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)

Sufficient quantities of human leukocyte interferon have become available for small-scale clinical studies during the past years. The present status of the interferon treatment of respiratory infections, herpes keratitis, hepatitis B, osteogenic sarcoma, and some other tumours is surveyed. The pharmaco-kinetic and toxicological data obtained are summarized. The first clinical experiments with human fibroblast interferon have also been started. The prospects for mass production of human interferons for clinical use are discussed briefly.
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PMID:Prospects for the clinical use of exogenous interferon. 19 14

Fifteen patients with chronic hepatitis B were treated with adenine arabinoside (Ara-A) or human leukocyte interferon (HLI). Cellular immune response to hepatitis B virus surface antigen and antigens prepared from herpes simplex virus, varicella zoster virus, and cytomegalovirus was measured by a lymphocyte blast transformation assay and an assay for interferon production. Measurements were made before, during, and after antiviral treatment. Unlike patients convalescing from acute hepatitis B, only 2 of 15 patients with chronic hepatitis B had significant blast transformation to hepatitis B surface antigen. One such response occurred during the pretreatment period of HLI therapy, and the other was in a patient undergoing low-dose (<10(5) U/kg per day) HLI therapy. Mononuclear cell cultures were tested for interferon production in the presence of hepatitis B surface antigen. Cells from only 1 of 15 patients produced detectable levels of interferon. In contrast, all of these patients had normal cellular immune responses to herpesvirus antigens. Transformation responses to herpes antigens decreased three- to fivefold after patients were treated with >10(5) U of HLI per kg per day. Antiviral therapy with <10(5) U of HLI per kg per day or Ara-A did not produce a detectable depression of transformation response. Ara-A produced marked lymphocytopenia and a marked lymphocyte fragility after 5 or more days of therapy. In vitro Ara-A was toxic to lymphocytes at concentrations as low as 0.5 mug/ml. These changes in lymphocyte parameters may affect the outcome of antiviral therapy.
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PMID:Effects of interferon and adenine arabinoside treatment of hepatitis B virus infection on cellular immune responses. 53 59

Four patients with chronic hepatitis B infection and chronic active hepatitis were treated with human leukocyte interferon. Three of them had consistently elevated levels of circulating Dane-particle markers, including Dane-particle-associated DNA polymerase activity, hepatitis B core antigen and Dane-particle-associated DNA. Parenteral interferon administration at a dosage between 6.0 X 10(3) and 17 X 10(4) U per kilogram per day was associated with a rapid and reproducible fall in all Dane-particle markers in the three patients. The suppressive effect was transient when the interferon was given for 10 days or less but appeared to be more permanent when administration was prolonged for a month or more. In addition, long-term interferon therapy was associated with a marked fall in hepatitis B surface antigen in two of three patients and a disappearance of e antigen in two of two patients. Interferon may be useful in limiting carrier infectivity or eradicating chronic infection.
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PMID:Effect of human leukocyte interferon on hepatitis B virus infection in patients with chronic active hepatitis. 95 Sep 57

In a randomized controlled trial of recombinant alpha-2a interferon for chronic hepatitis B, interferon antibodies developed in 21 (39%) of 54 Chinese adults who received IFN. No correlation was observed between sex, age, pretreatment serum ALT level or liver histological findings and the development of interferon antibodies. Antibodies were significantly more likely to develop in patients who received lower doses (2.5 or 5 MU/m2) of alpha-2a interferon than in those who received a higher dose (10 MU/m2): 53% vs. 11% (p = 0.006). The development of interferon antibodies appeared to reverse the initial antiviral response to treatment, with reappearance of hepatitis B virus DNA in serum in 12 patients and HBeAg in three patients. Sustained clearance of HBeAg was achieved in only one (5%) patient but was achieved in seven (21%) patients without interferon antibodies. The mere presence of interferon antibodies did not preclude an antiviral response to interferon therapy, but patients with high titer neutralizing antibodies were less likely to respond. These findings suggest that interferon antibodies may negate the antiviral effects of alpha-2a interferon. A higher incidence of interferon antibodies in Chinese vs. white patients with chronic hepatitis B may contribute to the poorer antiviral response in Chinese patients.
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PMID:Interferon antibodies may negate the antiviral effects of recombinant alpha-interferon treatment in patients with chronic hepatitis B virus infection. 225 42

We previously described a cytoplasmic antigen, detected by monoclonal antibodies, in hepatocytes of chimpanzees experimentally infected with the parenterally transmitted form of non-A, non-B hepatitis virus or with the hepatitis delta virus. The expression of this antigen appears to be a host-specified response to infection with these two hepatitis viruses but not with hepatitis A virus, hepatitis B virus or enterically transmitted non-A, non-B hepatitis virus. To determine whether this antigen, found in parallel with the hepatocyte cytoplasmic structures described previously, is associated with interferon, as suggested by others, we studied by immunofluorescence liver biopsies from chimpanzees treated with an interferon inducer or exogenous interferon for the presence of the antigen. In two hepatitis B virus carrier chimpanzees and one normal chimpanzee treated with the interferon inducer polyinosinic-polyribocytidylic acid-poly-l-lysine carboxymethylcellulose, the antigen became detectable in hepatocytes within 2 weeks of initiation of the treatment, remained detectable throughout the treatment and disappeared within 4 weeks after treatment was terminated. Electron microscopy revealed that the biopsies positive for the antigen exhibited the hepatocyte cytoplasmic changes; convoluted membranes and microtubular aggregates, identical to those described originally for chimpanzees infected with non-A, non-B hepatitis virus. The antigen was not detected in any of the biopsies from a control chimpanzee that received only the carboxymethylcellulose used to stabilize the interferon inducer. In addition, liver biopsies obtained from a hepatitis B virus carrier chimpanzee during treatment with exogenous human leukocyte interferon were found to be positive for the antigen as well.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytoplasmic antigen in hepatocytes of chimpanzees infected with non-A, non-B hepatitis virus or hepatitis delta virus: relationship to interferon. 247 36

Five patients with hepatitis B surface antigen (HBsAg) positive chronic hepatitis and histologically confirmed primary hepatocellular carcinoma (PHC) were treated with 3 X 10(6) units/day of partially purified human leukocyte interferon intramuscularly for 2 consecutive months. During interferon therapy, one patient had stable disease, while the remaining four patients had progressive disease. Following interferon therapy no changes were noted in the hepatitis B viral markers or in serum alphafetoprotein levels. Data on the effects of human leukocyte interferon on lymphocyte subpopulations and on the cytotoxic activity of peripheral blood mononuclear cells against a hepatitis B surface antigen expressing primary hepatocellular carcinoma cell line are presented.
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PMID:Clinical, serologic, and immunologic effects of human leukocyte interferon in HBsAg-positive primary hepatocellular carcinoma. 299 Jun 62

Twelve male patients with chronic hepatitis B were treated by the combination of recombinant human alpha-interferon and cyanidanol. They received 3 million units of interferon twice a week and 2,250 mg of cyanidanol daily for 24 weeks. Four patients had sustained clinical improvement in which hepatitis B e antigen and DNA polymerase disappeared from sera and aminotransferase activities fell to normal levels. Elevated pretreatment aminotransferases were associated with the response to therapy. Also, decreased number of OKT4-positive cells prior to treatment were observed among responders. Side effects were minimal and all patients tolerated treatment on an outpatient basis. Twice weekly administration of recombinant leukocyte interferon with cyanidanol may be effective in treating chronic hepatitis when patients are appropriately selected.
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PMID:Treatment of chronic hepatitis B with recombinant leukocyte interferon and cyanidanol. 335 Feb 78

Fourteen out of 28 HBsAg/HBeAg-positive carriers with chronic persistent and active hepatitis were randomly assigned to human leukocyte interferon (a-IFN) treatment for three months. The remaining 14 patients served as controls. Each treated subject received a standard i.m. dose of 0.7-1.0 X 10(5)/kg/day reference units of a-IFN for 28 consecutive days, and then the same dose twice a week for two months. This treatment regimen was well tolerated, and no remarkable side effects were recorded. At six months the number of patients who permanently lost HBV-DNA from serum was significantly higher in the treated group (p = 0.006) than in the untreated group. These results suggest that a less expensive and well tolerated treatment regimen based on low dosage of a-IFN may be as effective in producing permanent inhibition of hepatitis B virus replication as a treatment regimen based on larger dosage.
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PMID:Permanent inhibition of viral replication induced by low dosage of human leukocyte interferon in patients with chronic hepatitis B. 337 47

Disappearance of proteinuria was observed in a patient with hepatitis B-associated chronic glomerulonephritis after treatment with leukocyte interferon. The decrease of proteinuria was preceded by the disappearance of both deoxyribonucleic acid polymerase activity and hepatitis B e antigen from the patient's sera.
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PMID:Improvement of proteinuria in a case of hepatitis B-associated glomerulonephritis after treatment with interferon. 379 87

Seven children with chronic active hepatitis (CAH) and one child with persistently abnormal results of liver function test due to hepatitis B virus (HBV) infection were treated with human leukocyte interferon (Hu-alpha-IFN). Five of them were positive for eAg and two of the three who were measured for DNA polymerase (DNAP) activity in sera showed moderate elevations of its levels. Hu-alpha-IFN was injected intramuscularly daily or once weekly at doses of 0.05-1 X 10(6) IU. The total dose per patient varied from 10.5-54 X 10(6) IU. After administration of Hu-alpha-IFN, rapid loss of eAg was observed in two of the five eAg patients, and DNAP activity reverted to normal ranges in the two patients with moderate elevations of its levels. One of the patients who lost eAg has retained normal serum glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase levels for more than 2 years after therapy with Hu-alpha-IFN. Serial hepatic biopsies were performed in only one patient. In the second biopsy, 3 months after therapy with Hu-alpha-IFN, infiltration of inflammatory cells in the portal region was improved compared with earlier findings. Immediate and/or prolonged adverse side effects were not observed during or after administration of Hu-alpha-IFN. For the present, we propose these six conditions for use of Hu-alpha-IFN in children with HBV infection. Children should: (a) be more than 1 year old; (b) have abnormal liver function for more than 6 months; (c) have a liver biopsy demonstrating CAH; (d) have moderate elevation of DNAP activity; (e) be eAg positive; and (f) be unresponsive to other treatments.
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PMID:Therapeutic effects of human leukocyte interferon on chronic active hepatitis B in children. 398 64


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