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)

In the present study we have investigated and also compared the biochemical nature of the platelet phospholipids in patients with portal liver cirrhosis and in normals. Normal platelets contained 10.88 +/- 0.83 microgram of phospholipid phosphorus per 10(9) platelets whereas the cirrhosis platelets contained 7.63 +/- 1.29 microgramP/10(9) platelets. In cirrhosis there was a 29.87% decrease of phospholipids compared to normal. However the percentage distribution of phospholipids in cirrhosis was similar to normal. But each phospholipid value in cirrhosis was found lower then normal. Estimated as microgram phosphorus per 10(9) platelets decreased amounts of phosphotidyl inositol (PI) (0.29 +/- 0.16), phosphotidyl serine (PS) (0.49 +/- 0.12), phosphotidyl ethanolamine (PE) (2.0 +/- 0.43) and spingomyelin (SPH) (1.42 +/- 0.31) and phosphotidyl choline (PC) (3.25 +/- 0.62) and total lipid phosphorus (7.63 +/- 1.29) were found in the patient group.
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PMID:Platelet phospholipids in liver cirrhosis. 60 16

The effect on free plasma amino acids before and after infusion of 1 mg glucagon was studied at rest after an overnight fast in seven patients with compensated liver cirrhosis and in seven healthy controls. Total aminoacidaemia in cirrhotic patients is significantly higher than in controls. Elevated basal levels in cirrhotics are found particularly in tyrosine, citrulline, tryptophane, threonine, phenylalanine, and methionine whereas ornithine and serine levels are decreased. Save for the redox couple cystine-cysteine which increases, glucagon elicits an decrease in most amino acids that is proportionate to their initial level. Total aminoacidaemia decreases in controls and cirrhotics by 14.6 and 9.1 per cent respectively. Serum ammonia level rises significantly in both groups, urea increases only in controls, uricaemia remains virtually unchanged.
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PMID:The effect of glucagon on free plasma amino acids in cirrhotics and healthy controls. 63 37

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

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 aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.
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PMID:Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis. 289 85

Storage of alpha-1-antitrypsin (AAT) has been found in a small number of bile duct cells in liver tissue specimens from patients with Pi MZ, Pi SZ and Pi ZZ phenotypes. The storage appeared in the form of intracellular AAT immunoreactive inclusions. On EM investigation, AAT-like material was detected within cisternae of the RER and SER. Such AAT inclusions were found in proliferating bile ductules in conditions such as cirrhosis, focal nodular hyperplasia and extrahepatic obstruction. They were also observed in normal biliary structures at the level of the canals of Hering, bile ductules and interlobular ducts in 13 out of 47 cases. These findings are interpreted as indicating that the intrahepatic bile duct cells are a further source of AAT, and that in case of defective export of AAT from the cell, as is the case for the Z protein, the protein accumulates not only in hepatocytes but in biliary cells as well.
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PMID:Storage of alpha-1-antitrypsin in intrahepatic bile duct cells in alpha-1-antitrypsin deficiency (Pi Z phenotype). 298 2

A 59-year-old female was admitted to our hospital because of massive ascites and increasing jaundice, suggesting a severe decompensated state of liver cirrhosis. On the third hospital day, she was diagnosed as disseminated intravascular coagulation (DIC) from a coagulofibrinolytic study and developed renal failure. Continuous drip infusion of gabexate mesilate, a synthetic inhibitor of serine-protease, was found to be successful in managing DIC, followed by the restoration of renal function. During the clinical course, blood endotoxin, assayed by the chromogenic method, was initially 11 pg/ml and increased, in accordance with the elevation of serum FDP, to a level of 110 pg/ml when renal failure occurred. A proportional relationship was observed between changes in blood endotoxin and serum FDP throughout the course. This finding may be an important clue in studying the mechanism of DIC and non-septic endotoxemia both developing in liver cirrhosis.
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PMID:A case of liver cirrhosis complicated with endotoxemia and disseminated intravascular coagulation: a case report. 310 73

We determined by the ninhydrin method the plasma amino acid (AA) levels prior to, during and following, a 1-hour i.v. infusion of 1 U/kg body weight each of secretin and pancreozymin in patients with normal (n = 74) or reduced (n = 39) exocrine pancreatic function, as assessed by the duodenal aspiration test. The results of the two tests correlated significantly with each other (p less than 0.001). A maximum AA decrease of greater than or equal to 12% was observed in all patients with a normally functioning pancreas (specificity 100%), and of less than 12% in all patients with medium to high-grade impairment of pancreatic function (sensitivity 100%). Since, however, low-grade pancreas insufficiency (20-40% of the mean normal enzyme output) is recognized in fewer than one-half of the cases, the overall sensitivity of the AA-consumption test decreases to 69%. The results can, however, be improved by: 1) Calculating the mean percentage AA decrease with a limit value of 5% (sensitivity 90%); 2) determining individual AA with pancreas-specific absorption, such as serine (sensitivity 92%); 3) dropping the lower normal value of exocrine pancreatic function to 25% of the normal mean enzyme output (sensitivity 96%). Diseases that may be associated with the most common condition that causes pancreatic insufficiency--chronic pancreatitis--and which have an influence on AA metabolism, such as cirrhosis of the liver and diabetes mellitus, have no influence on the accuracy of the AA consumption test, which, considered overall, represents a competitive alternative to other tubeless tests of pancreatic function.
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PMID:[Amino acid level in plasma--expressed as alpha-amino-nitrogen--reaction to stimulation of the exocrine pancreas: approaches to a new pancreatic function test]. 343 Oct 32

The purpose of our study was to evaluate the effect of somatostatin (500 microgram/h intravenously) upon insulin, c-peptide, glucagon and plasma amino acids concentrations in patients with and without cirrhosis of the liver. The typical plasma amino acid pattern in cirrhosis is characterised by increased concentrations of the aromatic amino acids and decreased concentrations of the branched chain amino acids and of alanine and glycine. After administration of somatostatin insulin, c-peptide and glucagon concentrations decreased and those of the branched chain amino acids in both groups increased; in addition in patients with cirrhosis the plasma concentrations of threonine, serine, glycine, alanine, lysine, and arginine increased also. Infusion of somatostatin plus insulin in patients with cirrhosis succeeded in preventing the increase in the branched chain amino acid concentrations, while the infusion of somatostatin plus glucagon decreased threonine, serine, glycine, alinine, phenylalanine, tyrosine, lysine and arginine concentrations. It is therefore suggested that the effect of somatostatin on the plasma amino acids may be because of the reduction of insulin and glucagon concentrations; however, other effects of somatostatin cannot be excluded at present.
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PMID:Correction of altered plasma amino acid pattern in cirrhosis of the liver by somatostatin. 614 82

By means of a radioimmunoassay, which utilized [125I]-epiglycanin and anti-epiglycanin antiserum induced in rabbits by injections of viable TA3-Ha ascites cells with Freund's complete adjuvant, picogram quantities of epiglycanin could be detected. Anti-epiglycanin antiserum was similarly produced in allogeneic mice. Unlabeled epiglycanin lost the capacity to compete with [125I]epiglycanin in the radioimmunoassay as a result of periodate oxidation or incubation with endo-alpha-N-acetyl-D-galactosaminidase (Diplococcus pneumoniae), an enzyme found to cleave only the disaccharide beta-D-galactopyranosyl-(1----3)-2-acetamido-2-deoxy-D-galactose chain from serine or threonine residues in epiglycanin. Glycosylhydrolases known to cleave alpha-D-mannose, beta-D-galactose (1,4-linked), beta-N-acetyl-D-glucosamine, and alpha-N-acetyl-D-galactosamine did not reduce the activity of epiglycanin. Neuraminidase enhanced the activity twofold to fivefold. The finding that little or no activity was demonstrated by the disaccharide, the reduced disaccharide, or other glycoproteins containing the same disaccharide chain suggested that the antigenic determinant probably involved the disaccharide and a unique amino acid sequence at the site of its attachment. By means of the radioimmunoassay epiglycanin cross-reactive antigens were detected in the peritoneal or pleural fluid and in the sera of patients with metastatic cancer. Lower concentrations of epiglycanin-like antigen(s) were found in the peritoneal fluid of patients with hepatitis or liver cirrhosis but not in normal serum.
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PMID:Antibody to epiglycanin and radioimmunoassay to detect epiglycanin-related glycoproteins in body fluids of cancer patients. 620 3


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