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)

Administrations of hepatotoxicants namely carbon tetrachloride (CCl4:0.4 ml in 1.2 ml of liquid paraffin) and ANIT (1 ml of 1.5% solution in liquid paraffin) in Charles foster rats (force fed) and D-galactosamine (8 mg in water per swiss albino mouse, ip) induce the release of TNF-alpha in case of CCl4 and D-galactosamine. High TNF-alpha level was observed up to 48 hr in CCl4 and up to 24 hr in D-galactosamine treated animals. Elevated levels of biochemical like ALP and SGPT are also recorded. TNF-alpha level can be measured of tissue damage and prognosis in case of hepatitis.
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PMID:Induction of tumour necrosis factor alpha in experimental animals treated with hepatotoxicants. 145 48

Serum CA 19-9 was determined in 83 control subjects, 99 patients with pancreatic cancer, 104 with chronic pancreatitis and 137 with extra-pancreatic diseases mainly of gastrointestinal origin in order to evaluate whether hepatic factors can influence circulating CA 19-9 in pancreatic cancer. Sensitivity, specificity and accuracy of this test in determining pancreatic malignancy were: 74%, 83% and 57%. We divided patients into two groups: group A (159 cases) and group B (181 cases) with and without anatomical liver damage (presence of primary or metastatic cancer, cirrhosis, hepatitis, steatofibrosis, cholangitis). Group A presented higher CA 19-9 values as compared to group B. Significant correlations were found in group B but not in group A between CA 19-9 and ALT, ALP and total bilirubin. Multiple regression analysis (CA 19-9 dependent and ALT, ALP and total bilirubin predictor variables) was significant only in group B. The standardized partial regression coefficients found to be significant were those of ALP and total bilirubin. We can conclude that CA 19-9 is an index of pancreatic cancer with satisfactory sensitivity and specificity. The presence of anatomical liver damage seems to increase the value of this index, probably releasing CA 19-9 into the bloodstream. Extra-hepatic cholestasis may also be an important factor in elevating CA 19-9 probably by reducing the hepatic catabolism of this glycoprotein.
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PMID:How does liver dysfunction influence serum CA 19-9 in pancreatic cancer? 213 20

We report an easy, rapid method for quantifying bone isoenzyme of alkaline phosphatase (EC 3.1.3.1., ALP) in serum. The original method described by Rosalki and Ying Foo (Clin Chem 1984;30:1182-6) was somewhat simplified. In contrast to their results, we found that bone ALP is precipitated quantitatively by wheat-germ lectin. To check the clinical plausibility of the method, we used samples from several comparison groups (blood donors, children, pregnant women, patients with neoplasms but without skeletal involvement) and a large number of patients suffering from bone diseases and diseases of the liver and biliary tree. Measured activities of bone ALP nearly always correlated with the clinical diagnosis. Only patients with hepatitis often had pathological bone activities not in accord with the other findings. Possible reasons for this observation are discussed.
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PMID:Quantification of bone alkaline phosphatase in serum by precipitation with wheat-germ lectin: a simplified method and its clinical plausibility. 375 20

ALP activity has been studied during hepatitis (infection) in two genetically controlled mouse strains having different degrees of susceptibility ot MHV3 virus: A/JAX (resistant) and DBA/2 (susceptible). During the 8 days following viral infection we have compared ALP activity in serum and liver homogenates with ALP cytological localization in liver tissue (light and electron microscopy). Firstly, liver ALP activity has been demonstrated in the Disse's spaces, on the membrane of the hepatocytes microvilli whilst serum ALP was still very low. The serum ALP activity begins to increase markedly since the third day in sensitive mice (DBA/2), i.e., when the electron microscopy hepatocytes look very damaged; hepatocytes have lost most of their microvilli; necrotic vesicles, degenerative cytoplasmic organelles, lipid vesicles occurred in numerous hepatocytes. ALP activity has disappeared at the biliary pole of the cells whilst it increased at the vascular pole. Moreover, electron microscopic studies demonstrated that ALP positive cells are exclusively of lymphoid type whereas Kupffer cells remain ALP negative.
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PMID:The alkaline phosphatase activity in DBA/2 and A/JAX mouse strains injected with mouse hepatitis virus 3: a morphological and biochemical comparative study. 608 29

The lysosomal enzyme beta-hexosaminidase was elevated in different forms of hepatitis. The enzyme level was correlated to the aminotransferases in the acute stage of hepatitis A and B. In hepatitis B there was also a correlation to ALP and bilirubin. In chronic hepatitis B a significant correlation was found only to ALAT. The elevated beta-hexosaminidase levels are attributed to defective non-parenchymal liver cell function in hepatitis.
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PMID:beta-Hexosaminidase level in serum from patients with viral hepatitis as a measure of reticuloendothelial function. 645 81

Following a three-week administration of alpha-interferon (IFN-alpha), a 62-year-old woman with chronic hepatitis C manifested fever and dyspnea and showed diffuse infiltrative opacities on chest roentgenograms. Her laboratory data included results of anemia with reticulocytosis, a decreased complement level and hepatitis with elevated ALP, LDH and gamma-GTP. Because laboratory data also revealed a positive lymphocyte stimulation test for IFN-alpha, this cytokine was considered to be responsible for the development of interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction due to its immunomodulatory effects. Although these three disorders have been reported to develop singly after IFN-alpha therapy, this is the first report of a patient in whom these disorders occurred simultaneously.
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PMID:A patient with chronic hepatitis C who simultaneously developed interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction after alpha-interferon administration. 791 19

Rubella was accompanied by hepatic dysfunction in a 28-year-old male. Serum aminotransferase levels were moderately elevated and LDH markedly increased, especially LDH isoenzyme 5, whereas total bilirubin and ALP remained almost normal. GOT, GPT and LDH levels were completely normalized by the 21st hospital day. Paired antibody titers of viruses which may cause hepatitis, other than rubella, were of no significance. Laparoscopy showed enlarged, red liver. Histologic and electron microscopic findings of the liver were consistent with acute hepatitis. Hepatic damage with rubella is rare, and it is possible that the hepatic dysfunction seen in adult rubella may be mediated by an immunopathologic mechanism.
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PMID:Hepatitis in an adult with rubella. 828 39

The toxicological correlation between blood biochemical parameters and liver histopathological findings was summarized mainly in rats and dogs on the basis of our experiments and published papers. In rats and dogs with hepatocytic necrosis, GPT and GOT increased with a good correlation to necrotic severity. In dogs with cholestasis, ALP, gamma-GTP, T.BIL and BSP retention rates increased. In mixed types of hepatitis or cholestasis and hepatic necrosis, GPT, GOT and ALP increased in rats and dogs and additionally gamma-GTP and BSP retention rates increased in dogs. In hepatic steatosis, CHOL and TRIG decreased in rats and dogs. In hepatic injury due to accumulation of foreign materials or cell components and sinusoidal cell injury, no specific correlation with biochemical parameters was noted.
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PMID:Toxicological correlation between changes in blood biochemical parameters and liver histopathological findings. 927 20

We describe the clinical course of a group of patients with primary sclerosing cholangitis who at presentation were diagnosed to have autoimmune hepatitis. The history of one such patient is described in detail. We also compare this atypical sclerosing cholangitis (group I) to typical sclerosing cholangitis (group II) and to autoimmune hepatitis with (group III) and without (group IV) cholestasis. At presentation, mean AST in groups I and III was similar and significantly higher than in group II (P < 0.05). Mean ALP was higher in sclerosing cholangitis than in autoimmune hepatitis but not significantly so. Triaditis was present in all patients in groups I, III, and IV. Piecemeal necrosis and multilobular collapse/fibrosis were equally frequent in groups I, III, and IV. Only the response to corticosteroids helped differentiate among groups. Groups III and IV responded by normalizing AST. In group I, AST improved, but never became normal. As ALP became disproportionately abnormal (ALP-predominant pattern), cholangiography was performed, and the diagnosis of primary sclerosing cholangitis was made in all group I patients. We recommend that cholangiography be performed early in patients with suspected autoimmune hepatitis who partially respond to corticosteroids and develop an ALP-predominant pattern.
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PMID:An atypical presentation for primary sclerosing cholangitis. 936 27

The aim of the present study was to investigate the impact of the combined administration of Vitamin C and silymarin on lead toxicity. Male albino rats were subdivided into three groups: the first was a control group, the second received lead acetate in diet as 500 mg/kg diet daily, the third received the same lead acetate dose and supplemented with Vitamin C (1 mg/100g body weight) and silymarin (1 mg/100g body weight) by gastric tube three times per week. Blood samples were taken after 2, 4 and 6 weeks of treatment. Significant lead-induced elevations in serum ALT, AST, GGT and ALP activities were observed after different periods of treatment. However, serum LDLc was decreased. The intensities of RNA and apoptotic fragments of DNA were measured as optical density by Gel-pro program. Lead acetate decreased the intensity of DNA at 6 weeks and induced apoptotic DNA fragments reversibly with time. After 2 weeks of lead administration dilation and congestion of terminal hepatic veins and portal vein branches were observed. Lead also induced hepatocyte proliferation without any localized distribution among zones 1-3. Portal inflammatory infiltrate with disruption of the limiting plates (interface hepatitis), steatosis, apoptosis and mild fibrosis were detected especially by sixth week of lead administration. Combined treatment of lead-exposed animals with Vitamin C and silymarin showed marked improvement of the biochemical, molecular and histopathological findings. These experimental results strongly indicate the protective effect of Vitamin C and silymarin against toxic effects of lead on liver tissue.
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PMID:Amelioration of lead toxicity on rat liver with Vitamin C and silymarin supplements. 1559 Jan 5


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