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)

Following a longitudinal study of chronic non-A, non-B hepatitis in Italy and Spain, we evaluated the epidemiologic and clinical features of chronic hepatitis C in 77 consecutively observed children (35 male; mean age, 4 years) without underlying systemic diseases. All subjects were positive for antibody to hepatitis C virus in serum by second-generation tests. Forty-six patients had received blood transfusions in the perinatal period; 12 had a mother with antibodies to HCV in serum (five of these mothers were drug users or partners of a drug user); seven had a history of putative percutaneous exposure; and 12 had not been exposed to any risk factors for viral hepatitis. At presentation, only 22% were symptomatic, mean alanine-aminotransferase levels were three times the upper normal value, and liver histology showed active disease in only nine of 28 cases (32%). During a mean observation period of 6 years, only 11 of 57 patients (19%) complained of symptoms and 11 of 40 cases (27%) had histologic features of active hepatitis. Two patients had severe hepatitis with associated cirrhosis. However, only six of 57 cases (10%) achieved sustained biochemical remission. The clinical features and the outcome were similar in both the posttransfusion and the community-acquired cases. These results indicate that transfusions in the perinatal period are the single most important cause of hepatitis C in otherwise healthy children. Community-acquired cases represent an heterogeneous epidemiologic group in which maternal transmission, whether perinatal or postnatal, could be relevant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Posttransfusion and community-acquired hepatitis C in childhood. 1074 29

The impact of hepatic and renal failure on the metabolism of L-alanyl-L-glutamine (Ala-Gln) and glycyl-L-glutamine (Gly-Gln) was investigated in 11 healthy volunteers, five patients with liver cirrhosis, and six patients with chronic renal failure. The clearance (mL.kg-1.min-1) of Ala-Gln was significantly higher than that of Gly-Gln in all three groups. Renal failure significantly reduced clearances of both Ala-Gln and Gly-Gln (13.27 +/- 0.71 and 3.06 +/- 0.28) when compared with control values (21.68 +/- 1.21 and 7.08 +/- 0.38). Liver failure had no significant influence on the clearances of Ala-Gln and Gly-Gln (22.62 +/- 2.89 and 6.20 +/- 0.88). Liver failure delayed and renal failure almost abolished the increases in plasma concentrations of free amino acid residues after peptide injection. It is concluded that other organs can substitute for the peptide-clearing function of the liver, but not of the kidney. Kidney is the most important organ for the clearance of dipeptides and the release of amino acid residues into circulation. Our data show that clearance rates of both Ala-Gln and Gly-Gln are sufficient to avoid accumulation of either peptide if infused in the presently recommended doses. Both Ala-Gln and Gly-Gln could therefore be used as sources for glutamine in parenteral nutrition even in patients with chronic renal failure.
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PMID:Importance of liver and kidney for the utilization of glutamine-containing dipeptides in man. 808 85

The aim of the study was to evaluate the effect of ursodeoxycholic acid (UDCA) oral administration on alanine aminotransferases (ALT) levels in cirrhotic patients with chronic hypertransaminasemia. Ninety consecutive patients with histologically proven liver cirrhosis and ALT levels higher than twice the upper limit of normal for at least six months, were admitted to the study. All the patients were treated with UDCA 10 mg/kg/day for one year. At the end of this period they were randomized to placebo or to continue UDCA therapy for three further months. ALT levels were evaluated before the beginning of UDCA therapy, at twelve and fifteen months by standard methods. After 12 months of UDCA, ALT decreased significantly (-39 UI, 95% confidence intervals -27 to -52 UI). At the 15 th month ALT did not vary with respect to its values at the 12th month in 36 patients randomized to continue UDCA, while it increased significantly in patients taking the placebo (+11 UI 95% confidence intervals +2 to +19). The results of this study suggest that UDCA is effective in controlling the biochemical activity of the liver disease in cirrhotic patients.
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PMID:[The effect of ursodeoxycholic acid in patients with liver cirrhosis and chronic hypertransaminasemia]. 820 3

A three compartment mathematical model was used to analyse the urea response to an alanine infusion in six control subjects, and in 15 patients with liver cirrhosis and variable degree of hepatocellular failure. Model-derived coefficients were used to calculate two parameters (Ymax and Tmax), able to describe the theoretical response of the conversion of amino acid derived nitrogen into urea, in response to a unit impulse in alanine concentration. They correspond to the maximum rate of conversion of nitrogen from an intermediary pool into urea and to the time delay between the impulse and Ymax, respectively. In cirrhosis, the apparent volume of distribution of infused alanine was smaller than in controls, while the conversion of alanine nitrogen into an intermediary pool of nitrogen and finally into urea nitrogen were both reduced. Also Ymax was reduced by 50% in cirrhosis, whereas Tmax was increased by 50%, and both significantly correlated with galactose elimination capacity (GEC; R2 = 0.706 and R2 = 0.505, respectively) and with antipyrine clearance (Ap Cl; R2 = 0.823 and R2 = 0.576, respectively). Model-derived assessment of urea appearance in response to alanine infusion is able to quantify the functional liver cell mass, and may prove useful for the study of nitrogen metabolism in cirrhosis, mainly in relation to encephalopathy.
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PMID:Model-derived assessment of urea appearance in response to alanine infusion: a quantitative measure of liver function in cirrhosis. 828 Aug 43

Energy metabolism was studied in fed and fasted rats with carbon tetrachloride (CCl4)-induced cirrhosis. In situ liver perfusion experiments were performed under basal conditions (no substrate added to the perfusate) and after stimulation with glucagon (2 nM) and L-alanine (20 mM). Under basal conditions, oxygen consumption per gram of liver was reduced in cirrhotic rats irrespective of the metabolic state. After addition of glucagon/L-alanine to the perfusate, oxygen consumption increased significantly in fed and fasted control and cirrhotic rats. Under basal conditions, glucose production was reduced by 76% in cirrhotic rats, averaging 0.75 +/- 0.19 vs. 0.18 +/- 0.15 mumol.g liver-1.min-1 in control and cirrhotic livers, respectively (means +/- S.E.M., P < 0.05). After addition of glucagon/L-alanine to the perfusate, glucose production increased in both groups and was reduced by 65% in fed cirrhotic as compared with fed control rats, averaging 3.63 +/- 0.27 vs. 1.27 +/- 0.17 mumol.g liver-1.min-1 in control and cirrhotic rats, respectively (P < 0.05). Stimulated glucose production was linearly correlated with the fractional aminopyrine elimination rate constant (ABT-k), a measure of hepatic function in vivo. After 12 h of fasting, stimulated glucose production was decreased by 15% in control and by 65% in fed cirrhotic rats compared with the fed state, averaging 3.07 +/- 0.22 vs. 0.33 +/- 0.03 mumol.g liver-1.min-1 in control and cirrhotic rats, respectively (P < 0.05). After 24 h of starvation, glucose production was not significantly different between control and cirrhotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased hepatic glucose production in rats with carbon tetrachloride-induced cirrhosis. 830 Oct 44

The absolute and relative concentrations of 16 plasma amino acids in 48 mostly dystrophic infants and children (median of age 1 1/2 years) with extrahepatic biliary atresia and mainly stable preterminal cirrhosis were compared with those of controls. Patient plasma amino acid data were analysed statistically for diagnostic usefulness and correlated with standard biochemical quantities of liver function and of liver perfusion. In the patients the total amounts of non-essential and essential amino acids were reduced by 19% and with the same significance (p < 0.0005). Plasma tyrosine was increased (+40%), while taurine (-44%) and branched chain amino acids (+28.8% to -34.7%) were decreased. Methionine values varied widely. In the molar fractional plasma amino acid profile, only alanine, valine, and leucine were decreased, while threonine, methionine, tyrosine, phenylalanine, ornithine, and serine were increased. Discriminate function analysis showed that the plasma amino acid data discriminated 93.8% of the patients from controls. The concentrations of some amino acids in plasma seemed to have been influenced by protein-calorie deficiency in the patients. The valine/tyrosine ratio and the Fischer index (ratio branched chain/aromatic amino acids) were significantly reduced in the patients versus controls (1.54 +/- 0.55 vs 3.08 +/- 0.55 and 1.66 +/- 0.39 vs 3.00 +/- 0.48). A number of significant correlations (range of r: 0.37-0.59, p < 0.05, 30-48 data pairs) were calculated between plasma amino acid data and several standard biochemical quantities of liver function. The statistical analyses also showed that the Fischer index began to decrease gradually and linearly early in the progression of liver failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The plasma amino acid profile and its relationships to standard quantities of liver function in infants and children with extrahepatic biliary atresia and preterminal liver cirrhosis. 831 65

Glucagon exerts an up-regulatory effect on hepatic nitrogen metabolism in healthy subjects, but its potential role in the presence of liver failure is uncertain. The effects of glucagon on urea synthesis and hepatic nitrogen clearance during alanine infusion were studied in five control subjects and six cirrhotic patients in paired experiments at spontaneous glucagon concentrations and at high physiological glucagon levels (approximately 300 to 500 pmol.L-1) induced by a 7.5-hr continuous glucagon infusion. In all experiments the urea nitrogen synthesis rate increased linearly with increasing alpha-amino-nitrogen concentrations. At spontaneous glucagon concentrations the dynamics of alpha-amino nitrogen to urea nitrogen conversion (functional hepatic nitrogen clearance) were significantly reduced in cirrhosis (23.2 +/- 6.7 L.hr-1 vs. 35.3 +/- 8.0 L.hr-1, p < 0.05) in relation to decreased liver function. Glucagon superinfusion caused a 63% increase in the dynamics of the process in controls (57.7 +/- 11.0 L.hr-1; p vs. spontaneous glucagon, p < 0.01), whereas in cirrhosis it increased on average by only 15% (26.7 +/- 10.7; p = NS). The glucagon-induced change in functional hepatic nitrogen clearance significantly correlated with galactose elimination capacity and antipyrine clearance (r = 0.905 and 0.964, respectively). Glucagon, in high physiological concentrations achieved with glucagon infusion, does not produce significant effects on hepatic nitrogen metabolism in cirrhosis. The reduced sensitivity of the cirrhotic liver to glucagon seems to be dependent on decreased hepatocellular function. These data do not support the role of glucagon as a "catabolic" hormone in cirrhosis.
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PMID:Unresponsiveness of hepatic nitrogen metabolism to glucagon infusion in patients with cirrhosis: dependence on liver cell failure. 832 18

Hepatitis C virus (HCV) is responsible for most cases of chronic non-A, non-B hepatitis in multi-transfused children, but has been also implicated in at least one third of cases without history of parenteral exposure. We have recently evaluated the natural history of chronic hepatitis C in 37 children without underlying systemic diseases. None of the patients had a history of acute hepatitis and only 22 were symptomatic at presentation. Liver histology was consistent with active liver disease of mild to moderate activity in 42% of cases (one child had cirrhosis) and with persistent or lobular hepatitis in the remaining cases. During a mean follow-up period of 3.4 +/- 3.2 years symptoms were rarely observed and none of the patients developed liver failure, but 97% maintained abnormal alanine-aminotransferase levels. These results suggest that chronic hepatitis C in children, at least in its early stage, is a mild disease infrequently associated with severe liver lesions; however the persistence of liver damage over the years raises questions about the long-term outcome of the illness and about the rationale of antiviral therapy.
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PMID:Hepatitis C in childhood: epidemiological and clinical aspects. 837 55

Among 211 patients who, between 1985 and 1990, underwent liver resection in Kyushu University Hospital, uncontrollable ascites occurred in 53 (25%). A univariate analysis revealed that postoperative death with liver failure occurred more frequently in patients with intractable ascites (p < 0.05). Alanine amino transferase levels were significantly higher in patients with intractable ascites (p < 0.05), but serum bilirubin, alkaline phosphatase and serum albumin levels did not differ significantly. Portal pressure (p < 0.05), the operation time (p < 0.01) and blood loss (p < 0.01) were significantly higher in patients with intractable postoperative ascites. A multiple analysis showed a correlation between the operation time, portal hypertension and postoperative intractable ascites. Postoperative histology revealed that a larger number of patients with cirrhosis had intractable ascites (p < 0.05). We conclude that cirrhosis, portal pressure and operating time are the most important factors related to intractable ascites in the case of hepatectomy. Areas of the liver to be resected should be limited in cirrhotic patients with portal hypertension.
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PMID:Liver resection and intractable postoperative ascites. 846 21

People with genetic variants of cholinesterase (ChE) have been reported to have prolonged apnea with the use of myorelaxant succinylcholine. For the silent type variant ChE, two cases of mutation have been reported. In one case, the exon 2 of ChE gene was disrupted by a 342 bp insertion of Alu element. In the other case, a frame shift mutation was identified at Gly-117 (GGT-->GGAG) to create a stop codon at nucleotide 384. Dibucaine resistant ChE was examined and found to have a point mutation at nucleotide 209 (A-->G) that converted Asp-70 to Gly, and consequently reduced the affinity of ChE for choline esters. In addition, another two types of a point mutation reducing ChE activity were reported on K variant (Ala-539-->Thr) and a case of (Gly-365-->Arg) in a patient with liver cirrhosis.
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PMID:[Gene analysis of human cholinesterase variants]. 846 62


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