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)

To measure human serum ferritin and rat plasma ferritin a non-competitive enzyme-linked immunoassay has been developed using horseradish peroxidase as the enzyme. In this assay it proved necessary to use heated rat plasma to obtain reproducible ferritin values. The heating procedure caused a loss of 38% of the plasma ferritin. Rat plasma ferritin values have been corrected for this loss. The standard deviation, from duplicate normal human and rat samples is 10 ng ferritin/ml serum and 69 ng/ml plasma, respectively. (The mean ferritin concentrations are: in human sera, 82 ng/ml and in rat plasma 762 ng/ml.) Mean recovery of added liver ferritin in the human serum is 104% +/- 4% (+/-S.E.M') and in the rat plasma 101% +/- 3% (+/- S.E.M.). Normal ferritin concentrations varied in the human material between 30 ng/ml and 300 ng/ml serum, and in the rat plasma between 500 ng/ml and 1300 ng/ml. During increased body iron and acute hepatitis the ferritin concentrations, in patients as well as in rats, exceeded the upper limit of the normal values in most cases. During human hepatitis high serum ferritin levels combined with high serum iron levels were measured. The high serum iron concentrations could not be explained by the high serum ferritin concentrations, even if the iron content of the ferritin is supposed to be high.
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PMID:An enzyme-linked immunoassay for ferritin in human serum and rat plasma and the influence of the iron in serum ferritin on serum iron measurement, during acute hepatitis. 67 92

Human liver contains an acid cholesterol ester hydrolase (CEH) of presumed lysosomal origin, but its significance is unknown. We developed a modified CEH radioassay suitable for needle biopsy specimens and measured hepatic activity of this enzyme in 69 patients undergoing percutaneous liver biopsy. Histologically normal livers hydrolyzed 5.80 +/- 0.78 SEM mumoles of cholesterol ester per hr per g of liver protein (n, 10). Values were similar in alcoholic liver disease (n, 17), obstructive jaundice (n, 9), and miscellaneous hepatic disorders (n, 21). In contrast, mean hepatic CEH activity was more than 3-fold elevated in 12 patients with acute hepatitis, 21.05 +/- 2.45 SEM mumoles per hr per g of protein (P less than 0.01). In 2 patients studied serially, CEH returned to normal as hepatitis resolved. CEH activity in all patients paralleled SGOT levels (r, 0.84; P less than 0.01). There was no correlation with serum levels of free or esterified cholesterol nor with serum activity of lecithin-cholesterol acyltransferase, the enzyme responsible for cholesterol esterification in plasma. These studies confirm the presence of CEH activity in human liver and show markedly increased activity in acute hepatitis. The pathogenesis and clinical significance of altered hepatic CEH activity in liver disease require further study.
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PMID:Hepatic cholesterol ester hydrolase in human liver disease. 68 May 3

In a clinical series of 148 patients with acute hepatitis, serological analysis of hepatitis A and hepatitis B markers revealed 16% of the cases as hepatitis type non-A, non-b. Hepatitis A was diagnosed in 27% of the patients with drug addicts as the predominating category, while serological evidence of hepatitis B infection was found in 57%, again with drug addicts in the majority. Drug addicts also predominated among the non-A, non-B cases, and possibly this category of patients is today the main reservoir not only of hepatitis B but also of hepatitis A and non-A, non-B.
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PMID:The epidemiological pattern of hepatitis A, B, and non-A, non-B in Sweden. 72 9

A solid-phase radioimmunoassay using anti-HBe-coated polysterence beads and iodine-125-labeled anti-HBe of human origin was developed for the detection of HBeAg. Anti-HBe could be determined by a blocking test. Both assays were about 500-fold more sensitive than immunodiffusion. Few nonspecific positive results for HBeAg could be recognized in the anti-HBe test by increase in cpm over that of the negative control. HBeAg was not found in acute hepatitis A and non A-non B hepatitis or in a control group of accident patients. On admission to the hospital 12 of 48 (25%) acute hepatitis B patients from Greece and 17 of 20 (85%) acute hepatitis B patients from Germany were HBeAg-positive. All 39 initially HBeAg negative sera were already anti-HBe positive. Tests of the acute stage and follow-up sera of the 20 German patients indicated that HBeAg is regularly present in the incubation period and early acute phase of hepatitis B. After onset of disease the antigen is cleared from the serum very rapidly in uncomplicated cases and is usually followed by the appearance of anti-HBe. Like anti-HBc, anti-HBe can serve as a tool for the diagnosis of hepatitis B after the disappearance of HBsAg.
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PMID:Detection of HBeAg and anti-HBe in acute hepatitis B by a sensitive radioimmunoassay. 73 Dec 22

The probable etiology and outcome of bridging hepatic necrosis found on a liver biopsy performed within three months of the onset of clinical illness was evaluated in 42 consecutive patients with this finding. Eighteen of the patients (43%) had a probable drug etiology for their hepatitis. Ten patients had HBSAG-positive acute hepatitis. Fourteen patients had neither drug-induced disease nor proven HBSAg-positive hepatitis. One patient from the drug-induced group died, but the other 17 had complete clinical recovery. Eight of ten in the hepatitis B antigen-postive group cleared their antigen and had complete clinical recovery. Chronic hepatitis developed in two who remained persistently HGSAg positive. Eight of the patients in the group with unknown etiology recovered, while six developed evidence of active chronic liver disease. This incidence of active chronic liver disease is significantly greater than that found in the drug-induced group (P less than 0.02). We conclude that drug-induced hepatitiis accounts for a significant proportion of patients of acute hepatitis who have bridging hepatic necrosis on liver biopsy. However, in these drug-induced cases the finding of bridging hepatic necrosis does not appear to be associated with an increased risk of development of active chronic liver disease.
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PMID:Bridging hepatic necrosis. Etiology and prognosis. 73 15

Stokke has described a lysosomal cholesterol ester hydrolase (CEH) in human liver. To clarify the significance of this enzyme, we first modified Stokke's assay to enable CEH determination in hepatic needle biopsies. Studies established optimal pH of 4.6--5.2 and linearity of hydrolysis for at least 12 hours, using homogenates containing about 2 mg liver and radiolabeled cholesterol oleate as substrate. The assay was then applied to patients undergoing percutaneous needle biopsy. Hepatic CEH activity in alcoholic liver disease, obstructive jaundice and a variety of other hepatic disorders was not significantly different from that in histologically normal livers. In patients with acute hepatitis, however, mean CEH activity was more than 3-fold increased (P less than 0.01). Values paralleled SGOT levels, returned to normal as hepatitis resolved, and were unrelated to serum cholesterol levels or to lecithin:cholesterol acyltransferase activity. In contrast to CEH, activity of acid phosphatase, a standard lysosomal marker enzyme, was the same in hepatitic as in normal livers. We conclude that CEH can be assayed in needle biopsies of human liver, that its activity increases in acute hepatitis, and that this is probably not simply due to a nonspecific general increase in lysosmal enzymes.
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PMID:Studies on human hepatic cholesterol ester hydrolase in liver disease. 74 52

To determine the clinical significance of serum bile acid measurements, changes in the serum bile acid composition in liver diseases and endogenous bile acid clearance due to test meal loads were investigated. In the case of changes in the serum bile acid composition, a characteristic pattern of a remarkable increase of chenodeoxycholic acid (CDCA) was found in fulminant hepatitis. In patients with acute hepatitis, increases in CDCA were somewhat greater than those of cholic acid (CA) and there was tendency for these changes to precede changes in other liver function tests. In cases of extrahepatic obstructive jaundice, the CA/CDCA ratio was a large value exceeding 1.0. In investigations of endogenous bile acid clearance, serum bile acid concentration two hours after the text meal load clearly reflected the hepatic disorder and it was useful in differentiating between active and inactive form in chronic hepatitis and compensation and decompensation in liver cirrhosis.
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PMID:Clinical significance of serum bile acid measurement in liver diseases. 74 93

The clinical course and histological changes in the liver during a presumed adverse reaction to the drug dantrolene sodium are described in four patients. After a typical prodrome one developed a moderately severe hepatitis-like illness. Another also had a prodrome but never became jaundiced. In the other two, abnormal liver function tests were detected on routine screening. In each case liver biopsy showed changes typical of an acute hepatitis, but the severity was unrelated to the clinical presentation. In addition, there were also changes in the portal tracts resembling ascending cholangitis. In each case liver function tests returned to normal after withdrawing treatment with dantrolene.
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PMID:Hepatitis from dantrolene sodium. 76 34

Chronic hepatitis was diagnosed on liver biopsy of 76 patients; 52 (68%)had HBsAg. Of the 52 patients with HBsAg, 23% had HBsAg shown by immunofluorescence on the liver, while it could not be detected with radioimmunoassay on the serum; 77% had HBsAg detectable in liver and in serum, and none had HBsAg in serum only. HBsAg was detected more frequently in chronic aggressive hepatitis and active cirrhosis than in chronic persistent hepatitis and cirrhosis with little activity. No correlation was found in the different forms of chronic hepatitis between the HBsAg status on the one hand, and levels of transaminases, gammaglobulins, and auto-antibodies on the other. Acute hepatitis was diagnosed on liver biopsy of 24 patients; 50% had HBsAg. Liver tissue positivity was very low in the fully developed stage compared to serum positivity. In 146 patients with other liver ailments, both liver and serum were negative for HBsAg.
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PMID:Hepatitis B surface antigen (HBsAg) in the liver of patients with hepatitis; a comparison with serological detection. 77 38

One hundred liver biopsies from 100 hepatitis patients were examined by the indirect immunofluorescent technique for the detection of HBsAg. Of the 60 positive specimens 52 were diagnosed as various types of chronic hepatitis and 8 were acute hepatitis. Four main distribution patterns of HBsAg were obtained: full cytoplasmic fluorescence with diffuse lobular distribution; cytoplasmic fluorescence with spotty distribution; peripheral fluorescence in the cell membrane and/or cell peripheries; and focal cytoplasmic positivity. There was an inverse relationship between the number of positive hepatocytes and the extent of liver cell necrosis. The distribution patterns of HBsAg were distinctive in each type of chronic hepatitis and in acute hepatitis. Homogeneous full cytoplasmic fluorescence, distributed diffusely in the whole liver lobule, was observed in chronic persistent hepatitis and in cirrhosis with little activity whereas peripheral liver cell membrane and/or peripheral cytoplasmic fluorescence associated with cytoplasmic positivity in a smaller number of hepatocytes was a characteristic finding in chronic aggressive hepatitis, active cirrhosis, and acute hepatitis with possible transition to chronicity. Focal cytoplasmic fluorescence was observed in acute hepatitis and a group of biopsies in chronic hepatitis in which HBsAg was detected in the liver but no antigen was detectable in the serum. The results show that the different patterns of distribution of HBsAg in the liver biopsy are helpful for the histological diagnosis of different types of HBAg positive viral hepatitis and are consistent with the hypothesis of the role of specific immune response in the pathogenesis of type B viral hepatitis.
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PMID:Distribution patterns of hepatitis B surface antigen (HBsAg) in the liver of hepatitis patients. 77 39


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