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)

400 unselected liver biopsies were stained with aldehyde-thionin (AT) and examined for ground-glass hepatocytes (GGH). 1) AT-positive GGH were found in about half of all HBSAg-positive patients but were never seen in HBSAg-negative patients. 2) AT-positive GGH were observed in healthy HBSAg carriers and in all forms of chronic hepatitis but never in acute HBSAg-positive hepatitis. 3) AT-negative GGH were occasionally seen in HBSAg-negative patients under drug treatment. 4) Ultrastructurally GGH showed proliferation of smooth endoplasmic reticulum which only in AT-positive GGH contained filaments, 20-25 nm in diameter, within its cisternae.
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PMID:Ground-glass hepatocytes in unselected liver biopsies. ultrastructure and relationship to hepatitis B surface antigen. 5 36

A 35-year-old woman who had used Non-Ovlon for 3 1/2 years was treated for anicteric hepatitis and underwent vaginal extirpation of the uterus due to carcinoma. Point biopsies were taken of the liver at this time and 1 year later, and histological and electron microscopic studies were also performed. The examination of the hepatocytes revealed intracisternal, hyaloplasmic, and mitochondrial hyalin, i.e. protein deposits in the endoplasmic reticulum, the cytoplasmic ground substance, and the mitochondria ("Giant mitochondria"), respectively. Coagulation necrosis of the hepatocytes was also observed. These abnormal protein deposits could not be related to abnormal alpha-1-antitrypsin synthesis in the liver. No regression in the protein deposits was observed 5 months after Non-Ovlon use was discontinued. It was also ascertained that the histological discovery of globular hyaline bodies can indicate that any or all of the various hyalins or cell mecrosis can exist simultaneously.
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PMID:[Intracisternal hyalin and giant mitochondria in hepatocytes and oral contraceptives (author's transl)]. 9 11

After intraperitoneal inoculation with mouse hepatitis virus (MHv) into mice, the excretory cells of the pancreas showed a marked vacuolar degeneration concomitantly with hepatitis. MHV-specific antigen was evidenced in the cytoplasm of infected cells. Electron microscopy revealed a number of virions within the matrix, spaces of the endoplasmic reticulum and areas of focal cytoplasmic necrosis. The virus titer of the pancreas was equal or superior to that of the liver at least in early stage of infection.
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PMID:[Mouse pancreas involvement in murine hepatitis virus infection]. 17 Oct 39

Mice infected with JHM strain of mouse hepatitis virus develop a demyelinating encephalomyelitis. Myelin sheaths are stripped off axons by invading macrophages after degeneration of the infected oligodendrocytes. The derivation of the virus from granular cytoplasmic particles that condense around and bud into endoplasmic reticulum is demonstrated. The infected oligodendrocytes undergo hypertrophic changes prior to degeneration. Hypertrophic cells are characterized by abundant microtubules, filaments, mitochondria, aggregates of electron-dense particles, and numerous, unusual plasma membrane connections to myelin lamellae. Vacular and hydropic changes are prominent in degenerating cells. The significance of finding infected oligodendrocytes with altered myelin-plasma membrane connections is discussed with reference to the pathogenesis of recurrent, postinfectious demyelination known to develop subsequent to acute virus infections.
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PMID:Oligodendrocytes and their myelin-plasma membrane connections in JHM mouse hepatitis virus encephalomyelitis. 17 79

Indirect immunoperoxidase stainings for hepatitis B core and surface antigens (HBc&s Ag) were applied to formalin-fixed paraffin sections in 113 liver specimens from 56 patients. Many cytomorphologic staining characteristics of HBc&s Ag were illustrated, and the percentages of the cellular population positive for HBc&s Ag were estimated for all specimens in order to provide the basis for general analyses. The quantitative expressions and the topographic distribution of HBc&s Ag were assessed with respect to their significance and implication in histopathologic reactions. A definitive relationship or relevance was neither established nor completely excluded due to the size of samples. However, cytomorphologically the membranous expression of HBc&s Ag was shown often in association with acute lobular hepatitis and chronic active hepatitis. This observation supports the concept that the membranous expression may be the prerequisite for immune mediated hepatitic injury in viral hepatitis. In this study we also carried out indirect immunoferritin and immunoperoxidase electron microscopy for HBc&s Ag on formalin-fixed liver specimens. The results assured the validity of the light microscopic immunohistologic procedures. The immunoelectron microscopy confirmed the presence of core antigen in the Dane particles formation that takes place in the cisternae of endoplasmic reticulum. The significance of the cytoplasmic core antigen and the possible role of immunoelectron microscopy in the elucidation of mechanisms of hepatitic injury were discussed.
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PMID:Immunohistologic demonstration of hepatitis B viral antigens in liver with reference to its significance in liver injury. 36 33

Electron microscopical studies were carried out on coded liver biopsy specimens from chimpanzees inoculated with human hepatitis A or B virus. Hepatitis B was recognized by the presence of hepatitis B core particles in hepatocellular nuclei. Hepatitis A was characterized by unidentified large, dense, and more irregular heterochromatin-like particles in hepatocellular nuclei coincidental with peak aminotransferase activities. As type A hepatitis illness became manifest in the chimpanzees, mitochondrial cristae were curled and attenuated, and clusters of endoplasmic reticulum were tightly packed. In contrast, the livers in viral hepatitis B showed mainly hypertrophy of tubular smooth endoplasmic reticulum. This suggested different pathogenetic mechanisms in A and B chimpanzee viral hepatitis.
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PMID:Chimpanzee livers after infection with human hepatitis viruses A and B: Ultrastructural studies. 40 99

Electron microscopic findings made on microsomal fractions of rat liver after treatment with microsomal antibodies obtained from the blood of patients diagnosed as having chronic aggressive hepatitis and liver cirrhosis and after incubation with peroxidase-labelled antihuman IgG are described and presented in this paper. Interpretation of these findings as the substrate of an antibody reaction directed against membranes of the endoplasmic reticulum of hepatocytes is discussed.
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PMID:The immunoelectron-microscopical demonstration of antibodies against endoplasmic reticulum (microsomes) in chronic aggressive hepatitis and liver cirrhosis. 88 90

A novel compound N-(2-hydroxyethyl)-maleopimarimidyl morpholide (RU 18 492), was investigated for its effect against galactosamine induced hepatitis in rats. It was found to be active in reducing both serum transaminase levels and morphological changes due to the hepatotoxin. The protection was shown to be dose related and a significant reduction in liver damage was seen at doses of 50-400 mg/kg p.o. RU 18 492 was ineffective against carbon tetrachloride induced hepatitis in rats. It was suggested that the protective effect of RU 18 492 was due to its ability to stimulate the smooth endoplasmic reticulum thus inducing a more rapid detoxification of galactosamine.
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PMID:The protective effect of a novel compound RU 18492, on galactosamine-induced hepatotoxicity in the rat. 103 74

This study reproduces in experimental animals the sequential development of all the liver lesions seen in the human alcoholic: in 15 baboons fed ethanol, all developed fatty liver, five progressed to hepatitis, and five had cirrhosis. Maintenance of a nutritionally adequate regimen despite the intake of inebriating amounts of ethanol (50% of total calories) was achieved by incorporation of the ethanol in a totally liquid diet. Upon ethanol withdrawal, signs of physical dependence, such as seizures and tremors, developed. Ultrastructural changes of the mitochondria and the endoplasmic reticulum were already present at the fatty liver stage and persisted throughout the hepatitis and cirrhosis. The lesions were similar to those observed in alcoholics (including the inflammation and the central sclerosis) and differed from the alterations produced by choline and protein defiencies. At the fatty liver stage, some "adaptive" increases in activity of microsomal enzymes [aniline hydroxylase (EC 1.14.14.1) and the microsomal ethanol oxidizing system] were observed, but these tended to disappear with the development of hepatitis and cirrhosis. Fat accumulation was also much more pronounced in the animals with the hepatitis as compared with those with simple fatty liver (an 18-fold compared with 3- to 4-fold increase in liver triglycerides). The demonstration that these lesions can develop despite an adequate diet indicates that in addition to correction of the nutritional status, control of alcohol intake is mandatory for the management of patients with alcoholic liver injury.
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PMID:Sequential production of fatty liver, hepatitis, and cirrhosis in sub-human primates fed ethanol with adequate diets. 105 27

The morphological and functional alterations of the smooth endoplasmic reticulum of the liver cell related to biliary stasis have brought attention to drug biotransformation during cholestasis. The metabolism of meprobamate, pentobarbital and tolbutamide was assessed in subjects with intrahepatic recurrent cholestasis (3), cholestatic hepatitis (6), extrahepatic biliary obstruction (7) and normal controls (16). In the patients with recurrent intrahepatic cholestasis no differences in drug metabolism were noted as compared to the control group. In cholestatic hepatitis the plasma half-lives of meprobamate (828 +/- 422 min.) and pentobarbital (39+-65) were significantly longer than in in controls (444 +/- 37 and 25.4 +/- 1.1 respectively). Tolbutamide plasma half-life appeared unchanged. The most striking variations were observed in the patients with extrahepatic biliary obstruction. In such cases while meprobamate half-life was unchanged, pentobarbital half-life was significantly prolonged (31.2 +/- 2.5) and the in vitro metabolism of the drug, using liver preparations, was decreased to less than 50% of the control value. In contrast the metabolism of tolbutamide was accelerated as evidenced by a significant decrease of plasma half-life (165 +/- 48 min. versus 384 +/- 76 of the controls) and an enhanced urinary excretion of the drug's metabolites. However the metabolism of tolbutamide in vitro did not show any difference between normal and cholestatic liver. Whatever the mechanism of the peculiar behaviour of tolbutamide in extrahepatic biliary obstruction it seems to be related to the increased bile dalt concentration during cholestasis. In fact the low values of plasma half-life increase significantly either relieving the biliary obstruction or producing a bile salt depletion with cholestyramine. Preliminary results in vitro suggest the bile salt could displace tolbutamide from albumin binding thus increasing the amount of free drug available for biotransformation by the liver. In conclusion cholestasis may affect drug metabolism depending on the degree of biliary stasis, liver cell injury and the type of drug tested. The mechanism could be that of an impaired biotransformation in the smooth endoplasmic reticulum or could involve extrahepatic factors.
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PMID:Alteration of drug metabolism during cholestasis in man. 120 63


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