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)

Fifty-one patients with metastatic colorectal carcinoma confined to the liver received intraarterial chemotherapy through the hepatic artery via a subcutaneous pump. The chemotherapy consisted of sequential 14-day infusions of floxuridine (FUDR) and dichloromethotrexate (DCMTX) or a 14-day infusion of FUDR and bolus mitomycin (MMC). Twenty-four patients (47%) developed hepatitis with an elevation of hepatic serum transaminase (serum glutamic oxaloacetic transaminase, SGOT, or serum glutamic-pyruvic transaminase, SGPT). The median time to develop hepatitis was 11 weeks after initiation of chemotherapy. The morphologic effects of chemotherapy were evaluated in eight patients with hepatitis. All the patients with hepatitis had normalization of the serum transaminases after temporary cessation of chemotherapy. There was a trend toward a greater chance of remission in patients who developed hepatitis. Sixty-seven percent of the patients with a therapeutic response had hepatitis, whereas only 33% of the patients without a response had hepatitis. However, this difference was not statistically significant. The occurrence of hepatitis was not related to FUDR dose, drug program (FUDR-DCMTX vs. FUDR-MMC), pump flow rate, hepatic arterial anatomy, sex, or age of the patients.
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PMID:Hepatitis in patients receiving intraarterial chemotherapy for metastatic colorectal carcinoma. 295 Jul 52

A guinea pig model of halothane hepatitis was used to explore the humoral immune response induced by multiple halothane exposures and the potential role this response might play in contributing to liver damage. Three different strains of guinea pigs (Strain 2, Amana, and Hartley) were exposed to 1% halothane under either 21 or 80% oxygen for 4 hr at 2-week intervals. In each strain, halothane induced the appearance of an antibody cross-reactive with trifluoroacetylated guinea pig serum albumin (TFA-GSA). Three of six Strain 2 guinea pigs demonstrated an association between antibody titer and serum glutamate pyruvate transaminase levels. However, the possible cause and effect relationship between these two factors requires more investigation. Hartley guinea pigs had a 4- to 11-fold higher level of anti-TFA antibody than the other two strains because of either a "higher responder" genetic background or exposure conditions that favored oxidative metabolism of halothane. Immunization of Amana guinea pigs with TFA-GSA evoked a specific anti-TFA antibody response. However, the presence of this antibody before halothane exposure did not potentiate the transient liver damage induced by exposure. Thus, these results demonstrate that in guinea pigs multiple exposures to halothane induce the formation of an antibody that recognizes a reactive intermediate of halothane formed during the anesthetic's metabolism.
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PMID:Generation of halothane-induced immune response in a guinea pig model of halothane hepatitis. 368 90

Pharmacological investigations were carried out to evaluate the hepatoprotective effects of Crepis rueppellii and Anisotes trisulcus. Ethanolic extracts of these plants were investigated for their ability to reduce mortality of mice after ethanol intoxication and to lower the activities of plasma glutamic-pyruvic transaminase (GPT) after carbon tetrachloride-induced hepatitis in rats. Crepis and Anisotes extracts and a 50:50 mixture of both at 200 mg/kg presented significant hepatoprotective effects in both experimental situations. The traditional therapeutic indications of these plants have been largely confirmed.
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PMID:Hepatoprotective properties of Crepis rueppellii and Anisotes trisulcus: two traditional medicinal plants of Yemen. 374 59

To study the clinical course and biochemical features of congenital syphilitic hepatitis, the records of all 22 pediatric patients admitted to North Carolina Memorial Hospital between 1969 and 1979 with a positive maternal, cord blood, or serum VDRL were reviewed. Of the seven infants identified with symptomatic congenital syphilis, five had clinical and biochemical evidence of liver dysfunction. All five were jaundiced (peak bilirubin ranged from 8.4 to 29.8 mg/dl, in each case greater than 40% conjugated). Peak transaminase elevation ranged from seven to 150 times normal. Serum glutamic-oxaloacetic transaminase exceeded serum glutamic-pyruvic transaminase in each infant, the difference ranging to 7,400 U. The onset of illness did not occur until after treatment had been initiated in two of these five cases. Liver dysfunction increased with treatment in all four infants with serial enzyme determinations. Liver dysfunction also persisted for more than 6 weeks after adequate treatment in two cases. Liver biopsy 5 weeks after treatment in another infant showed giant cell hepatitis. These observations suggest that treatment can potentiate liver dysfunction in congenital syphilis and that viable treponemes are not necessarily essential in the pathogenesis of the hepatitis.
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PMID:Clinical manifestations of congenital syphilitic hepatitis: implications for pathogenesis. 648 65

The molecular mechanisms responsible for hepatocyte death and the events leading to viral clearance in hepatitis B virus (HBV) infections are not well understood. Elucidation of the mechanisms involved have been complicated by the difficulty of infecting human hepatocytes with HBV in vitro and the lack of an appropriate animal model. We report an animal model of human HBV infection by in vivo transfection. We have directly introduced a replication-competent, cloned HBV construct into rat liver by using a membrane fusion-promoting cationic lipid. HBV mRNA and 3.2-kb HBV DNA were expressed in the liver by this in vivo transfection method. In the majority of rats, HBV virions and hepatitis B e antigen were found in the blood 3-7 days after transfection, after which antibody to the e antigen appeared. Two to three weeks after the transfection, glutamic-pyruvic transaminase levels were elevated in serum, hepatocyte death and lymphocyte infiltration were observed in the vicinity of the portal vein of liver, and HBV virions were no longer detected in the serum. Thus, transfection of HBV into rats resulted in histological and serological changes comparable to HBV-induced acute hepatitis in humans. In contrast, no hepatocellular injury was observed in T-lymphocyte-deficient nude rats transfected with the same HBV construct, and viremia was substantially prolonged, providing direct evidence that T lymphocytes play an essential role in liver cell injury and in the clearance of HBV. This rat hepatitis model will be useful for studying pathogenesis of HBV infection.
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PMID:Acute hepatitis in rats expressing human hepatitis B virus transgenes. 787 2

Intercellular adhesion molecule-1 (ICAM-1) is expressed on the hepatocyte membrane in patients with chronic hepatitis B and C. We assayed levels of the soluble form of this molecule (sICAM-1) in serum by an enzyme-linked immunosorbent assay method; we then analyzed the results in relation to hepatitis activity. Fifty-one patients with chronic hepatitis (22 with type B and 29 with type C) and 10 normal controls were examined. The serum levels of sICAM-1 in hepatitis B and C were significantly higher (P < 0.01) than in normal controls. The serum level of sICAM-1 was correlated with serum glutamic-pyruvic transaminase level (P < 0.01), and the level of sICAM-1 in patients in whom exacerbation was seen was significantly higher (P < 0.05) than that in patients in a remission. There was no relationship between the serum level of sICAM-1 and the degree of ICAM-1 expression on the hepatocyte membrane. These results suggest that the serum level of sICAM-1 reflects the degree of activity of chronic hepatitis B and C.
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PMID:Soluble intercellular adhesion molecule-1 in serum in chronic hepatitis B and C. 795 56

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

Four patients with acute viral hepatitis complicated by pure red cell aplasia were clinically evaluated. Two patients with hepatitis type A, one with hepatitis type B, and one with posttransfusion non-A non-B hepatitis had pure red cell aplasia. Only the patient with posttransfusion hepatitis was female, and the mean age of the four patients was 37.8 yr (31-51 yr.) The mean interval from the onset of hepatitis to the appearance of pure red cell aplasia was 30.5 days (27-37 days), and the development of hematopoietic disorders coincided with decreases in transaminase levels. Laboratory findings included peak serum glutamate pyruvate transaminase levels of 1305-3160 KU and decreases in the prothrombin time to about 50% in the two patients with hepatitis type A. Pure red cell aplasia was successfully treated by prednisolone or transfusion in all patients.
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PMID:Clinical evaluation of four cases of acute viral hepatitis complicated by pure red cell aplasia. 830 14

We previously developed a method for introducing foreign genes into liver tissue using liposomes with incorporated hemagglutinating virus of Japan (HVJ, Sendai virus), and found that liver cells transfected with the E. coli beta-galactosidase gene or the gene for hepatitis B virus (HBV) surface protein (HBsAg) expressed these proteins in vivo. Here, we analyzed cellular reactions leading to hepatitis in the liver by expressing the genes of HBV in vivo. Lymphocytes were eluted directly from liver transfected with the HBsAg genes and shown to be cytotoxic only to cells expressing HBsAg in vitro. These lymphocytes were identified as cytotoxic T lymphocytes with the CD4- CD8+ phenotype. Transfer of these lymphocytes to transgenic mice with the whole HBV genome led to elevation of the serum glutamic-pyruvic transaminase (SGPT) level, indicating the induction of hepatitis due to the cytotoxic T lymphocytes in vivo. Similarly, direct transfer of the gene for the HBV secretory core protein (HBeAg) induced expression of HBeAg in hepatocytes and the appearance of antibody against HBeAg in the serum. However, using this system, we found that the lymphocytes infiltrating the transfected liver showed no cytotoxicity specific for HBeAg. These results indicate that expression of HBsAg, one of the components of virions, in animal liver induced hepatitis efficiently through generation of specific cytotoxic T lymphocytes (CTL) without any expression of the other viral components. This in vivo experimental system should be useful for evaluating how expression of a given gene induces cellular reactions and intrinsic functions in the living body.
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PMID:Use of the hemagglutinating virus of Japan (HVJ)-liposome method for analysis of infiltrating lymphocytes induced by hepatitis B virus gene expression in liver tissue. 839 62

The male (NZW x BXSB)F1 (W/BF1) mouse, a murine model for autoimmune diseases, shows hepatosplenomegaly with lymphoid cell infiltration in the liver by 20 weeks of age. The majority of infiltrating cells are T cells, B cells and plasma cells, as seen in autoimmune hepatitis. Together with the increase in serum glutamate pyruvate transaminase (GPT) levels, anti-dsDNA antibody (Ab) and circulating immune complex (CIC) levels increase with age. These findings are compatible with those of autoimmune hepatitis in humans. In addition, a unique finding in this mouse is the accumulation of CD4+ Mac-1+ Class II+ cells in the sinusoidal space. The cells have the capacity to proliferate and differentiate into macrophages in vitro, indicating that they are the precursors of macrophages. This W/BF1 mouse provides a useful tool for not only analyzing the pathogenesis of autoimmune hepatitis but also establishing a new therapeutic strategy for it. In addition, we discuss the significance of the appearance of abnormal cells in autoimmune-prone mice.
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PMID:The appearance of unusual phenotypic cells (CD4+ Mac-1+ class II+) in the liver of (NZW x BXSB)F1 mice is possibly an animal model for autoimmune hepatitis. 924 29


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