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 amino acid solution, Aminofusin hepar, was evaluated for treatment of hepatic encephalopathy and for parenteral nutrition of patients with liver cirrhosis in correlation to changes in amino acid levels. In contrast to amino acid solutions used for the parenteral nutrition of patients without liver disease, this solution contains an increased proportion of branch chained amino acids and of arginine and ornithine, and a reduced proportion of phenylalanine, methionine, glycine and threonine. The changes in the plasma amino acid levels after infusion of this solution were measured in 4 cirrhotics. The concentration of leucine, isoleucine, valine, ornithine and arginine increased markedly, whereas phenylalanine, methionine, tyrosine, glycine and threonine decreased. The ammonia level in venous blood increased slightly. 4 cirrhotics with encephalopathy were treated for 7 days. In 3 of them the neuropsychiatric symptoms were completely reversed, whereas in the remaining 1 no clinical improvement was achieved in spite of normalization of the plasma aminogramm. In this patient a constant rise of blood ammonia was noted. The indications for special amino acid solutions in liver diseases are discussed.
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PMID:[Parenteral feeding of patients with liver cirrhosis with hepatic encephalopathy]. 677 52

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

To elucidate the relative contribution of parenchymal liver damage and spontaneous portal-systemic shunting to the reduction of peripheral insulin degradation rate and the decrease in plasma concentrations of three branched chain amino acids (valine, leucine, and isoleucine), plasma insulin, C-peptide, and amino acid concentrations were measured during oral glucose tolerance tests in 17 patients with liver cirrhosis, 10 with idiopathic portal hypertension, 5 hospitalized controls, and normal subjects. None of the patients had evidence of hepatic encephalopathy. Patients with idiopathic portal hypertension had histologically minimum hepatic fibrosis in spite of the existence of extensive exophageal varices. The molar ratio between plasma concentrations of C-peptide and insulin was significantly decreased in patients with cirrhosis, but not in those with idiopathic portal hypertension. In both patients with cirrhosis and idiopathic portal hypertension, the three branched chain amino acid levels were significantly decreased and the molar ratio between the concentrations of the three branched chain amino acids and two aromatic amino acids (tyrosine and phenylalanine) were markedly reduced. These results suggest that spontaneous portal-systemic shunting does not primarily contribute to the reduced degradation of insulin, but has a close relationship with the decrease in branched chain amino acid levels and in the molar ratio of plasma amino acids. In addition, the present data indicate that decreased branched chain amino acid levels in patients with cirrhosis is not merely ascribed to hyperinsulinemia and that the decrease in the molar ratio of plasma amino acids is not specific to the presence of hepatic encephalopathy.
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PMID:Effect of spontaneous portal-systemic shunting on plasma insulin and amino acid concentrations. 698 17

1. Intravenous infusions of L-valine (600 mumol/min), L-isoleucine (150 mumol/min), L-leucine (300 mumol/min) and a mixture of the three branched-chain amino acids (70% L-leucine, 20% L-valine, 10% L-isoleucine; 270 mumol/min) were given to four groups of healthy volunteer subjects. Whole-blood concentrations of amino acids and glucose and serum insulin were measured before and during the infusions. 2. Valine and isoleucine infusions resulted in twelve- and six-fold increases in the respective amino acid. During valine infusion, tyrosine was the only amino acid for which a decrease in concentration was seen (25%, P less than 0.05). With isoleucine administration, no significant changes were found. In contrast, leucine infusion (during which the leucine concentration rose about sixfold) was accompanied by significant decreases in tyrosine (35%), phenylalanine (35%), methionine (50%), valine (40%) and isoleucine (55%). The arterial glucose concentration fell slightly (5%) and the insulin concentration increased 20% during leucine infusion. 3. Infusion of the mixture of the three branched-chain amino acids resulted in marked decreases in tyrosine (50%), phenylalanine (50%) and methionine (35%). The decreased amino acid levels remained low for 2 h after the end of the infusion. 4. The present findings demonstrate that intravenous infusion of leucine (not infusion of valine or isoleucine) results in marked reductions in the concentrations of the aromatic amino acids and methionine. Infusion of a mixture of the three branched-chain amino acids gives results similar to those obtained with leucine infusion alone. Thus a mixed branched-chain amino acid solution with leucine as its main constituent seems to be the best alternative in the treatment of patients with hepatic cirrhosis and encephalopathy.
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PMID:A comparison of the effects of intravenous infusion of individual branched-chain amino acids on blood amino acid levels in man. 701 2

The changes induced by active tilting in arterial pressure, plasma renin activity, norepinephrine and its precursors phenylalanine and tyrosine were evaluated in 8 patients with liver cirrhosis and 6 healthy controls. The results suggest the inability of the adrenergic system, though hyperstimulated, to maintain arterial pressure homeostasis in cirrhosis with a compensatory hyperactive renin-angiotensin system. Derangements in catecholamine synthesis, possibly due to altered utilisation of precursors to alternative final products (weak neurotransmitters?) can be taken into account.
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PMID:[Catecholamine and renin-angiotensin system in blood pressure control in patients with liver cirrhosis]. 702 55

Multivariable physiologic studies of cardiovascular, respiratory, and metabolic functions were performed in 341 patients (884 studies). Eighty patients had cirrhotic liver disease, 64 had sepsis, 87 had nonseptic cariogenic syndromes, and 110 had nonseptic general surgical or traumatic injury. The group with cirrhosis had the highest cardiac index and ejection fraction. When compared with the group with nonseptic surgery or trauma, vascular tone was reduced in the patients with cirrhosis or sepsis and was lowest in patients with both conditions. Ventricular function was good in the groups with cirrhosis or sepsis, due to the additive effect in reducing vascular tone that allowed ejection fraction to increase, but caused the ratio of alveolar ventilation to perfusion (VA/QT) to fall, resulting in a greater perfusion of a decreased pulmonary vascular bed. The falls in vascular tone and VA/QT in patients with cirrhosis or sepsis result from the reduced oxygen consumption that occurs due to metabolic imbalance (B state). This B state seems to reflect a hepatic inability to metabolize aromatic amino acids, so that levels of tyrosine, phenylalanine, and the false neurotransmitter octopamine increase. These mechanisms are pathologically synergistic when sepsis and cirrhosis occur together.
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PMID:Pathologic synergy in cardiovascular and respiratory compensation with cirrhosis and sepsis. A manifestation of a common metabolic defect? 705 35

Plasma amino-acid concentrations were measured in 167 patients with liver disease of varying aetiology and severity, all free of encephalopathy, and the results compared with those in 57 control subjects matched for age and sex. In the four groups of patients with chronic liver disease (26 patients with chronic active hepatitis, 23 with primary biliary cirrhosis, 11 with cryptogenic cirrhosis, and 48 with alcoholic hepatitis +/- cirrhosis) plasma concentrations of methionine were significantly increased, while concentrations of the three branched chain amino-acids were significantly reduced. In the first three groups of patients plasma concentrations of aspartate, serine, and one or both of the aromatic amino-acids tyrosine and phenylalanine were also significantly increased, while in the patients with alcoholic hepatitis +/- cirrhosis plasma concentrations of glycine, alanine, and phenylalanine were significantly reduced. In the three groups of patients with minimal, potentially reversible liver disease (31 patients with alcoholic fatty liver, 10 with viral hepatitis, and 18 with biliary disease) plasma concentrations of proline and the three branched chain amino-acids were significantly reduced. Patients with alcoholic fatty liver also showed significantly reduced plasma phenylalanine values. Most changes in plasma amino-acid concentrations in patients with chronic liver disease may be explained on the basis of impaired hepatic function, portal-systemic shunting of blood, and hyperinsulinaemia and hyperglucagonaemia. The changes in patients with minimal liver disease are less easily explained.
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PMID:Plasma amino-acid patterns in liver disease. 707 13

Serum amino acid patterns in patients with different types of hepatic encephalopathy were investigated. Marked elevations in most of serum amino acids observed in untreated patients with acute type of fulminant hepatitis were not remarkable in the patients who have already treated; particularly branched chain amino acids (BCAA), phenylalanine and tyrosine were much lower in the latter group. However, elevation of serum methionine levels and lower ratio of BCAA/(phenylalanine + tyrosine) were similarly observed in both groups. In encephalopathic patients with decompensated cirrhosis, many amino acids such as phenylalanine, tyrosine and methionine were elevated with a slight depressed levels of serum BCAA. Highly significant decrease in serum BCAA levels and no elevation of phenylalanine and methionine with a minimal increase of tyrosine were observed in patients with chronic type of hepatic encephalopathy; other amino acids except for glutamine and arginine were much lower as compared to those in decompensated cirrhotics and even to the control values.
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PMID:Characteristics change in serum amino acid levels in different types of hepatic encephalopathy. 711 80

Femoral arterio-venous (A-V) differences of blood free amino acids and plasma ammonia (NH3) were simultaneously determined after an overnight fast in 16 patients with decompensated liver cirrhosis in the absence and presence of encephalopathy, as compared with those in 8 control subjects. In spite of increased releases of phenylalanine (Phe) and tyrosine (Tyr) from the peripheral tissue, releases of isoleucine (Ile) and leucine (Leu) as well as alanine (Ala) were found to be significantly reduced in decompensated liver cirrhosis, particularly in the presence of hepatic encephalopathy. Furthermore, NH3 was found to be significantly taken up by the skeletal muscle of these patients, and a positive correlation was observed between arterial NH3 level and the A-V differences of Leu, of Ile and of Ala. These findings strongly suggest that net degradation (or utilization) of branched-chain amino acids (in particular, Leu and Ile) is enhanced in the muscle for detoxication of ammonia (i.e., glutamine synthesis) by supplying the carbon skeleton and energy in cirrhosis of the liver.
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PMID:Augmented utilization of branched-chain amino acids by skeletal muscle in decompensated liver cirrhosis in special relation to ammonia detoxication. 722 60

Hepatic encephalopathy in liver cirrhosis is due to several factors, including amino acid imbalance and hyperammonemia. Lactitol [correction of lactilol], a non adsorbable disaccharide, improves hepatic encephalopathy increasing bowel movements, modifying colonic bacteria and pH, and reducing blood ammonium. Ten patients with liver cirrhosis and longstanding stable hepatic encephalopathy were treated, after a period of drugs wash-out, with lactitol. A significant improvement of hepatic encephalopathy was observed, with a significant decrease of blood ammonium, related with the increase of stool frequency/day. Atrial natriuretic peptide decreased as well. Moreover, an increase of the ratio of plasma aliphatic amino acids (valine, leucine and isoleucine)/aromatic amino acid (tyrosine and phenylalanine) was observed. Lactitol is an effective drug in the treatment of chronic hepatic encephalopathy; its mechanism of action involves not only a decrease of blood ammonium but also modifications of the degree of plasma amino acid imbalance, and fluid and circulatory adjustments.
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PMID:Effects of lactitol [correction of lactilol] on hepatic encephalopathy and plasma amino-acid imbalance. 756 87


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