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)

In this paper we report on anti-HBc-titers, HBcAg, DNApolymerase activity in the serum and intracellular HBsAg in healthy HBsAg-carriers and patients with HBsAg-positive inflammatory liver diseases. 32/44 patients with acure virus-B-hepatitis were negative for anti-HBc in the first week of the disease. Anti-HBc-titers in healthy HBsAg-carriers varied between 1:10 and 1:32,000 (medium titer 1:4,000). In HBsAg-positive CAH we found a medium titer between 1:32,000 and 1:64,000, in cases with CPH of about 1:16,000. All autoimmune type CAH showed anti-HBc-titers less than 1:10. By immunofluorescence we could demonstrate in a group of 71 asymptomatic HBsAg-carriers in none of the healthy HBsAg-carriers HBcAg in the liver cell nuclei. In contrast HBcAg could only be found in 4/5 HBsAg positive CAH- and 6/9 CPH patients. No elevated DNApolymerase activity could be demonstrated in healthy HBsAg-carriers. Out of 44 patients with virus-B-hepatitis only 3 showed elevated DNApolymerase activity. On the other hand DNApolymerase elevation was demonstrable in 17/37 cases with CAH and 9/15 with CPH. The investigations showed a strong correlation between the demonstration of HBcAg in the serum and the DNApolymerase activity. The characteristic findings enabled us to differentiate between "healthy" HBsAg-carriers and HBsAg-carriers with inflammatory liver diseases.
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PMID:Anti-HBc, HBeAg and DNApolymerase activity in healthy HBsAg carriers and patients with inflammatory liver diseases. 64 1

A specific and sensitive radioimmunoassay was used to measure the levels of antibody to a liver-specific membrane lipoprotein in patients with acute and chronic liver disease. Antibody was detected in 29 of 30 patients with chronic active hepatitis (all of 15 HBsAg-negative and 14 of 15 HBsAg-positive cases), and in 10 of 17 patients with chronic persistent hepatitis but at significantly lower titer. The titer of antibody to the lipoprotein showed a significant correlation with activity of disease as judged histologically and biochemically. Transiently elevated levels were found in 20 of 21 patients with acute viral hepatitis, but there was no correlation with the degree of liver damage. Antibody to liver-specific membrane protein may be part of the final common pathway of liver-cell damage in both HBsAg-positive and HBsAg-negative chronic activite hepatitis, whereas other immune mechanisms determine the liver-cell injury in acute viral hepatitis.
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PMID:Detection of antibodies directed against a liver-specific membrane lipoprotein in patients with acute and chronic active hepatitis. 66 44

Thirty-four persistent healthy carriers of HBsAg (serum HBsAg detectable for longer than 3 months with normal liver function tests and normal liver histology or slight aspecific abnormalities) were discovered by routine testing of household relatives of B virus hepatitis patients. The carriers were followed-up for 11 to 37 months by clinical control, liver function tests and liver needle biopsy. None carrier had previous jaundice. During the follow-up period, in 17 of the 34 subjects, was there no evidence of deterioration in either clinical state, liver function of pathological findings. In 5 of the 34 carriers, HBsAg disappeared from serum after a period ranging from 6 to 12 months. The remaining 12 cases developed clinical and histological picture of acute viral hepatitis after 6 to 29 months (mean 12 months). Of these 12 patients, 6 recovered and become HBsAg; 2 remained HBsAg healthy carriers despite normalization of biochemical and histological abnormalities; 3 progressed from the acute stage to antigen positive CAH. The remaining one case could not be followed-up after the acute hepatitis. Our data indicate that the outcome of the HBsAg carrier state is unpredictable and stress the need of long-term follow-up surveillance.
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PMID:The significance of the Australia antigen (HBsAg) persistent healthy carrier "status": a long-term follow-up study of 34 cases. 66 17

58 patients with acute hepatitis type B, including 13 with fulminant hepatitis, were tested on presentation for HBeAg. Positive results were obtained in 24%. The frequency was highest in those with fulminant hepatitis (46% positive), and this was probably related to the earlier presentation of patients with this condition. Patients with acute hepatitis who were HBeAg-positive had had a significantly shorter duration of symptoms than those who were HBeAg-negative at presentation. HBeAg was still detectable more than 3 weeks after the onset of symptoms in only 2 patients, both of whom progressed to chronic active hepatitis. The early detection of HBeAg in patients with acute hepatitis is of no prognostic significance, but its persistence may provide the earliest evidence of potential chronicity.
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PMID:HBeAg in viral hepatitis type B. 66 77

Membrane-fixed IgG on isolated hepatocytes from biopsy material could be demonstrated by direct immunofluorescence in nine of thirty-four patients with acute virus-B hepatitis and in seventeen of forty-nine cases with chronic active hepatitis (CAH). Patients with acute virus-A hepatitis, chronic persistent hepatitis (CPH) or metabolic liver diseases did not show this phenomenon. Cases with CAH and IgG on the hepatocytes-HBsAg-positive as well as HBsAg-negative-had high inflammatory activity. Antibodies against HBsAg were not present in any serum. Autoimmune phenomena (antibodies against smooth muscle, mitochondria and nuclei) were only rarely demonstrable. The findings suggest that an antibody- or immune complex-mediated lymphocyte cytotoxicity may be involved in the pathogenesis of chronic liver diseases.
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PMID:Studies on the pathogenesis of chronic inflammatory liver diseases. I. Membrane-fixed IgG on isolated hepatocytes from patients. 76 15

The histopathology of acute and chronic infections associated with viral hepatitis is reviewed and illustrated. Particular attention is directed to changes that help to differentiate chronic persistent from chronic active viral hepatitis. Features that help to identify the intravenous drug abuser who has hepatitis, whether acute or chronic, include the presence of particulate birefringent material (usually talc) in reticuloendothelial cells, as well as tissue eosinophilia. Ground-glass hepatocytes are characteristic of the HBAg carrier. They may be present in chronic persistent and chronic active hepatitis and in cirrhotic livers with or without hepatocellular carcinoma. Ground-glass cells which contain the surface component of the HBAg, can be stained specifically by a number of stains that include aldehyde fuchsin and orcein. The cirrhotic liver of the HBAg-seropositive patient may show liver-cell dysplasia, a premalignant change.
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PMID:Light microscopic morphology of viral hepatitis. 80 46

The heterogeneity of the clinical responses to hepatitis A and B infection is well known, and may in part relate to different etiologic agents (hepatitis A, B, "C", etc.) as well as to the individual hosts' immune responses. The spectrum of disease ranges from anicteric asymptomatic infections to fulminant hepatic necrosis with hepatic failure and death. Although the clinical presentation is varied, there are essentially two patterns of necrosis that can be seen histologically during the first few weeks of clinical symptoms. The more common pattern is focal, and necrosis is scattered throughout the hepatic lobule. Less commonly, zones of necrosis that bridge between the portal--portal or portal--central areas of the lobule develop. When the latter process (bridging necrosis) is extensive, confluent lobules may be destroyed. Patients with focal patterns of necrosis eventually recover without sequelae, whereas a sizable proportion (30-60%) of patients who have bridging or multilobular necrosis progress to chronic active hepatitis, postnecrotic cirrhosis, or progressive hepatocellular failure. There is increasing evidence that these widely differing clinical and histologic responses to hepatitis infection may be related to differences in the immune response.
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PMID:The diagnosis and pathogenesis of clinical variants in viral hepatitis. 80 49

The incidence of HBAg in viral hepatitis, in chronic active hepatitis and in cirrhosis has been investigated by using immunological methods and a solid-phase radioimmunoassay. RIA demonstrated as positive: 90% of 20 patients with posttransfusion hepatitis; 88% of 50 patients with acute viral hepatitis; 100% of 13 patients with chronic active hepatitis and 35% of 20 patients with cirrhosis; whereas the frequency of HBAg in the same patients appeared to be lower by AGD, CIEP and CF. The measure of antigenaemia has been obtained by use of HBAg (ad) dose response standard curve. The quantitative HBAg data of an eight-week follow-up of fully recovered 15 patients with acute hepatitis are reported. In the first week it appeared a distribution of the HBAg levels into three classes of values. The concentration of HBAg in the serum became lower week by week and in 8th week the antigen was no longer detectable. The radioimmunoquantitation of HBAg in the serum of patients suffering from chronic acitve hepatitis and cirrhosis showed wide levels of antigenaemia ranging between 17 and 5100 ng ad equivalent/ml. The use of a dose response standard curve in order to quantify HBAg in the serum represents a further increased sensitivity of RIA.
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PMID:Hepatitis B virus antigen quantitation by radioimmunoassay (RIA) in viral hepatitis and in chronic liver diseases. 80 25

89 randomized liver patients (42 with chronic hepatitis, 25 with hepatic cirrhosis, 14 with hepatitis of protracted evolution, 8 with alcohol-toxic adiposis hepatica, stage II) are reported, in whom considerable functionally and histologically identifiable therapeutic results were achieved by combined i.v. and oral treatment with thioctic acid. According to expectation, the most favourable results were found in alcohol-conditioned chronic liver diseases; however, also in chronic active hepatitis, resistant to treatment, a therapy could be promising. The oral therapy with thioctic acid, producing no side effects, is especially suited for the long-term outpatient treatment of chronic hepatitis and hepatic cirrhosis of toxic and posthepatic etiology.
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PMID:[A contribution to the treatment of chronic liver diseases (author's transl)]. 82 8

With an immunofluorescence technique using rabbit hepatocytes isolated by a non-enzymatic method an autoantibody directed against liver-cell-membrance was identified. Sera from 361 patients with various liver diseases and 274 patients with primary non-hepatic diseases-many associated with non-organ-specific auto-antibodies-were examined. The antibody (LMA) was found in 27 out of 72 patients with hepatitis-B-surgace antigen (HBsAg)-negative chronic active hepatitis and in 17 out of 28 patients with HBsAg-negative non-alcoholic cirrhosis. Only two patients had LMA and HBsAg, and both had chronic active hepatitis. One patient with extrhepatic disease was found to have LMA, and this patient had biochemical evidence of liver disease. Hence there is a close correlation between the presence of LMA and HBsAg-negative chronic inflammatory liver diseases and its detection may help in diagnosis.
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PMID:Liver-cell-membrane autoantibody specific for inflammatory liver diseases. 83 76


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