Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of anti-HBcAg antibodies in the blood as determined by indirect immunofluorescence and its relation to the occurrence of HBsAg in the cytoplasm and of HBcAg and IgG in the nuclei of hepatocytes were studied in the following groups of patients (total of 123 biopsies): I. 64 HBAg-negative patients with various liver diseases; II. 51 HBAg-positive patients without therapeutical immunosuppression (6 acute hepatitis, 10 nonspecific reactive and 10 chronic persistent hepatitis, 19 chronic aggressive hepatitis, 6 "Hippie"-hepatitis); III. 8 kidney transplant recipients. It could be shown that nuclear IgG is found only if both parameters can be demonstrated at the same time: HBcAg in liver cell nuclei and anti-HBcAg antibodies in the serum in titers higher than 1:64. Accordingly, all types of hepatitis with excess formation of nuclear HBcAg (early phase of acute hepatitis, chronic aggressive hepatitis and chronic non-aggressive forms with generalized core formation, i.e. carrier state or chronic persistent hepatitis of the HBc type) may show nuclear fluorescence for IgG. All forms of hepatitis B without detectable core formation (acute hepatitis in the elimination phase, chronic non-aggressive hepatitis with isolated HBsAg expression, i.e. carrier state or chronic persistent hepatitis of the HBs type, posthepatitic phase) do not present nuclear IgG despite eventual anti-HBcAg formation. Finally, lack of anti-HBcAg or very low titers associated with lack of IgG in hepatocytic nuclei do not exclude generalized core formation in liver cell nuclei in chronic persistent hepatitis of effectively immunosuppressed patients. Although the demonstration of nuclear IgG has several diagnostic and prognostic consequences in common with the demonstration of HBcAg, a specific search for the core antigen in the tissue is needed for the correct appraisal of the HBcAg- and HBsAg tissue expression pattern and the associated disease.
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PMID:Nuclear fluorescence of liver cells for IgG in viral hepatitis B: significance and relation to hepatitis B-core and anti-hepatitis B-core formation. 32 65

Seven liver biopsies (6 chronic aggressive hepatitis B, 1 kidney transplant recipient with chronic persistent hepatitis B) are described showing differential distribution patterns of HBcAg in liver cells (with gradual transitions): pure nuclear, mixed nuclear/cytoplasmic, and pure cytoplasmic (diffuse and/or submembraneous). This was combined with spotty expression of HBsAg (cytoplasm and liver cell membrane) and with Dane particles (DP) in blood. A phasic nuclear formation and release of cores from the nucleus and of DP from the cell, respectively, is suggested. Electron microscopy (EM) of one biopsy indicates a secretory disturbance as a possible cause for HBcAg accumulation in liver cells the tolerance of which is attributed to immunosuppression therapeutically induced in 4 patients and suspected in 3 (2 dialysis patients, 1 spontaneous chronic aggressive hepatitis B).
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PMID:Evidence for phasic sequences in nuclear HBcAg formation and cell membrane-directed flow of core particles in chronic hepatitis B. 33 81

In a study of persistent abnormalities of liver-function tests in hemophilic patients deficient in factor VIII or IX and treated with factor VIII or IX concentrates, we examined 14 liver biopsies from 13 anti-HBs-positive patients. None had any symptoms of liver disease. All had chronically abnormal levels of alanine aminotransferase. Histologic studies showed chronic persistent hepatitis in eight patients, chronic active hepatitis in four and fatty infiltration with portal fibrosis in one. Indirect immunofluorescence of antiserums containing anti-HBs or anti-HBc (or both) revealed nuclear and cytoplasmic fluorescence in the hepatocytes of eight of 12 patients. Specificity testing of these antiserums confirmed that hepatitis B viral markers are present in the hepatocytes of these anti-HBs-positive patients. These histologic derangements are probably related to frequent treatment with blood products obtained from multiple donors and to the persistance of hepatitis B virus in hepatocytes despite the presence of circulating anti-HBs.
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PMID:Asymptomatic structural liver disease in hemophilia. 34 86

The 'e antigen' (eAg) is specifically associated with hepatitis B virus infections and appears to be a marker for the infectivity and a prognostic indicator of the chronicity of liver disease. Therefore we examined by immunodiffusion the presence of eAg in the seum of HBsAg-positive patients on maintenance dialysis. The dialysis patients had a significantly higher incidence of positive eAg compared with a group of unselected HBsAg-positive patients without renal failure. In most of the dialysis patients the microscopic findings in the liver revealed only 'minimal changes'. Three eAg-positive patients received a renal transplant. Afterwards they displayed an appreciably increased eAg-yield on immunodiffusion and histology revealed chronic persistent hepatitis. It is assumed therefore that the immunodeficiency of patients undergoing chronic haemodialysis is possibly a supporting factor in the synthesis of eAg, and will perhaps induce a more subscute and prolonged course of hepatitis. The synthesis of eAg after renal transplantation may be enhanced by the additional immunosuppressive therapy.
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PMID:E antigen in the serum of HBs antigen-positive patients on maintenance dialysis and after transplantation. 36 77

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.
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PMID:Hepatitis B core antigen immune complexes in the liver of hepatitis B patients. 38 86

Twenty-six untreated patients with chronic persistent hepatitis were followed prospectively for one to 17 years (mean 5.6 years). The patients developed no clinical features of chronic liver disease. Raised serum transaminase levels were usually, but not consistently, the only biochemical abnormality; gamma globulin values were normal. Serum markers of past or present hepatitis B infection were found initially in 14 patients: another two developed markers during their follow-up. Nine patients progressed to a mild or moderate chronic active hepatitis as shown by serial needle liver biopsies but there was no evidence of cirrhosis. This progression was not associated with any clinical or biochemical deterioration. Seven of these patients had presented with insidious symptoms, seven had serum markers of hepatitis B infection, and the four who were HBsAg positive had relatively lower serum HBsAg concentrations than did those patients who continued with chronic persistent hepatitis.
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PMID:Chronic persistent hepatitis: hepatitis B virus markers and histological follow-up. 46 67

Immune complexes (IC) were investigated in sera from 208 individuals with various clinical types of viral hepatitis diagnosed by clinical and laboratory criteria, including liver biopsy. Immune complexes were assessed by platelet aggregation (PI A) and by radioimmunoassay (RIA). The data were related to autoimmune phenomena (especially rheumatoid factors) and to the role that the IgM class of hepatitis B (HB) antibody might have in IC formation. Although the highest frequency of P1 A was in the few sera from patients with cirrhosis or hepatoma, the next highest was in sera from acute hepatitis patients (71%), and the lowest in sera from chronic active (57%) and chronic persistent (46%) hepatitis patients. A proportional number of patients with IC's were positive for hepatitis B surface antigen (HBs). A parallel prevalence was noted between P1 A and autoantibodies, with anti-Ig's being found more frequently in sera from acute hepatitis and chronic active hepatitis patients. The relationship between RIA results for complexes and RIA results for anti-IgG was inverse, as though anti-IgG interfered with IC reactivity by RIA. Anti-IgM pre-incubated with sera increased the amount of P1 A in sera from patients with acute hepatitis as well as in those from patients with chronic persistent hepatitis, suggesting a more frequent IgM involvement in IC's in these diseases than in chronic active hepatitis. Whereas liver cell damage in acute and active hepatitis may reflect elevated autoantibodies, the IgM class of HBs antibody may be involved in acute as well as chronic persistent hepatitis.
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PMID:Autoimmune implications of immune complexes in clinical variants of hepatitis B. 49 83

Eight patients with chronic hepatitis B infection (seven with chronic active hepatitis and one with chronic persistent hepatitis) were treated with daily intramuscular injections of human leucocyte interferon for periods of 5 to 8 weeks and in one case for 5 months. In one patient there was a marked fall in virus-associated DNA polymerase activity and in the number of DNA containing viral particles during each of two courses of interferon. Hepatitis Be antigen (HBeAg) also disappeared, the aspartate transaminase levels fell and liver histology improved. In the four other patients with detectable DNA polymerase activity there was an early fall but this was transient and in one of these patients there was a continuing rise in activity despite treatment. One other patient became HBeAg negative but hepatitis B surface antigen (HBsAg) titres were mostly unaffected by treatment. A marked decrease in T-lymphocyte mediated cytotoxicity towards HBsAg coated target cells was demonstrated and raises the possibility that an immunosuppressant action of interferon may offsets its direct anti-viral action but may also account for the improvement in liver function which occurred in some patients.
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PMID:Effects of human leucocyte interferon on hepatitis B virus replication and immune responses in patients with chronic hepatitis B infection. 50 26

Ten cases of hepatitis B virus infection were identified among asymptomatic male homosexuals. These patients shared a number of characteristics: A subclinical origin and course of infection; Persistence of HGsAg for periods exceeding six to 25 months; Persistent GPT elevation of two to five times upper normal limit; Morphological changes in the liver with portal and parenchymal inflammation (chronic persistent hepatitis, six cases; non-specific reactive hepatitis, 2 cases; cirrhosis and acute hepatitis with signs of chronicity, one case each). HBeAg was found in six cases, anti-HBe in none. These results indicate that screening for hepatitis B should be performed whenever these individuals come under medical attention in order to detect asymptomatic chronic liver diseases and to detect these silent vectors of an infection that presently shows an increased frequency among homosexuals.
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PMID:Chronic hepatitis B infection in male homosexuals. 51 38

372 children with suspected liver disease were examined for serum HBsAg. Six (three boys, three girls) were found to be positive (1.6%). Further studies of these patients for up to three and a half years revealed elimination of HBsAg in one case only. Biopsies were performed in five patients. Three showed mild chronic hepatitis (two chronic persistent hepatitis, one unspecific reactive hepatitis). Chronic aggressive hepatitis was diagnosed in one patient. One child seemed to be normal on light microscopy, but the findings on electron microscopy were abnormal, the liver cell nuclei being filled with core particles. Two thirds of the family contacts of these children showed hepatitis B marker. Two pregnancies were observed in HBsAg-positive mothers. An infection of the babies was not demonstrable.
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PMID:[Hepatitis B markers in paediatric patients (author's transl)]. 51 42


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