquantitative nitrogen balance increased during both treatments, with a tendency of a larger increase during branched chain amino acid treatment. At the same time ammonia concentration tended to decrease during branched chain amino acid treatment. Taking into account the crossover design, significant improvements attributable to branched chain amino acid treatment could be demonstrated in psychomotor functions (line tracing, tapping, steadiness, auditory reaction time), attention (digit table), and practical intelligence (digit symbol, number connection test).
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PMID:Branched chain amino acids in the treatment of latent portosystemic encephalopathy. A double-blind placebo-controlled crossover study. 388 9

An orally administered branched-chain amino acid (BCAA) rich supplement (T), Travasorb-Hepatic was compared to a casein based supplement (E), Ensure, in a randomized double-blind cross-over study in eight malnourished, stable cirrhotics unable to achieve a daily dietary protein intake of 1.0 g/kg. Doses of antiportal systemic encephalopathy drugs remained constant and a baseline 1000 kcal, 40 g dietary protein intake was encouraged. To this diet, supplemental protein was added in daily 20-g increments to a maximum of 60 g supplemental protein. Mental status, asterixis, and number connection tests were assessed daily and an antiportal systemic encephalopathy index calculated. There was no significant difference in the mean intake of dietary protein (T, 33.7 +/- 4.0 g; E, 26.7 +/- 10.8 g), supplemental protein (T, 43.1 +/- 8.3 g; E, 47.9 +/- 7.1 g), or N2 balance (T, 4.2 +/- 3.7 g; E, 3.4 +/- 4.4) between treatment trials. The antiportal systemic encephalopathy index improved on E, with no significant change in the BCAA:aromatic acid molar ratio. This ratio improved on T (1.02 +/- 2.0 to 2.7 +/- 1.1), but was not accompanied by improvement in the antiportal systemic encephalopathy index. The improved protein tolerance in both groups was not further increased by a highly enriched BCAA formula compared to one with a moderate BCAA content from a natural dietary protein source. Thus, both conventional casein-based supplements and enriched BCAA formulas are well tolerated and can be safely and effectively used as an integral part of diet therapy.
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PMID:Enriched branched-chain amino acid formula versus a casein-based supplement in the treatment of cirrhosis. 390 62

When normal individuals eat 0.33 g protein N/kg body weight (BW)((3/4)) per day, they excrete 10-15 mg urea N/h per kg BW((3/4)). If they now ingest (at 0 h) 0.27 (dose A), 0.40 (dose B), 0.53 (dose C), 0.94 (dose D), or 1.33 (dose E) g protein N/kg BW((3/4)) (in the form of casein, ovalbumin, or lactalbumin), the rate of urea N excretion accelerates within 4 h. At dose C a maximal rate of urinary urea N excretion (MRUE) is reached, which averages 55 mg urea N/h per kg BW((3/4)) and which persists for 16 h. Higher doses of protein do not further accelerate urea excretion, but prolong the duration of MRUE to 28 h (after dose E). Blood urea N (BUN) rises by 7-20 mg/100 ml during the first 8 h after dose C to E, and remains stable within +/-5 mg/100 ml during the ensuing 8-28 h of MRUE. Each increment of protein above dose C causes a further increment in plasma alpha-amino N. During infusion of free amino acids at a rate of 110 or 165 mg amino acid N/h per kg BW((3/4)) for 12 h, rate of urea excretion increases to the MRUE value produced by dose C-E of oral protein.These findings indicate that MRUE corresponds to a period of maximal rate of urea synthesis (MRUS). MRUS is greater than MRUE because one fraction of newly formed urea is hydrolyzed in the gastrointestinal tract, and another fraction may accumulate temporarily in body water during the MRUE period. Oral neomycin reduces the proportion of urea hydrolyzed in the gut to less than 20%; its extent is measured by recovery in the urine of a tracer dose of [(14)C]urea injected intramuscularly during determination of MRUE. Accumulation of urea in body water is estimated from increment in BUN during the period of MRUE measurement (8-24 h after dose E of casein) and from body water measured with (3)H(2)O. Then MRUS is calculated as: ([mg urea N excreted between 8 and 24 h after dose E] + [BUN at 24 h - BUN at 8 h] x [body water]) x (100/% recovery [(14)C]urea) x (1/kg BW((3/4))) x (1/16 h).MRUS in 10 normal subjects averaged 65 mg urea N/h per kg BW((3/4)) (range 55-76), and in 34 cirrhotics 27 mg urea N/h per kg BW((3/4)) (range 6-64). Among 19 cirrhotic patients fed 40, 60, 80, or 100 g protein daily for successive 10 day periods, the occurrences of hyperammonemia, hyperaminoacidemia, and encephalopathy at each level of protein intake were inversely related to MRUS value.
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PMID:Maximal rates of excretion and synthesis of urea in normal and cirrhotic subjects. 472 56

Hepatic-Aid is purported to ameliorate encephalopathy and promote positive nitrogen balance in protein-intolerant, cirrhotic patients by correcting their imbalanced amino acid profile. This study evaluated Hepatic-Acid by comparing a 50-g Casein diet with an identical diet with 20-g Casein/30-g Hepatic-Aid per day in a cross-over study. Four patients with biopsy-proven stable cirrhosis, encephalopathy, and under-nutrition were studied. Each study period included three days of equilibration and eight days of metabolic balance, with the following measured at baseline and on balance days 5 and 8: routine biochemistry, fasting ammonia, psychometric tests, EEG, and plasma amino acid profiles. There was no significant change in clinical status, routine biochemistry, fasting ammonia, psychometrics or EEG between the two study periods. Mean (+/-SD) nitrogen balance on the Casein diet at 1.5 +/- 1.5 g/day was not significantly different from that on the Hepatic-Aid diet at 1.5 +/- 1.2 g/day. Plasma amino acid profiles showed a significant fall (p less than 0.05) in fasting and intraprandial tyrosine (tyr) and phenylalanine (phe) on Hepatic-Aid, but only intraprandial leucine (leu), isoleucine (ile), and valine (val) were significantly increased (p less than 0.05) on Hepatic-Aid. The ratio leu + ile + val to tyr + phe was significantly increased (p less than 0.05) on Hepatic-Aid. It is concluded that Hepatic-Aid, as given in this study, maintains N balance similar to Casein, alters the amino acid profile towards normal, but does not ameliorate encephalopathy.
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PMID:Comparison of the effects of Hepatic-Aid and a Casein modular diet on encephalopathy, plasma amino acids, and nitrogen balance in cirrhotic patients. 683 Mar 37

Previous investigations showed that Schistosoma mansoni infection aggravates protein malabsorption in undernourished mice and this can be reverted by administration of casein hydrolysate. The present study was undertaken to evaluate the effects of ingestion of casein hydrolysate for long periods. Albino Swiss mice were divided into eight groups. Diets contained 5% (undernourished) or 20% (controls) casein levels. For each group there were sub-groups ingesting whole or hydrolysed casein for 12 weeks. Infection with S. mansoni developed in half of the animals under each diet. All undernourished mice developed malabsorption. Low albuminemia was detected in infected animals independently of the protein level in the diet. However, albuminemia was lower in infected controls than in undernourished non-infected mice, suggesting a deficient liver protein synthesis. Infected mice fed on a 20% protein hydrolysed diet exhibited low weight gain and high mortality rates. On the other hand, non-infected mice ingesting the same diet had the highest body weights. We are investigating the hypothesis that infected mice, even when fed normal diets, are unable to metabolise large amounts of amino acids due to the liver lesions related to schistosomiasis and as a result die of hepatic coma. In some of them, the excessive accumulation of ammonia in the blood enhances the outcome of an encephalopathy.
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PMID:A long-term intake of a protein hydrolysate seems to increase the risk of encephalopathy in mice infected with Schistosoma mansoni. 992 50