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)

Serum gamma-glutamyl transpeptidase (gamma-GT) level was estimated in 132 patients with different liver diseases (chronic persistent and chronic active hepatitis, postnecrotic cirrhosis, chronic alcholic hepatitis and alcoholic cirrhosis, cholestasis syndrome, fatty liver, Gilbert disease) and malignancies with and without liver involvement. The gamma-GT levels were compared with the values for serum bilirubin, transaminases (GOT, GPT) and alkaline phosphatase in the same patients. gamma-GT values were normal in chronic persistent hepatitis and increased in chronic active hepatitis. Very high activities were measured in chronic alcoholic cirrhosis in contrast to postnecrotic cirrhosis. gamma-GT proved to be more sensitive than alkaline phosphate as an index of cholestasis and liver involvement in malignancies. It is suggested that gamma-GT activity offers valuable aid in differential diagnostics of liver-diseases. gamma-GT being an inducible enzyme, its activity may be raised by enzyme inducing drugs also in subjects without liver disease.
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PMID:Serum gamma-glutamyl transpeptidase: its clinical significance. 2 44

In 7 unselected necropsy cases of clinically diagnosed periarteritis nodosa, the detection of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) in the cytoplasm and nuclei of hepatocytes indicated an ongoing infection with hepititis B virus (HBV). In all these cases histologic changes found in the liver varied from "minimal" to chronic aggressive hepatitis. In all the cases, deposits of HBsAg, immunoglobulins, beta1C-globulin and C1q were detected in vascular lesions. That these deposits could represent HBsAg-anti-HBs immune complexes was supported by demonstrating their strong binding of guinea pig complement and by the successful elution of all HBsAg and part of the immunoglobulin from these deposits by treatment with buffers known to dissociate antigen-antibody bonds but not with phosphate-buffered saline, pH 7.6 (PBS). Glomerulonephritis associated with these immune complexes was found in 6 cases. The presence of larger masses of HBsAg immune complexes, chiefly in recent insudative and fibrinoid vascular lesions, their lesser amounts in lesions undergoing involution, and their absence from healed lesions strongly suggest that these complexes play a primary role in the pathogenesis of acute vascular damage in periarteritis nodosa.
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PMID:Immune complexes of hepatitis B surface antigen in the pathogenesis of periarteritis nodosa. A study of seven necropsy cases. 2 42

41 heterozygoes and 4 homozygotes with a deficiency of galactose 1-phosphate uridyl transferase and also 3 heterozygotes and 1 homozygous patient with galactokinase deficiency were subjected to intravenous galactose loading tests with a dose of 350 mg/kg body weight in order to answer the question whether it is possible to detect the heterozygotes of both types of galactosemia by this method. For comparison, 38 healthy children and adolescents, 24 children with epidemic hepatitis and 4 children with cirrhosis of the liver, which was verified by histology, were included in the study. The elimination half-life (and also the other pharmacokinetic parameters as inaugurated by Dost) was the same for all the heterozygotes for both types of galactosemia almost without exception, and for the healthy cs, children in the acute stages of hepatitis and patients with cirrhosis of the liver was prolonged 2 to 5 times the normal. In patients with hepatitis, however, the elimination half-life was normal before the transaminases. Accordingly, the galactose clearance was decreased to half and one-fourth of the normal. Hence, heterozygotes with galactosemia cannot be detected with galactose loading tests.
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PMID:Biokinetics of galactose in the homozygotes and heterozygotes of both forms of galactosemia. 18 90

1-beta-D-Ribofuranosyl-1,2,4-triazole-3-carboxamide 5'-phosphate (2) was prepared and converted into the following derivatives: the 5'-phosphoramidate 3, the 5'-diphosphate 4, the 5'-triphosphate 5, and the cyclic 3',5'-phosphate 6. The cyclic 2',3'-phosphate 7 was prepared from the parent nucleoside, 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide (1), and was opened to the 2'(3')-phosphate 8. These compounds were found to exhibit significant antiviral activity against several viruses in cell culture. Ribavirin 5'-phosphate (2) was shown to be effective when tested against lethal infections in mice caused by influenza A2, influenza B, and murine hepatitis viruses.
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PMID:Synthesis and antiviral acticity of some phosphates of the broad-spectrum antiviral nucleoside, 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide (ribavirin). 21 Dec 34

Four strains of the coronavirus murine hepatitis virus were examined for the presence of phosphorylated proteins. The nucleocapsid protein was determined to contain phosphate covalently linked to serine but not to threonine residues. The nucleocapsid protein was the only phosphorylated protein detected in these strains of murine hepatitis virus.
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PMID:Phosphoproteins of murine hepatitis viruses. 22 84

Re/coagulan was compared to the standard calcium chloride (CaCl2) method for effectiveness of recalcification of plasma and whole blood. The time required for clot formation was determined. The effect of Re/coagulan on the specificity of hepatitis tests, direct antiglobulin tests, indirect antiglobulin tests, and agglutination tests were investigated. Hepatitis testing was performed on untreated serum and Re/coagulan-treated ethylenediamine tetraacetic acid (EDTA) plasmas by radioimmunoassay, reversed passive latex agglutination, and reversed passive hemagglutination methods. Direct antiglobulin tests were performed on untreated, CaCl2 treated, and Re/coagulan treated EDTA, acid-citrate-dextrose (ACD), and citrate-phosphate-dextrose (CPD) samples of whole blood. Red cell antibody specificity and titer were determined before and after clot formation by both the CaCl2 and Re/coagulan methods. Examples of agglutinating and sensitizing antibodies were tested. Antibodies directed against antigens in the Rh, Kell, MNS, Lewis, P, Kidd, Duffy, and Lutheran blood groups systems were investigated. Re/coaglulan didnot have a detrimental effect on the tests performed and compared favorably to the standard recalcification method.
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PMID:An evaluation of Re/coagulan for blood center tests. 51 59

Metabolism of calcium and magnesium may be disturbed in hepatobiliary disease because of deficient or absent bile flow into the gut, since bile is important for the intestinal absorption of these elements. In the present paper the tubular reabsorption of phosphate (TRP), calcium (TRCa), and magnesium (TRMg) were determined in an attempt to evaluate the parathyroid function of infants and children with hepatobiliary disease. In unrepaired biliary atresia TRP was conspicuously reduced (mean 49.8%, SD 15.1). In successfully repaired biliary atresia the value was increased near the normal range (mean 80.7%, SD 8.1). In neonatal hepatitis the value was variable in individual cases, but significantly lower than the normal (mean 47.6%, SD 19.9). TRCa was reduced in one third of the patients with unrepaired biliary atresia and in one fifth of the cases of neonatal hepatitis. The value was within the normal range in repaired biliary atresia. TRMg was decreased in both unrepaired and repaired biliary atresia and in neonatal hepatitis. The effect of intravenous calcium infusion on TRP, TRCa and TRMg was evaluated in 3 patients with unrepaired biliary atresia. TRP was conspicuously enhanced after infusion. TRCa was decreased in 3 to a variable extent. TRMg was moderately increased in 2 and greatly decreased in 1. These results indicate that infants with hepatobiliary disease are in a state of secondary hyperparathyroidism because of deficient or absent bile flow into the intestines.
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PMID:Hyperparathyroidism in hepatobiliary disease in infancy. 81 5

A method for the large-scale preparation of a coagulation factor IX concentrate from human plasma is described. The method includes absorption of the coagulation factors from cryosupernatant plasma to DEAE-Sephadex, extensive washing of the gel and elution of the coagulation factors with 0.5 M phosphate buffer at 6.85, followed by desalting of the eluate in a column of Sephadex G-25, then by lyophilization, dissolving and sterile filtration, and finally by freeze-drying of the final product. Experiments performed with HBsAg-positive plasma demonstrated a decrease in the HBsAg content by a factor of 10(-5) during the process. The product is inactive in a Na-PTT assay. The process yields an about 100-fold purified factor IX concentrate containing also factors II, VII, and X, but in relatively smaller amounts. The average yield relative to factor IX is 60%. The batch size has been from 16 to 150 litres of plasma and about 300 batches of the concentrate have been prepared. About 5,100 bottle (about 4.0 X 10(6) U of factor IX) of the concentrate have been used in the treatment of patients with haemophilia B. The clinical effect has always been good and the in vivo response to factor IX was 1.15 +/- 0.30%/U/kg body weight. Two cases of HBsAg-negative hepatitis that may have been caused by the concentrate, were detected. No thrombotic complications were found.
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PMID:Preparation and properties of a therapeutic factor IX concentrate. 88 44

A permature male infant required intravenous alimentation for six weeks following extensive surgery for ileal and cecal necrosis. At 3 months he developed evidence of hepatitis. Subsequently osteoporosis and the Fanconi syndrome appeared. Urine phosphate clearance was 83 percent of creatinine clearance at a serum phosphate concentration of 1.6 mg/dl. Concentration of plasma immunoreactive parathyroid hormone was elevated at 550 pg/ml. 25-Hydroxycholecalciferol was given at 240 mug/day. Aminoaciduria disappeared and bone healing occurred. Serum phosphate rose to 6.5 mg/dl and phosphate clearance fell to 2 percent of creatinine clearance. Upon cessation of 25-OHCC therapy, the Fanconi syndrome recurred despite administration of vitamin D2. 25-OHCC was then administered at 40 mug/day, and the urine abnormalities were reversed. The patient probably developed hyperparathyroidism, secondary malabsorption, and hepatitis. The Fanconi syndrome was the consequence of the hyperparathyroidism. 25-OHCC therapy was more effective than vitamin D in reversing the disordered state, possibly because of impaired hepatic metabolism of vitamin D2.
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PMID:Fanconi syndrome following bowel surgery and hepatitis reversed by 25-hydroxycholecalciferol. 112 25

Isaxonine phosphate or Nerfactor (2-isopropylaminopyrimidine) has been implicated in several cases of hepatitis which is reversible after withdrawal of the drug. In order to understand the cause of such hepatitis, the metabolic activation of isaxonine phosphate with different liver microsomes was investigated. The major metabolites were 5-hydroxyisopropylaminopyrimidine and 2-aminopyrimidine. Covalent binding to microsomal proteins was also detected. In vitro metabolic activation required intact microsomes, NADPH and O2 as cofactors and was cytochrome P-450 dependent. A sensitive fluorimetric assay of 5-hydroxyisaxonine was developed. The metabolism of isaxonine phosphate was compared in liver microsomes from rat, rabbit, dog, monkey and man and found to be qualitatively similar. Treatment of rats with phenobarbital increased the formation of 5-hydroxyisaxonine, while treatment with 3-methylcholanthrene increased the formation of 2-aminopyrimidine but decreased that of 5-hydroxyisaxonine. Inhibition and reconstitution experiments demonstrated that 5-hydroxylation of isaxonine was catalyzed by a cytochrome P-450. Metabolic oxidation of isaxonine phosphate using 5-[3H]isaxonine phosphate led to a total loss of tritium in 5-hydroxyisaxonine and partial loss of tritium in 2-aminopyrimidine and covalent binding to proteins.
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PMID:In vitro metabolism of isaxonine phosphate: formation of two metabolites, 5-hydroxyisaxonine and 2-aminopyrimidine, and covalent binding to microsomal proteins. 139 69


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