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)

To determine whether long-term therapy with recombinant interferon-alpha can improve the course of chronic delta hepatitis, 61 Italian patients with this disease were randomly assigned to receive either interferon-alpha-2b three times a week (5 MU/m2 for 4 mo and then 3 MU/m2 for another 8 mo) or no treatment. At the end of the 12-mo study, all patients were followed-up for 12 additional months. Normalization or decrease of more than 50% from baseline of serum ALT levels occurred in 42% of treated patients the fourth month of therapy, 26% the twelfth month and 3% the twenty-fourth month vs. 7%, 7% and 0%, respectively, in the control group. However, relapses occurred in 7 of 8 (87.5%) responders 1 to 10 mo (mean = 3.5 mo) after cessation of therapy. Liver biopsies were carried out at baseline and during the twelfth month of treatment. Histological improvement, mostly caused by decrease of portal inflammation, was observed in 57% of treated and 36% of untreated patients. Measures of antiviral activity (serum hepatitis delta virus RNA and intrahepatic hepatitis delta antigen) showed similar levels in treated and control patients. In treated patients the percentage of patients who were negative for HDV RNA never exceeded that of baseline. Although interferon-alpha in the dosage given in this study had no antiviral effect on patients with chronic hepatitis D, it reduced hepatic inflammation as measured by ALT levels. Whether a longer duration or reinstitution of interferon-alpha therapy would achieve long-term control of ALT levels and prevent chronic liver damage is not known.
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PMID:A randomized controlled trial of a 12-month course of recombinant human interferon-alpha in chronic delta (type D) hepatitis: a multicenter Italian study. 205 Mar 21

The frequency and clinical features of acute hepatitis B virus (HBV) infection with and without a hepatitis D virus (HDV) co-infection was investigated retrospectively in the Stockholm region during two different time periods, September 1977-October 1978 and November 1984-October 1986. Totally, 31/229 (14%) patients with acute HBV infection had a HDV co-infection. No change in the frequency of co-infections, 12% and 15%, respectively, was observed between the 1970s and 1980s. Among the 31 HDV co-infected patients 74% were intravenous drug addicts. Totally 23/66 (35%) intravenous drug addicts with acute HBV infection had HDV co-infection. Clinically a biphasic rise of the serum levels of alanine aminotransferase and bilirubin was noted among 63% of the HDV co-infected patients but only among 8% of the solely HBV infected patients (p less than 0.001). A clinically more severe hepatitis was seen significantly more often among the HDV co-infected patients than among the solely HBV infected.
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PMID:Acute hepatitis B and hepatitis D co-infection in the Stockholm region in the 1970s and 1980s--a comparison. 207 8

In general, the biological and structural properties of the hepatitis delta virus resemble those of the viroids and related satellite RNA viruses of plants. This resemblance has been strengthened by the discovery that, in analogy to the self-cleaving of some plant RNA viruses, hepatitis delta virus RNA possesses autocleaving and autoligating sites located in sequences that are homologous with highly conserved domains in the viroids. The catalytic properties identify the hepatitis delta virus as the first mammalian ribozyme. The current interpretation of the pathobiology of delta hepatitis rests on the postulates that the hepatitis delta virus invariably requires hepatitis B virus for infection and is highly pathogenic. Accordingly, delta hepatitis is thought to occur when hepatitis delta virus coinfects with hepatitis B virus or when it superinfects hepatitis B virus carriers. However, new evidence from the liver transplantation model suggests that hepatitis delta virus is capable of establishing latent, asymptomatic infections without the apparent assistance of hepatitis B virus: in this model, disease was only reactivated when hepatitis B virus also returned to the graft. Thus, hepatitis B virus superinfection on a latent hepatitis delta virus state may be a third pathobiological mechanism conducive to delta hepatitis.
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PMID:Hepatitis delta: the virus and the disease. 207 73

In this pilot study, 12 patients with chronic delta hepatitis were studied. The diagnosis was based on the presence of antibodies to the hepatitis delta antigen in the serum and hepatitis delta virus RNA and hepatitis delta antigen in the serum and liver. All patients were also positive for hepatitis B surface antigen. The infection was presumed to have been transmitted by intravenous drug abuse in six of the patients, blood transfusion in one and by sexual contact in four (two had antibodies to human immunodeficiency virus in their serum, but did not show signs of acquired immunodeficiency syndrome). In one further patient, the source of infection was unknown. Interferon alfa-2b (INTRON A, Schering-Plough Corporation) was initiated at 5 million units per day subcutaneously for at least 4 months, being reduced by half if side effects occurred. Serum alanine aminotransferase levels, hepatitis delta virus RNA and hepatitis delta antigen were measured at monthly intervals for up to 12 months in some patients. Interferon therapy resulted in decreased serum levels of these three markers. On cessation of therapy, most patients experienced a relapse over 6 months, but alanine amino transferase levels could be normalized once more by restarting interferon therapy. In conclusion, interferon decreased hepatic inflammation by the inhibition of hepatitis delta virus replication, although relapse occurred when interferon was stopped and long-term therapy is required to achieve permanent control of the disease. Care will be required when treating patients with advanced or decompensated liver disease.
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PMID:Therapy of chronic delta hepatitis with interferon alfa-2b. 207 75

In view of the recognized importance of necroinflammatory episodes in chronic hepatitis B virus (HBV) infection, chimpanzees, either HBV surface antigen (HBsAg) carriers or noninfected (naive), were infected with other primary hepatotropic viruses to evaluate histologic alterations and changes in virologic and biochemical markers of infection. The advantages of studies on chimpanzees are the availability of serial biopsy specimens and the viral type-specific histologic lesions, not as well recognized in humans. Infection with hepatitis A and non-A, non-B (NANB) agents produced more severe lesions in chronic HBsAg carrier chimpanzees than in naive animals. During this superinfection, the specific expression of the second agent was predominant, indicating that the exacerbation is caused by the second agent, but that carriers are prone to more severe disease than the naive chimpanzees. Hepatitis delta virus (HDV) infections were always coexistant with HBV and superinfection of carriers produced histologic changes more severe than those seen in any other type of viral hepatitis. Such HDV infections revealed less evidence of lymphocytotoxicity but rather of cytotoxicity, and sometimes resembled in appearance the histopathology of NANB. Coinfection of HDV and HBV and superinfection of HBV-carriers with NANB resulted in hepatitis that was far less severe than superinfection of HDV in HBV carriers, greatly in keeping with human experiences. HBV replication was suppressed transiently in both NANB and HDV superinfection. This implies that in exacerbations during chronic HBV infections of humans, suppression of HBV replication markers indicates superinfection, for instance, by NANB for which markers are so far not widely available; by contrast, elevated markers of HBV replication suggest reactivation of the original HBV infection.
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PMID:The significance of infections with two types of viral hepatitis demonstrated by histologic features in chimpanzees. 210 49

In the light of the present serological tests, the etiology, clinical features and course of acute viral hepatitis were reviewed in 423 consecutive male patients. Follow-up started less than 15 days after the onset of jaundice and continued until recovery or for at least six months if recovery did not occur before them. The incidence of type A viral hepatitis decreased in France but remained high in North Africa and tropical areas. During the acute phase it differed from hepatitis type B by a lower aminotransferase level. Relapse, however, was more common, as was protraction of longer than six months. Recovery ultimately occurred. The specific IgM antibody persisted throughout the condition. Type B hepatitis differed from type A hepatitis by a mean quicker normalization of the biochemical disturbances. In the absence of superinfection by delta hepatitis virus or by a non-A, non-B virus, the progression to chronic liver disease was rare. The course of non-A, non-B hepatitis was very dissimilar according to the circumstances of occurrence. In epidemic cases rapid recovery occurred and no progression to chronicity was noted. In the other cases, relapse and chronicity were more frequent than for type A or B hepatitis. Type D hepatitis was characterized by more pronounced biochemical disturbances during the acute phase and by more frequent progression to chronicity in case of superinfection.
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PMID:[Acute icteric viral hepatitis type A, B, D and non-A non-B. Etiologic, clinical and developmental aspects in the young man. Apropos of 423 cases]. 211 81

Zone electrophoresis on agarose gel was performed in serum samples from patients with chronic viral hepatitis. On the basis of the clinical, serological, and biochemical evaluation, the patients were divided into three categories: chronic type B hepatitis; chronic type delta hepatitis; and chronic non-A-non-B (NANB) hepatitis. The results of the electrophoretic analysis showed a high incidence of oligoclonal immunoglobulin bands (OIBs) in patients with chronic B hepatitis and chronic delta hepatitis and a low incidence of OIBs in patients with NANB. Since other biochemical and serological characteristics are variable and do not correlate with clinical symptoms of disease, we suggest that oligoclonal immunoglobulins could be used as a marker to aid in studies of the natural history and pathologic course of the various types of chronic hepatitis.
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PMID:Oligoclonal immunoglobulins in serum of patients with chronic viral hepatitis. 211 95

Hepatitis may be caused by hepatitis A virus, hepatitis B virus, hepatitis C virus (classic non-A non-B viral hepatitis), hepatitis D virus (delta agent), and hepatitis E virus (epidemic non-A non-B viral hepatitis). Cytomegalovirus, Epstein-Barr virus, and herpes simplex virus may also occasionally cause hepatitis. Some forms of hepatitis carry the risks of chronic infection, cirrhosis, or hepatocellular carcinoma. Treatment options for viral hepatitis are limited and, in many cases, still under investigation. Prophylaxis is available for many forms of hepatitis and should be offered to those at risk.
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PMID:Viral hepatitis. The new ABC's. 212 Jun 86

One hundred and fifteen patients with chronic type B, D and non-A, non-B hepatitis treated with recombinant alpha-interferon were tested for six different autoantibodies prior to or during therapy, and the course of treatment was compared in autoantibody-positive and -negative patients. Three out of 25 (12%) hepatitis B patients, 14 out of 30 (47%) hepatitis D patients and 19 out of 60 (32%) chronic non-A, non-B hepatitis carriers had baseline or post-therapy autoantibodies. The rate of response between patients with and without autoantibodies among B, D and non-A, non-B patients was, respectively, 67 vs. 79%, 23 vs. 25%, 70 vs. 61% (p = N.S.). No adverse reaction was observed in the 36 patients who had or developed nuclear, smooth muscle, parietal cells and thyroid autoantibodies during therapy. A patient with baseline antibodies against liver and kidney microsomes developed an icteric acute hepatitis at the fourth month of therapy, but five other patients with this reactivity responded to therapy uneventfully. The presence of autoantibodies before therapy or their induction following therapy is not a contraindication to the use of interferon in patients with chronic viral hepatitis.
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PMID:Autoantibodies and response to alpha-interferon in patients with chronic viral hepatitis. 212 54

The 19S and 7-8S forms of IgM antibody to hepatitis B core antigen (IgM anti-HBc) were separated by rate-zonal centrifugation from the serum of 20 Greek hepatitis B surface antigen (HBsAg) carriers with a superimposed acute icteric hepatitis positive for IgM anti-HBc by a radioimmunoassay. Serological markers of hepatitis A virus (HAV), hepatitis B virus (HBV) and hepatitis D virus (HDV) infections were detected with radioimmunoassays and serum HBV DNA was detected with molecular hybridization techniques. Eighteen of the 20 carriers showed a predominance of one or the other form of IgM anti-HBc. Low molecular weight (7-8S) IgM anti-HBc was observed more frequently in HDV superinfection (5/9) and was related to a low mortality (1/9). In contrast, 19S IgM anti-HBc was observed more frequently in reactivation of chronic hepatitis B (6/9) and was related to a high mortality (5/9). These preliminary data show that in HBsAg carriers with a superimposed acute icteric hepatitis, predominance of 19S IgM anti-HBc is frequently associated with a severe clinical course; the opposite is true for predominance of 7-8S IgM anti-HBc.
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PMID:19S and 7-8S forms of IgM antibody to hepatitis B core antigen in acute icteric hepatitis superimposed on hepatitis B surface antigen carriage. 212 87


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