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

A study was made of latent hepatic diseases in university students. 1.4% to 1.6% of the students were positive for hepatitis B surface antigen (HBsAg), and 10.3% for anti-HBs. Of 28 students with HBs-antigenemia, 2 had chronic persistent hepatitis, and 3 minimal hepatitis, 23 being healthy carriers. Hepatitis B e-antigen (HBeAg) was detected in 44% of the students with HBsAg, and anti-HBe in 13%. Anti-HBe was significantly more frequently found in female students with HBsAg than in male students. Though most of the students with HBsAg had high titer of antibody to hepatitis B core antigen (anti-HBc), there were a small number of cases showing low titer. HBsAg and anti-HBs was detected in the same serum specimens of 2 carrier students. Liver damage was also found in 3 students without HBs-antigenemia.
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PMID:Chronic hepatitis B and hepatitis B surface antigen carriers in university students. 66 37

Twelve patients on haemodialysis for 6 months to 3 years contracted AgHBs positive hepatitis, 9 being also Ag e positive. They continued to carry the same antigens. Histological surveillance was begun from the 6th month of the disease onwards, with 2 to 4 repeated biopsies in 1,5 to 3,5 years in 9 patients, the last 3 having only one biopsy between the 8th and the 15th month. In 6 patients, the first biopsy revealed chronic persistent hepatitis (CPH) and in other 6 (5 male and 1 female) chronic aggressive hepatitis (CAH). Subsequent biopsies revealed cirrhosis in a patient treated with alphamethyldopa (Ag e +), the absence of any changes in 7 other patients (4 CPH including 3 Ag e + and 3 CAH including 2 Ag e +), and an improvement in the last. Long term surveillance of hepatitis B by repeated biopsies in haemodialysed patients reveals that histological lesions are stable at 2 years, that certain drugs may have an aggravating role and that Ag e has no prognostic value.
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PMID:[B virus chronic hepatitis in the haemodialysed uraemic patient. Correlation between hepatic lesions and the presence of antigen e in 12 patients (author's transl)]. 71 64

Serum desialylated glycoprotein level was tested for chronic hepatitic patients. The level was significantly elevated in patients with chronic aggressive hepatitis but not in chronic persistent hepatitis comparing to normal subjects. In chronic aggressive hepatitis, severe type (2B), serum desialylated glycoprotein levels were significantly enhanced but not in moderate type (2A) when compared to chronic persistent hepatitis. Sera taken serially from patients with chronic aggressive hepatitis, severe type (2B), demonstrated a slight correlation between circulating desialylated glycoprotein level and serum glutamic-pyruvic transaminase activity.
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PMID:Serum glycoproteins in the liver diseases. V. Desialylated glycoproteins in chronic hepatitis. 74 94

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

Evidence of chronic hepatitis was found on histological examination in nine out of 15 patients positive for hepatitis-B surface antigen (HBsAg) who had either chronic renal failure or a functioning renal transplant. Cirrhosis had already developed in three of the patients, who deteriorated rapidly and died. Liver biopsies from the remaining 12 patients showed the features of chronic aggressive hepatitis in two, chronic persistent hepatitis in four, and minor histological lesions in six. The persistence of HBsAg in patients with renal failure or in those receiving immunosuppressive drugs after a transplant must indicate some impairment of the normal immune response to hepatitis-B viral antigens. Nevertheless, cellular or humoral immunity to HBsAg was detected in all eight patients with chronic hepatitis tested compared with only one out of five with minimal liver lesions, which suggests that the severity of the liver damage may be directly related to the degree of immunocompetence.
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PMID:Immune response to HBsAg and the spectrum of liver lesions in HBsAg-positive patients with chronic renal disease. 77 35

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

129 blood donors found to be HBsAg-positive on routine testing were studied for evidence of hepatic disease. Twelve had already lost the antigen from the serum when histologically examined. None of these has had clinical or histological evidence of inflammatory liver disease. Two of the 129 patients showed mild icteric hepatitis, cleared the antigen during the follow up and became anti-HBs positive. The remaining 115 patients who appeared clinically healthy and who had no history of previous icteric liver disease remained HBsAg positive during a mean follow up period of 17.3 +/- 3.0 months. Forty patients from these had a normal liver histology and 37 mild to distinct steatosis but no signs of inflammatory liver disease. 11 patients a mild nonspecific mesenchymal activity but no focal necrosis, 16 patients had mild infiltration in portal tracts and a few necrotic parenchymal cells with mesenchymal reaction, 6 patients had chronic persistent hepatitis, 4 chronic aggressive hepatitis, and 1 definite posthepatic cirrhosis.
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PMID:[The characterization of clinically healthy hepatitis-b-surface-antigen (HBsAg)-carriers. Clinical, biochemical, histiological and immunological investigations in 129 case of a prospective study (author's transl)]. 78 93


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