Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic effects of selected and branched-chain amino acid (BCAA)-enriched parenteral solutions were studied in liver cirrhosis. After 3 days of an oral protein-free diet with balanced amino acid (AA) infusion, 36 cirrhotic patients without encephalopathy were randomly divided into four groups. Groups A and B were infused for 5 days with BCAA (valine, leucine, isoleucine) at doses of 0.5 and 1.0 g/kg/day, respectively, as the only nitrogen source. Group C received 0.8 g/kg of essential and nonessential AA solution with a prevalence of BCAA; the last group (D) continued the basic standard diet, as control. Routine chemistry, urinary nitrogen losses, nitrogen balance, and the whole plasma AA pattern were detected before and after the treatment period. BCAA alone led to an impressive and significant improvement in the basic AA pattern in both the A and B groups. The same results were obtained in group C for plasma AA. In particular, the ratio of BCAA to aromatic amino acids in groups A, B, and C was significantly increased (p less than 0.01, less than 0.02, less than 0.02, respectively). In group D the AA pattern and the BCAA/aromatic amino acid ratio remained unchanged. The negative nitrogen balance of the base state remained unchanged after 0.5 g of BCAA (A); it improved significantly and became positive during and after the infusions of a double dose of BCAA (B), as it did in the case of selective solutions (C), although to a lesser extent; the negative nitrogen balance of the control group showed only a slight improvement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Standard or branched-chain amino acid infusions as short-term nutritional support in liver cirrhosis? 392 19

Evidence from several sources suggest that blood-brain transport of the large neutral amino acids (NAA) is abnormal in animals with a portacaval anastomosis (PCA) and in patients with liver cirrhosis and portal-systemic shunting and encephalopathy, but the underlying mechanisms are unknown. After PCA, the concentration of glutamine (Gln) in brain is markedly increased as a by-product of cerebral ammonia detoxification, and the rate of efflux of Gln from brain is also increased. The following studies were undertaken to clarify the relationships among plasma and brain concentrations of NAA after PCA in rats and to examine the relationship of brain Gln concentration to plasma and brain NAA concentrations. After PCA plasma phenylalanine, tyrosine and histidine were elevated and leucine, isoleucine and valine were lowered. In brain, phenylalanine, tyrosine, histidine and methionine were markedly elevated after PCA and their concentrations in brain far exceeded the concentrations in plasma. Analyses of single, partial and multiple correlations of plasma NAA ratios expressed as plasma competitor function (PCF), brain NAA and brain Gln showed significant correlations between PCF nd brain NAA in shunted rats. A better correlation was found between brain NAA and brain Gln. Correlation coefficients obtained from multiple correlation analysis equalled or exceeded those obtained in the partial correlation or in the single correlation, suggesting that the effects of PCF and brain Gln on brain NAA were separate and additive. Gln was shown to compete with other NAA for blood brain transport by inhibiting brain 14C phenylalanine uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of brain glutamine and brain neutral amino acid concentrations after portacaval anastomosis in rats. 393 Feb 56

Administration of total parenteral nutrition (TPN) solutions high in branched chain amino acids (BCAA) is thought to improve metabolic support during stress. This prospective, randomized, double blind study compared 45 per cent BCAA with 25 per cent BCAA in 12 patients. Seven patients had multiple trauma; two, gastrointestinal surgery; one, pancreatitis; and two, cirrhosis. The TPN regimen was 1.0-1.5 gm/kg/day amino acids and 30-45 glucose kcal/kg/day. The BCAA formula used was high in isoleucine and valine, but not leucine. Amino acid plasma levels, blood chemistries, 3-methylhistidine excretion, and nitrogen balance were studied. Control studies showed negative nitrogen balance (-7.1 +/- 2.9 gm) (mean +/- SEM), elevated insulin (61 +/- 21 microunit/ml), and elevated 3-methylhistidine (3MH) excretion (688 +/- 309 micromol); plasma leucine (93 +/- 11 nmol/ml) and isoleucine (37 +/- 23) were low, and valine (155 +/- 20) was elevated. Plasma methionine (40 +/- 9) and tyrosine (70 +/- 12) were high normal. Phenylalanine (85 +/- 5) was elevated. Both groups showed increased nitrogen excretion and positive nitrogen balance during the study (25 per cent, 2.0 +/- 1.4 gm/day; 45 per cent, 1.2 +/- 2.6 gm/day). Three-methylhistidine excretion changed little in either group (557 +/- 149, 414 +/- 91), insulin rose (135 +/- 27, 65 +/- 19), and plasma leucine (82 +/- 4, 71 +/- 9) changed little. Plasma isoleucine (51 +/- 3, 155 +/- 16) and valine (173 +/- 11, 691 +/- 23) both rose, more in the 45 per cent group. Methionine (67 +/- 12, 37 +/- 4) and tyrosine (51 +/- 6, 50 +/- 10) changed little.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of total parenteral nutrition with 25 per cent and 45 per cent branched chain amino acids in stressed patients. 393 93

Low plasma levels of branched-chain amino acids, leucine, isoleucine, and valine are postulated to play an etiologic role in hepatic encephalopathy. Supplementation is advocated to reverse encephalopathy and improve nutritional status and survival. We measured in vivo leucine metabolism in normal individuals (n = 5) and in two groups of patients with cirrhosis (n = 8) with a primed continuous infusion of L-[15N, 1-13C] leucine to quantitate the following parameters of leucine metabolism: nitrogen and carbon fluxes, oxidation, contribution to protein synthesis, breakdown of endogenous protein to leucine, deamination and reamination to/from ketoisocaproate. Studies were performed in the fasting and fed states with a conventional enteral diet (Propac) and a branched chain-enriched diet (one third Propac plus two thirds Hepatic-Aid). In vivo leucine metabolism was similar in the fasting and fed states in normal individuals in patients with cirrhosis and with both diets when studied at a protein intake of 0.6 gm/kg ideal body weight/day. When fed these diets, oxidation increased (p less than 0.05) and breakdown decreased (p less than 0.05). The Hepatic-Aid diet increased (p less than 0.05) nitrogen and carbon fluxes significantly more than did the standard diet. Four additional patients with cirrhosis on a diet with more protein were studied (0.75 gm/kg ideal body weight/day). Carbon and nitrogen fluxes, oxidation, synthesis, and deamination were increased (p less than 0.05) when patients with cirrhosis were fed the Propac diet compared with those who fasted. The Hepatic-Aid diet further increased (p less than 0.05) all parameters except synthesis and did not decrease protein breakdown. These data show that patients with cirrhosis metabolize leucine in vivo in a manner identical to that of normal subjects and that leucine-enriched formulas increase oxidation to CO2 without improving protein synthesis.
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PMID:In vivo measurement of leucine metabolism with stable isotopes in normal subjects and in those with cirrhosis fed conventional and branched-chain amino acid-enriched diets. 403 63

3-Methylbutanal is a volatile aldehyde which in the rat is derived, at least in part, from colonic bacterial breakdown of leucine. It has been proposed as a toxin of importance in the pathogenesis of hepatic encephalopathy in man. A rapid, reliable and highly reproducible method for estimating 3-methylbutanal in plasma is described using a gas-chromatograph with a head space-sampler. The mean plasma 3-methylbutanal concentration in non-fasting patients with hepatic encephalopathy, 0.244 mumol/litre (range 0-1.30) was not significantly different from the mean value in controls, 0.116 mumol/litre (0-0.349). Oral leucine feeding resulted in significant increases in plasma 3-methylbutanal concentrations in both control subjects and patients with cirrhosis. Peak leucine and 3-methylbutanal values occurred at approximately the same time and usually within 120 min of leucine ingestion. Pre-treatment with neomycin had no effect on the results of leucine feeding. No changes occurred in the clinical condition or psychometric performance of patients with cirrhosis fed leucine despite increases in plasma 3-methylbutanal of up to 700% over basal values. In man plasma 3-methylbutanal, at least in part, derives from ingested leucine independently of the action of colonic bacteria. The role of this compound in the pathogenesis of hepatic encephalopathy in man needs further exploration.
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PMID:Plasma 3-methylbutanal in man and its relationship to hepatic encephalopathy. 403 37

The AA. have studied behaviour of the LAP (leucine-amino-peptidase) in the serum of blood in subjects affected of cirrhosis of the liver in stage ascitical, of cause toxic-alcoholic excluding about of the casuistry the cirrhosis of the another cause and the cirrhosis that are compled white an obstruction in and extrahepatic standard biliary cirrhosis 1 degree e 2 degree. After the exposition of the casuistry in the registred normality of the test (seric-LAP) in some cases of hepatic-alcoholic cirrhosis, the AA. concluded considering the LAP an indicator only of the obstruction in and extra-hepatic, consistent with hepatic-organ well operating; do not be a secure test to follow development of a chronic hepatitis of any kind, even if in the hepatic disease is present an infiltration and an overturning of the hepatic-lobule, like it is normally in the hepatic alcoholic diseases.
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PMID:[Behaviour of the LAP (leucine-amino-peptidase) in the serum of blood in subjects affected of cirrhosis of the liver in stage ascitical (author's transl)]. 610 56

In order to investigate disturbances in glycoregulation and plasma amino acids and their possible relationship in alcoholic liver diseases, plasma concentrations of insulin, C-peptide, glucagon and branched-chain (valine, leucine, isoleucine) as well as aromatic (phenylalanine, tyrosine) amino acids were measured during an arginine test (i.v infusion of arginine chloride 0.5 g/kg over 30 min) in 21 alcoholic patients: 11 with cirrhosis (group C) and 10 with steatosis (group S). Insulin responses to arginine was reduced in both groups, whereas glucagon response was increased in group C and reduced in group S. Plasma concentrations of branched-chain amino acids were reduced in both groups, irrespective of the degree of hyperinsulinism. Plasma concentrations of aromatic amino acids were increased only in cirrhotic patients; the increase was independent of the degree of hyperglucagonism and of the plasma insulin/glucagon molar ratio. These results suggest that disturbances of glycoregulation in plasma amino acids imbalance do not play a major role in alcoholic cirrhosis and steatosis.
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PMID:[Disturbances in glycoregulation and plasma amino acids in alcoholic hepatopathies. Study using the arginine test]. 623 16

In 14 patients with cirrhosis of the liver and portal-systemic shunts the effect of a branched-chain amino acid-enriched elemental diet on portal systemic encephalopathy, routine laboratory parameters and plasma amino acids was investigated. In addition to the standard therapy including protein restriction (40 g/day) the patients received 44 g of an amino acid-protein mixture containing 30% of branched-chain amino acids and placebo over 3 months in a crossover regimen. Plasma valine and leucine increased significantly, whereas all other amino acids, including the ratio (formula: see text), remained unchanged. The electroencephalogram, number connection test, clinical state and laboratory parameters were not influenced by therapy with branched-chain amino acids. Thus, orally administered branched-chain amino acids probably have no influence on hepatic encephalopathy but are an adequate source of nitrogen in patients with cirrhosis of the liver.
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PMID:Branched-chain amino acid-enriched elemental diet in patients with cirrhosis of the liver. A double blind crossover trial. 636 43

Plasma amino acid concentrations and plasma glucagon and serum insulin levels were studied in male patients with compensated alcoholic and nonalcoholic liver cirrhosis. Age, nutritional status, and liver function tests were similar in both groups; none of the patients presented hepatic encephalopathy. Plasma valine and leucine concentrations were lower, and tyrosine, higher in alcoholic than nonalcoholic liver cirrhosis. As a result, the molar ratios of branched-chain amino acids (BCAA) to aromatic amino acids (AAA) were reduced markedly in this group. Although correlation coefficients comparing BCAA/AAA ratios and KICG in alcoholic and nonalcoholic liver cirrhosis were similar, a steeper regression line was observed in alcoholics. Plasma glucagon and proline levels were significantly higher in alcoholic than nonalcoholic liver cirrhosis, the former correlated with AAA concentrations only in alcoholic liver cirrhosis, but not with BCAA levels. These results indicated that alcoholic liver cirrhosis presented a more deranged plasma amino acid pattern than nonalcoholic, and the amino acid imbalances, except for depressed BCAA and elevated proline, were derived, in part, from the hyperglucagonemia.
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PMID:Plasma amino acid imbalance in alcoholic liver cirrhosis. 639 76

Repeated plasmaphereses were done in 7 patients with acute hepatic failure (5 of them with coma stage IV and two with stage III). Acute liver insufficiency was induced by fulminant viral hepatitis in 4 cases, by drugs in one case, and was caused by a dystrophic exacerbation of liver cirrhosis in two further cases. Four of the 7 treated patients have survived. Beginning improvement of hepatic function was evidenced by an increase of factor VII and prothrombin in plasma. Significant lowering of bilirubin could be observed in all cases. While ammonia values decreased continuously in the four successfully treated patients while on plasmapheresis, the opposite behaviour was observed in the decreased patients. The influence of plasmapheresis on the pathologically altered aminoacid pattern in hepatic coma was investigated in two patients: Before treatment clearly to excessively increased values of methionine and aromatic aminoacids (phenylalanine and tyrosine) were seen. Branched-chain aminoacids leucine, isoleucine and valine were normal to moderately decreased. After termination of plasmapheresis methionine and aromatic aminoacids were significantly lower, branched-chain aminoacids were slightly below the initial values. Improvement of consciousness correlated with increase of the quotient (val+leu+ile)/(phe+tyr).
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PMID:[Treatment of acute liver failure by plasmapheresis]. 640 57


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