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)

Ammonia concentrations were measured in 152 plasma samples taken from patients with liver cirrhosis or from intensive care patients. For each sample, a new reflectometric procedure (AC-System) as well as the enzymatic method (Monotest) were used. There was a high and significant correlation between the values obtained with the two methods (r = 0.98, p less than or equal to 0.001). Ammonia determination by means of the reflectometric procedure can also be done in whole blood.
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PMID:[A new micromethod for the determination of ammonia concentrations in whole blood and plasma]. 667 19

A controlled study was carried out in two groups of 20 patients with cirrhosis of the liver and deep coma in order to compare the efficacy of intravenous branched-chain amino acid solutions in 20% glucose (group A) vs lactulose plus glucose in isocaloric amount (group B). There were 3 drop-outs from each group. Plasma amino acids and ammonia were assayed at fixed intervals throughout the 10-day observation period. Routine tests were assayed daily. Complete mental recovery was obtained in 70% of patients in group A and in 47% in group B. The difference was not significant, likely due to the lack of placebo group. With the exception of free tryptophan/all competing amino acids ratio, the modifications in plasma amino acid levels showed no correlation with the clinical course under either treatment. Ammonia, like free tryptophan, decreased significantly upon mental recovery, paralleling the clinical course throughout the study. In conclusion, branched-chain amino acids are at least as effective as lactulose in deep hepatic coma. It is suggested that branched-chain amino acids may reverse coma either by competing with brain entry of the aromatic amino acid or by metabolically decreasing free tryptophan and ammonia.
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PMID:Branched-chain amino acids vs lactulose in the treatment of hepatic coma: a controlled study. 674 58

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

[13N]Ammonia produced by the cyclotron was instilled intrarectally in patients with cirrhosis and other liver diseases to study the turnover of rectally absorbed [13N]ammonia. A positron camera connected to an on-line computer system was used for the measurement of sequential changes of 13N activity in blood and for coincidence positron imaging of the liver and heart. 13N activity over the head was also recorded. Chromatographic analysis of 13N-labeled substances in blood was carried out using a Dowex 50Wx8 column at varying times after the administration. In the control, [13N]ammonia was absorbed quickly and visualized the liver, whereas in patients with cirrhosis, the lungs and heart were first visualized, and 13N activity over the head was also higher. It was suggested that a large proportion of absorbed [13N]ammonia bypassed hepatocytes and reached peripheral tissues in cirrhosis. The heart/liver ratio of 13N and 13N over the head were correlated with various indices of portal hypertension. The relative proportion of nonammonia 13N metabolites in blood was lower at 5 and 15 min after administration in cirrhosis, suggesting a reduced capacity of the liver to remove and metabolize ammonia.
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PMID:A dynamic study of rectally absorbed ammonia in liver cirrhosis using [13N]ammonia and a positron camera. 743 57

Lactitol, a non-absorbable synthetic disaccharide, was administered at a dose of 36g/day for 3-4 weeks to 8 patients with liver cirrhosis and hepatic encephalopathy in order to investigate its effects on fecal bacterial flora and clinical symptoms of hepatic encephalopathy. Lactitol significantly increased occupation ratio (ratio to total bacterial number) of anaerobic Bifidobacterium (before administration 7.1% --> after 4 weeks 46.0% (p < 0.05) as well as bacterial count of Lactobacillus. On the other hand, bacterial counts of Bacteroides and Clostridium, which are considered to be NH3-producing bacteria, and that of total aerobic bacteria were not markedly changed, but their occupation ratio were decreased after the administration. Further, tendencies toward decreased fecal pH, increased frequency of defecation and soft stools were observed. As for clinical efficacy, a decrease in blood ammonia concentration, improvement in mental state and flapping tremor were also observed.
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PMID:[Effects of lactitol on fecal bacterial flora in patients with liver cirrhosis and hepatic encephalopathy]. 764 58

Urease is an enzyme found in plants and bacteria, but not mammals. It catalyzes the conversion of urea to carbon dioxide and ammonia. Ammonia shortens the life span of cells; and higher concentrations cause tissue necrosis and cytolysis. Twenty percent of total body urea is converted to ammonia by bacterial urease in the colon. Small injections of urease immunize animals by producing antiurease, a gamma globulin, which inactivates urease. Immunization eliminates the colonic conversion of urea to ammonia. Injection of urease produces ammonia intoxication making immunization hazardous. Although previously impossible, a non enzymatic urease antigen was synthesized by covalently bonding jack bean urease with glutaraldehyde. This antigen stimulated the production of antiurease that inactivates native urease. Helicobacter pylori, a potent urease producer, has been implicated in peptic ulcer, gastritis and other inflammatory bowel lesions. The pathogenicity of H pylori is dependent on its urease production. Immunization to urease can render H pylori non pathogenic. Cirrhotics develop encephalopathy and hyperammonemia because their livers fail to convert all the ammonia in portal venous blood to urea and collaterals develop by passing the liver. Colonic ammonia increases the turnover rate of colonic mucosa. Ammonia absorbed into the portal venous system is transported to the liver where it is reconverted to urea. Absorbed ammonia adversely influences liver function. Infections with urease producing organisms destroy the renal parenchyma and produce struvite stones. Urease immunization aids colonic healing and prevents uremic colitis. Absorbed ammonia is a noxious influence on the liver. Animals immunized to urease regenerate the liver faster and are less susceptible to hepatotoxins. Immunization to urease ameliorates cirrhosis. Proteus and other urease producers become non toxic and do not damage the renal parenchyma. Urease is responsible for the pathogenicity of infections with urease producing organisms. Immunization to urease renders urease producing organisms non pathogenic.
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PMID:Awakenings to the pathogenicity of urease and the requirement for continuous long term therapy. 799 80

Over the 1st postoperative yr, distal splenorenal shunt (DSRS) in cirrhotic patients is followed by a reduction in portal perfusion resulting from a spontaneous opening of portal-systemic collaterals. This can influence plasma levels of insulin and glucagon. Fasting plasma glucose, insulin, C-peptide, and glucagon and their 5-h responses to a protein meal (which directly stimulates the hormone secretions) were measured before and 3 and 12 mo after DSRS in 10 cirrhotic patients. Hormone effectiveness and pancreatic alpha- and beta-cell sensitivities to ammonia (NH3), amino acids, and glucose were also calculated. Liver function and portal vein diameter were assessed before each study. Seven cirrhotic patients treated with injection sclerotherapy of esophageal varices served as a control group. Liver function did not deteriorate in either patient group. An increase in fasting glucagon (from 181 +/- 22 to 242 +/- 22 and 255 +/- 22 pg/ml, p = 0.02) and NH3 (from 57 +/- 8 to 84 +/- 11 and 97 +/- 14 micrograms/dl, p = 0.04) and a decrease in glucagon effectiveness (from 0.56 +/- 0.06 to 0.39 +/- 0.05 and 0.035 +/- 0.03, p = 0.047) and portal vein diameter (from 16.0 +/- 1.1 to 11.3 +/- 0.8 and 9.4 +/- 0.6 mm, p < 0.001) was found only in DSRS patients. The elevation in glucagon was correlated with that of NH3 at 3 mo (r = 0.83, p = 0.003) and with the reduction of portal vein diameter at 1 yr (r = -0.81, p = 0.005). In cirrhosis, DSRS does not influence insulin secretion or its plasma level and effectiveness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distal splenorenal shunt and insulin secretion, plasma glucagon, and glucose homeostasis in cirrhosis. 848 25

Liver cirrhosis is associated with malnutrition in 10 to 90% of cases, following different authors. This prompted us to compare our previous studies with recent literature data in order to review this topic from a practical standpoint. Several pathophysiological factors are blamed for this state and mainly protein and lipid-restricted diets from among these. Some lean and fat body mass indices predictive of malnutrition are proposed taking into account the influence of liver disease in their evaluation. Nitrogen balance derangements and liposoluble vitamins and carotenoids plasma decrease are highlighted as sensitive nutritional parameters. After a brief review of amino acid, glucose and lipid metabolic derangements, some nutritional guidelines are provided by distinguishing oral selective supports from the parenteral nutrition. The latter, being reserved to moderate-severe encephalopathy or to hemorrhagic conditions, is proposed following an algorithm which takes into account different nutritional principles as a function of the severity of the clinical condition. During the first period (24-48 hrs) parenteral fluids, electrolytes, dextrose and whole blood or derivatives (when necessary) are provided; lactulose or lactitol via nasogastric tube, or by enema, are started as well. During the following 48-72 hrs branched-chain amino acids alone or enriched solutions are added taking into account an optimum calorie/nitrogen ratio. Finally, vegetable lipids, vitamins and oligoelements can be added if intravenous nutrition must be maintained, with a view of warranting the most complete nutritional approach to these severely malnourished patients.
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PMID:[Nutrition and malnutrition in hepatic cirrhosis]. 851 55

Hepatic encephalopathy (HE) is associated with elevated arterial ammonia levels. The relationship is variable, in part due to ammonia methodology. One method, based on the indophenol reaction (IPh), is interfered with a number of amino acids including all aromatic amino acids. We have determined arterial ammonia simultaneously with the Blood Ammonia Checker II (BAC) as reference method and with the IPh method. The difference BAC-IPh, mumol/l, was assumed to express the interference in the indophenol method (IFI) by amino acids. It may be positive or negative. The aim was to establish the value of BAC in comparison with IPh in the diagnosis of liver disease and overt HE and to assess any added value of IFI. Of two reference groups without disturbances, A (n = 39) had not and B (n = 13) had encephalopathy. Group C consisted of 125 liver patients (34 no cirrhosis, 91 cirrhosis) of which 55 had no manifest HE (C:HE-) and 70 had HE (C:HE+). Median BAC ammonia nitrogen (NH3-N), mumol/l: A 21, B 35, C 80, C:HE - 57 and C:HE+ 98 (A < B < C and A < B < C:HE - < C:HE +, P < 0.001). Median IPh NH3-N, mumol/l: A 27, B 30, C 30, C:HE - 25 and C:HE + 35 mumol/l (A = B = C and C:HE - < C:HE+, P < 0.01). IFI medians: A -6, B 3, C 40, C:HE - 29 and C:HE + 58 mumol/l (A < B (P < 0.05) < C (P < 0.0001); A, B < C:HE - and C:HE+; C:HE- < C:HE + (all P < 0.0001)). While BAC correlated weakly with IPh in the (sub)groups C, C:HE-, C:HE+ (r = 0.3, 0.3, 0.4, P < 0.05), it correlated strongly with IFI (r = 0.9, 0.9, 0.8, P < 0.0001). There was no correlation between IPh and IFI. BAC, as well as IFI, could discriminate all liver patients (C) from both reference groups A and B with 100% positive likelihoods. BAC, IPh and IFI could discriminate between HE- and HE+. To differentiate cirrhosis from non-cirrhosis the specificity of IPh was uniformly high and the sensitivity satisfactory, whereas BAC had a high sensitivity but an insufficient specificity. In conclusion, in blood, BAC is the ammonia determination of choice. It differentiates between reference groups (encephalopathic or not) and liver disease and the more so HE. The combination of BAC and IPh (indicating IFI) may eventually be shown useful to rapidly assess the severity of underlying liver disease in HE patients. In other biological fluids, IPh is excellent when the inhibiting influence of non-protein nitrogen substances is absent or can be eliminated.
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PMID:Arterial ammonia with Blood Ammonia Checker II and with indophenol reaction to assess presence of hepatic encephalopathy. 881 63

In hepatocellular carcinoma (HCC), autoantibodies to intracellular antigens are detected in 30-40% of patients. Patients with chronic hepatitis or liver cirrhosis develop HCC, and when this occurs, some patients exhibit autoantibodies of new specificities. It has been suggested that these novel autoantibody responses may be immune system reactions to proteins involved in transformation-associated cellular events. One HCC serum shown to contain antibodies to unidentified cellular antigens was used to immunoscreen a cDNA expression library, and a full length cDNA clone was isolated with an open reading frame encoding 556 amino acids with a predicted molecular mass of 62 kD. The 62-kD protein contained two types of RNA-binding motifs, the consensus sequence RNA-binding domain (CS-RBD) and four hnRNP K homology (KH) domains. This protein, provisionally called p62, has close identity (66-70%) to three other proteins at the amino acid sequence level, and all four proteins may belong to a family having CS-RBD in the NH2-terminal region and four KH domains in the mid-to-COOH- terminal region. The homologous proteins are: KH domain-containing protein overexpressed in cancer (Koc); zipcode binding protein, a protein which binds to a conserved nucleotide element in chicken beta-actin mRNA (ZBP1); and a protein which binds to a promoter cis element in Xenopus laevis TFIIIA gene (B3). p62 protein is cytoplasmic in location, and autoantibodies were found in 21% of a cohort of HCC patients. Patients with chronic hepatitis and liver cirrhosis, conditions which are frequent precursors to HCC, were negative for these autoantibodies, suggesting that the immune response might be related to cellular events leading to transformation. However, the possible involvement of p62 autoantigen as a factor in the transformation process remains to be elucidated.
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PMID:A novel cytoplasmic protein with RNA-binding motifs is an autoantigen in human hepatocellular carcinoma. 1019 Sep 1


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