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)

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

The characterization of the hepatitis C virus (HCV) and the development of an anti-HCV antibody test have closed a further gap in the etiological diagnosis of viral hepatitis, but at the same time new questions have been raised. It has been shown that HCV is by far the most frequent source of the parenterally transmitted form of non-A, non-B hepatitis (NANBH). The anti-HCV test is reactive in the majority of cases with chronic NANBH. However, seroconversion is delayed by weeks or even months and therefore the test is inappropriate for confirmation of acute NANBH. Most patients with autoimmune hepatitis and some with alcoholic liver injury were shown to be anti-HCV reactive, giving rise to a debate on the specificity of the anti-HCV test. The significance of these findings has not yet been explained, since a confirmation test is currently lacking. Alpha-interferon has been shown to be the first promising drug for treatment of chronic viral hepatitis. In a high percentage of patients with chronic NANBH, treatment with interferon induces biochemical and histological remission. Nevertheless, about half of the patients had relapses under the treatment regimens currently used. The aim of ongoing studies is to improve results by optimizing the dosage and duration of interferon treatment.
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PMID:[Non-A, Non-B hepatitis: advances in diagnosis and therapy]. 164 47

To assess the effect of interferon therapy on posttransfusion non-A, non-B acute hepatitis, we examined the appearance of serum hepatitis C virus antibody (anti-HCV) and abnormal serum aminotransferase levels after the onset of hepatitis in 12 patients treated with interferon and in 46 patients treated conservatively. Eleven patients were given 3 million units of human fibroblast beta-interferon three times weekly for 4 wk and 1 was given one million units of human lymphoblastoid alpha-interferon daily for 3 months. In the interferon-treated patients, the effect of therapy on hepatic histology was also assessed. Detection of anti-HCV within 6 and 12 months after the onset of hepatitis was less common in interferon-treated patients than in control patients (6/12 vs 35/46 and 5/12 vs 35/46, both p = NS). At 24 months after the onset of hepatitis, anti-HCV levels were significantly lower in interferon-treated patients (0/10, p less than 0.05), but had not changed significantly in control patients (34/46). Abnormal serum aminotransferase levels at 6, 12, and 24 months after the onset of hepatitis were significantly less common in interferon-treated patients than in controls (25% vs 78.3%, p less than 0.005; 25% vs 71.7%, p less than 0.01; and 0% vs 67.4%, p less than 0.001). The percentage of abnormal serum aminotransferase levels at 6, 12, and 24 months after onset of hepatitis was also less in interferon-treated patients than in control patients, both among anti-HCV-positive patients (50% vs 85.7%, p = NS; 50% vs 80%, p = NS; and 0% vs 77.1%, p less than 0.01) and among anti-HCV-negative patients (0% vs 54.5%, p = NS; 0% vs 45.5%, p = NS; and 0% vs 27.3%, p = NS). Immediately after interferon therapy, the histological activity index dropped from 6.0 +/- 4.2 to 4.8 +/- 2.5 in anti-HCV-positive patients (p = NS) and from 4.2 +/- 4.3 to 2.6 +/- 1.7 in anti-HCV-negative patients (p = NS). Biopsy specimens obtained from four patients 12-23 months after interferon therapy revealed normal histology in one anti-HCV-positive patient and two anti-HCV-negative patients, and marked improvement in the other anti-HCV-positive patient. These results indicate that short-term, low-dose interferon therapy may be effective for posttransfusion non-A, non-B acute hepatitis (both anti-HCV-positive and anti-HCV-negative).
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PMID:Interferon therapy for acute posttransfusion non-A, non-B hepatitis: response with respect to anti-hepatitis C virus antibody status. 165 Jan 29

The regulation of gamma-interferon-induced major histocompatibility complex (MHC) class II antigen expression on mouse cerebral endothelial cells by the neurotropic mouse hepatitis virus (MHV-4, JHM) was studied in vitro. The results presented demonstrate that MHV-4 can selectively block gamma-interferon-induced class II antigen expression on cerebral endothelial cells. The blocking effect of class II expression occurs in a strain-dependent manner, and is limited to virus-susceptible mouse strains. Virus replication is not required to obtain the blocking effect since UV-inactivated MHV-4 produces the same result. MHV-4 blocking of gamma-interferon-induced class II antigen expression is observed at both the cell surface (flow cytometry) and transcriptional level (Northern analysis).
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PMID:Mouse hepatitis virus (MHV-4, JHM) blocks gamma-interferon-induced major histocompatibility complex class II antigen expression on murine cerebral endothelial cells. 165 58

We report the results of our study on 8-week consecutive interferon (IFN) treatment for chronic non-A, non-B hepatitis. In the 6 MIU/day group, most cases had continuously normalized alanine-aminotransferase (ALT) levels even after IFN treatment was discontinued. In responders whose ALT levels remained normal, not only the degree of inflammation, as seen from HAI scores, but also liver histopathological features were improved. Moreover, antibody to hepatitis C virus (anti-HCV) titer in responders was continuously decreased. Antiviral effects of IFN were observed by detection of HCV-RNA using the PCR technique. HCV-RNA became negative with IFN treatment, however, in some patients who relapsed after discontinuation of IFN treatment, re-elevation of ALT levels was usually preceded by re-appearance of HCV-RNA.
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PMID:Interferon therapy for non-A, non-B chronic hepatitis. 165 64

Forty-nine Japanese patients were enrolled in a randomized, placebo-controlled, double-blind trial of alpha-interferon for chronic non-A, non-B hepatitis: 24 patients received 3 million units of recombinant human alpha alpha-interferon (alpha-2a) thrice weekly for eight weeks, and 25 patients received placebo in a similar schedule. The mean serum alanine aminotransferase (ALT) dropped from 155 +/- 91 (SD) to 69 +/- 72 during interferon treatment, but remained unchanged (158 +/- 140 to 147 +/- 130) during placebo treatment (P less than 0.001). Serum ALT level fell to the normal range in 29% of interferon-treated patients, but in only 4% of placebo-treated patients. Pre- and posttreatment liver biopsies were obtained in all but one case. Average histological activity indices (HAI) were markedly improved in the interferon-treated group (9.5 +/- 3.7 to 7.0 +/- 4.3), but were unchanged in the placebo group (8.5 +/- 4.3 to 8.5 +/- 4.9). In addition, we compared the efficacy of interferon treatment between anti-hepatitis C virus (HCV) antibody positive and negative groups. Biochemical and histological improvements were similar and statistically significant in patients with and without antibody to hepatitis C virus. These data indicate that a eight-week course of alpha-interferon induces biochemical and histological improvement in more than half the patients with chronic non-A, non-B hepatitis.
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PMID:Randomized, double-blind, placebo-controlled trial of eight-week course of recombinant alpha-interferon for chronic non-A, non-B hepatitis. 165 40

This study was carried out on 33 patients who were sero-positive for liver-kidney microsomal antibodies (LKM) in order to examine clinical features and the presence of underlying hepatitis C virus infection. Twenty-four sera were positive for antibodies against HCV (anti-HCV) as detected by enzyme immunoassay and confirmed by recombinant immunoblot assay. These patients had chronic liver disease and the majority of those treated with interferon responded favourably. Three of the nine anti-HCV-negative patients had idiopathic chronic hepatitis and two responded favourably to steroids. Two patients were diagnosed as having toxic hepatitis and the other four had various extrahepatic disorders without evidence of liver involvement. The immunoblotting analysis showed reactivity with a 50 kDa microsomal protein which presumably corresponded to cytochrome P-450 db1 both in anti-HCV-positive and -negative sera. In addition a few anti-HCV-positive sera also reacted with a 35 kDa microsomal antigen. Autoimmune markers different from LKM were absent in both groups. The high prevalence of antibodies to the hepatitis C virus among LKM-positive sera confirms that this infection plays a role in forms of chronic hepatitis that had previously been labelled autoimmune. In patients with LKM the presence of anti-HCV may help to forecast a therapeutic response to interferon, while its absence may forecast response to steroid therapy.
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PMID:Hepatitis C virus-related chronic liver disease with autoantibodies to liver-kidney microsomes (LKM). Clinical characterization from idiopathic LKM-positive disorders. 165 68

Hepatitis C virus has been shown to be responsible for most cases of posttransfusion hepatitis, as well as for sporadic non-A, non-B viral hepatitis. Hepatitis C virus has also been implicated in the development of primary hepatocellular carcinoma, autoimmune hepatitis, and fulminant viral hepatitis. Although the role of the parenteral transmission of hepatitis C virus is well established, its route of transmission in cases of sporadic infection remains unclear. Sexual transmission is suspected but not confirmed. Recent work regarding treatment has shown interferon alfa to be effective, but the discontinuation of therapy is associated with a 50% relapse rate.
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PMID:Hepatitis C virus. A review. 165 11

Earlier studies from this laboratory showed that infection of BALB/cByJ mice by a natural route with mouse hepatitis virus, strain JHM (MHV-JHM), results in functional splenic T cell suppression in vitro. This was evidenced by reduced concanavalin A-driven spleen cell proliferation and interleukin (IL)2 production measured after conventional intervals of cell culture (72 and 24 h, respectively). The purpose of the present work was to determine whether MHV-induced T cell dysfunction is kinetic or absolute and whether production of other T-cell derived cytokines is defective. Bioassays revealed that production of IL2, gamma interferon, and IL4 by spleen cells from acutely infected mice is suppressed and that some of the defects are kinetic as well as absolute. Proliferative responses of both CD4+ and CD8+ T cells were depressed, but neither cell type contained infectious virus. Cells that proliferated poorly in response to concanavalin A were fully capable of responding to specific virus stimulation. These results further emphasize the potential complications that MHV infection may pose to immunologic research using mice.
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PMID:Infection of BALB/cByJ mice with the JHM strain of mouse hepatitis virus alters in vitro splenic T cell proliferation and cytokine production. 165 57

48-1 and S-1 antibodies produced by lymphoblastoid cells transformed with Epstein-Barr virus were reported to be associated with infection by not only the hepatitis non-A, non-B (NANB) virus but also hepatitis delta virus. Appearance of the antigens reacting with these antibodies in the liver of chimpanzees was recently found to be a host response to alpha-interferon induced by infections of both viruses. To investigate organ specificity of these antigens, various organs obtained from chimpanzees with hepatitis C (NANB) were examined. In addition to the liver, the adrenals and spleen were found to be positive by immunofluorescence. The positive reactions of these three organs were also confirmed by radioimmunoassay. By electron microscopy, microtubular aggregates similar to those observed in the liver were detected in the adrenals, but not in the spleen. The results suggested that these antigens existed in the liver, adrenal, and probably spleen of chimpanzees infected with hepatitis C.
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PMID:Organ specificity of the antigens reacting with the 48-1 and S-1 antibodies in chimpanzees infected with hepatitis C virus. 166 Feb 98


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