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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hospitalized patients with hepatic insufficiency often suffer from severe catabolic states and are in urgent need of nutritional support during their acute illness. Protein intolerence, however, remains a significant problem with respect to the provision of adequate nutrition, either enterally or parenterally. The following report is an anecdotal series of 63 consecutive patients in a large urban hospital treated prospectively with nutritional support using a prototype high branched-chain amino acid solution (FO80) given by technique of total parenteral nutrition by the subclavian or internal jugular route with hypertonic dextrose. Sixty-three patients, of which 42 had chronic liver disease (cirrhosis) with acute decompensation and 17 with acute hepatic injury as well as four with hepatorenal syndrome, are the subject of this report. All required intravenous nutritional support and were either intolerant to commercially available parenteral nutrition solutions or were in hepatic encephalopathy at the time they were initially seen. The cirrhotic patients had been hospitalized for a mean of 14.5 +/- 1.9 days before therapy, had a mean bilirubin of 13 mg/100 ml, and had been in coma for 4.8 +/- 0.7 days despite standard therapy. Patients with acute hepatitis had been in the hospital for 16.2 +/- 4.1 days before therapy, had a mean bilirubin of 25 mg/100 ml, and had been in coma 5.2 +/- 1.6 days before therapy. Routine tests of liver function, blood chemistries, amino acids, EEGs, and complex neurological testing including Reitan trailmaking tests were used in the evaluation of these patients. Up to 120 grams of synthetic amino acid solution with hypertonic dextrose was tolerated in these patients with improvement noted in encephalopathy of at least one grade in 87% of the patients with cirrhosis and 75% of the patients with hepatitis. Nitrogen balance was achieved when 75 to 80 grams of synthetic amino acids were administered. Survival was 45% in the cirrhotic group and 47% in the acute hepatitis group. Encephalopathy appeared to correlate with individual amino acids differentially in the various groups and with the ratio between the aromatic and the branched-chain amino acids. Ammonia did not correlate with either the degree of encephalopathy or improvement therefrom. In 24 Patients therapy for hepatic encephalopathy was limited to infusion of the branched-chain enriched amino acid solution only, with wake-up in 66% of this group. The results strongly suggest that in protein intolerant patients requiring nutritional support, infusion with branchedchain enriched amino acid solutions is well tolerated with either no worsening of or improvement in hepatic encephalopathy coincident with the achievement of nitrogen equilibrium and adequate nutritional support.
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PMID:Infusion of branched-chain enriched amino acid solution in patients with hepatic encephalopathy. 628 73

Two size classes of O-glycosidically linked oligosaccharides were liberated from glycoprotein E1 of mouse hepatitis virus (MHV) A59 by reductive beta-elimination and separated by h.p.l.c. The structures of the reduced oligosaccharides were determined by successive exoglycosidase digestions and by methylation analyses involving combined capillary gas chromatography-mass spectrometry and mass fragmentography after chemical ionization with ammonia. Oligosaccharide A (Neu5Ac alpha 2----3 Gal beta 1----3 GalNAc) comprised 35% of the total carbohydrate side chains, while the remaining 65% of the oligosaccharides of E1 had the branched structure B: Neu5Ac alpha 2----3 Gal beta 1----3 (Neu5Ac alpha 2----6) GalNAc. Both oligosaccharides were linked to the E1 polypeptide via N-acetylgalactosamine, and 20% of the sialic acids present in E1 glycopeptides were found to consist of N-acetyl-9-mono-O-acetylneuraminic acid. The reported structures of the O-linked glycans are discussed in the context of the amino acid sequence of E1, which exhibits a cluster of four hydroxyamino acids (Ser-Ser-Thr-Thr) as potential O-glycosylation sites at the amino terminus. Oligosaccharides with identical structures and an identical O-glycosylated tetrapeptide sequence are present in the blood group M-active glycophorin A of the human erythrocyte membrane.
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PMID:The carbohydrates of mouse hepatitis virus (MHV) A59: structures of the O-glycosidically linked oligosaccharides of glycoprotein E1. 632 80

A 26-month-old child was admitted to the pediatric intensive care unit for treatment of apparent fulminant hepatitis. While hospitalized, he underwent eight exchange transfusions to decrease ammonia concentrations. The patient received intravenous phenobarbital (Pb) for the treatment of cerebral edema. To determine the effects of exchange transfusion on Pb clearance, serum Pb concentrations were obtained before, after, and between exchanges. Preexchange and postexchange serum Pb concentrations were obtained on three separate exchanges. Pb concentrations also were examined between two exchange transfusions. The amount of Pb actually removed during one exchange transfusion was determined by analyzing serum obtained from the discarded blood resulting from the procedure. All Pb concentrations were analyzed by the Emit system. Results indicate that Pb was cleared at a mean rate of 433 ml/h during the exchange periods examined, with a mean overall elimination constant of 0.20 h-1. The Pb actually removed by the exchange transfusion on day 10 of hospitalization was determined to be 17 mg, while the calculated amount was 8 mg. A mean of 22.3 mg of Pb was calculated to be removed over an average exchange time of 2.2 hours. Pb clearance during exchange transfusion has not been reported previously. This case has shown that small amounts of Pb can be removed by exchange transfusion; therefore, patients undergoing this procedure may require serum monitoring after exchange.
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PMID:The effects of exchange transfusion on the pharmacokinetics of phenobarbital. 665 6

An assay for the estimation of guanosine deaminase is described. The method employs guanosine as substrate and after incubation of serum and substrate at 22 degrees C for 18 h the ammonia liberated is estimated using the Berthelot reaction. Absorbance is measured as 625 nm and the catalytic activity read from a standard curve obtained using ammonia standards. The method provides reproducible measurements of serum guanosine deaminase. The results obtained using 'normal' sera have been used to calculate the 'normal range' for the enzyme in serum. Preliminary results suggest that guanosine deaminase is increased in hepatitis and in patients with liver metastases but normal in all other liver diseases including cirrhosis and obstructive jaundice.
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PMID:The estimation of serum guanosine deaminase activity in liver disease. 666 43

560 patients with hepatic coma were treated during the years 1958 to 1982 in Homburg and Bad Kissingen . 82 patients had an endogeneous and 478 an exogeneous hepatic coma. Endogeneous hepatic coma was caused most frequently by fulminant virus hepatitis, intoxication, and hepatorenal syndrome accompanying serum hepatitis. Exogeneous hepatic coma in patients with cirrhosis of the liver was caused in most cases by gastrointestinal bleeding, by a diet too high in protein, or by excessive diuresis. Early clinical symptoms are changes in writing tests and ability to concentrate, whereas hepatic foetor occurs in coma stage III and IV. Clinical chemistry findings pointing to imminent hepatic coma are increase of arterial ammonia in exogeneous hepatic coma, and increase of free phenols in endogeneous hepatic coma. The increase of prothrombin time is prognostic for imminent hepatic coma in both types. Prognosis of endogeneous hepatic coma is still rather bad; 87% of the patients suffering from it died; in exogeneous hepatic coma prognosis has improved for stage I and II in the last 23 years, whereas however the total prognosis for all 4 stages is still unchanged, letality being 55%.
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PMID:[Causes and diagnostic criteria of hepatic coma--an analysis of 560 cases]. 667 13

Hepatic encephalopathy in patients with severe liver disease was associated with marked elevation of either serum methionine or blood ammonia levels or with simultaneous moderate increases in both parameters. CSF methionine levels also increased in encephalopathic patients with fulminant hepatitis and liver cirrhosis. Increased influx of methionine into the brain over the theoretical values predicted from Pardridge's equation suggested that accelerated transport of serum methionine across the blood-brain barrier was observed in these cases with hepatic encephalopathy. Hepatic encephalopathy in acute carbon tetrachloride liver injury could be obtained experimentally following intraperitoneal injection of ammonium acetate in rats, which already received intragastric administration of methionine. However, similar encephalopathy could not be observed by the administration of glycine or leucine in place of methionine. These results suggest at least that methionine and ammonia act synergistically on inducing hepatic encephalopathy.
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PMID:Impaired metabolism of methionine in severe liver diseases. II. Clinical and experimental studies on role of impaired methionine metabolism in pathogenesis of hepatic encephalopathy. 710 99

In 19 acute hepatitis patients with severe coagulopathy who were fully alert and oriented without any changes of mood or behavior, the P300 latency and the arterial blood ketone body ratio (KBR) were assessed as predictors of fulminant hepatitis. All 5 patients developing fulminant hepatitis had a corrected P300 latency longer than 345 msec and 4 of them had a KBR below 0.6. There was a significant negative correlation between the KBR and the blood ammonia level and between the KBR and the corrected P300 latency, while there was a positive correlation between the blood ammonia level and the corrected P300 latency. These data suggest that hepatic encephalopathy develops when loss of hepatic detoxifying activity allows toxic substances to reach the brain and induce cerebral edema. Our findings also suggest the clinical value of using the P300 latency combined with the KBR as predictors of fulminant hepatitis.
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PMID:Long-latency event-related potentials in acute hepatitis patients with severe coagulopathy. 768 66

Fulminant hepatic failure (FHF) is a poorly understood condition in which total liver failure occurs and is thought to be caused by a variety of conditions including Reye's syndrome, hepatitis, drug overdoses, and vascular insufficiency. While this condition is an uncommon one, it carries with it a high fatality rate and must therefore be diagnosed as rapidly as possible. Six patients have been observed over a two-year period with biopsy and/or autopsy-confirmed FHF: one with acute hepatitis B-delta; three with histories of alcoholism, two of them with cirrhosis; one with acute tylenol overdose; and one with hepatic vascular insufficiency. All of these patients, except one, exhibited a rapid, fatal downhill course after onset of symptoms. In all of these patients, a consistent elevation was observed in serum levels of aspartate aminotransferase (AST) or serum glutamate oxaloacetate transaminase (SGOT) and alanine aminotransferase (ALT) or serum glutamate pyruvate transaminase (SGPT) such that the ratio of AST to ALT was significantly greater than 1 and in serum levels of ammonia. Other liver function tests were found to be abnormal but not in so consistent a pattern, although total protein and albumin were found to be significantly decreased in all of these patients. The stereotypical elevation of the transaminases with high AST-to-ALT ratios and the rise in ammonia appear to characterize this life-threatening illness most reliably.
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PMID:Serum analyte pattern characteristic of fulminant hepatic failure. 820 19

Toxic liver diseases coincide with oxidative stress correlating positively with the seriousness of the course of disease. For the purpose of elucidating the pathogenic significance of an increased radical generation. 56 patients suffering from acute alcohol-toxic hepatitis of the clinical grade of seriousness B and C according to Child/Pugh were classified randomly into antioxidant subgroups (n = 31) and control groups (= 25). The basis therapy being identical, the patients of the antioxidant group received additionally 600 mg of D-alpha tocopherol per day, 200 micrograms of selenium and 12 mg of zinc. Due to the supplementation of antioxidants there were quicker significant changes in the concentration of bilirubin, malondialdehyde and of ammonia in the serum. In comparison with the control group the length of stay in hospital could be reduced by 6 days. In the control group the mortality rates amounted to 40% (10 of 25), in the antioxidant group to 6.5% (2 of 31). The results confirm the pathogenic significance of oxidative stress in alcohol-toxic liver disease because a distinct improvement of prognosis could be achieved by using a low-cost adjuvant antioxidant supplementation.
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PMID:[Alcohol-induced toxic hepatitis--a "free radical" associated disease. Lowering fatality by adjuvant antioxidant therapy]. 825 68

We describe three children with transaminase elevations and hepatic insufficiency who were given the diagnosis of cryptogenic hepatitis after the more common viral and metabolic diseases of the liver had been excluded. However, further laboratory investigations showed hyperammonemia, low blood urea levels, elevated plasma glutamine levels, and low citrulline levels. Urinary excretion of orotic acid was higher than normal, with absent urinary homocitrulline and normal fractional tubular reabsorption of lysine, ornithine, and arginine. These findings suggest the diagnosis of ornithine transcarbamylase deficiency. We emphasize the importance of investigating possible urea cycle disorders by determining ammonia plasma levels, both at baseline and after a protein load; urinary and plasma amino acids; and urinary orotic acid in all patients with liver disease of indeterminate etiology.
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PMID:Cryptogenic hepatitis masking the diagnosis of ornithine transcarbamylase deficiency. 873 1


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