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)

The occurrence of infectious hepatitis in patients with coexistent glucose-6-phosphate dehydrogenase (G6PD) deficiency may present a clinical picture similar to that of fulminant hepatitis. To determine the factors which enable a rapid diagnosis of this disease combination, the clinical and biochemical findings in 14 patients were compared with those in 50 patients with uncomplicated hepatitis and those in 14 patients with fulminant hepatitis. Similarities with the latter group included persistence of fever, tachycardia, leukocytosis and hyperbilirubinemia of greater than 340 mumol/liter (20 mg/dl). A rise in bilirubin values of more than 50 mumol/liter (3 mg/dl) per day in patients with viral hepatitis strongly suggested the presence of G6PD deficiency. Despite the severity of the illness, prothrombin activity was well maintained in G6PD-deficienct patients.
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PMID:Infectious hepatitis and glucose-6-phosphate dehydrogenase deficiency. 88 12

Nitrofurantoin is a widely utilized urinary antimicrobial drug which has been associated with pulmonary fibrosis, neuropathy, and hepatitis as well as hemolytic anemia in glucose-6-phosphate dehydrogenase-deficient individuals. Incubation of freshly isolated rat hepatocytes with nitrofurantoin caused oxygen activation as a result of futile redox cycling. Glutathione disulfide (GSSG) was formed and rapidly exported from the cell resulting in complete glutathione (GSH) depletion followed by cell death. However, fructose prevented the export of GSSG from the cell and GSH levels recovered rapidly without cytotoxicity occurring. Fructose did not affect nitrofurantoin metabolism but rapidly depleted cellular ATP levels by approximately 80% which remained depressed during the incubation period. Fructose, however, did not protect hepatocytes from nitrofurantoin-induced cytotoxicity if GSH was depleted beforehand. Protection by fructose only occurred at concentrations which caused ATP depletion. These results suggest that fructose prevents nitrofurantoin-induced toxicity by depleting ATP and thereby preventing the ATP-dependent GSSG efflux. GSSG is retained enabling NADPH and glutathione-reductase to reduce the GSSG back to GSH, thereby protecting the cell from nitrofurantoin-induced oxidative stress.
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PMID:Prevention of nitrofurantoin-induced cytotoxicity in isolated hepatocytes by fructose. 189 74

Chronic infection of woodchucks with woodchuck hepatitis virus (WHV) was associated with the development of hepatitis, foci of altered hepatocytes and hepatocellular adenomas and carcinomas. The cytomorphological and cytochemical analysis permitted the identification of three different types of focal lesions; namely, glycogen-storage foci, mixed-cell foci and intermediate-cell foci, each showing a characteristic pattern. The cells of the glycogen-storage foci had clear to acidophilic cytoplasm, and were overloaded with glycogen. They showed a marked elevation in the activity of glucose-6-phosphate dehydrogenase (G6PDH) and malate dehydrogenase (MDH), increased activity of succinate dehydrogenase (SDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and glycerol-3-phosphate dehydrogenase (G3PDH), reduction in the activity of glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and adenyl cyclase (ADC), and unchanged activity of glycogen synthase (SYN) and gamma-glutamyl transferase (GGT). The mixed-cell foci mainly consisted of basophilic cells poor in glycogen, but were intermingled with cells containing glycogen. These foci were characterized by a marked decrease in activity of PHO, SYN, G6Pase, G6PDH, ATPase and ADC, and increased activity of GGT, SDH, MDH and GAPDH. The intermediate-cell foci consisted of cells with both basophilic and glycogenotic cytoplasmic compartments, and showed a similar enzyme histochemical profile to the mixed-cell foci, with slight differences in the degree of elevation or reduction of some enzymes. The phenotypic similarities and the close spatial relationship between the foci of altered hepatocytes, and the hepatocellular adenomas and carcinomas in WHV-infected woodchucks, suggest that these lesions are preneoplastic. The focal morphological and metabolic aberrations emerging during hepatocarcinogenesis in WHV-infected woodchuck, are in principle similar to those identified in the course of chemical hepatocarcinogenesis in various species. The focal metabolic aberrations apparently represent a general biological response of the liver parenchyma to oncogenic agents and are closely linked to neoplastic transformation of the hepatocytes.
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PMID:Phenotypic patterns of preneoplastic and neoplastic hepatic lesions in woodchucks infected with woodchuck hepatitis virus. 215 41

Thirty-six wild-caught woodchucks (Marmota monax) were characterized according to sex, weight, trapping locality, liver pathology, and serum or hepatic markers of woodchuck hepatitis virus. Liver subcellular fractions were assayed for microsomal cytochromes P-450, aryl hydrocarbon hydroxylase, glutathione, cytosolic enzymes involved in its metabolism (glutathione S-transferase, glutathione peroxidase, and glutathione reductase), in the hexose monophosphate shunt (glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase), NADH- and NADPH-dependent diaphorases, and DT diaphorase. Moreover, liver postmitochondrial fractions were assayed for their ability to activate procarcinogens [i.e., a tryptophan pyrolysate product, aflatoxin B1, 2-aminofluorene, and trans-7,8-dihydrobenzo(a)pyrene] to mutagenic metabolites in the Ames reversion test and to decrease the activity of direct-acting mutagens [i.e., 4-nitroquinoline N-oxide, 2-methoxy-6-chloro-9-[3-(2-chloroethyl)aminopropylamino]acridine X 2HCl, and sodium dichromate]. A considerable interindividual variability in metabolism was observed among the examined woodchucks. Some of the investigated parameters were more elevated in virus carriers, especially in those suffering from chronic active hepatitis, but only a few of the recorded differences (i.e., oxidized glutathione reductase and NADPH-dependent diaphorase) were statistically significant. The comparison of the monitored activities in woodchucks and in other rodent species (rat and mouse) led to the conclusion that the liver metabolism of mutagens and carcinogens in woodchucks is more oriented in the sense of activation, while detoxification mechanisms are more efficient in rats and mice.
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PMID:Metabolism of mutagens and carcinogens in woodchuck liver and its relationship with hepatitis virus infection. 360 50

Severe neonatal hyperbilirubinemia can occur without apparent reason in term healthy breast-fed infants and some develop kernicterus. The aim of our study was to assess the incidence of severe hyperbilirubinemia in term healthy newborns discharged from the hospital. From January 1 through December 31, 1994, 6705 infants were delivered at Bikur-Cholim and Misgav-Ladach Community Hospitals. All 1448 newborns discharged with a serum bilirubin level > 10.0 mg/dL were instructed to return to the hospital within 3 days for follow-up, as well as bilirubin determination. Twenty-one newborns with a bilirubin level > 18.0 mg/dL were identified and readmitted at mean +/- standard deviation (SD) 5.5 +/- 1.8 (range, 5 to 10 days of life). This represents 1.7% of the 1220 infants who returned for follow-up examination. Mean +/- SD serum bilirubin levels at readmission were 19.6 +/- 2.5 mg/dL. All but one of the infants were breast-fed. No cases of ABO incompatibility were found and two newborns were glucose-6-phosphate dehydrogenase (G6PD)-deficient. Sepsis work-up and direct Coomb's tests were negative in all cases. None had hemolysis or were found to have any cause for hyperbilirubinemia other than breast-feeding. Phototherapy was provided in all but two cases, and an exchange transfusion was performed in one case. Three additional infants, with bilirubin levels < 10 mg/dL at discharge, were readmitted due to hyperbilirubinemia. One was diagnosed with neonatal hepatitis. We conclude that, based on our study population, 0.36% of term infants may subsequently develop severe neonatal hyperbilirubinemia in the first postnatal week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hospital readmission due to neonatal hyperbilirubinemia. 756 38

Galactosamine-induced hepatitis caused a marked increase in plasma lactate and pyruvate, but completely abolished the increase in ketone bodies in the rat exposed to an 8000 m simulated altitude. Plasma free fatty acid as the precursor of ketone bodies was higher in the galactosamine-treated rats during and after an exposure to 8000 m altitude. Treatment of the rat with galactosamine markedly reduced activities of citrate synthase, fumarase, glutamate dehydrogenase and fructose 1,6-bisphosphatase, but increased hexokinase and glucose 6-phosphate dehydrogenase in the liver. The effect of galactosamine-induced hepatitis on the energy metabolism can be explained by a reduction of mitochondrial oxidative enzymes and gluconeogenesis, and involves a shift of the aerobic metabolism to anaerobic glycolysis at high altitude.
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PMID:Effect of galactosamine-induced hepatitis on the aerobic and anaerobic metabolism of the rat exposed to high-altitude hypoxia. 774 7

Content of lipids in blood serum and membranes of liver tissue endoplasmic reticulum, functional activity of microsomes, antitoxic activity of liver tissue as well as collagen production in rat liver tissue were studied in experimental hepatitis after administration of exogenous lipids (equine erythrocyte phospholipids and ganglioside GM3, bovine spinal cord phospholipids). All the preparations studied inhibited the functional activity of the liver cells which was expressed as a decrease of the lipids content in the microsomes, inhibition of glucose-6-phosphate dehydrogenase activity and impairment of the liver tissue antitoxic functions. Distinct inhibition of these reactions caused an increase of the collagen content in the liver tissue.
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PMID:[The effect of exogenous lipids on the functional activity of the liver in experimental hepatitis]. 849 69

Influence of a new sorbent based on the AU-L lignin on the hepatic enzyme spectrum has been investigated in rats with experimental toxic hepatitis. The intact animals were in control group. There was a shift in lactate dehydrogenase (LDH) isoenzymic spectrum to the LDH5 side, glucose-6-phosphate dehydrogenase (G-6-PDH) activity increased to 144.7% against the control. Aspartate aminotransferase (AsT) activity reduced 2 times and alanine aminotransferase (ALT) activity enhanced 1.3 times, LDH2 activity increased 2.8 times in the liver of rats with toxic hepatitis which received sorbent for 7 days versus the untreated animals. The LDH4 and LDH5 fractions activity lowered to the level of the intact animals. G-6-PDH activity continued to increase, aminotransferase activity reduced up to the level less than control. The aerobic shifts in the LDH isoenzymic spectrum in which LDH4 and LDH5 fractions' activity completely returned to the control level evidence for glycolysis conversion to the aerobic type that apparently was promoted by positive effects of enterosorbent.
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PMID:[Effect of enterosorption effects on hepatic enzyme spectrum in experimental toxic hepatitis]. 947 96

The effect of perftoran on the course of experimental acute hepatitis in albino rats was studied on the hepatitis models induced by allyl alcohol or P. acnes culture with typhoid fever endotoxin. Perftoran (10 ml/kg) favored more rapid cytolytic syndrome elimination by affecting the lipid peroxidation in rat liver. The drug inhibits the activity of prooxidant enzymes (xanthine oxidase and myeloperoxidase of Kupffer cells) and induces the synthesis of factors accounting for the antiperoxidation protection in hepatocytes such as catalase, glucose-6-phosphate dehydrogenase, and reduced glutathione.
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PMID:[Effect of perftoran on experimental hepatitis]. 1156 5

Melatonin administered to intact animals increased glutathione concentration and activities of glutathione peroxidase, glutathione reductase, NADP-isocitrate dehydrogenase, and glucose-6-phosphate dehydrogenase in the liver. In animals with toxic hepatitis melatonin treatment decreased glutathione concentration and enzyme activities, which was probably associated with inhibition of free radical oxidation under the influence of this hormone.
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PMID:Glutathione system and activity of NADPH-generating enzymes in the liver of intact rats and animals with toxic hepatitis receiving melatonin. 1622 50


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