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)

Interferon therapy is useful for decreasing the serum ALT level and improving liver histology in patients with chronic non-A, non-B hepatitis. This study examined the effect of interferon therapy in acute cases of posttransfusion hepatitis C. We report on three cases in which interferon alpha was administered at 100-220.5 million units. HCV RNA became undetectable during interferon administration and the ALT level declined to the normal range. However, after the cessation of the therapy, the ALT level began to fluctuate and HCV RNA reappeared in two patients. We concluded that interferon therapy for the acute phase of posttransfusion hepatitis is useful for suppressing viral replication and quickly improving the ALT level, but it can not always prevent the development of chronic hepatitis. Furthermore, there was a close correlation between the profile of HCV RNA and that of the ALT level, indicating that the replication of HCV plays an important role in liver injury.
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PMID:Three cases of posttransfusion hepatitis C treated with interferon-alpha. Confirmation of a carrier state by detection of hepatitis C virus RNA after interferon therapy. 131 23

Serial serum samples from cardiac patients with a history of chronic or resolved post-transfusion non-A, non-B hepatitis were analyzed by a combination of cDNA synthesis and the polymerase chain reaction (cDNA/PCR) to amplify HCV RNA. Analysis of sera drawn after the acute hepatitis episode from 8 of the patients who had an acute, resolving HCV infection showed no detectable levels of HCV RNA when primers from the NS3 region were used. Evaluation of these sera with primers from the 5'-untranslated (5'-UT) region revealed that one patient was positive for HCV RNA. Further analysis of serial serum samples available from two of these patients indicated that a resolved infection was associated with a disappearance of detectable HCV RNA after a peak level during the acute phase of the disease. In contrast, post-acute samples from 4 of 6 patients with symptomatic acute HCV infection evolving to chronicity were positive for HCV RNA using primers from the NS3 region, however, upon retesting with primers from the 5'-UT region, all 6 patients were found to be positive. Analysis of serial serum samples from 2 of these patients showed the persistence of HCV RNA in 70% of the samples. These two patients were subsequently treated with interferon alpha-2b. One patient resolved his disease and normalized his aminotransferase level during treatment and thereafter, while the other relapsed upon cessation of treatment. In these two patients, normalization of ALT levels was consistent with the absence of HCV RNA while relapse of disease was confirmed by the reappearance of detectable levels of HCV RNA. These results indicate the utility of HCV RNA as a marker for persisting HCV viremia and in differentiating patients with ongoing active HCV infection from those with an acute resolving disease.
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PMID:Detection of hepatitis C viral RNA by the polymerase chain reaction in serum of patients with post-transfusion non-A, non-B hepatitis. 131 77

We treated four cases of acute unresolving non-A, non-B hepatitis, and eleven cases of chronic non-A, non-B hepatitis with recombinant interferon alpha-2a for up to one year. The dose of interferon was initially 3 million units daily, and was gradually decreased to 1 million units three times weekly. The overall response rate was 80 percent (twelve out of fifteen cases) at the end of treatment. Relapse occurred after the cessation of treatment in seven of the eight cases of chronic disease responding to interferon therapy. In contrast, three of the four cases of acute unresolving hepatitis became (sero)negative for antibody to hepatitis C virus, and in three completely normal serum aminotransferase levels persisted for more than one year after therapy. It is urged that early recognition of non-A, non-B hepatitis should be striven for, because interferon therapy may lead to an improved prognosis of the disease, particularly in cases of possible transitional phase from acute to chronic disease.
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PMID:Interferon therapy for non-A, non-B hepatitis: a pilot study and review of the literature. 133 37

To evaluate cost-effectiveness and response predictors of treatment with recombinant interferon alpha-2a in chronic non-A, non-B hepatitis, 263 consecutive patients were enrolled in a multicenter long-term study. A pre-planned analysis aimed at identifying predictors of early response was carried out when all patients had completed the initial 3 months of treatment with 6 MU thrice weekly. Sixty-three percent of the patients enrolled were classified as responders. At multivariate logistic regression analysis, baseline gamma-glutamyltranspeptidase levels and cirrhosis were the only independent variables significantly associated with response. The risk of no response after 3 months of treatment was 3.9 times higher (95% confidence interval, 1.6 to 7.2) in patients with high baseline levels of gamma-glutamyltranspeptidase as compared with patients showing low baseline levels, and it was 2.0 times higher (1.1 to 3.8) in patients with cirrhosis as compared with those without it. We expect that results from this and other studies on large patient populations may help to select those patients who are more likely to benefit from interferon administration.
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PMID:Factors predicting early response to treatment with recombinant interferon alpha-2a in chronic non-A, non-B hepatitis. Preliminary report of a long-term trial. 136 57

The effects of interferon therapy on liver histologic findings were assessed in a randomized controlled trial consisting of 80 patients with chronic non-A,non-B hepatitis. Twenty-eight patients received 1 million units of recombinant interferon alpha-2b; 25 patients received 3 million units, subcutaneously, three times a week for 24 weeks; and 21 patients were observed as untreated controls; all of them underwent liver biopsy within 6 months from the beginning of the study and on the last day of therapy. Six patients were withdrawn from the study because of inadequate liver biopsy specimens. Alanine aminotransferase levels were determined before, during, and after therapy. For each biopsy, a semiquantitative score of histologic features, the histologic activity index, and the overall histologic assessment were performed. Ninety-five percent of patients tested positive for hepatitis C virus antibody. Portal inflammation, piecemeal and spotty necrosis, and bile duct proliferation were significantly decreased in patients with normalized alanine aminotransferase. The effectiveness of therapy was dose dependent: piecemeal and spotty necrosis and the histologic activity index showed a significant decrease only in 3-million-unit-treated patients. Hepatocellular degeneration and fibrosis did not change significantly after treatment.
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PMID:Histologic changes in liver biopsy specimens produced by recombinant interferon alpha-2b therapy for chronic non-A,non-B viral hepatitis. A randomized controlled trial. 141 21

The case of a 52-year-old male with chronic active type B hepatitis in whom severe exacerbation of liver disease was associated with interferon alpha treatment is described. It seems that patients with very active forms of chronic hepatitis B may experience severe and symptomatic exacerbation of liver disease during interferon treatment.
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PMID:Severe exacerbation of chronic active hepatitis B during interferon alpha therapy. 142

A patient with chronic active hepatitis B was treated with interferon alpha. Inhibition of HBV replication was associated with severe exacerbation of hepatitis. Treatment of chronic hepatitis B with interferon may lead to transient decompensation of liver function, especially in patients with high activity of morphological changes.
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PMID:[Severe exacerbation of chronic hepatitis B following interferon therapy]. 144 31

269 orthotopic liver transplantations (OLT) were performed in 253 patients at our institution from September 1988 to May 1992. 121 patients had end-stage cirrhosis secondary to viral hepatitis type B, delta, or type non-A non-B and C respectively. Reinfection of the graft by persistent viruses is a potential complication in these cases. Passive immunization with anti-HBs hyperimmunoglobulin (HIg) can prevent clinically relevant reinfection of the graft in patients with hepatitis B virus (HBV) infection and low replication rates. Patients with high replication rates will rarely benefit from OLT. Patients with hepatitis delta virus (HDV) infection usually experience HDV reinfection of the graft with subsequent chronic hepatitis although prophylaxis with anti-HBs-HIg was performed. Treatment with interferon alpha had no apparent effect on the incidence of graft reinfection with HBV in this series, but the replication rate of HDV was reduced. Persistent hepatitis C viruses (HCV) usually infect the graft; this was demonstrated in 17 patients by means of the polymerase chain reaction. HCV infection usually causes a mild form of acute hepatitis with transition to a chronic course. Therefore the significance of persistent viral infection lies in the potential for chronic hepatitis in the transplanted organ rather than in the danger of acute injury of the allograft.
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PMID:[Orthotopic liver transplantation in hepatic cirrhosis: on the problem of infection of the transplant with persistent hepatitis viruses]. 144 5

A 39 years old homosexual male suffering from chronic type B hepatitis superinfected by HDV, and positive for anti-HIV1 was treated with zidovudine associated with high doses of recombinant interferon alpha for onset of an extensive cutaneous Kaposi sarcoma. Other than the long-lasting disappearance of Kaposi's lesions, this therapy was followed by complete recovery from hepatitis B and D. Serological and hepatic clearance of both viruses was marked by two successive cytolytic peaks separated by a 9 month interval. The patient's immunologic status has remained stable at 30 months. To our knowledge, such a success had never been reported in the literature and the clearance of both hepatitis B and D viruses in an AIDS patient stands in sharp contrast with the usual rapidly progressive evolution of those triple coinfections. This phenomenon illustrates the potential benefits of zidovudine in association with high dose of interferon alpha in HIV patients suffering from hepatitis D.
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PMID:[Recovery of chronic hepatitis B- delta infection by zidovudine and recombinant interferon alpha combination therapy in a patient with Kaposi's sarcoma associated with HIV infection]. 152 1

The histological outcome in liver biopsies following 9 months of interferon alpha-2b treatment was assessed in detail in 19 patients with chronic posttransfusion non-A, non-B hepatitis (PTH-NANB) and compared with 12 untreated PTH-NANB patients. Fourteen (74%) treated and 7 (58%) control patients were reactive for antibodies against hepatitis C virus (anti-HCV). Liver biopsies taken before and after the 9-month period were scored numerically for portal inflammation, piecemeal necrosis (PMN) and fibrosis, without knowledge of whether the specimens came from control or treated patients. There were no score differences in the initial biopsies between the treated and control group. In the follow-up biopsies the treated group showed significantly less portal inflammation, PMN and fibrosis than the control group (p less than 0.05-0.01). When paired samples from the treated group were compared, significantly regressed portal inflammation, PMN and fibrosis were noted in the follow-up biopsies (p less than 0.05-0.001). The presence or not of anti-HCV antibodies in serum had no impact on the histological response to interferon treatment. We conclude that a 9-month course of interferon alpha-2b treatment significantly diminishes not only inflammation but also fibrosis in the liver of patients with PTH-NANB whether they are anti-HCV reactive or not.
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PMID:Histological outcome in interferon alpha-2b treated patients with chronic posttransfusion non-A, non-B hepatitis. 164 69


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