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)

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.
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PMID:Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage. 70 Mar 29

A patient presenting with nephrotic syndrome was found to have hepatitis B surface antigen-positive chronic active hepatitis and membranoproliferative glomerulonephritis. Glomeruli stained positive for hepatitis B surface antigen, IgG, and C1q. After spontaneous clearance of hepatitis B surface antigen both the glomerulonephritis and the chronic active hepatitis improved. The natural history, pathogenesis, and treatment of this disease complex are discussed.
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PMID:Reversibility of hepatitis B virus-induced glomerulonephritis and chronic active hepatitis after spontaneous clearance of serum hepatitis B surface antigen. 71 Aug 68

Immunosuppressive treatment with prednisolone and/or azathioprine has been assessed in three chronic liver diseases with immunological features, namely chronic active hepatitis, cryptogenic cirrhosis and primary biliary cirrhosis. In chronic active hepatitis, controlled prospective clinical trials have shown clinical, biochemical and hepatic histological improvement when prednisolone with or without azathioprine is employed. Azathioprine alone has no advantage over placebo tablets. Cirrhosis is probably not prevented. Selection of patients for treatment, the response and therapeutic regimes are discussed. Patients with hepatitis B surface antigen positive chronic active hepatitis have a worse therapeutic response than those patients with chronic active hepatitis who are HBsAg negative. In primary biliary cirrhosis, corticosteroid treatment is contra-indicated on account of bone thinning. Azathioprine has been used in controlled clinical trials and is of only marginal benefit.
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PMID:Immunosuppressive therapy in chronic liver disease. 71 60

To localize immune complexes in viral hepatitis Type B and to assess their pathogenic role, we examined by the direct fluorescent-antibody technic 21 liver specimens with hepatitis B core antigen (HBc Ag) in hepatocytic nuclei from 10 patients with HBs Ag-seropositive acute viral hepatitis and from 11 patients with HBs Ag-seropositive chronic active hepatitis. IgG with in vitro fixation of complement was demonstrated in HBc Ag-containing hepatocytic nuclei of all patients with chronic active, but not in those with acute viral hepatitis. All patients except for one had antibody to HBc Ag in the serum as determined by indirect immunofluorescence. The evidence suggests that intranuclear IgG in chronic active hepatitis has anti-HBc specificity and forms immune complexes with HBc Ag. The binding of IgG to intranuclear HBc Ag might have pathogenic importance in chronic active hepatitis.
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PMID:Immune complexes in hepatocytic nuclei of HB ag-positive chronic hepatitis. 76 64

This paper describes immunofluorescence studies on liver cell surface localization of hepatitis B surface antigen (HBsAg) and of IgG in acute and chronic hepatitis and in cirrhosis. In acute hepatitis B, HBsAg was found at the surface of hepatocytes in an early phase of the disease, but not during the recovery. This finding is consistent with the hypothesis that immune reactions to HBsAg may be responsible for the liver cell lysis. In HBsAg-positive chronic hepatitis and cirrhosis the antigen was found in the cytoplasm, but not on the surface of the hepatocytes, while in HBsAg-negative cases the antigen could not be detected in the liver cells. Both in HBsAg-positive and in HBsAg-negative chronic active hepatitis (CAH) and cryptogenic cirrhosis IgG bound to the membrane of the hepatocytes could be detected, suggesting a role of antibodies in the pathogenesis of the disease.
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PMID:Liver cell surface localization of hepatitis B antigen and of immunoglobulins in acute and chronic hepatitis and in liver cirrhosis. 78 18

Anti-HBc, the antibody to core antigen of hepatitis B virions, was assayed by a new solid phase sandwich radioimmunoassay inhibition method in the sera of 26 patients with HBsAg-negative chronic active hepatitis (CAH) and 31 patients with primary biliary cirrhosis (PBC). The sensitivity of the method was validated by finding anti-Hb titers averaging greater than 1:1000 in a group of 8 chronically HBsAG-positive individuals, 4 of whom had chronic persistent hepatitis and 4 of whom had no histological or biochemical evidence of liver disease. However, anti-HBc was not detectable in any of the 26 patients with HBsAg-negative CAH. Sera from 2 of the 31 PBC patients contained anti-HBc but only in low titers, a distribution of anti-HBc similar to that found among a comparison group of medical personnel. Anti-HBc testing among PBC patients and control subjects identified a few persons in whom negative tests for HBsAg and anti-HBs failed to identify previous hepatitis B infections. Nevertheless, the uniformly negative tests for anti-HBc among our HBsAg-negative patients with CAH provide additional evidence that this subgroup, typically young-middle age females, seldom derive CAH from hepatitis B infection.
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PMID:Antibody to hepatitis B core antigen in chronic hepatitis and primary biliary cirrhosis: evaluation by a new autologous solid phase radioimmunoassay. 83 11

The Australia-antigen (HBSAG) is a simple detectable marker of an infection with hepatitis B virus. By demonstration of HBSAG an acute hepatitis B can be differentiated from other forms. Likewise the detection of HBSAG in chronic active hepatitis can differentiate the viral induced type from the autoimmune type. HBSAG is important with respect to the prognosis of an acute hepatitis B, because persistence for some months points at a transition to chronic hepatitis.
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PMID:[Significance of Australia antigen in the differential diagnosis and prognosis of hepatitis]. 84 84

The different types of immune responses occurring during hepatitis B virus infection are reviewed. The responses specific for HBsAg (hepatitis B surface antigen) are important in the pathogenesis of chronic liver disease. The cell-mediated immunity specific for this antigen seems to be responsible for cytolysis occurring when the antigen is located within the hepatocyte (acute and persistent hepatitis). It is also responsible for the subsequent elimination of the virus. Immune complexes in antibody excess probably provoke the lesion of fulminant hepatitis. Complexes in the zone of antigen excess, which are responsible for the extrahepatic lesions of the prodromic phase, may perhaps also play a pathogenetic role in some forms of chronic active hepatitis.
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PMID:[Immune mechanisms in hepatitis B. New aspects and consequent practices]. 85 20

There is as yet no specific treatment for viral hepatitis, and in an uncomplicated course no further action apart from moderate bedrest is necessary. The patient should however, be isolated in a special ward. In fulminant hepatic failure the benefit of glucocorticoid therapy is still controverted and appears to depend on an early beginning. Treatment with HBsAg-rich human serum in fulminant hepatitis B is still under evaluation. In chronic active hepatitis the administration of azathioprine in combination with glucocorticoids is highly effective, and it appears to be irrelevant whether HBsAg is present in plasma or not; however, the best results have been achieved in "lupoid" hepatitis. The use of transfer factor, laevamisol or thymosin to suppress T-cell action on antibody production of the B-cells cannot yet be finally evaluated with respect to its effectiveness in chronic active hepatitis. Prevention is of major importance in solving the problems involved in hepatitis B infections. Recent experience with active immunization using HBsAg-rich sera or purified formalin inactivated HBsAg preparations suggest the possibility of successful vaccination against hepatitis B in the near future, but the precondition for obtaining sufficient quantities of vaccine is to find suitable culture media for the virus.
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PMID:[Therapy of hepatitis B. Practical implications]. 85 9

108 adult patients and 34 children with chronic active hepatitis (CAH) are divided in four groups on the basis of presence and absence of hepatitis B surface antigen (HBsAg) and autoantibodies (AutoAb). There are significant differences in the numeric distribution among the four groups and the sex distribution between adult patients and children, but no differences in the frequencies of the HLA antigens tested. An increased frequency of HLA-B8 (and HLA-A1) compared with normal controls and the other groups is only found in autoimmune types of CAH, characterized as HBsAg-negative, AutoAb-positive CAH. HBsAg-negative, AutoAb-negative forms of CAH are called cyptogenic CAH and these are most likely non-hepatitis B virus induced types of CAH. In these and hepatitis B virus induced forms of CAH no significant deviation of any HLA antigen tested could be found.
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PMID:HLA in different forms of chronic active hepatitis. A comparison between adult patients and children. 86 30


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