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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Different forms of prophylaxis and therapy of HBsAg positive hepatitis are discussed. Prevention of HBsAg positive hepatitis has been attempted by passive and active immunisation. For passive immunisation against parenteral infections hepatitis B immunoglobulin (HBIG) of high titer has to be used. However, the protection provided by HBIG is incomplete and temporary. Therefore active immunisation is to be preferred for protection of high risk groups. Experiments using the 22 nm spheric particles prepared from plasma of chronic carriers showed the efficacy of this type of vaccine. The direct way to treat the different forms of hepatitis B is the eradication of the virus from the body. Success has been claimed with the use of interferon and adenine arabinoside. However, this antiviral therapy is still in an experimental stage. In some forms of HBsAg positive hepatitis the liver damage is supposed to be the result of an immune response against the virus. Immunosuppression in these conditions failed, however, to show a beneficial effect. Corticosteroids turned out to be harmful in all forms of acute hepatitis and are therefore contraindicated. Chronic hepatitis B seems to be caused by the inability of the immune system to clear the virus. Successful results have been claimed employing immune stimulative agents like BCG, levamisole, and transfer factor. Most of these reports, however, are anecdotycal and the more comprehensive studies are uncontrolled.
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PMID:Prophylaxis and therapy of HBsAg positive hepatitis. 48 86

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

To challenge the hypothesis that interferon (IF) production in chronic hepatitis-B virus liver disease is defective, lymphocytes from 14 patients with chronic active liver disease (CALD); from nine patients with chronic inactive liver disease (CILD), and from six healthy chronic carriers (HCC) were stimulated by Newcastle Disease virus. The patients with CILD showed a weak IF response by comparison with the controls (P less than 0.0005), whereas IF production by CALD patients and the HCC did not statistically differ from IF production in the healthy hepatitis-B surface antigen negative subjects who served as controls. These results indicate that IF treatment of CALD does not rely on a completely proved background.
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PMID:Normal lymphocyte interferon production in adult HBsAg-positive chronic active liver disease. 52 84

Potent sheep anti-mouse interferon globulin has been used to determine the role of virus-induced interferon in mouse hepatitis virus type 3-infected susceptible (C57BL/6), semiresistant (C3H/He), and resistant (A/J) strains of mice. Injection of anti-interferon globulin accelerated the onset of death in C57BL/6 mice, induced almost 100% mortality in C3H/He mice that usually do not die of acute disease, and caused death in 4- and 6-week-old A/J mice, but not in older mice. We conclude that interferon is an important host defense factor in the initial response of different strains of mice to MHV-3 infection. Other factors, however, such as the capacity of macrophages to restrict viral multiplication probably underlie the genetically determined susceptibility or resistance of mice to MHV-3 infection.
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PMID:Role of interferon in the pathogenesis of viral diseases of mice as demonstrated by the use of anti-interferon serum. V. Protective role in mouse hepatitis virus type 3 infection of susceptible and resistant strains of mice. 65 66

Hepatitis B antigen (HBAg) positive sera became negative after in vitro incubation with homogenates of human faeces or intestinal mucosa. This was found to occur in all sera tested by various methods. These findings suggest the existence in the human intestine of a substance able to inactivate the HBAg and that it is not an antibody or of the nature of interferon. The presence of an inhibitor could explain why B-type hepatitis is seldom if ever faecally transmitted and also the low oral infectiousness of the B virus.
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PMID:[New pathogenetic aspects of hepatitis B in relation to finding HBAg inhibitor in the intestinal mucosa and human feces]. 122 51

A quantitative polymerase chain reaction (PCR) assay for hepatitis C viral RNA (HCV-RNA) was used to monitor viraemia levels in six patients at multiple time points before, during, and after interferon therapy for chronic non-A, non-B hepatitis (NANBH). Prior to therapy, serum HCV-RNA was detected in all patients at approximately 10(4)-10(5) HCV genomes/ml. HCV viraemia became undetectable within 1 month of commencing interferon in three of the five patients whose alanine aminotransferase (ALT) levels decreased to normal on therapy. In the remaining two responder patients, viraemia levels declined more slowly, becoming undetectable after a period of several months. Recurrence of viraemia during therapy was observed in two cases. The one patient whose serum ALT levels remained elevated throughout therapy showed no decline in viraemia. On stopping interferon after a 6 months course, HCV genome titres climbed rapidly in all patients, reaching higher levels than had been observed prior to therapy. Biochemical relapse occurred within 7 months of ending interferon treatment in all but one of the patients who demonstrated this viraemia "rebound" phenomenon.
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PMID:Hepatitis C viraemia rebound after "successful" interferon therapy in patients with chronic non-A, non-B hepatitis. 127 10

The identification of the Hepatitis C virus using molecular cloning techniques, besides making the term Non-A Non-B Hepatitis obsolete, enables the development of specific assays for the detection of antibodies in HCV-infected individuals, thus making it possible to obtain sero-epidemiological data of the disease. The carriage of Hepatitis C antibody varies worldwide. The disease is most prevalent in intravenous drug abusers or haemophiliacs. Parenteral transmission is the most important route of transmission. Sexual, intra-familial and perinatal transmissions are uncommon. About 40% could be community-acquired (sporadic). Diagnostic tests include enzyme-linked immunosorbant (ELISA) anti-HCV assay, recombinant immunoblot assay, HCV-RNA by polymerase chain reaction and HCV-Ag. More than 50% of acute cases becomes chronic and runs a benign and indolent course. About 20% progress to cirrhosis and some of these develop hepatocellular carcinoma. Several published trials have consistently shown that treatment with interferon in some patients is useful. There is however a relapse rate of 50%. Further trials with interferon and other anti-viral agents like ribavirin are awaited for more effective treatment.
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PMID:Hepatitis C: an update. 128 40

We describe a case of exacerbated mixed cryoglobulinemia in a patient previously treated with alpha-interferon, for chronic active hepatitis. The possible pathogenesis of this exacerbated mixed cryoglobulinemia and the relationship between cytokines, hepatitis viral infections and immune reactions is discussed.
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PMID:[Can alpha-interferon exacerbate a case of mixed cryoglobulinemia?]. 128 57

To evaluate the histological effects of alpha Interferon (IFN) therapy, serial liver biopsy specimens from 30 patients with chronic hepatitis were studied. The biopsies were examined using a scoring system. After 12 mths of IFN therapy responders were 8 out of 11 HBV infected patients, 10 out of 12 HCV infected patients and only 1 out of 7 patients with cryptogenetic hepatitis. As spontaneous improvement of hepatic changes is infrequent, our data indicate that in terms of histological patterns interferon therapy is effective in chronic viral hepatitis.
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PMID:Histological behaviour of chronic hepatitis in patients treated with alpha interferon. 128 64

Since the detection of hepatitis B virus (HBV) in the 1960s and hepatitis A virus in the 1970s, a considerable proportion of infections of (probably viral) hepatitis could not be classified. About 90% of transfusion-related hepatitis was identified as non-A/non-B. In 1988 investigators from the Chiron Company (USA) detected the non-A, non-B agent and named it hepatitis C virus (HCV). An anti-HCV antibody assay (ELISA) and subsequently confirmation tests (immunoblot and polymerase chain reaction) were developed. HCV infection results in a chronic carrier state of the virus in about 80%. Almost all HCV carriers have, irrespective of their liver function tests, histologic signs of chronic hepatitis and/or liver cirrhosis. Chronic HCV infection is, like HBV, also associated with the development of hepatocellular carcinoma. Most HCV carriers are infected by parenteral routes (intravenous drug use, blood transfusion, tattooing). Intravenous drug users and haemophilia patients have the highest risk (80-90%) of becoming infected. Sexual and perinatal transmission does not play an important role in spreading the infection. Antiviral therapy (alpha-interferon) in patients with chronic hepatitis C will normalize liver function tests in about 25% of the cases, but it is unclear if the HCV carrier state will disappear and if liver cirrhosis will be prevented. At present no specific immunoglobulin or vaccine preparations are available to prevent the HCV infection.
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PMID:New developments in hepatitis C. 129 54


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