Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytostatic-treated persons and cases of severe hepatic failure under corticoid therapy are predisposed to disseminating Aspergillus infections. Constant exposure to Aspergillus spores may result in a fatal Aspergillus infection. The triad of hepatic failure, corticoid therapy and constant exposure to Aspergillus spores is described in a 70-year-old female patient. A painless icterus was clinically diagnosed as non-A non-B hepatitis, with a protracted cholestatic course. She had been treated with an oral corticoid preparation. After leaving the hospital at her own insistance when still in the icteric stage, severe pneumonia due to Aspergillus developed within 14 days; this was confirmed radiologically. The autopsy results showed unexpected infarction, similar to pneumonic foci, in all lobes and dissemination in the myocardium, stomach, kidneys and brain. The liver showed subacute dystrophy. Constant exposure to the conidia of A fumigatus came about as a result of the soil of potted ornamental plants in the patient's living room. The fungus could only be successfully cultured by putting infected tissue particles on Sabouraud dextrose agar; it was not possible by the common method of fractionated streaking.
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PMID:[Peracute disseminated course of fatal Aspergillus fumigatus infection in liver failure and corticoid therapy. A case report on the epidemiology, pathogenesis and diagnosis of the systemic course of Aspergillus infections]. 392 20

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

N-acetyl-beta-D-glucosaminidase is a lysosomal glycosidase, which participates in the catabolism of the mucopolysaccharides and of the glycoproteins. For the determination of this enzyme the production of the substrate and a modified methodology are described. Measurements of the activity were performed by 4-nitrophenyl-alpha-D-galactopyranoside and 4-nitrophenyl-N-acetyl-beta-D-glucosaminide as substrates. Examinations of this enzyme were performed in patients with acute virus hepatitis, chronic hepatitis, liver cirrhosis and healthy test persons. In acute hepatitis and liver cirrhosis and significant increase of enzyme is provable, but not in protracted hepatitis.
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PMID:[Clinical value of N-acetyl-beta-D-glucosaminidase and alpha-galactosidase in liver diseases]. 626 8

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

The intracellular sites of biosynthesis of the structural proteins of murine hepatitis virus A59 have been analyzed using cell fractionation techniques. The nucleocapsid protein N is synthesized on free polysomes, whereas the envelope glycoproteins E1 and E2 are translated on the rough endoplasmic reticulum (RER). Glycoprotein E2 present in the RER contains N-glycosidically linked oligosaccharides of the mannose-rich type, supporting the concept that glycosylation of this protein is initiated at the co-translational level. In contrast, O-glycosylation of E1 occurs after transfer of the protein to smooth intracellular membranes. Monensin does not interfere with virus budding from the membranes of the endoplasmic reticulum, but it inhibits virus release and fusion of infected cells. The oligosaccharide side chains of E2 obtained under these conditions are resistant to endoglycosidase H and lack fucose suggesting that transport of this glycoprotein is inhibited between the trans Golgi cisternae and the cell surface. Glycoprotein E1 synthesized in the presence of monensin is completely carbohydrate-free. This observation suggests that the intracellular transport of this glycoprotein is also blocked by monensin.
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PMID:Post-translational glycosylation of coronavirus glycoprotein E1: inhibition by monensin. 632 72

In 33 patients with acute hepatic encephalopathy due to toxic or viral hepatitis the following analyses were performed: (24-14C)cholic acid conjugation and sulfation, plasma phenazone clearance, galactose elimination capacity, and concentrations of glycocholic acid and glycolithocholic acid sulfate in plasma. The (24-14C)cholic acid conjugation in patients with viral hepatitis was significantly lower in fatal cases than in patients who survived (p less than 0.002). In these patients the galactose elimination capacity and the plasma phenazone clearance were insignificantly lower. Tauro-(24-14C)cholic acid was the predominant metabolite of (24-14C)cholic acid in six patients, but in four patients with toxic hepatitis this metabolite was only found in trace amounts. Sulfation after 3 h of (24-14C)cholic acid accounted for 0-8.2% of the administered dose. The sulfate of glycolithocholic acid was found in the plasma of all patients. No survival limit with regard to the capacity for the (24-14C)cholic acid conjugation could be defined.
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PMID:Cholic acid conjugation test and quantitative liver function in acute liver failure. 666 44

Studies by Liehr et al. suggest that endotoxins are important in the pathogenesis of galactosamine hepatitis (Gal-N hepatitis) in rats. Lactulose (9.1 gm per kg per day) prevents hepatic lesions induced by Gal-N; an antiendotoxin effect of lactulose is postulated. However, commercial preparations of lactulose are contaminated with galactose, which shows a competitive action to Gal-N. To analyze the effect of galactose, male Wistar rats were pretreated with lactulose (Duphalac, 9.1 gm per kg per day) and given Gal-N (375 mg per kg i.p.). After 24 hr, serum was analyzed for glutamic pyruvate transaminase, glutamate dehydrogenase, and sorbitol dehydrogenase activities. Pretreatment with Duphalac, even 1 hr before Gal-N, abolished toxicity. Duphalac contains 10 gm galactose per 100 ml. Galactose was given in a similar concentration and similar inhibition occurred. Pretreatment with purified lactulose (9.1 gm per kg for 5 days) diminished the effects of Gal-N but did not normalize enzyme concentrations. Because small doses of galactose (80 and 300 mg per kg) showed similar inhibitory effects, we conclude that the protective effect of commercial lactulose preparations is mainly due to galactose contamination and not to an antiendotoxin effect.
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PMID:Galactosamine hepatitis, endotoxemia, and lactulose. 683 15

Glucan, a macrophage stimulant, was evaluated for its ability to alter survival and phagocytic dysfunction in mice challenged with mouse hepatitis virus strain MHV-A59. Administration of glucan before the mice were challenged with the virus significantly prolonged median survival time but did not modify overall mortality compared with control mice given dextrose. Maximal effectiveness was achieved when glucan was administered both before and after the viral challenge. In contrast to the marked hepatic parenchymal cell necrosis observed in the control mice, glucan-treated mice exhibited reduced pathology. Intraperitoneal administration of MHV-A59 resulted in a significant depression of phagocytic activity compared with controls that were not exposed to the virus. The enhancement in phagocytic function in glucan-treated control mice was unaltered in virus-challenged, glucan-treated mice. Thus glucan is capable of increasing survival, inhibiting hepatic necrosis, and maintaining an activated state of phagocytic activity in mice challenged with MHV-A59. Macrophage stimulants may have a significant role in the modification of virally induced hepatic lesions.
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PMID:Glucan-induced modification of murine viral hepatitis. 736 Nov 8

The galactose elimination capacity and the plasma clearance of phenazone were investigated in 24 patients with uncomplicated acute hepatitis and in 8 patients who survived and in 26 who died of fulminant hepatitis. The galactose elimination capacity was 52% of the normal mean value on admission to the hospital in uncomplicated hepatitis, 47% in patients who survived fulminant hepatitis, and 22% in the fatal cases, while the plasma clearance of phenazone was 43%, 22%, and 10%, respectively. Both quantitative liver function tests showed rapid improvement in most cases of uncomplicated acute hepatitis and in the patients who survived fulminant hepatitis. They did not improve in the fatal cases of fulminant hepatitis, among whom the patients with the lowest initial values died first. Both the galactose elimination capacity and the plasma clearance of phenazone were significantly higher in survivors than in non-survivors of fulminant hepatitis. The results indicate that the loss of functioning liver cell mass is about 60-70% in the acute stage of uncomplicated hepatitis and 80-85% in patients who survive fulminant hepatitis, whereas patients who die of fulminant hepatitis have nearly total loss of functioning liver cell mass.
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PMID:Functioning liver mass in uncomplicated and fulminant acute hepatitis. 736 24

Syncytial giant cell hepatitis (SGCH) has recently been reported to be a cause of severe hepatitis, with little chance of patient recovery without orthotopic liver transplantation. We have recently seen a patient with multisystem disease and histologic features of SGCH. Upon reaching stage IV coma, she was treated with an extracorporeal liver assist device containing 200 g of cultured liver cells. There was an immediate improvement in her galactose elimination capacity, and her own liver recovered to the point that therapy could be discontinued after 58 h. The patient recovered slowly from her multisystem disease and was discharged with mildly elevated transaminases and biochemical evidence of cholestasis. All laboratory values are normal at 2 yr, and the patient appears to have no sequelae of her disease.
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PMID:A case of syncytial giant-cell hepatitis treated with an extracorporeal liver assist device. 751


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