Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferon-gamma (IFN-gamma) was induced from a human peripheral mononuclear fraction by incubation with a streptococcal preparation stabilized with penicillin G (OK432). This IFN-gamma-producing activity was significantly reduced in patients with chronic hepatitis and hepatocellular carcinoma. In patients with liver cirrhosis it was also reduced but not significantly. Serum hepatitis B virus DNA and skin tests for the purified protein derivative of tuberculin, phytohemagglutinin-P and a polysaccharide fraction prepared from streptococcus pyogenes Su strain were determined to have no significant relation to this IFN-gamma-producing activity. Although the addition of interleukin 2 (IL-2) to the culture medium enhanced the IFN-gamma-producing activity, there was no difference in this enhancement between normal control and chronic hepatitis. Therefore reduction of the IFN-gamma-producing activity observed in chronic hepatitis seems to be caused by a decreased number of IFN-gamma-producing activity cells or hypofunction of these cells or both. Since HBeAg became negative in patients whose IFN-gamma-producing activity was increased by the administration of the immunopotentiator OK432 or IFN-beta, the IFN-producing system in the patients with B type hepatitis may contribute to the elimination of HBV. Adenine arabinoside suppressed IFN-gamma-producing activity both in vivo and in vitro.
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PMID:In vitro interferon producing activity of peripheral mononuclear cells in patients with chronic liver disease. 303 38

The current status of therapy for chronic HBsAg positive hepatitis is reviewed. Corticosteroid therapy usually has little, if any, benefit; in fact, in addition to its customary side-effects, it may enhance viral replication. Corticosteroids are indicated only in the rare case of life-threatening HBsAg-positive severe chronic active hepatitis with immune features. Clinical studies on antiviral treatment are continuing. Today interferon, ARA-A, and acyclovir appear the most promising agents under investigation. Patients with HBeAg-positive chronic hepatitis should be referred to centers evaluating antiviral treatment, particularly in the case of progressive liver dysfunction, relapsing activity or psychological imbalance because of contagious blood. There are at present few prospects of eradicating hepatitis B virus in patients with HBsAg, antiHBe positive cirrhosis, who remain at risk of developing hepatocellular carcinoma. With the exception of the above-mentioned categories, patients with chronic HBsAg-positive hepatitis should be encouraged to pursue as normal a life as possible. To define the natural history of the disease more precisely, they should be followed carefully after being adequately informed about their disease and the proper preventive measures.
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PMID:Treatment of chronic hepatitis type virus B. 619 73

The association of glomerulonephritis and persistent HBs antigenemia is reported in 4 adults with nephrotic syndrome: 2 cases of membranous glomerulonephritis associated with chronic persistent hepatitis and 2 cases of membrano-proliferative glomerulonephritis associated with active cirrhosis. In 3 patients, all positive for HBsAg, anti-HBc and HBeAg by radioimmunoassay, indirect immunofluorescent study was performed on kidney and liver biopsies. Glomerular deposit of HBcAg was detected in two cases. HBsAg and HBcAg were not found in the liver. The pathogenesis of such glomerulonephritis remains uncertain and the role of HBs antigen-antibody circulating immune complexes is not clearly proved. Two patients were treated with vidarabine intravenously. Vidarabine produced a transitory decrease of HBsAg concentration in 2 cases and a transitory loss of DNA-polymerase activity associated with a decrease of HBeAg concentration in one case. Neither seroconversion nor improvement of the glomerular disease were ascertained.
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PMID:[Glomerular nephropathies and B virus: apropos of 4 cases in adults, with an immunofluorescence study and review of the literature]. 634 98

Vaccine therapy is now used in various infectious diseases. The hepatitis B virus (HBV) leads to chronic infection in around 5% of patients with a high risk of chronic active hepatitis which may result in cirrhosis and hepatocellular carcinoma. The partial efficacy of antiviral therapies (40% of sustained inhibition of HBV replication), their cost, their possible side effects and the immune-mediated pathology of HBV infection explain the need of new immune therapies in treating HBV infection. Experimental and clinical evidences suggest the usefulness of vaccine therapy in HBV chronic infection. In a pilot and opened study, forty-six consecutive chronic HBsAg carriers with chronic hepatitis and detectable serum HBV DNA were given 3 standard injections of the GenHevac B vaccine at one month interval. Six months after the first injection, 12 patients (26.1%) had undetectable HBV DNA while 8 others showed significant decrease (more than 50%) in HBV DNA titers. Six of these 12 responders received a standard course of alpha-Interferon (5 MU thrice weekly subcutaneously for 4 months) and all six had still undetectable HBV replication at the end of follow-up. Among the 34 non responders to vaccine, 20 were given alpha-interferon and 2 the monophosphate derivate of Vidarabine: 12 of these 22 patients stopped HBV replication and in all 12, vaccine therapy had induced a significant decrease of HBV replication before the antiviral treatment with a decrease of mean serum HBV DNA from 392 pg/ml before to 217 pg/ml after vaccine therapy. In an ongoing controlled study, using the same vaccine schedule, serum HBV DNA disappeared more frequently after 6 months, in patients who were given a preS2/S vaccine (7/35) than in patients who received a S vaccine (1/21) or no vaccine (1/32). In responders to vaccine, an induction of specific proliferative responses was observed and this may contribute to the potential efficacy of anti-HBV vaccine therapy. No side-effect or vaccine-induced escape-mutants occurred during the follow-up. In summary, serum HBV DNA disappeared in 28 of the 46 patients (60.9%) who were given vaccine therapy, with (64.2%) or without (55.6%) Interferon. These results are not different at 6 months and at the end of follow-up from those of 43 HBsAg chronic carriers who were given only an antiviral treatment. Active immune therapy against HBV appears efficient and less expensive than antiviral therapies in stopping HBV replication. Such results need to be confirmed by the completed results of our controlled, randomized trial which is now conducted in our unit.
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PMID:Immunotherapy of chronic hepatitis B by anti HBV vaccine. 965 16