Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We studied the effects of infusion of a branched chain enriched amino acid mixture versus glucose on acute hepatic encephalopathy in patients with cirrhosis. Sixty-five patients were randomly treated with 1 g/kg per day of an amino acid mixture with 40% branched chain contents (32 patients), or isocaloric glucose (33 patients) for a maximum of 16 days. The regimens further included glucose infusion to a total of 26.5 kcal/kg per day and lactulose. The patients took part in the study for 5-6 days. In each group 17 patients woke up. In the amino acid group eleven died and four developed renal failure. In the glucose group ten died, three developed renal and two respiratory failure, and one remained encephalopathic. The coma score worsened in three of the patients who died in the amino acid group, but in all patients who died in the glucose group. The negative nitrogen balance on entry reversed in the amino acid group, but not in the glucose group. Thus, the branched chain enriched amino acid supplement did not change the prognosis for wake-up, but had other effects on the cerebral state and on nitrogen homeostasis.
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PMID:Branched chain enriched amino acid versus glucose treatment of hepatic encephalopathy. A double-blind study of 65 patients with cirrhosis. 219 6

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

Effects of differentiated diet with reduced proteins or diet without proteins with simultaneous use of lactulose or the preparation enriched with aliphatic amino acids with aminosteril-hepa chain on the clinical results and the ammonia, phenols, alpha-amino nitrogen, tyrosine, phenylalanine and tryptophan++ concentrations in the serum have been studied. It has been demonstrated that limitations of proteins in the diet or diet without proteins with the use of lactulose or amino acids mixtures above does not influence significantly the clinical amelioration or biochemical indices of encephalopathy or coma during the liver cirrhosis course. Homogenates of the liver and brain of patients who died due to encephalopathy and liver cirrhosis showed high contents of ammonia, tyrosine, phenylalanine and tryptophan++.
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PMID:[Effect of differentiated diet therapy on the clinical results and biochemical indicators in chronic hepatic encephalopathy]. 228 19

Liver cirrhosis is characterized by low plasma levels of branched chain amino acids (BCAA) and high concentrations of aromatic amino acids (AAA), and this imbalance has been implicated in the pathogenesis of hepatic encephalopathy by the synthesis of altered neurotransmitters. Contrasting results on intravenous or oral BCAA efficacy and metabolic impact have already been reported, but studies reported in the literature were never longer than a few weeks. After oral administration of BCAA and a standard diet to 28 cirrhotic patients for 1 year, no modifications in plasma concentrations of BCAA could be observed up to 3 months of therapy. Our data and an accurate analysis of the current literature lead us to propose the hypothesis that in the impaired nitrogen metabolism following cirrhosis there are neither single metabolic presentations nor many perturbations, but numerous 'subpopulations' of patients who present a homogeneous pattern of alterations that may distinguish them in terms of therapeutic approach.
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PMID:Effects of chronic oral branched-chain amino acid supplementation in a subpopulation of cirrhotics. 236 52

The authors studied gastric juice ammonia and urea nitrogen levels to determine how they are altered by gastric Campylobacter pylori (CP) infection. Patients with chronic gastritis (20), peptic ulcer (24), hepatic cirrhosis (10), chronic renal failure (13), or gastric remnant (20) were included. Endoscopic biopsy specimens stained with the Warthin-Starry stain were evaluated for the presence of CP. Blood and gastric juice analysis was performed for 11 of the patients with chronic renal failure and 37 patients from the remaining groups. CP was identified in gastric biopsies from 50 of 87 (57.5%) patients, including 87.5% with peptic ulcer and 40-50% of those with chronic gastritis, cirrhosis, chronic renal failure, or gastric remnant. CP infection had no effect on blood urea nitrogen or blood ammonia levels in any group of patients. The urea nitrogen level of gastric juice was higher in patients with chronic renal failure than in other groups but was not related to CP infection. CP infection was associated with a significant increase in gastric juice ammonia levels, both in patients with chronic renal failure (23.3 mmol/L vs. 2.90 mmol/L; [P less than 0.05]) and in other groups (5.48 mmol/L vs. 1.26 mmol/L [P less than 0.0001]). The authors conclude that elevation of gastric juice ammonia level is an indicator of gastric CP infection.
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PMID:The gastric juice urea and ammonia levels in patients with Campylobacter pylori. 237 72

Following a single oral dose of 10 mg/kg of [15N]glycine, plasma [15N]glycine kinetics and urinary 15N excretion were measured in 12 cirrhosis patients and in 6 control subjects. Cirrhosis patients were divided into two groups of 6 patients with and without a history of hepatic encephalopathy designated as group II and group I, respectively. Thirty minutes after oral administration of labeled glycine, the plasma concentration of [15N]glycine was significantly higher in both cirrhosis groups than that in the control group (P less than 0.05 and P less than 0.01). The elimination constant of plasma [15N]glycine slightly decreased in group II, but not significantly. Urinary 15N excretion did not differ among the three groups, but the rate of urinary ammonia 15N in urinary 15N was significantly increased in group II (P less than 0.05). The whole-body protein flux did not differ among the three groups, but whole-body protein breakdown was significantly increased in group II cirrhosis patients (P less than 0.05). These findings indicated that the kinetics of glycine were substantially altered in severe cirrhosis patients. Because hepatic uptake and oxidation of glycine was well maintained even in group II, increased endogenous protein breakdown seemed to be responsible for hyperglycinemia and also for the negative nitrogen balance seen in this group.
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PMID:[15N]glycine metabolism in normal and cirrhotic subjects. 238 24

A study was conducted to investigate effects of oral supplementation with branched-chain amino acids (BCAA) on protein-nutritional status in rats with liver cirrhosis. Liver cirrhosis was induced in male strain Sprague-Dawley rats by simultaneously administrating carbon tetrachloride (500 mg/kg, twice a week, intracutaneously) and phenobarbital (0.05% in drinking water, ad libitum) for 30 weeks. Following treatment with carbon tetrachloride and phenobarbital, cirrhotic rats received oral supplementation of BCAA with varying ratio among isoleucine (Ile), leucine (Leu) and valine (Val), or with varying content of total BCAA in the diet (Final content of total nitrogen was kept consistent by addition of glutamine). Nutritional efficacies of diets as described above were evaluated employing those protein-nutritional parameters as nitrogen balance and plasma levels of total protein, albumin and free neutral amino acids. Following results were obtained: 1. Compositional ratio of Ile:Leu:Val at 1:2:1.2 or at 2:1:1 was found to be more effective on diets which contained ILe:Leu:Val at 1:1:2 or either Val, Ile or Leu alone. 2. As to content of total BCAA in the diet (0, 2.5, 5, 10%), supplementation level of 2.5% was found to be most appropriate in terms of effects on nitrogen balance and on plasma protein concentration. In conclusion, 2.5% BCAA in the diet with the ratio of Ile:Leu:Val at 1:2:1.2 or 2:1:1 seems to be recommended to improve the impaired protein-nutritional status in liver cirrhosis.
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PMID:[Effects of supplementation with branched-chain amino acids on protein-nutritional status in rats treated by carbon tetrachloride]. 258 90

The liver participates in the turnover rate of free fatty acids (FFA) with a third. A severe disruption of liver function that occurs in cirrhosis leads therefore to a pathogenetic relevant hyperlipacidaemia respectively increases that. With regard to its clinical relevance a survey is given of the FFA metabolism of the liver. The factors are described which influence the FFA uptake by this organ. In this connection the metabolic fate of the FFA in dependence on the hormonal nutritive state is depicted. The author deals with the relation of the hepatic FFA metabolism to that of triglycerides, cholesterol, ketone bodies, carbohydrates, amino acids and insulin. The importance of these relatons for the caloric homeostasis and for the pathogenesis of various acute and chronic functional disturbances (ketoacidosis, negative nitrogen-balance, hyperlipoproteinaemia, hyperinsulinism, atherosclerosis) is described.
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PMID:[The metabolism of free fatty acids in the liver]. 266 56

Diet-induced thermogenesis after ingestion of a mixed meal was investigated in eight patients with documented liver cirrhosis and in eight age- and sex-matched healthy controls. Respiratory gas exchange was measured continuously for one hour in the basal state and for three hours after ingestion of a mixed liquid meal, consisting of 17% kJ protein, 28% kJ lipids and 55% kJ carbohydrates and dispensed to correspond to 60% of the individually computed energy expenditure. Arterial substrate and hormone concentrations were determined before and at timed intervals for three hours after the meal. Urine was collected for determination of nitrogen excretion. The patients' oxygen uptake, energy expenditure and respiratory quotient were similar to those of the controls in the basal state. After the meal, pulmonary oxygen uptake and energy expenditure rose markedly in both groups during the first hour and were subsequently stable. The average increase in oxygen uptake above basal during the whole study period was 21.2 +/- 1.8% and 22.3 +/- 1.2% (NS) in patients and controls, respectively. The corresponding increase in energy expenditure was 24.8 +/- 2.0% in the patients and 24.9 +/- 1.4% in the controls (NS). The respiratory quotient was elevated throughout the postprandial period in both groups but the quotient was significantly higher in the patients (P less than 0.05-0.001), suggesting a greater proportion of carbohydrate oxidation. The basal arterial concentrations of insulin and glucagon were significantly higher in the patients. After the meal the insulin level increased 10- to 20-fold in both groups. Glucose concentration rose significantly in both groups to a maximum of 8.82 +/- 1.00 and 8.03 +/- 0.95 mmol/l in patients and controls, respectively, at 60 min after the meal. This was accompanied by a fall in the levels of glycerol and ketone bodies in both groups, indicating decreased lipolysis. It is concluded that both the basal energy expenditure and the thermogenic response to a mixed meal are similar in patients with liver cirrhosis and in healthy controls. The patients' carbohydrate oxidation rose to a greater extent after the meal, probably as a consequence of excessive increases in insulin concentration, demonstrating that insulin resistance in these patients may be compensated for by postprandial hyperinsulinaemia.
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PMID:Diet-induced thermogenesis in patients with liver cirrhosis. 272 Nov 26

Soluble interleukin 2 receptors (sIL 2R) in the sera of patients with viral liver diseases were quantified with a solid-phase enzyme immunoassay using two monoclonal antibodies against the receptors. The sIL 2R levels in patients with acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma were significantly higher than those in control subjects. In acute hepatitis patients, the high levels of sIL 2R observed during the florid stage returned to normal during remission. Levels in patients with chronic active hepatitis were significantly higher than in those with chronic persistent and lobular hepatitis, and levels observed during the exacerbation phase of chronic hepatitis were higher than they were during remission. Thus, in chronic hepatitis, sIL 2R levels increased in proportion to the inflammatory activity, and correlated well with serum transaminase (glutamic oxaloacetic transaminase: SGOT, glutamic pyruvic transaminase: SGPT) activities, but not with blood urea nitrogen or creatinine concentrations. In patients with a high degree of focal and piecemeal necrosis, serum sIL 2R levels increased further during recombinant interleukin 2 therapy. In post-hepatitic liver cirrhosis and hepatocellular carcinoma, sIL 2R levels correlated with serum cholinesterase and creatinine concentrations, but not with transaminase activities. Measurement of serum sIL 2R levels in patients with liver disease but without renal injury, may help in the diagnosis of inflammation in hepatitis, a process in which interleukin 2 may participate.
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PMID:Increased serum soluble interleukin 2 receptor levels in patients with viral liver diseases. 306 11


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