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)

Serial determinations of e antigen and e antibody were made in 20 patients with chronic active liver disease and hepatitis-B surface antigen (HBsAg) or antibody (anti-HBs). The presence of e antigen was associated with failure to clear HBsAg, produce anti-HBs, or respond to treatment with steroids. It is proposed that the presence of the e antigen is associated with impaired host immune responses to hepatitis-B virus infection and a poor prognosis.
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PMID:Behaviour of e antigen and antibody during chronic active liver disease. Relation to HB antigen-antibody system and prognosis. 5 88

One patient with hepatitis-B surface antigen (HBsAg)-positive chronic aggressive hepatitis, and two chimpanzee carriers of HBsAg, were each given seven doses of 10(7) I.U. of human fibroblast interferon over two weeks. The main differnce observed after treatment was a depression of the nucleocapsid hepatitis-0 core antigen in the liver, indicating that hepatitis-B virus infection is sensitive to interferon. Except for a short febrile reaction, no undesirable effects were seen after the administration of human fibroblast interferon which has not been previously given to man.
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PMID:Administration of human fibroblast interferon in chronic hepatitis-B infection. 6 May 13

Chimpanzees chronically infected with hepatitis-B virus showed transient changes in several markers of infection when treated with the interferon inducer polyriboinosinic-polyribocytidylic acid-poly-l-lysine carboxymethyl cellulose. Serum Dane-particle-associated D.N.A. polymerase, e antigen and hepatitis-B surface antigen, and intrahepatic hepatitis-B surface and core antigens diminished during treatment. Defective (D.N.A.-polymerase-negative) Dane particles increased in titre transiently during treatment; these may play a role in the modulation of hepatitis-B virus infection. Humoral immune responses in chronic hepatitis-B carrier chimps were unaffected. Interferon inducers (or exogenous interferon) may be useful for the treatment of chronic hepatitis-B virus infection.
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PMID:Modification of chronic hepatitis-B virus infection in chimpanzees by administration of an interferon inducer. 6 40

One hundred patients on chronic haemodialysis were studied prospectively over one year for evidence of hepatitis and of infection with hepatitis A or B virus. Five patients developed transient elevations of SGPT, accompanied by a consistent pattern of clinical manifestations, including low-grade fever, anorexia, nausea, hepatomegaly, and hypotension during dialysis. None of these patients had a positive test for A or B virus infection. Non-A non-B hepatitis appears to cause a specific syndrome in uraemic patients, and its transmission in a dialysis unit seems unrelated to blood transfusions.
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PMID:Non-A, non-B hepatitis: a new syndrome in uraemic patients. 12 59

The classification, clinical course, etiology and treatment of chronic hepatitis are discussed. The clinical manifestations of chronic hepatitis are of limited diagnostic use. Diagnosis must be made by liver biopsy. The disease is classified as chronic persistent or chronic active hepatitis. The prognosis for chronic persistent hepatitis is excellent, and no treatment is required. Chronic active hepatitis may progress to cirrhosis and is associated with a poor prognosis if untreated. Recognized causes of chronic active hepatitis are hepatitis-B virus infection, post-transfusion hepatitis not associated with hepatitis-B virus, and certain drugs. For drug-induced hepatitis, discontinuation of the medication is indicated. For other types of chronic active hepatitis the recommended treatment is prednisone 10 mg and azathioprine 50 mg daily.
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PMID:Drug therapy reviews: chronic hepatitis. 35 29

Seventeen mothers, all apparently healthy carriers of hepatitis-B surface antigen (HBsAg) during pregnancy, and their children were studied for four to five years to determine the transmission rate of hepatitis-B virus infection. All the mothers had antibody against hepatitis-B core antigen in addition to HBsAg. One of them, a renal transplant recipient, was persistently positive for hepatitis-B-associated e antigen (HBeAg), while the remaining 16, who were detected during screening of healthy pregnant women were positive for anti-HBe. Evidence of infection was found in the child and husband of the woman positive for HBeAg, while none of the 29 children and five husbands of the anti-HBe-positive women became infected.
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PMID:Transmission of hepatitis type B from healthy HBsAg-positive mothers. 76 11

In confirmation of earlier descriptions by Huang et al. (Huang S-N, Millman I, O'Connell A, Aronoff A, Gault H, Blumberg BS: Am J Pathol 67: 453, 1972) nuclear eosinophilic inclusions due to excess HBcAg particles have been identified in cases of chronic hepatitis B virus infection. As the euchromatin space of affected nuclei is "sanded" by numerous core particles with concomitant dissolution of the chromatin network, spiky, finely granular, and eosinophilic inclusions without a limiting membrane become visible in hematoxylin and eosin-stained paraffin sections. These HBcAg inclusions stain greyish pink with chromotrope aniline blue and are negative for orcein, the periodic acid-Schiff reaction, and the Feulgen reaction for DNA. Sanded nuclei were detected, although not always and only few in number, exclusively in HBAg-positive patients when a focal (as in chronic aggressive hepatitis) or a generalized core formation (as in immunosuppressed kidney transplant recipients) could be demonstrated by electron microscopy or immunofluorescence. Therefore, the positive finding of sanded nuclei in a persistent hepatitis B virus infection indicates an excessive core formation the extent of which should be verified by specific methods.
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PMID:Sanded nuclei in hepatitis B: eosinophilic inclusions in liver cell nuclei due to excess in hepatitis B core antigen formation. 78 2

The AusRIA 2 test has been modified for HBs antibody detection. This technique is about 7 to 8 dilution steps more sensitive for antibody detection than the IPE. Using this modified radioimmunological technique investigations have been carried out on blood donors, patients with acute and chronic liver disease and on haemophiliacs. An HBs antibody incidence of 11% was found among voluntary blood donors. Intensive clinical investigation of blood donors positive for HBs antibodies by IPE demonstrated that the Serum GOT was elevated in 11% of cases and the liver biopsy showed histological changes of different severity in 16 out of 22 cases. Investigation of 22 cases of acute HBs antigen-positive hepatitis confirmed that nearly all the patients developed HBs antibodies within 10 weeks following the disappearance of HBs antigen. The HBs antibodies persist over years. The appearance of HBs antibodies after an acute HBs antigen-negative hepatitis can be taken as an indication of a hepatitis-B virus infection also in these cases. Among 22 HBs antigen-negative chronic hepatitis cases, HBs antibodies were detectable in 52%. Sera of 111 patients with HBs antigen-negative liver cirrhosis of varying aetiology showed HBs antibodies in 29.7% of cases. The incidence was higher in males. HBs antibodies were found in 98% of patients with haemophilia. These results reveal new aspects with regard to the importance of the hepatitis-B viurs, especially in chronic liver disease. Apart from a description of the newly-developed HBs antibody test and a discussion of the results obtained using this technique, a survey is given of the importance of HBs antibody determination by means of sensitive methods for clinical and epidemiological purposes.
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PMID:[Hepatitis-B-surface-antibodies (detection, incidence, clinical importance)]. 106 4

The hepatitis-B surface antigen (HBsAG) may be persistently present in the serum in a few cases of active chronic hepatitis but the cause of the disease in most patients is unknown. In a study of 39 HBsAg-negative cases cell-mediated immunity to HBsAg was observed in 24 (62%), suggesting a high frequency of previous infection with the hepatitis-B virus. Hepatitis-B surface antibody was detectable by radioimmunoassay in six patients, in all of whom complexes of HBsAg were present in the serum on electron microscopy. Out of 12 patients with HBsAg-positive active chronic hepatitis who were also studied eight, including all those untreated at the time, showed a cellular response to the antigen. Evidence of sensitization to a liver-specific cell surface lipoprotein was found with similar frequency in the two groups. These results are consistent with the hypothesis that hepatitis-B virus infection is important in initiating the disease in many cases of active chronic hepatitis and that sensitization to the liver cell membrane antigen is the autoimmune process responsible for the perpetuation of the liver injury.
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PMID:Cellular and humoral immunity to hepatitis-B surface antigen in active chronic hepatitis. 112 73

Hepatocyte expression of pre-S1 and pre-S2 in relation to hepatitis B virus replication (hepatitis B virus-DNA in serum and HBcAg in the liver), histological activity and hepatitis delta virus superinfection was studied by indirect immunofluorescence on frozen sections of liver specimens from 68 patients with chronic hepatitis B virus infection. All 44 patients with chronic type B hepatitis had pre-S1 and pre-S2 display in the liver. The distribution of pre-S1 in the liver was membranous in one, mixed membranous and cytoplasmic in 12, and cytoplasmic in 31. The distribution of pre-S2 was membranous in one, mixed membranous and cytoplasmic in 26, and cytoplasmic in 17. Membranous expression of pre-S1 was significantly more prevalent in patients with active hepatitis B virus replication than in those without (13/28 v 0/16, p < 0.001), regardless of the histological activity, as was membranous expression of pre-S2 (27/28 v 0/16, p < 0.001). In contrast, a significantly higher extent of cytoplasmic expression of pre-S1 and pre-S2 was noted in patients without active hepatitis B virus replication than in those with. Of 24 patients with chronic type D hepatitis virus, eight had active hepatitis B virus replication, and the other 16 did not. The distribution and quantitative expression of pre-S1 and pre-S2 in the liver in these patients also correlated significantly with the status of hepatitis B virus replication and, moreover, showed little or no difference from those without hepatitis delta virus infection. In conclusion, all patients with chronic type B hepatitis had synthesis and display of pre-S1 and pre-S2 in the liver. The distribution and quantitative expression of pre-S1 and pre-S2, however, were closely related to the status of hepatitis B virus replication, but not to the histological activity. Hepatocyte expression of pre-S1 and pre-S2 in chronic type D hepatitis also correlated significantly with status of hepatitis B virus replication, and was not modulated by concurrent hepatitis delta virus infection.
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PMID:Intrahepatic expression of pre-S1 and pre-S2 antigens in chronic hepatitis B virus infection in relation to hepatitis B virus replication and hepatitis delta virus superinfection. 145 81


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