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)

Whether the plasma concentration of beta endorphin was increased in hepatic cirrhosis like that of smaller opioid peptides methionine enkephalin and leucine enkephalin was determined. Its concentration in chronic renal failure was also measured. Plasma beta endorphin was not significantly raised in cirrhotic patients with or without ascites (medians 5.2 pmol/l and 4.7 pmol/l respectively) compared with disease control subjects (4.9 pmol/l) and healthy control subjects (4.9 pmol/l). In contrast, the peptide was increased 2.5 fold (p less than 0.001) in chronic renal failure (12.4 pmol/l) and was found in many of these patients' urine. The data are compatible with the hypothesis that the liver may play an important role in the elimination of opioid peptides of octapeptide size or less but not the larger peptides such as beta endorphin.
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PMID:Plasma beta endorphin in cirrhosis and renal failure. 201 26

Plasma amino acid and venous blood ammonia concentrations were measured in six patients with well-compensated cirrhosis and in six healthy volunteers, both in the fasting state and serially for 5 h following ingestion of 30 g mixed protein and 30 g amino acid mixture, administered on separate occasions. Mean fasting plasma concentrations of threonine, serine, proline, glycine, and of the three branched-chain amino acids, valine, isoleucine and leucine, were significantly reduced in the cirrhotic patients compared with the control subjects, while mean (+/- 1 s.d.) fasting venous blood ammonia concentrations were comparable 71.2 +/- 31.4 cf. 56.0 +/- 25.4 mumol/L. Following the oral protein and amino acid loads, increases were observed in plasma amino acid concentrations in the majority of subjects with a return to baseline values by the end of the study. Changes in the circulating concentrations of most amino acids were independent of their concentration in the oral protein and amino acid loads, and their relative distribution in the circulation varied over time. The increases in the concentrations of the three branched-chain amino acids did, however, reflect their concentrations in the two nitrogen loads and did remain constant, relative to one another, over time. There were wide intra- and inter-individual variations in plasma amino acid concentrations following protein and amino acid ingestion in both study groups, and in general no significant differences in responses were observed between them. Similarly, no significant inter-group differences were observed in the ammonia response to the two nitrogen loads. No fundamental differences exist in the ways in which patients with well-compensated cirrhosis handle oral protein or amino acid loads of the magnitude employed in the present study.
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PMID:Amino acid tolerance in cirrhotic patients following oral protein and amino acid loads. 210 85

1. We investigated arteriovenous exchanges of tyrosine and 3-methylhistidine across leg tissue in the postabsorptive state as specific indices of net protein balance and myofibrillar protein breakdown, respectively, in eight patients with cirrhosis and in 11 healthy control subjects. Whole-body protein turnover was also measured using L-[1-13C]leucine. 2. Leg efflux of tyrosine was 45% greater in cirrhotic patients than in normal control subjects [-6.5(1.4 to -19.1) vs -4.2(-2.2 to -7.7) mumol min-1 100 mg-1 of leg, median (range), P less than 0.025]. 3-Methylhistidine efflux was not significantly altered. 3. In cirrhosis, whole-body leucine flux was normal but whole-body leucine oxidation was elevated so that whole-body protein synthesis was depressed by 17%. 4. The results indicate the predominant mechanism of muscle wasting in cirrhosis to be a fall in muscle protein synthesis, which is accompanied by an overall fall in whole-body protein turnover.
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PMID:Skeletal muscle and whole-body protein turnover in cirrhosis. 216 95

This study was conducted to determine whether an amino acid solution enriched with branched-chain amino acids altered protein catabolic rates and plasma ammonia in patients with cirrhosis. Nine stable subjects were given two peripheral intravenous infusions: a standard amino acid solution (solution A) and a branched-chain-enriched solution containing 97% more leucine (solution B). Each solution was given for separate 9-day (group 1, n = 6) or 3-day (group 2, n = 3) periods. Amino acid solutions delivered 0.7 gm protein.kg-1.day-1. Diets provided an additional 0.3 gm protein plus maintenance calories. Protein turnover was assessed by a primed continuous infusion of [1-14C] leucine in six patients (three patients in group 1 and three patients in group 2). Nitrogen balance and urinary 3-methyl histidine excretion were determined in group 1 patients. Compared with solution A, solution B increased leucine flux and leucine oxidation but had no significant effect on protein synthesis or catabolism based on the plasma specific activity of either leucine or alpha-ketoisocaproic acid. The additional leucine infused with solution B was quantitatively oxidized. Nitrogen balance did not differ with the two solutions and there was also no difference in the urinary excretion of 3-methyl histidine, suggesting that muscle protein catabolism was unchanged. Plasma ammonia concentration decreased significantly during the infusion of solution B and was associated with a slight fall in plasma glucagon concentration. The results indicated that a branched-chain-enriched amino acid solution did not alter protein synthesis or catabolism although it did lower the plasma ammonia when compared with a standard amino acid formula in stable cirrhotic patients.
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PMID:Effects of branched-chain amino acids on nitrogen metabolism in patients with cirrhosis. 219 23

Free amino acid (AA) concentrations in plasma and quadriceps femoris muscle were determined in 19 healthy volunteers and in 16 patients with hepatic cirrhosis and portal hypertension. Nutritional state was impaired as judged by overt muscle wasting (9/16), triceps skinfold thickness less than 70% of normal in 8/14 (57%), and creatinine-height index below 70% in 5/12 (42%). In the plasma of patients the typical amino acid pattern of cirrhosis was to be observed: Elevation of tyrosine and methionine (p less than 0.01), uniform reduction of branched chain amino acids (p less than 0.001) resulting in a decreased molar ratio of BCAA/AAA from 2.85 +/- 0.05 in normal individuals to 1.35 +/- 0.12 in cirrhotics (p less than 0.001). Levels of the gluconeogenic AA glutamine, glutamate, aspartate, alanine, glycine, threonine, serine and lysine were lowered (p less than 0.05). In muscle of cirrhotics, intracellular AA concentrations exhibited a similar pattern with two major exceptions: Tyrosine and phenylalanine were augmented (p less than 0.001). Surprisingly, BCAA levels were altered heterogeneously; those of gluconeogenic BCAA decreased: Valine from 0.34 +/- 0.03 to 0.20 +/- 0.03 mmol/l (p less than 0.001), isoleucine 0.09 +/- 0.01 to 0.05 +/- 0.02 mmol/l. However, the concentration of ketogenic leucine remained unaltered in muscle. Nevertheless, the molar ratio of BCAA/AAA was considerably reduced from 3.70 +/- 0.04 to 0.81 +/- 0.08 (p less than 0.001). Most of the gluconeogenic AA exhibited reduced intramuscular concentrations, but glutamine levels were normal. The pattern of plasma and muscle free AA in hepatic cirrhosis is thus characterized by accumulation of aromatic AA and by depletion of gluconeogenic AA, especially BCAA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characteristic pattern of free amino acids in plasma and skeletal muscle in stable hepatic cirrhosis. 231 39

The functional and phenotypic characteristics of carcinomatous pleural or peritoneal lymphoid cells cultivated with either rIL 2 or TCGF have been investigated. The cultivation of the lymphoid cells with cytokines was initiated by a mixture of coexisting, viable carcinoma cells for 14 days. Results have indicated that cytokine-activated lymphoid cells from malignant pleural and peritoneal effusions showed considerable cytolytic activity against K562 and Daudi cells. The cell population responsible for LAK and/or CTL effector cells of TCGF-activated lymphoid cells were CD8+ CD11- cells. Further, in rIL 2-expanded cultures from pleural and peritoneal lymphoid cells, the CD4+ Leu 8- population was found to contain effector cells of cytotoxic activity against the tumor cells. It further was seen that the TCGF-activated CD8+ CD11- T cells possessed a more potent killing activity, in comparison to the rIL 2-activated CD4+ Leu8- T cells. However, rIL 2-activated lymphoid cells from ascites in liver cirrhosis (used for a control) showed a higher tumoricidal activity.
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PMID:[In vitro induction of cytotoxic activity against carcinomatous pleural or peritoneal lymphoid cells cultivated with cytokines, and an immunological phenotypic analysis of the effector cells]. 232 66

In the present study, the first case of ruptured hepatoma followed by disseminated intravascular coagulation is reported. An elastase-like enzyme which possessed elastolytic and caseinolytic activities was confirmed from patient plasma. On the other hand, no elastase activity was detected in the plasma of patients with hepatitis, liver cirrhosis or hepatoma without disseminated intravascular coagulation. The patient plasma did not possess H-D-Val-Leu-Lys-p-nitroanilide hydrochloride, succinyl-L-alanyl-L-alanyl-p-nitroanilide, and pyro-Glu-Pro-Val-p-nitroanilide amidolytic activities. However, when chromatographed on Sephadex G-200, the presence of low-molecular weight plasminogen was confirmed. Its molecular weight was approximately 52,000. A slight decrease of alpha 2-plasmin inhibitor was noted, but no decrease of alpha 2-macroglobulin was detected.
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PMID:A case of ruptured hepatoma followed by elastase-induced disseminated intravascular coagulation. 241 97

A human B cell subpopulation identifiable by the expression of the cell surface antigen Leu-1(CD5) was examined in peripheral blood lymphocytes obtained from patients with various liver diseases by dual two-color fluorescence flow cytometry. A significantly high level of Leu-1 B cells in chronic hepatitis and in liver cirrhosis especially in hepatitis B surface antigen (HBsAg)-positive patients (hepatitis B virus carriers) was observed. However, there was no significant difference between the percentage in controls and those in patients with acute hepatitis and primary biliary cirrhosis. Moreover, we could not demonstrate a correlation between the incidence of these cells and positive IgM class rheumatoid factor in patients with liver diseases. The percentage of Leu-1 B cells in patients who had been receiving prednisolone at the time of this study was lower than that in healthy controls. These results suggested that Leu-1 B cells might be associated with the continuation of the HBsAg-positive state and that the presence of the Leu-1 B cell population might be modified by prednisolone administration.
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PMID:Leu-1(CD5) B cell subpopulation in patients with various liver diseases--special reference to hepatitis B virus carrier and to changes caused by prednisolone therapy. 246 4

Plasma methionine enkephalin is increased in liver disease and may contribute to some of the clinical manifestations of hepatic failure. To determine if another 'small' opioid peptide is increased in the plasma of patients with liver disease, leucine enkephalin was measured by radioimmunoassay. Its plasma concentration was raised approximately five-fold in patients with acute liver disease (median 1490 pmol/l, range 830-2420) and three-fold in patients with cirrhosis with ascites (960 pmol/l, 470-2900), compared with disease controls (325 pmol/l, 180-740) and healthy controls (305 pmol/l, 180-560). The increase in plasma leucine enkephalin was proportional to the degree of liver damage, as judged in the patients with acute liver disease by its correlation with the prothrombin time (r = 0.691, p less than 0.01) and alanine aminotransferase (r = 0.502, p less than 0.05), and in the patients with cirrhosis by its negative correlation with the plasma albumin (r = -0.743, p less than 0.001). It is unclear whether the raised plasma leucine enkephalin in liver disease is a consequence of diminished hepatic inactivation, increased secretion from sympathetic nerves and adrenal glands, or both.
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PMID:Plasma leucine enkephalin is increased in liver disease. 258 65

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


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