Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 20 patients with HBsAg-and HBeAg-positive chronic active hepatitis, we determined the long-term effect of human leukocyte interferon as well as placebo treatment. During the 2-year follow-up period, HBsAg remained present in all patients, but the Dane particle markers HBeAg and DNA polymerase disappeared in two of 10 patients who had received interferon, and in 4 of 10 patients from the placebo group. Patients, with loss of HBeAg initially had HBs antigenemia for a longer period as well as a lower serum concentration of both HBsAg and DNA polymerase, fewer HbcAg-containing hepatocyte nuclei, and higher serum transaminase levels than did the patients in whom HBeAg persisted. Disappearance of Dane particle markers was associated with a decrease in HBsAg titer, appearance of anti-HBe, normalization of the serum transaminases, and morphological transition to inactive chronic hepatitis. We conclude that, in HBsAg- and HBeAg-positive chronic active hepatitis, disappearance of Dane particle markers occurs in approximately 30% of the patients within a 2-year period and that arrest of active viral replication is associated with loss of activity of chronic hepatitis. Treatment with human leukocyte interferon in the doses used in this study did not change the natural course of the disease.
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PMID:Spontaneous disappearance of viral replication and liver cell inflammation in HBsAg-positive chronic active hepatitis: results of a placebo vs. interferon trial. 714 89

The concept of antiviral therapy with interferon for chronic hepatitis B emerged in the middle of the seventies and was supported by the suppressive effect of human interferon on HBV-DNA polymerase levels in 3 patients. This effect of leukocyte interferon was confirmed in a small controlled study of patients with HBeAg-positive chronic hepatitis B; however, no effect was found on other indices of hepatitis B. More than 10 years elapsed before one large RCT demonstrated clinically relevant virological responses in 35% vs. < 10% in placebo and led to registration of interferon for hepatitis B. Responses in HBeAg-negative chronic hepatitis B were very high during treatment but high relapse rates eliminated most of the long-time treatment effect. Interferon has now to compete with highly effective nucleoside analog therapy, but still has a prominent place as a limited duration therapy leading to sustained and sometimes complete responses. In the middle of the eighties, interferon was tested in 10 patients with non-A, non-B chronic hepatitis and ALT normalization was observed in the majority. After the discovery of the hepatitis C virus and the introduction of the HCVRNA PCR test it became clear that interferon therapy can cure hepatitis C infections. Widespread therapy was introduced after a co-drug ribavirin was found to reduce relapse rates and two pivotal trials with recombinant interferon showed sustained virological responses in about 50% of patients, with much higher positive outcomes in genotype 2 and 3. Therapy-induced sustained virological remission has been shown to reduce liver-related death, liver failure and to a lesser extent hepatocellular carcinoma. Interferon has become the key drug for hepatitis C.
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PMID:Clinical use of interferon in hepatitis B and C. 1973


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